CURRENT ISSUE

ABSTRACT: Background: Diabetic chronic kidney disease (DKD) is a leading cause of kidney failure and cardiovascular morbidity worldwide. Although albuminuria and estimated glomerular filtration rate (eGFR) remain central markers of risk stratification, early progression is frequently driven by a broader cluster of metabolic, hemodynamic, inflammatory, and cardiometabolic factors. Identification of simple clinical predictors may support earlier intensification of nephroprotective therapy. This study aimed to evaluate clinical, biochemical, and renal predictors associated with early DKD progression.
Methods: This prospective observational study included 112 patients with type 2 diabetes mellitus and established chronic kidney disease. Baseline assessment included age, sex, diabetes duration, body mass index, systolic and diastolic blood pressure, glycated hemoglobin (HbA1c), fasting plasma glucose, lipid profile, serum creatinine, eGFR, urinary albumin-to-creatinine ratio (UACR), hemoglobin, uric acid, C-reactive protein, smoking status, hypertension, obesity, dyslipidemia, and cardiovascular disease history. Early CKD progression was defined as clinically significant eGFR decline during follow-up. Patients were divided into early progression and stable/slow progression groups. Between-group comparisons and multivariable logistic regression were performed.
Results: Early DKD progression was observed in 34 of 112 patients (30.4%), while 78 patients (69.6%) had stable or slowly progressive disease. Patients with early progression had longer diabetes duration (12.8±4.1 vs 8.9±3.6 years; p<0.05), higher systolic blood pressure (148±16 vs 134±14 mmHg; p<0.05), higher HbA1c (8.7±1.1 vs 7.6±0.9%; p<0.01), greater UACR (286 [164–420] vs 118 [62–210] mg/g; p<0.01), and lower baseline eGFR (52.4±13.8 vs 64.7±15.2 mL/min/1.73 m²; p<0.05). Progressors also had higher body mass index (31.2±4.6 vs 28.7±4.2 kg/m²; p=0.006), triglycerides (2.3±0.7 vs 1.8±0.6 mmol/L; p<0.01 ), uric acid (421±76 vs 368±69 µmol/L; p=0.05), and C-reactive protein (5.8 [3.4–8.6] vs 3.1 [1.8–5.2] mg/L; p=0.002), with lower hemoglobin (118±14 vs 126±13 g/L; p=0.004). In multivariable analysis, independent predictors of early progression were UACR above 300 mg/g (odds ratio [OR] 3.42, 95% confidence interval [CI] 1.48-7.91; p=0.004), HbA1c at least 8.0% (OR 2.76, 95% CI 1.27-6.01; p=0.011), uncontrolled hypertension (OR 2.58, 95% CI 1.17-5.68; p=0.018), and hyperuricemia (OR 2.21, 95% CI 1.02-4.79; p=0.044).
Conclusion: Early DKD progression affected nearly one-third of patients. Albuminuria, poor glycemic control, uncontrolled hypertension, hyperuricemia, reduced baseline eGFR, obesity, dyslipidemia, inflammation, and anemia were associated with accelerated renal decline. These clinically accessible variables may improve early risk stratification and guide individualized nephroprotective management.

ABSTRACT: Background: Gastroduodenal lesions in patients with end-stage chronic kidney disease often present with nonspecific clinical manifestations. Standard esophagogastroduodenoscopy allows for the detection of macroscopic changes in the gastric mucosa; however, its ability to reflect the severity of chronic inflammation and structural changes in the stomach in hemodialysis patients has been poorly studied.
Aim of the study: To evaluate the correlation between clinical manifestations, endoscopic findings, and morphological changes in the gastric mucosa in patients with end-stage chronic kidney disease receiving programmatic hemodialysis.
Materials and Methods: This prospective comparative study included 92 patients with stage V chronic kidney disease who had been receiving hemodialysis for at least 6 months and had dyspeptic symptoms, as well as 60 patients with preserved renal function who were examined for dyspepsia. The groups were matched for gender and age. All participants underwent esophagogastroduodenoscopy with biopsy of the antral and corpus mucosa. Histological examination assessed chronic inflammation, disease activity, atrophy, and the presence of Helicobacter pylori.
Results: The clinical presentation in hemodialysis patients was dominated by episodic epigastric pain (61.9%), bloating (58.7%), and nausea (46.7%). Persistent epigastric pain and vomiting were significantly more common than in patients with preserved renal function (p=0.041 and p=0.008, respectively). However, the pattern of complaints remained nonspecific and did not allow us to determine the nature of the structural damage to the mucosa.
Endoscopically, gastritis was detected in 51.1% of patients on program hemodialysis and in 58.3% of patients in the comparison group; no statistically significant difference was found between the groups. Thus, the visual endoscopic picture did not reflect the more severe nature of mucosal damage in end-stage renal failure.
Fundamental differences were revealed by morphological examination. Atrophy of the gastric body mucosa was diagnosed in 34.8% of hemodialysis patients, significantly exceeding the rate in the comparison group (p=0.009). In patients with preserved renal function, active superficial inflammation without significant structural changes in the mucosa predominated. Atrophic changes in dialysis patients were associated with a longer duration of renal replacement therapy (p<0.001) and more pronounced acid-base imbalances (p=0.013). The detection rate of H. pylori in the corpus and antrum of the stomach was 48.9% and 57.6%, respectively, and did not differ significantly from the comparison group. Therefore, the observed morphological dissociation could not be explained solely by differences in the prevalence of infection.
Conclusion: In patients on program hemodialysis, the severity of morphological damage to the gastric mucosa does not correspond to the severity of dyspeptic symptoms and the standard endoscopic picture. A comparable frequency of endoscopically diagnosed gastritis with a significantly higher prevalence of atrophy indicates a systematic underestimation of uremic gastropathy when using visual EGDS alone. Biopsy of the corpus and antrum of the stomach should be considered a mandatory component of the evaluation of patients with a long history of dialysis, regardless of the severity of complaints and the macroscopic picture.

ABSTRACT: Background: Patients with end-stage chronic kidney disease have an increased risk of recurrent gastrointestinal bleeding due to a combination of uremic thrombocytopathy, anemia, nutritional deficiency, microcirculatory disorders, and regular anticoagulation during hemodialysis. However, the prognostic value of ulcer morphology and the intensity of acid-suppressive therapy in this population has not been adequately studied.
Aim: To determine endoscopic, laboratory, and therapeutic factors associated with ulcer recurrence in patients with end-stage chronic kidney disease receiving programmatic hemodialysis. Materials and Methods. A prospective observational analysis included 84 patients on program hemodialysis who experienced non-variceal ulcer bleeding. Recurrence was recorded in 22 patients, while no recurrence was observed in 62. The location and size of the ulcer defect, endoscopic stigmata of bleeding according to the Forrest classification, hemoglobin and total protein levels, mineral metabolism parameters, and proton pump inhibitor therapy regimen were assessed. Associations were assessed by calculating odds ratios with 95% confidence intervals.
Results: The most significant association with recurrence was found for ulcer defect size. Ulcers larger than 20 mm were detected in 36.4% of patients with recurrence and in 11.3% of patients without a recurrence; their presence increased the odds of recurrence by 4.49 times (OR = 4.49; 95% CI 1.39–14.49; p < 0.05). In contrast, ulcer defects smaller than 10 mm occurred in 18.2% and 53.2% of cases, respectively, and were associated with a lower likelihood of recurrence (OR = 0.20; 95% CI 0.06–0.66; p < 0.01).
Attached Forrest IIb thrombus was more often detected in patients with recurrence—54.5% versus 32.3% (OR = 2.52; 95% CI 0.93–6.81), while pigmented Forrest IIc spots were more often detected in patients with a favorable course—35.5% versus 13.6% (OR = 0.29; 95% CI 0.08–1.09). However, the confidence intervals for these features included unity, which does not allow them to be considered statistically confirmed independent predictors. Relapse was accompanied by more severe anemia: the median hemoglobin was 9.9 g/dL versus 12.0 g/dL in patients without relapse (p<0.01). A decrease in total protein was also observed: 4.8 g/dL versus 5.7 g/dL (p<0.05). Serum iron, calcium, phosphorus, cholesterol, and intact parathyroid hormone levels did not differ significantly.
In univariate analysis, the use of high-dose proton pump inhibitors was associated with a reduced odds of relapse (OR=0.31; 95% CI 0.11–0.85; p<0.05), while low-dose therapy was associated with an increased odds (OR=3.18; 95% CI 1.16–8.75; p<0.05). The initial treatment groups were comparable in terms of clinical and demographic characteristics, ulcer size and location, Forrest stigmata, comorbidities, and concomitant pharmacotherapy.
Conclusion: Ulcer recurrence in patients on scheduled hemodialysis is determined by the interaction of local morphological and systemic metabolic factors. The most compelling endoscopic predictor is ulcer size greater than 20 mm, while anemia and hypoproteinemia reflect a decrease in systemic reparative reserve. High-dose PPI therapy is associated with a lower risk of recurrence; however, the lack of multifactorial adjustment precludes the independent assessment of this effect. These results support a risk-adapted strategy combining intensive acid suppression in high-risk patients with mandatory correction of anemia and nutritional deficiencies.

ABSTRACT: Introduction: Polyorgan failure syndrome (POYES) remains the most common cause of death after surgical interventions. It is also one of the most common causes of death in intensive care units and intensive care units. The pathogenesis of the syndrome remains incompletely understood, but is probably associated with a combination of dysregulation of the inflammatory response, microcirculatory dysfunction, hypoperfusion ischemia, and immune dysregulation.
Objectives: To improve the effectiveness of predicting the outcome of acute renal failure against the background of dysfunction of other organs and systems during renal replacement therapy.
Materials and methods of the study: From January 2022 to December 2025, a retrospective and prospective analysis of clinical and laboratory indicators and methods of renal replacement therapy in patients with acute renal failure accompanied by dysfunction of other organs and systems was conducted based on data from the intensive care unit of the Tashkent State University of Medical Sciences and the National Children's Medical Center (NCMC). 150 patients aged 1 to 17 years (8.17±6.78) were included in the clinical study. The main contingent consisted of 130 (86.7%) (4-12 years old), of which 110 (73.3%) were boys and 40 (26.7%) were girls.
Research results: Based on the etiology of acute renal failure (ARF) and the associated dysfunction of other organ systems, the study cohort was categorized into five distinct groups:
Group I (26 patients): Individuals suffering from diffuse atherosclerotic cardiosclerosis, those who underwent cardiovascular surgery, patients with bacterial endocarditis, and those presenting with acute cardiovascular pathology or cardiogenic shock.
Group II (55 patients): Patients who underwent emergency thoracic or abdominal surgery, as well as those with traumatic brain injuries or polytrauma.
Group III (18 patients): Patients diagnosed with hemorrhagic destructive pancreonecrosis complicated by diffuse enzymatic peritonitis.
Group IV (25 patients): Patients suffering from acute poisoning.
Group V (26 patients): Patients with generalized sepsis and bilateral septic pneumonia.
Beyond the primary diagnosis, the involvement of additional organ systems defined the criteria for Multiple Organ Dysfunction Syndrome (MODS). The most frequent clinical presentation involved the concurrent failure of the renal, respiratory, and cardiovascular systems, with central nervous system impairment occurring less frequently.
The distribution of organ failure within the groups was as follows:
Group I: 11.6% (3 patients) had three systems involved, 50% (13 patients) had four, 34.6% (9 patients) had five, and 3.8% (1 patient) had six systems affected.
Group II: The majority showed four or five-system involvement (27.3% and 32.7%, respectively). Three systems were involved in 23.6% (13 patients), six systems in 14.6% (8 patients), and two systems in 1.8% (1 patient).
Group III: Four and five-system involvement occurred in 27.8% (5 patients each), three systems in 33.3% (6 patients), and two systems in 11.1% (2 patients).
Group IV: Two-system involvement was most common at 44% (11 patients). Three and four-system involvement occurred in 20% each (5 patients each), five systems in 12% (3 patients), and six systems in 4% (1 patient).
Group V: Three, four, and five-system involvement were each observed in 23.1% (6 patients each). Two systems were involved in 26.9% (7 patients), and six systems in 3.8% (1 patient).
Renal replacement therapy was administered as follows: 109 patients (72.7%) underwent hemodialysis, 25 (16.7%) received hemofiltration, and 16 (10.6%) were treated with a combination of both methods. Renal function recovery, marked by the transition to the polyuric phase of acute kidney injury (AKI), was observed in 81 patients (54%), while the remaining 69 (46%) failed to regain kidney function.
Mortality rates varied by clinical condition: 76.9% (20 patients) among those with cardiovascular pathology, 76.4% (42 patients) in the group undergoing emergency abdominal surgery or suffering from polytrauma, and 77.8% (14 patients) in cases of destructive hemorrhagic pancreonecrosis. Mortality for patients with acute poisoning and disseminated sepsis stood at 48% (12 patients) and 69.2% (18 patients), respectively. The overall mortality rate reached 70.7% (106 patients), with acute cardiovascular failure identified as the primary cause of death in 96% of cases (144 patients). Notably, among the 81 patients who showed renal recovery, 37 still succumbed to their condition.
Our analysis indicates that the prognosis for survival is influenced by several factors, including the number of failing organ systems, the severity of the patient's condition, hemodynamic stability, level of consciousness, and the success of renal recovery. Consequently, we conducted further research to evaluate how specific clinical and laboratory markers impact AKI outcomes. These criteria were categorized into three groups: general clinical indicators, clinical-biochemical parameters, and urinalysis/daily diuresis data.
The findings demonstrate that the outcome of AKI is significantly affected by the number of affected organ systems—particularly the involvement of the cardiovascular and central nervous systems—as well as the duration of the oligoanuric phase, the timing of renal replacement therapy initiation, and specific laboratory values such as plasma sodium, platelet count, fibrinogen levels, and proteinuria. While individual markers hold some prognostic value, the accuracy of predicting AKI outcomes is substantially higher when utilizing a combination of these clinical and laboratory indicators.
Conclusions: The development of acute kidney injury (AKI) in the context of multi-organ dysfunction syndrome (MODS) is primarily triggered by cardiovascular diseases, post-cardiac surgery states, bacterial endocarditis, acute vascular events, major thoracic or abdominal surgeries, traumatic brain injuries, polytrauma, severe enzymatic peritonitis, acute poisoning, and systemic sepsis. In cases of MODS involving AKI, the involvement of four or five organ systems is most frequent (29.4% and 27.3%, respectively), while the involvement of three systems occurs in 22% of cases, two systems in 14%, and six systems in 7.3%. Renal function recovery is observed in 54% of patients. The prognosis for recovery is most favorable when only two or three systems are affected, with success rates of 66.7% and 78.8%, respectively. Conversely, recovery rates drop to 45.5% for four affected systems, 43.5% for five, and 27.3% for six. For patients undergoing renal replacement therapy, survival probability can be predicted with 86% accuracy using a mathematical-statistical model. This model incorporates critical clinical and laboratory parameters, including the number of failing organs, Glasgow Coma Scale scores, the need for inotropic hemodynamic support, mechanical ventilation requirements, and serum levels of bilirubin, urea, and creatinine. Similarly, the likelihood of renal function recovery can be forecasted with 85.3% accuracy using a separate statistical model. This model accounts for key prognostic factors such as the presence of cardiovascular failure, the depth of coma, the total number of impaired systems, platelet and fibrinogen counts, plasma sodium levels, proteinuria, and the duration of the oligoanuric phase.

ABSTRACT: Introduction: Advances in dialysis, kidney transplantation, and conservative kidney care have significantly increased the life expectancy of patients with chronic kidney disease (CKD) and end-stage kidney disease (ESKD). At the same time, technological progress has created complex ethical dilemmas related to the initiation or withdrawal of dialysis, informed consent, quality of life, end-of-life care, organ transplantation, and equitable allocation of limited healthcare resources. These issues require not only clinical assessment but also philosophical reflection on autonomy, human dignity, justice, and moral responsibility.
Aim: To analyze the main bioethical challenges arising in nephrology and to determine the philosophical principles that can improve decision-making in the management of patients with CKD and ESKD.
Materials and Methods: A philosophical and comparative bioethical analysis of scientific literature published between 2008 and 2025 was conducted. Peer-reviewed publications in nephrology, bioethics, palliative medicine, and philosophy of medicine were examined. The study used critical literature review, conceptual analysis, comparison of ethical approaches, and synthesis of the principles of autonomy, beneficence, non-maleficence, justice, and respect for human dignity.
Results: The analysis demonstrated that the traditional individualistic interpretation of patient autonomy is insufficient for resolving many contemporary ethical problems in nephrology. Patients with advanced CKD may experience cognitive impairment, emotional distress, severe comorbidity, and dependence on family and healthcare professionals. Therefore, treatment decisions are rarely made in complete social isolation.
The concept of relational autonomy provides a more comprehensive ethical framework. It recognizes that patient preferences and choices are formed within family, cultural, social, and institutional relationships. Accordingly, nephrologists should ensure meaningful communication among patients, relatives, and members of the multidisciplinary team while preserving the patient’s right to self-determination.
The initiation or withdrawal of dialysis represents one of the most difficult ethical decisions. Dialysis may prolong life but can also increase treatment burden without providing a meaningful improvement in functional status or quality of life. Ethical decision-making should therefore consider clinical prognosis, treatment benefits and burdens, patient values, expected quality of life, psychosocial consequences, and family perspectives. Shared decision-making is considered the most appropriate approach because it combines professional medical judgment with the informed preferences of the patient.
Justice is another fundamental challenge, particularly in settings with limited access to dialysis and kidney transplantation. Transparent allocation criteria are required to prevent discrimination based on age, ethnicity, socioeconomic status, disability, or social position. Palliative and conservative kidney care should also be recognized as ethically acceptable patient-centered options rather than as abandonment of treatment.
Conclusion: Contemporary nephrology requires an integrated ethical model that combines autonomy, beneficence, non-maleficence, justice, human dignity, and relational responsibility. Relational autonomy offers a more realistic framework than an exclusively individualistic approach because it considers the social and cultural context of decision-making. The proposed approach may improve communication, support shared decision-making, reduce non-beneficial treatment, and promote patient-centered care in CKD and ESKD. Further research should focus on adapting this model to different cultural traditions and healthcare systems.

ABSTRACT: Introduction: Obstetric thrombotic microangiopathies (TMAs) are rare but potentially life-threatening disorders that include HELLP syndrome, thrombotic thrombocytopenic purpura, and atypical hemolytic uremic syndrome (aHUS). Their overlapping clinical features often complicate timely diagnosis. Differentiating HELLP syndrome from aHUS is particularly challenging when TMA persists and acute kidney injury (AKI) progresses after delivery. Early recognition of aHUS is crucial because targeted complement-inhibitory therapy may significantly improve outcomes.
Case Presentation: A 41-year-old woman (gravida 5, para 3) with a high-risk pregnancy, including a history of preeclampsia complicated by placental abruption and recurrent pregnancy loss, was admitted at 28 weeks' gestation with severe preeclampsia complicated by obstetric TMA. On admission, she presented with hypertension (150/90 mmHg) and proteinuria (1.0 g/day), while hemoglobin, platelet count, and kidney function were within the normal range.
On the fourth day of hospitalization, an emergency cesarean section was performed because of progressive placental abruption. The postoperative course was complicated by HELLP syndrome, sepsis, massive hemorrhage, disseminated intravascular coagulation, microangiopathic hemolytic anemia, thrombocytopenia, and severe anuric AKI. Peak laboratory values included hemoglobin 48 g/L, platelet count 48 × 10⁹/L, serum creatinine 563 μmol/L, aspartate aminotransferase 560 U/L, lactate dehydrogenase 5,844 U/L, schistocytes detected on two peripheral blood smears, and a negative direct Coombs test.
Despite elimination of the obstetric trigger by delivery, followed by relaparotomy and hysterectomy, TMA manifestations and dialysis-dependent AKI persisted, prompting differential diagnosis between severe HELLP syndrome and aHUS. The patient underwent hemodiafiltration followed by 24 hemodialysis sessions and remained on maintenance hemodialysis for 2.5 months after discharge. Subsequently, kidney function partially recovered, allowing discontinuation of dialysis, although significant renal impairment persisted (serum creatinine 250–300 μmol/L).
Conclusion: This case highlights the diagnostic challenge of distinguishing HELLP syndrome from aHUS in obstetric TMA. Persistence of TMA for more than 48–72 hours after removal of the obstetric trigger, together with ongoing microangiopathic hemolysis, thrombocytopenia, and severe AKI, should prompt evaluation for aHUS, including assessment of ADAMTS13 activity, complement abnormalities, and genetic risk factors to guide timely initiation of complement-inhibitory therapy. The case emphasizes the importance of early multidisciplinary management and long-term nephrology follow-up, even in patients who achieve partial recovery of kidney function.

ABSTRACT: Patient T., 43 years old. End-stage chronic kidney disease (CKD) was diagnosed in 2013, and emergency kidney replacement therapy with maintenance hemodialysis was initiated. Prior to this, the patient had not been followed by a nephrologist. Throughout the course of hemodialysis treatment, the patient failed to comply with medical recommendations regarding regular laboratory monitoring of mineral metabolism.
In 2024, a markedly elevated parathyroid hormone (PTH) level (>1,935 pg/mL; October 2024) was detected for the first time. The patient had not received any specific medical therapy. Clinical manifestations included generalized weakness, bone and joint pain, impaired mobility (waddling gait), and skeletal deformities involving the sternum and tibial bones.
Scintigraphy performed on December 13, 2024, demonstrated increased functional activity of all four parathyroid glands (Figure 1). Despite prolonged combined medical therapy with cinacalcet 90 mg/day and paricalcitol 15 μg three times weekly, laboratory markers of calcium-phosphate metabolism continued to deteriorate, with the PTH level rising to 2,338 pg/mL. Bone mineral density assessment by dual-energy X-ray absorptiometry (DXA) revealed a Z-score of −5, consistent with severe secondary osteoporosis (Figure 2).
In December 2024, the patient underwent cervical exploration with removal of the hyperplastic left superior, left inferior, and right inferior parathyroid glands at Poytaxt Medical Clinic. In the postoperative period, a significant reduction in serum PTH was observed, decreasing to 492 pg/mL (December 27, 2024) compared with the preoperative level of 2,338 pg/mL.
During the one-year follow-up after parathyroidectomy, the patient's condition remained stable, with no recurrence of hyperparathyroidism. As replacement therapy, the patient has been receiving long-term calcium supplementation and alfacalcidol.
Biochemical blood tests performed in August–September 2025 demonstrated total serum calcium levels ranging from 1.79 to 2.71 mmol/L (reference range: 2.1–2.6 mmol/L) and serum phosphorus levels of 1.0–1.15 mmol/L (reference range: 0.81–1.45 mmol/L).
In November 2025, dysfunction of the patient's arteriovenous fistula (AVF) resulted in complete loss of vascular access. The exact etiology could not be established because of insufficient diagnostic evaluation; however, vascular wall calcification was considered a possible contributing factor. A temporary central venous catheter was inserted for hemodialysis, followed by successful creation of a new arteriovenous fistula.
According to the most recent laboratory evaluation performed on January 7, 2026, the PTH level remained within the target range (200 pg/mL), serum phosphorus was 0.98 mmol/L, and alkaline phosphatase was 410.5 U/L.
Conclusion: This clinical case illustrates the consequences of delayed diagnosis and inadequate management of secondary hyperparathyroidism, resulting from both poor patient adherence to treatment and systemic healthcare limitations, including insufficient long-term follow-up, limited access to regular laboratory monitoring, and shortcomings in the standard management of maintenance hemodialysis patients.
Although parathyroidectomy is effective in improving quality of life and reducing cardiovascular mortality, it is associated with postoperative complications and is generally performed only in advanced stages of the disease, when irreversible disorders of mineral and bone metabolism have already developed.
Therefore, early diagnosis and timely initiation of long-term medical therapy remain the cornerstone of secondary hyperparathyroidism management, allowing better disease control and reducing the need for surgical intervention.

ABSTRACT: Introduction: Diabetic kidney disease is a major cause of end-stage kidney disease and is frequently accompanied by cardiovascular and metabolic complications. Patients receiving maintenance hemodialysis remain at high risk of life-threatening complications, particularly when multiple comorbidities are present. We present a case of severe metabolic decompensation in a patient with end-stage diabetic kidney disease receiving maintenance hemodialysis.
Aim: To describe the clinical presentation, laboratory abnormalities, emergency management, and short-term clinical response in a patient with end-stage diabetic kidney disease and multiple comorbidities receiving maintenance hemodialysis.
Methods: A clinical case was analyzed based on the patient's medical records, including clinical presentation, laboratory investigations, comorbid conditions, treatment, and clinical course during hospitalization.
Results: A 59-year-old woman with type 2 diabetes mellitus complicated by diabetic kidney disease and end-stage chronic kidney disease (CKD stage 5) had been receiving maintenance hemodialysis three times weekly since March 2026. Her comorbidities included rheumatoid arthritis, congestive heart failure, diabetic polyneuropathy, anemia of chronic disease, bilateral secondary gonarthrosis, cholelithiasis without cholecystitis, hemorrhoids, and a stage III pressure ulcer. She was admitted in a severe condition with marked weakness, poor appetite, nausea, vomiting, and impaired consciousness. Laboratory evaluation demonstrated severe azotemia, with a creatinine level of approximately 1154 µmol/L and urea of 47.7 mmol/L, accompanied by hyperkalemia (6.3 mmol/L). The clinical picture was consistent with severe uremic and metabolic decompensation in the setting of end-stage kidney disease. Emergency hemodialysis and comprehensive supportive treatment were performed. Following treatment, serum creatinine, urea, and potassium levels decreased, accompanied by clinical stabilization.
Conclusion: This case highlights the high risk of severe metabolic complications in patients with end-stage diabetic kidney disease receiving maintenance hemodialysis, particularly in the presence of substantial cardiovascular and systemic comorbidity. Early recognition of uremic and electrolyte disturbances and timely initiation of hemodialysis are essential for preventing life-threatening complications and achieving clinical stabilization.

ABSTRACT: Background: Pregnancy in women with kidney disease is associated with an increased risk of maternal and obstetric complications, including preeclampsia, preterm delivery, and deterioration of kidney function. The magnitude of risk increases with advancing chronic kidney disease (CKD) stage and is further influenced by hypertension and proteinuria. However, evidence describing the spectrum of kidney disease and predictors of adverse pregnancy outcomes in Central Asian populations remains limited. This study aimed to characterize the clinical and laboratory features of pregnant women with kidney disease and identify factors associated with adverse pregnancy outcomes.
Methods: We conducted a retrospective single-center cohort study including 80 hospitalizations of 79 pregnant women with kidney disease between 2022 and 2026. Demographic characteristics, kidney disease categories, comorbidities, laboratory parameters, and available pregnancy outcomes were analyzed. A combined adverse outcome was defined as at least one of the following: CKD progression, dialysis initiation, preeclampsia, eclampsia, HELLP syndrome, pregnancy termination for medical indications. Bias-reduced logistic regression was used to identify factors associated with adverse outcomes.
Results: Urinary tract infections accounted for 49.4% of kidney-related diagnoses and glomerular diseases for 35.4%. Hypertension was present in 28.8% and anemia in 61.8% of cases. Women with glomerular diseases had significantly higher 24-hour proteinuria than women with other kidney disorders (1.3 [0.6–3.3] vs 0.1 [0.0–0.5] g/day; p<0.001). A combined adverse outcome occurred in 10/80 (12.5%) hospitalizations. The incidence was markedly higher in women with CKD stage ≥3 than in those with CKD stage <3 or without CKD (83.3% vs 7.2%; p<0.001). In univariable analysis, CKD stage ≥3 (OR 43.00; 95% CI 5.07–364.80), hypertension (OR 24.68; 95% CI 3.93–154.88), higher admission creatinine (OR 2.70 per 1 SD; 95% CI 1.43–5.09), and higher 24-hour proteinuria (OR 2.20 per 1 SD; 95% CI 1.17–4.16) were associated with adverse outcomes. In the multivariable model, CKD stage ≥3 (OR 20.29; 95% CI 1.58–260.05) and hypertension (OR 18.62; 95% CI 2.61–132.74) remained independently associated with adverse outcomes.
Conclusion: Advanced CKD and hypertension were the strongest predictors of adverse pregnancy outcomes. Assessment of kidney function, blood pressure, and quantitative proteinuria may facilitate early risk stratification and identify women requiring intensive multidisciplinary nephrology and obstetric surveillance.
 

ABSTRACT: Introduction: The development of amyloidosis in primary membranous nephropathy (PML) is extremely rare and is reported in medicine as isolated clinical cases. These two diseases have completely different development mechanisms. Primary membranous nephropathy is an autoimmune kidney disease caused by antibodies (most often to PLA2R receptors). Amyloidosis is a protein metabolism disorder in which abnormal fibrillar protein is deposited in tissues.
Case presentation: Patient M, woman, 69 years old.
Complaints: swelling throughout the body, decreased urine output, and increased blood pressure. History: In January 2026, the patient suddenly began to experience swelling throughout the body and decreased urine output. Due to the development of CHD, the patient received treatment in cardiology departments. Since the patient's condition did not improve for two months, the patient applied to nephrology center in May. Objective examination: Overall condition is moderately severe. Swelling is observed throughout the body. BP 110/70mmHg, HR-82bpm. BR-20bpm. Laboratory tests: CBC: Hemoglobin-125g/l, RBC-4.2, platelet-345.0, WBC-14.7, neutrophil-82, lymphocyte-9, ESR-14. Urine: color-yellow, protein-2.31g/l, epithelium-4, WBC-16, RBC-6, hyaline cylinder-8, granular-4. BA: 12.02.2026. Total protein-40.0, urea-5.4, albumin-23.0, creatinine-72.0. 17.02.2026. Total protein-37.0, albumin-22.0. 24.02.2026. Total protein-34.0, urea-5.0, albumin-16.0, creatinine-69.0. 10.03.2026. Total protein-32.0, albumin-17.0, creatinine-89.0. ANTI PLA2R-33.6 RU/ml (positive). Immunogram: CD3-44.38, CD4-61.69, CD8-35.06, CD19-21.61, CD16+-78.96, CD56+ -17.29. Compliment C3-1,19. C4-0.348.
The patient was diagnosed with primary membranous nephropathy because of the positive AntiPLA2R. Monoclonal antibody (rituximab) was chosen for pathogenetic treatment. The patient received 500 mg once a week for 4 weeks, a total of 2000 mg of the drug. However, the biochemical blood test showed no increase in total protein and albumin, the proteinuria hasn't decreased and the patient remained edematous. To clarify the diagnosis, the patient was recommended a kidney biopsy, and after the patient agreed, the procedure was performed (04.2026). Biopsy result: Kidney biopsy shows features of a deposit glomerulopathy with lambda immunoglobulin light chain restriction in glomeruli suggestive of an AL amyloidosis.
The patient was referred to a hematologist to confirm the diagnosis. The patient was diagnosed with Multiple myeloma from, System amyloidosis by hematologists. Then CyBorD (cyclophosphamide 400mg, bortezomid 2.5mg, dexamethasone 20mg) treatment was performed. The patient received 4 courses of chemotherapy. The patient's general condition improved clinically. Swelling throughout the body decreased. Laboratory tests showed hypoproteinemia and hypoalbuminemia. The patient's general condition improved over time. However, biochemical tests did not show an increase in total protein and albumin levels.

ABSTRACT: Introduction: Effective follow-up of patients with kidney disease requires systematic patient registration, monitoring of kidney function, assessment of disease progression risk, and timely referral. Proper organization of medical information and reducing the risk of human error are also important. There are no published data on a functioning chronic kidney disease registry at the primary health care level in Kazakhstan. This study presents the experience of implementing a nephrology registry in Viamedis LLP city polyclinics.
Aim: To develop and implement a nephrology registry at the PHC level for data management, active identification of kidney function abnormalities, risk assessment, and improvement of patient follow-up.
Materials and Methods: The registry was developed according to current regulations of the MHRK, including Order No. 149. It includes data from the population registered at four large city polyclinics of Viamedis LLP.The registry includes patients already under follow-up and patients actively identified based on available laboratory data. For patients with previous serum creatinine results, estimated glomerular filtration rate is automatically calculated using the CKD-EPI equation and classified according to eGFR categories.The registry also includes the 4-variable Kidney Failure Risk Equation to estimate the individual 2- and 5-year risk of kidney failure. Data on eGFR, urine albumin-to-creatinine ratio, medication availability, and sodium-glucose cotransporter-2 inhibitor therapy are also recorded.
Results and Discussion: At the time of analysis, 3036 patients were under follow-up. During one month, the registry additionally identified 3051 patients outside the existing follow-up register based on previous serum creatinine results. 1462 patients (47,9%) had eGFR<60 ml. This shows a large potential for active identification of previously unregistered kidney function abnormalities and possible undiagnosed CKD requiring further confirmation and follow-up.KFRE-4 was used to assess the risk of kidney failure. Based on the 2-year risk calculation, 91 patients were identified, while 176 patients were identified using the 5-year risk calculation. These patients may require closer monitoring and timely referral to a nephrologist.The active identification results were obtained over one month. If these results are conditionally extrapolated to one year, the potential number of identified patients may increase substantially, highlighting the value of the registry as a tool for active kidney disease detection.The registry also included ACR results: 12861-A1, 1777-A2, and 67-A3 results. This allows albuminuria to be monitored over time and supports additional risk assessment.The integration of kidney function, ACR, laboratory monitoring, medication availability, and SGLT2 inhibitor therapy provided a more complete assessment of nephrology workload. Nephrology nurses supported data updating and patient follow-up, improving registry completeness.
Conclusion: The nephrology registry at the PHC level allowed a shift from monitoring only known patients to active identification of previously unregistered kidney function abnormalities. Automated CKD-EPI calculation, ACR assessment, and KFRE-4 support risk stratification and timely referral. Integration of clinical, laboratory, and treatment data improves structured follow-up and provides a more objective assessment of nephrology workload. The registry provides a basis for a proactive approach to kidney disease management at the PHC level.

ABSTRACT: Background: Alport syndrome is an inherited disorder of the glomerular basement membrane caused by pathogenic variants in COL4A3, COL4A4, or COL4A5. The disease is characterized by persistent microscopic hematuria, progressive proteinuria and chronic kidney disease, with possible hearing and ocular involvement. Early recognition is important for timely nephroprotective management and family screening.

ABSTRACT: Background: Evidence on chronic kidney disease (CKD) in Central Asia remains limited, particularly for community-based detection using both kidney function and albuminuria. This study assessed the frequency of CKD markers among adults in three cities of Kazakhstan and examined whether point-of-care (POC) creatinine testing could support community screening.
Methods: Adults were recruited through community screening events in Astana, Ust-Kamenogorsk, and Turkestan. Laboratory serum creatinine was used to calculate eGFR with the CKD-EPI 2021 equation, and urine albumin-to-creatinine ratio (ACR) was measured to identify albuminuria. Participants were classified as having screening-detected CKD markers if eGFR was <60 mL/min/1.73 m² and/or ACR was ≥30 mg/g on a single assessment. Multivariable logistic regression was used to examine associated factors. Capillary POC creatinine was compared with laboratory creatinine, and its diagnostic performance for identifying eGFR <60 mL/min/1.73 m² was evaluated.
Results: Of 1,022 participants with complete laboratory kidney measurements, 100 (9.8%; 95% CI 8.1–11.8) had screening-detected CKD markers. Albuminuria was identified in 7.7%, while reduced eGFR was present in 3.4%. Among participants with CKD markers, 52.0% reported no previous awareness of abnormal kidney findings. Hypertension was associated with approximately twice the adjusted odds of CKD markers (aOR 2.05, 95% CI 1.24–3.41). POC and laboratory creatinine were available for 987 participants. POC creatinine exceeded laboratory values by an average of 18.5 µmol/L, with wide limits of agreement. For identifying laboratory-defined reduced eGFR, POC-derived eGFR had 84.4% sensitivity, 83.4% specificity, 14.5% positive predictive value, 99.4% negative predictive value, and an AUC of 0.919.
Conclusions: CKD markers were detected in roughly one in ten screened adults, and albuminuria accounted for a substantial proportion of identified abnormalities. The high proportion of previously unrecognized findings supports greater use of combined eGFR and ACR assessment in CKD case-finding. POC creatinine may be useful for triage because of its strong rule-out performance, but positive findings should be confirmed with standardized laboratory testing.

ABSTRACT: Background: Paroxysmal nocturnal hemoglobinuria (PNH) is a rare acquired clonal hematopoietic disorder characterized by complement-mediated intravascular hemolysis and thrombosis. Renal involvement is clinically relevant: impaired renal function (eGFR <90 mL/min/1.73 m²) was reported in 42.8% of 4,439 patients in the International PNH Registry. Pregnancy is a high-risk setting. A 2025 meta-analysis of 190 pregnancies in 135 women with PNH reported fetal survival of 82% with eculizumab versus 69% without it, while preterm birth occurred in 32% and 44%, respectively. Coexisting hemolysis, thrombocytopenia, and renal dysfunction during pregnancy may mimic thrombotic microangiopathy (TMA).
Case Presentation: A 33-year-old woman in her third pregnancy had longstanding thrombocytopenia previously considered immune/idiopathic. In March 2025, she developed acute kidney injury (AKI), with serum creatinine 143 μmol/L and eGFR 42.8 mL/min/1.73 m². Nephrology admission revealed dark urine, anemia, thrombocytopenia, proteinuria up to 5 g/L, hematuria, and 24-hour proteinuria of 1.98 g/day. Marked intravascular hemolysis was demonstrated by LDH >2136 U/L, indirect bilirubin 20.9 μmol/L, and haptoglobin 0.1 g/L. Renal function subsequently recovered. TMA was initially suspected, including thrombotic thrombocytopenic purpura (TTP) and atypical hemolytic uremic syndrome. ADAMTS13 activity was 93%, arguing against severe ADAMTS13 deficiency. Persistent hemolysis prompted flow cytometry, which identified a PNH clone: type II erythrocytes 0.14%, type III erythrocytes 38.24%, FLAER−/CD24− granulocytes 7.8%, and FLAER−/CD14− monocytes 34.4%. Urinary hemosiderin was positive, reticulocytes were 8.9%, and LDH remained >1684 U/L. PNH with chronic intravascular hemolysis was diagnosed. At approximately 19 weeks, a multidisciplinary team considered eculizumab; because renal function was preserved and there was no transfusion dependence, anticoagulant prophylaxis and close monitoring were chosen. At approximately 27 weeks, pregnancy was complicated by severe preeclampsia and subsequently resulted in preterm delivery with antenatal fetal death.
Conclusion: PNH should be considered in pregnant patients with unexplained AKI and/or proteinuria accompanied by thrombocytopenia and intravascular hemolysis. Preserved ADAMTS13 activity and identification of a PNH clone were pivotal in distinguishing PNH from TTP. Early recognition and multidisciplinary nephrology–hematology–obstetric management are essential because renal, thrombotic, and pregnancy-related complications may be severe.

ABSTRACT: Background: Iron deficiency anemia is common in patients with chronic kidney disease (CKD) and is associated with adverse clinical outcomes. Ferric carboxymaltose (FCM) is an effective and well-tolerated treatment for iron deficiency anemia in CKD. However, its potential effects on renal function remain insufficiently understood. This study aimed to evaluate changes in renal function following FCM administration in patients with CKD stages 3–4 and to assess whether these changes were associated with the administered dose.
Methods: This prospective study included patients with CKD stages 3–4, anemia, and iron deficiency (serum ferritin <100 μg/L or <200 μg/L with transferrin saturation <20%) who received intravenous FCM (Fercari) and were followed for 24 weeks. Patients were stratified according to the administered dose: 500 mg or 1000 mg. Clinical and laboratory parameters were assessed at baseline and after 24 weeks. Renal function was evaluated using estimated glomerular filtration rate (eGFR) calculated by the CKD-EPI equation.
Results: A total of 56 patients were included; mean age was 64.3 ± 6.7 years, and 25 (44.6%) were men. Diabetes mellitus, chronic heart failure, and arterial hypertension were present in 34 (60.7%), 31 (55.3%), and 45 (80.3%) patients, respectively. CKD stage 3 was present in 20 (35.7%) patients and stage 4 in 36 (64.3%). Thirty-two patients (57.1%) received 1000 mg FCM. Baseline mean hemoglobin was 98.3 ± 4.23 g/L and mean eGFR was 39.18 ± 15.14 mL/min/1.73 m². After 24 weeks, hemoglobin increased by 12.3 ± 1.51 g/L in the overall cohort (P=0.001), with increases of 15.6 ± 3.71 g/L in the 1000 mg group and 8.8 ± 1.5 g/L in the 500 mg group (both P=0.001). Mean eGFR increased by 5.86 ± 2.13 mL/min/1.73 m² in the overall cohort (P=0.042). In the 1000 mg group, eGFR increased by 6.64 ± 2.55 mL/min/1.73 m² (P=0.049), whereas no statistically significant change was observed in the 500 mg group.
Conclusions: FCM effectively improved hemoglobin levels in patients with CKD stages 3–4 and iron deficiency anemia. Treatment with 1000 mg FCM was associated with a modest improvement in eGFR over 24 weeks, whereas no significant change was observed with 500 mg. These findings suggest a possible dose-related association between FCM treatment and renal function; however, controlled randomized studies are required to determine whether this represents a true nephroprotective effect.

ABSTRACT: Introduction: Chronic kidney disease (CKD) is a progressive condition characterized by declining kidney function and altered urinary protein excretion. However, relationships between individual urinary proteins and kidney function remain incompletely understood. We aimed to compare urinary proteomic profiles between patients with CKD and healthy controls (HC) and identify proteins associated with estimated glomerular filtration rate (eGFR).
Methods: Urinary proteomics was performed in 79 patients with CKD and 54 HC using diaPASEF on a timsTOF Pro 2 platform. DIA-NN data were processed with MSstats using log2 transformation, median normalization, and Tukey's median polish without missing-value imputation. Differential abundance was assessed using limma models adjusted for log10 urinary creatinine and LC-MS run order with robust empirical-Bayes moderation. Protein associations with eGFR were evaluated separately in CKD and HC using Spearman correlation. Benjamini-Hochberg false-discovery rate (BH-FDR) <0.05 was used to define significance.
Results: CKD participants had lower eGFR and higher urine albumin-to-creatinine ratio than HC (both P < 0.001). Summed MaxLFQ intensity was higher in CKD (8.0 [7.7-8.2] vs 7.5 [7.4-7.6] log10; P < 0.001), despite fewer detected protein groups (4,338 vs 4,553) (Table 1).
Values are median (IQR), mean ± SD, n (%), or detected protein-group counts, as appropriate. P values compare HC with patients with CKD. Sex was compared using the Pearson chi-square test. Age, serum creatinine, urine ACR, and summed MaxLFQ intensity were compared using the Wilcoxon rank-sum test. Estimated GFR was compared using Welch’s two-sample t-test. Detected protein groups were reported descriptively and were not statistically tested. ACR, albumin-to-creatinine ratio; CKD, chronic kidney disease; eGFR, estimated glomerular filtration rate; HC, healthy controls; IQR, interquartile range; MaxLFQ, maximum label-free quantification.
Creatinine-adjusted differential abundance analysis showed broad bidirectional changes in the CKD urinary proteome. Among the most significantly upregulated proteins were A1AG1, TRFE, AFAM, A1AG2, and A1AT, whereas MUC18, BCAM, CD248, ROBO4, and IBP7 were among the most significantly downregulated proteins (Figure 1).
No protein-eGFR association remained significant after BH-FDR correction in HC (3,316 proteins tested). In CKD, 125 of 1,905 tested proteins showed significant associations with eGFR. The strongest FDR-ranked associations included positive associations for F16P1 (ρ = 0.60) and UROK (ρ = 0.49), and negative associations for CFAD (ρ = -0.59), VSIG4 (ρ = -0.57), SH3L1 (ρ = -0.65), FABP4 (ρ = -0.62), PEDF (ρ = -0.50), RET4 (ρ = -0.50), B2MG (ρ = -0.49), and FHR4 (ρ = -0.67) (Figure 2).
Conclusions: CKD was characterized by a distinct urinary proteomic profile and numerous proteins associated with kidney function. The presence of 125 eGFR-associated proteins in CKD, with none surviving FDR correction in HC, suggests disease-related variation in the urinary proteome. These findings support further evaluation of urinary proteins as potential CKD biomarkers.

ABSTRACT: Relevance: Urolithiasis is a widespread urological disease worldwide, characterized by the formation of stones in any part of the urinary tract, including the kidneys, ureters, bladder, and urethra. In CIS countries, the proportion of urolithiasis among urological diseases ranges from 33.9% in Russia to 58.2% in Kyrgyzstan, while in Tajikistan, Uzbekistan, and Kazakhstan it is at the level of 42.2–56.1%, showing an increasing trend in incidence. Globally, the prevalence of urolithiasis varies from 1% to 20%, with higher risk observed in regions with hot climates and high environmental pollution, which is associated with increased fluid loss and higher salt concentration in urine. Within the framework of this study, a retrospective analysis of 162,538 hospitalizations among 132,915 patients with urolithiasis in the Republic of Kazakhstan was conducted for the period 2014–2021. The overall hospitalization rate was 1.31 cases per 1,000 population. The highest rates were observed in the Turkestan region and Almaty city, corresponding to the geographical concept of the “stone belt.” The majority of hospitalizations were recorded among patients aged 50 years and older. A comparison of urban and rural populations showed a higher disease burden in urban areas, likely associated with lifestyle factors and better access to medical care. In conclusion, urolithiasis remains a significant medical and social problem in Kazakhstan. In 2021, approximately 106 million new cases were reported worldwide; despite the increase in absolute incidence, standardized rates and DALYs have decreased, and mortality remains consistently low (<0.5 per 100,000 population), indicating improvements in diagnosis, prevention, and treatment.
Aim of the study: To analyze the dynamics and regional characteristics of urolithiasis morbidity among the population of the Republic of Kazakhstan.
Study materials and objectives: A retrospective analysis was conducted using data from annual official health reports (National Bureau of Statistics of the Republic of Kazakhstan) for the period 2015–2024.To assess national trends in urolithiasis morbidity over the period 2015–2024.To compare urolithiasis incidence rates between urban and rural populations.To develop practical recommendations for the prevention, early detection, and management of urolithiasis.
Results: In Kazakhstan, the incidence of urolithiasis demonstrated a wave-like pattern: an increase during 2015–2018, a decrease in 2019–2021, and a renewed upward trend from 2022 onwards. By 2024, the indicators exceeded the average level of the studied period. Urban areas showed relatively stable dynamics, whereas rural areas demonstrated more pronounced fluctuations.
In 2024, the incidence rate among the urban population reached 85.9 cases per 100,000 population, showing a renewed increase after the decline observed in 2020–2021. A similar post-decline increase was observed in rural areas, with marked regional variability.The highest rural incidence was recorded in the Almaty region, exceeding 150 cases per 100,000 population in 2023–2024. In urban areas, the highest rate was observed in Atyrau city, reaching up to 198 cases per 100,000 population in 2024, while in Aktobe city it reached 153.5 cases per 100,000 population.
Conclusion: In recent years, an increase in the incidence of urolithiasis and pronounced regional differences have been observed. Therefore, it is necessary to strengthen preventive measures, improve early diagnosis, and enhance the control of risk factors in regions with high incidence rates.

ABSTRACT: Introduction: Chronic kidney disease (CKD) is frequently diagnosed after clinically meaningful loss of kidney function. Creatinine-based estimated glomerular filtration rate (eGFR) may fail to identify early renal dysfunction, while cystatin C, albuminuria and artificial intelligence (AI)-based prediction models may improve early detection and risk stratification. This umbrella review synthesizes current evidence regarding the diagnostic and prognostic value of these approaches and identifies limitations to their clinical implementation.
Methods: We synthesized published systematic reviews and meta-analyses evaluating adults with CKD or individuals at risk of CKD. Evidence addressing cystatin C, albuminuria, or AI/machine-learning models for CKD detection or progression was considered. Outcomes included diagnostic accuracy, sensitivity, specificity, area under the receiver operating characteristic curve (AUC), and prognostic associations. Findings were summarized descriptively according to reported pooled estimates and study limitations.
Results: A meta-analysis of 19 studies evaluating serum cystatin C for CKD detection reported pooled sensitivity of 0.85 (95% CI, 0.81–0.89), specificity of 0.87 (95% CI, 0.84–0.90), and AUC of 0.92 (95% CI, 0.90–0.94). Another meta-analysis including 35 studies and 23,667 participants found that the combined creatinine/cystatin C CKD-EPI equation achieved 7.50% higher accuracy than creatinine-based eGFR alone. A 2025 systematic review of risk-factor-based CKD screening included 24 studies from 11 countries; eGFR was used in 22 studies and albumin-creatinine ratio in 14, while confirmed CKD prevalence ranged from 4.4% to 17.1%. For AI, a systematic review identified 68 eligible studies from 648 records, but only 6/68 were conducted in clinical settings. A subsequent meta-analysis of 33 AI studies reported pooled sensitivity of 0.43, specificity of 0.92 and AUC of 0.89, with substantial heterogeneity.
Conclusion: Cystatin C and combined creatinine/cystatin C assessment demonstrate improved diagnostic performance compared with creatinine-based assessment alone. Albuminuria remains an important component of targeted CKD screening, while AI models show promising predictive performance but limited clinical validation. Prospective multicenter studies integrating biomarkers and interpretable AI models are warranted to establish whether these approaches improve clinically meaningful early CKD detection.

ABSTRACT: Introduction: Renal tubular acidosis (RTA) in adults remains an underdiagnosed condition, often masked by other diseases. Distal RTA is particularly challenging as it may present primarily with neurological symptoms for a long time, including muscle weakness, flaccid pareses, and episodes of paralysis against the background of hypokalemia. In clinical practice, such patients are often initially hospitalized and monitored in neurological departments with suspected primary neurological pathology, which leads to delays in establishing the correct diagnosis. The true cause of these symptoms is metabolic and electrolyte disturbances caused by RTA.
Late diagnosis increases the risk of complications such as nephrocalcinosis, nephrolithiasis, and progression of chronic kidney disease. Thus, reporting clinical cases of RTA with “neurological masks” is important to raise awareness among doctors of various specialties and ensure timely differential diagnosis.
Objective: To analyze a clinical case of distal RTA in an adult patient who presented with neurological symptoms at onset.
Clinical case: A 19-year-old male was admitted with severe weakness in all limbs and inability to move independently. He had been monitored by a cardiologist for mitral valve prolapse and was one of triplets. At 17, he experienced two episodes of muscle weakness progressing to severe movement restriction after physical exertion. At 18, he was hospitalized twice for periodic paralysis with hypokalemia (1.6–3.3 mmol/L). Treatment included potassium supplements and metabolic therapy.
On admission, potassium was 1.6–2.8 mmol/L and chloride 126–127 mmol/L, while sodium remained normal (140–143 mmol/L). Immunological and hormonal tests, including ANA, anti-dsDNA, ANCA, antiphospholipid antibodies, thyroid hormones, and anti-TPO, were normal. CT showed bilateral renal microcalculi and right-sided pyeloectasia. Neurological evaluation was performed, and AChR and MuSK antibodies were ordered to exclude myasthenia gravis.
Severe hypokalemia was corrected with intravenous KCl. Considering hypokalemia, hyperchloremia, and nephrolithiasis, distal renal tubular acidosis was suspected.
Conclusions: Distal RTA in adults can present initially with pronounced neurological symptoms, mimicking primary nervous system diseases.
The presence of hypokalemia combined with hyperchloremia requires exclusion of RTA, especially in cases of recurrent episodes of muscle weakness.
Detection of nephrolithiasis or kidney microcalculi is an important diagnostic marker supporting distal RTA.
The presented case highlights the need for interdisciplinary approach and increased vigilance among physicians to consider metabolic causes of neurological disorders.

ABSTRACT: Introduction: Kidney transplantation has been actively developing in Kazakhstan, data on outcomes remain limited. This study aimed to evaluate recipient characteristics, patient survival, causes of ESKD, and renal graft function after KT.
Methods: We retrospectively analyzed 37 consecutive kidney transplant recipients who underwent KT between January 2020 and July 2025. Body mass index (BMI), etiology of ESKD, donor type, pre-transplant hemodialysis, mortality, and renal graft function were evaluated. Renal graft function was assessed using serial serum creatinine measurements during follow-up. Some recipients were lost to follow-up, which limited assessment of long-term graft function in these patients.
Results: In the available follow-up data, renal function was generally satisfactory and remained stable in most recipients with observations. Graft survival was 86.5%, with graft loss documented in five recipients: three surviving recipients experienced rejection-associated graft loss, and two patients died following rejection.
Among the five deaths, two were associated with confirmed COVID-19 infection, one was attributed to cerebral infarction caused by cerebral arterial thrombosis, and two were related to graft rejection. Among the three recipients with rejection-related complications, all experienced adverse effects associated with immunosuppressive therapy, including significant infectious complications.
Discussion: An important consideration is that the study period overlapped with the COVID-19 pandemic. Registry data showed substantially increased infection-related mortality among kidney transplant recipients receiving chronic immunosuppression during 2020, with infection and COVID-19 accounting for a major proportion of excess deaths. Therefore, mortality and survival outcomes should be interpreted in the context of the pandemic, limiting direct comparison with pre-COVID-19 cohorts.
Conclusion: Kidney transplantation at our center demonstrated favorable medium-term outcomes, with improvement in renal function and satisfactory outcomes in most recipients. Overall patient survival was 86.5%, and graft survival was also 86.5%. Continued monitoring of immunosuppression-therapy, complications, and long-term follow-up is important for improving patient and graft outcomes.

ABSTRACT: Background: Long-term graft survival in solid organ transplantation directly depends on the degree of human leukocyte antigen (HLA) compatibility between the donor and the recipient. Along with the cellular immune response, the humoral component—specifically, the presence of pre-existing circulating HLA antibodies—plays a critical role in the pathogenesis of both acute and chronic rejection. Monitoring the level of allosensitization in patients on the transplant waiting list is essential to mitigate the risk of post-transplant immunological complications.
Objective: To evaluate the structure and level of sensitization to HLA Class I and Class II antigens in potential kidney transplant recipients using high-sensitivity Luminex multiplex bead array technology.
Materials and Methods: A retrospective analysis of 1043 serum samples from patients on the kidney transplant waiting list for one year was performed. The mean age of the cohort was 53 years. HLA antibody screening was conducted via solid-phase bead-based immunoassay (Luminex technology) using commercial LabScreen Mixed (LSM12) detection kits (One Lambda, USA). The level of sensitization and antibody specificity were evaluated based on Mean Fluorescence Intensity (MFI).
Results: Screening revealed that 69.3% of the samples (n = 723) were negative for HLA antibodies. Reactive HLA antibodies (positive results) were verified in 30.7% of the patients (n = 320). Among the positive samples, isolated sensitization to HLA Class I antigens was detected in 143 recipients (44.7%), isolated sensitization to HLA Class II antigens in 36 recipients (11.2%), and combined sensitization to both classes (I and II) was identified in 113 cases (35.3%). The panel-reactive antibody (PRA) levels within the cohort ranged from 11% to 97%, with MFI values varying from 399.06 to 175,982.52.
Conclusion: Screening on the Luminex platform serves as a highly sensitive tool for pre-transplant monitoring. Assessing HLA status allows for the timely stratification of waitlist patients into specific immunological risk groups. Detecting high levels of allosensitization (MFI) justifies the need for tailored, selective donor matching, as well as the preemptive implementation of desensitization protocols including extracorporeal hemocorrection and targeted immunosuppressive therapy.

ABSTRACT: Objective: To assess dietary practices and challenges in managing hyperphosphatemia in CKD patients from nephrology specialists’ perspective.
Methods: An online survey of 68 nephrologists, hemodialysis physicians, and nurses at the Republican Specialized Medical Center of Nephrology and Kidney Transplantation (Tashkent, Uzbekistan) evaluated dietary habits, phosphorus awareness, and adherence difficulties. Descriptive statistics were applied.
Results: 64.7% reported increased consumption of ready-to-eat foods, 70.6%—phosphate-containing products, and 82.4% noted higher patient awareness. Adherence challenges were greatest among hemodialysis patients (51–75%). Most specialists (76.5%) emphasized equal importance of protein intake and phosphorus restriction.
Conclusion: Despite improved awareness, dietary adherence remains difficult. Increased processed and phosphate-rich food consumption complicates hyperphosphatemia management, highlighting the need for enhanced dietetic support.

ABSTRACT: Introduction and Aim: Atypical hemolytic uremic syndrome (aHUS) is an ultra-rare orphan disease that requires differential diagnosis from other thrombotic microangiopathies (TMAs). The aim of this study was to determine the diagnostic value of ADAMTS13 activity levels, anti‑complement factor H (anti‑CFH) antibody titers, and genetic screening in verifying aHUS subtypes among the pediatric population in Kazakhstan.
Materials and Methods: A retrospective analysis was conducted on 15 children with aHUS (8 girls and 7 boys) from 8 regions of Kazakhstan between 2019 and 2025. The mean age was 7.2 ± 3.8 years. ADAMTS13 activity was measured in 7 patients (46.6%), and anti‑CFH titers were assessed in 10 patients (66.7%). In the remaining patients, these tests were not performed because they had received fresh frozen plasma transfusions prior to testing. Genetic testing was completed for 10 out of 15 children (66.7%); the remaining 5 patients (33.3%) died before testing could be carried out.
Results: In all patients tested (n = 7, 100%), ADAMTS13 activity was >10%, effectively ruling out thrombotic thrombocytopenic purpura (TTP). Autoimmune aHUS associated with anti‑CFH antibodies was diagnosed in 4 out of 10 children (40%), of whom 3 were of Asian descent and 1 was Caucasian. Genetic testing in 10 children revealed pathogenic variants in complement system genes in 2 patients (20%): one child had a CFHR3/CFHR1 deletion, and another had a CFHR1/CFHR4 microdeletion; both exhibited high anti‑CFH titers (up to 11,490 U/mL). Additionally, one child was found to have a clinically insignificant heterozygous autosomal recessive mutation in the ADAMTS13 gene.
The comprehensive laboratory workup allowed for the stratification of aHUS subtypes and personalized therapy. Patients with idiopathic forms received complement‑blocking therapy with eculizumab alone, while children with anti‑CFH antibodies received combined treatment with eculizumab and immunosuppressive agents.
Conclusions: This is the first comprehensive diagnostic data report on pediatric aHUS in Kazakhstan. Genetically determined aHUS was identified in 20% of the cohort. Anti‑CFH–associated aHUS appears to occur more frequently in the Asian population (reported as 50–60% in Indian cohorts by Khandelwal et al.) compared to Caucasians (5–25%). Our findings represent an intermediate frequency between European and Asian populations, which is consistent with the mixed ethnic composition of the Kazakhstani cohort.

ABSTRACT: Background: Patients with type 2 diabetes mellitus (T2DM) on maintenance hemodialysis represent one of the highest-risk populations in nephrology practice. End-stage kidney disease (ESKD) and T2DM create a state of profound immunosuppression that predisposes patients to life-threatening infections.
Central venous catheters (CVCs), frequently required for hemodialysis access, are a well-recognized gateway for bacteremia. When bacteremia is complicated by coagulopathy, the clinical course can rapidly evolve toward disseminated intravascular coagulation (DIC).
Case Presentation: A 58-year-old woman was admitted with a 3-day history of nausea, vomiting, and body pain. Examination revealed anasarca, lower-extremity purpura, and petechial rash, with concern for coagulopathy. T2DM diagnosed in 2007 and ESKD on maintenance hemodialysis since October 2025 (three 4-hour sessions weekly). Vascular access was a right internal jugular CVC.
On admission, hemoglobin 62 g/L, RBC 2.02 ×10¹²/L, platelets 93 ×10⁹/L, WBC 11.18 ×10⁹/L, glucose 24.28 mmol/L, total protein 63 g/L, D-dimer 2,680 ng/mL, procalcitonin (PCT) 14.8 ng/mL, creatinine 405 μmol/L, urea 13.9 mmol/L, INR 1.46, Prothrombin Index 66%, fibrinogen 4.0 g/L, APTT 28.2 sec. Antibiotics had been started at home without improvement. In hospital, broad-spectrum therapy was escalated to a carbapenem plus a fluoroquinolone, with packed red blood cell and fresh frozen plasma transfusions. Hemoglobin increased to 87 g/L, PCT decreased to 1.78 ng/mL, and D-dimer to 1,178 ng/mL; thrombocytopenia persisted. After treatment, creatinine 592 μmol/L, urea 20.7 mmol/L, glucose 16.55 mmol/L, albumin 26 g/L, total protein 53 g/L, INR 1.39, Prothrombin Index 69%, fibrinogen 7.55 g/L, APTT 25.4 sec.
On days 5–6, livedo reticularis, worsening dyspnea, and persistent coagulopathy prompted chest MSCT. It revealed bilateral peribronchial foci with formed cavities, consistent with abscessing (necrotizing) pneumonia. The bilateral cavitary pattern suggested hematogenous dissemination, likely from the indwelling CVC. Patient transferred to the ICU with sepsis-associated DIC.
Linezolid 600 mg IV twice a day was added to provide coverage for possible methicillin-resistant Staphylococcus aureus and other gram-positive organisms. Following treatment escalation, hemoglobin reached 118 g/L, PCT decreased to 0.9 ng/mL, INR normalized to 0.92, and Prothrombin Index increased to 117%.
Conclusion: CVC-related bacteremia should be considered early in hemodialysis patients with unexplained coagulopathy or bilateral pulmonary infiltrates. Purpura followed by livedo reticularis may indicate DIC progression and should prompt urgent reassessment. Cavitation despite antibiotics signals treatment failure and need to reassess pathogen coverage, including biofilm-forming gram-positive organisms. T2DM and ESKD create a multiplicative immunocompromised state, requiring multimodal management and glycemic control.

ABSTRACT: Background: Immunoglobulin light-chain (AL) amyloidosis is a rare plasma cell dyscrasia caused by deposition of misfolded monoclonal light chains, with the kidneys and heart among the most frequently affected organs. Kidney biopsy is the diagnostic gold standard; however, in patients with severe hypoalbuminemia, coagulopathy, and high bleeding risk, an alternative tissue site may be required. We present a case of severe renal involvement in AL amyloidosis in which diagnosis was established despite an initially negative surrogate-site biopsy and contraindication to kidney biopsy.
Case Presentation: A 70-year-old woman initially presented with urticaria, fever, arthralgia, epistaxis, leukopenia, eosinophilia, and severe thrombocytopenia (13×10⁹/L). Bone marrow examination excluded hematological malignancy, and the thrombocytopenia subsequently resolved without specific therapy. Three months later, she developed generalized edema, hypotension, oliguria, dyspnea, pleural effusions, and ascites. Severe nephrotic syndrome was identified, with proteinuria up to 49.5 g/day, serum albumin 12–17.4 g/L, creatinine 170 μmol/L, and eGFR 28 mL/min/1.73 m². Urine immunofixation revealed lambda Bence–Jones protein (3.9 g/day), while serum immunofixation was negative. Extensive autoimmune testing was unrevealing.
AL amyloidosis was suspected because of nephrotic-range proteinuria and monoclonal lambda light-chain secretion. Rectal mucosal biopsy was Congo red-negative. Kidney biopsy was considered high-risk because of profound hypoalbuminemia, coagulation abnormalities, previous severe thrombocytopenia, and bleeding risk. Repeat bone marrow examination and flow cytometry subsequently demonstrated a minor monoclonal plasma-cell population without criteria for active multiple myeloma.
Bone marrow histology showed no amyloid deposits. However, abdominal subcutaneous fat pad biopsy demonstrated Congo red-positive deposits with characteristic apple-green birefringence under polarized light, confirming systemic AL amyloidosis. Cardiac involvement was supported by elevated NT-proBNP (4731 pg/mL) and concentric left ventricular hypertrophy with preserved ejection fraction (58%).
Treatment with daratumumab, bortezomib, cyclophosphamide, and corticosteroid (Dara-CBorD) was initiated. Following early treatment, renal and cardiac parameters improved: urinary protein became undetectable, renal function improved, and NT-proBNP decreased from 4731 to 1180 pg/mL, representing a 75% reduction.
Conclusion: This case demonstrates that AL amyloidosis should remain strongly suspected despite a negative surrogate-site biopsy when clinical and laboratory findings indicate monoclonal light-chain–mediated disease. When kidney biopsy carries prohibitive bleeding risk, abdominal fat pad biopsy can provide definitive minimally invasive histological confirmation. Close collaboration between nephrologists, hematologists, and pathologists enabled diagnosis without kidney biopsy and facilitated early clone-directed therapy, resulting in rapid renal and cardiac improvement.

ABSTRACT: Background: Treatment of rheumatoid arthritis (RA) in patients with end-stage chronic kidney disease (CKD stage 5D) on maintenance hemodialysis is challenging because of limited therapeutic options and increased drug toxicity. Stevens–Johnson syndrome (SJS) is a rare, life-threatening drug reaction that may cause severe systemic complications. This case is noteworthy for severe SJS complicated by sepsis and progressive coagulation abnormalities in a patient with seropositive RA, secondary renal amyloidosis, and CKD stage 5D.
Case Presentation: A 61-year-old woman with seropositive RA (anti-CCP+, RF+), late-stage disease, high activity (DAS28 5.3), secondary renal amyloidosis, and CKD stage 5D had received maintenance hemodialysis since December 2025. From January 21 to February 2, 2026, she was hospitalized due to RA exacerbation. Before therapy, hemoglobin was 106 g/L, erythrocytes 3.64 × 10¹²/L, leukocytes 21.57 × 10⁹/L, hematocrit 32.4%, neutrophils 17.99 × 10⁹/L, ESR 30 mm/h. Creatinine was 405 μmol/L, urea 14.1 mmol/L, total protein 63 g/L, potassium 4.05 mmol/L, glucose 6.77 mmol/L, ALT 18 U/L, AST 16 U/L. Hemostasis lab tests: PTI 79%, INR 1.24, fibrinogen 684 mg/dL, aPTT 26.0 s. Therapy included methotrexate 15 mg, colchicine 1.0 mg, infliximab 200 mg, denosumab 60 mg, and prednisolone 10 mg. Subsequently, severe stomatitis and generalized skin eruptions developed. On March 24, she was hospitalized; on March 25, was diagnosed drug-induced SJS. On March 27, she was transferred to the intensive care unit. At admission, hemoglobin was 67 g/L, leukocytes 1.68 × 10⁹/L, platelets 88 × 10⁹/L, creatinine 605.3 μmol/L, urea 21.99 mmol/L, and total protein 53.6 g/L. By March 29, platelets decreased to 12 × 10⁹/L, total protein to 36.3 g/L, and albumin to 17.6 g/L. Hemostasis lab tests deteriorated: PTI 79%-74%-59%, INR 1.24-1.31-1.60, and aPTT 26.0-26.9-77.3 s (January 21, March 24, and March 29, respectively). Sepsis developed, requiring antibacterial and antifungal therapy, platelet concentrates, fresh frozen plasma, and maintenance hemodialysis. Despite intensive treatment, her condition progressively deteriorated. Treatment was stopped at her family's request.
Conclusion: This case highlights the high risk of severe drug-related complications in patients with RA and CKD stage 5D on hemodialysis. Individualized antirheumatic therapy, careful assessment of drug toxicity and renal status, early recognition of severe mucocutaneous reactions, and prompt multidisciplinary management of SJS, sepsis, and coagulation abnormalities are essential to improve outcomes. Early withdrawal of suspected offending agents and close monitoring of hematological and hemostatic parameters are critical to prevent progression.

ABSTRACT: Background: Systemic pseudohypoaldosteronism type 1 (PHA1B; OMIM 264350) is a rare autosomal recessive disorder caused by biallelic pathogenic variants in SCNN1A, SCNN1B, or SCNN1G, which encode epithelial sodium channel (ENaC) subunits. Aldosterone resistance causes neonatal salt wasting, hyponatremia, severe hyperkalemia, metabolic acidosis, and potentially multiorgan dysfunction. Because the presentation mimics salt-wasting congenital adrenal hyperplasia (CAH) and sepsis, early differentiation is critical. We report a genetically confirmed, life-threatening neonatal case of PHA1B.
Case Presentation: A full-term girl (38 weeks + 2 days) was admitted on day 8 of life in critical condition with an 11% weight deficit, severe hypoxic-ischemic encephalopathy, subarachnoid and intraventricular hemorrhage with cerebral edema, bilateral pneumonia, and grade II respiratory failure. In the pediatric intensive care unit, respiratory failure progressed, requiring mechanical ventilation. Cardiac manifestations included bradyarrhythmia to 80 beats/min, ventricular ectopy, and complete right bundle branch block. Laboratory tests showed K+ 13.6 mmol/L, Na+ 110 mmol/L, pH 7.20, and base excess -17.4 mmol/L.
Salt-wasting CAH was initially suspected; however, hydrocortisone and fludrocortisone produced no clinical or biochemical response. Cortisol (27.53 µg/dL), 17-hydroxyprogesterone (1.2 ng/mL), and adrenocorticotropic hormone (5.0 pmol/L) were within reference ranges, while plasma aldosterone was markedly elevated at 10,355 pg/mL (reference range, 28-376 pg/mL), supporting aldosterone resistance. Whole-exome sequencing identified a homozygous pathogenic nonsense variant in SCNN1A (exon 10; c.1474C>T; p.Arg492Ter), confirming systemic PHA1.
Management included mechanical ventilation, intravenous calcium, intensive enteral and intravenous sodium chloride replacement, antibacterial therapy, and peritoneal dialysis for refractory life-threatening hyperkalemia. Potassium decreased to 8.1 mmol/L, sodium increased to 128-135 mmol/L, and the metabolic crisis initially improved. Despite treatment, the patient died from progressive multiorgan failure and neurological complications.
Conclusion: PHA1 should be considered in neonates with severe hyponatremia, hyperkalemia, and metabolic acidosis, particularly when CAH markers are normal and glucocorticoid/mineralocorticoid therapy is ineffective. In this setting, markedly elevated aldosterone supports mineralocorticoid resistance. Prompt sodium replacement and emergency management of hyperkalemia, including early dialysis when medical therapy fails, are essential. Molecular testing confirms the systemic form, informs prognosis, and enables family genetic counseling.

ABSTRACT: Systemic Lupus Erythematosus; Lupus Nephritis; Belimumab; Acute Kidney Injury; Renal Replacement Therapy

ABSTRACT: Background: WNK1 encodes a serine/threonine kinase involved in renal electrolyte transport, blood-pressure regulation, and peripheral nervous system function. Pathogenic variants are associated with pseudohypoaldosteronism type II (PHAII; Gordon syndrome) and hereditary sensory and autonomic neuropathy type IIA. We report an unusual phenotype involving severe familial hypertension, mild autonomic manifestations, and recurrent seizure-like episodes.
Case presentation: A 39-year-old man presented with severe arterial hypertension and seizure-like episodes occurring daily, sometimes twice per day. Episodes began with hand tremor, progressing to generalized muscle rigidity, transient loss of consciousness, and facial and hand swelling. Observed sustained rigidity predominantly affected the upper body and thighs, with relative sparing of the gastrocnemius muscles. Psychological stress and blood-pressure elevations were common triggers. Blood pressure was 160/100 mmHg approximately five minutes before one attack; symptoms were less pronounced at systolic pressures of 130–140 mmHg. His mother and maternal grandfather had severe hypertension, whereas siblings were unaffected.
Brain 3-T MRI showed no explanatory structural abnormalities. Twenty-four-hour video-EEG monitoring demonstrated no convincing epileptiform activity, prompting consideration of a non-epileptic mechanism. Whole-genome sequencing identified a heterozygous WNK1 frameshift variant, NM_018979.4.1748dup (p.Gln584AlafsTer27), classified as pathogenic by AIRS and Franklin, with sequencing evidence supported by manual IGV review.
Biochemical findings were atypical for classical PHAII. Potassium (4.0 mmol/L), sodium (143 mmol/L), magnesium (0.78 mmol/L), total calcium (2.16 mmol/L), phosphate (0.89 mmol/L), and creatinine (70.25 μmol/L) were within reference intervals. Venous pH (7.39) and bicarbonate (23.7 mmol/L) were normal. Mild hyperchloremia (109 mmol/L), decreased ionized calcium (1.05 mmol/L), and vitamin D deficiency (12.11 ng/mL) were present, with normal PTH (28.07 pg/mL) and aldosterone (131.06 pg/mL). Twenty-four-hour urinary sodium excretion was elevated (232 mmol/day). Treatment comprised hydrochlorothiazide 12.5 mg once daily, calcium citrate 1,000 mg, and magnesium citrate 400 mg. At the two-month follow-up, the patient reported only one stress-triggered episode during the preceding month, compared with daily episodes before treatment.
Conclusion: This presentation raises the possibility of an atypical WNK1-associated phenotype, although the variant’s contribution requires further clarification. The absence of hyperkalemia and metabolic acidosis differs from classical Gordon syndrome, while ionized hypocalcemia may contribute to neuromuscular hyperexcitability. The reported reduction in episode frequency suggests clinical improvement following treatment. Long-term follow-up, including blood-pressure and electrolyte monitoring and further characterization of paroxysmal events, is required to evaluate sustained response and clarify the underlying mechanism.

ABSTRACT: Introduction: Catheter-related bloodstream infections remain a major cause of morbidity in patients receiving maintenance dialysis. Management becomes particularly challenging in kidney transplant recipients with failed allografts because of persistent immunosuppression, severe systemic inflammation, and a high risk of thrombotic complications. Hemoadsorption has emerged as a promising adjunctive extracorporeal therapy for sepsis by reducing circulating inflammatory mediators. We present a case of successful integration of HA-330 hemoadsorption into the treatment of severe catheter-related sepsis in a patient with end-stage kidney disease.
Case Presentation: A 28-year-old woman with kidney failure secondary to glomerular disease underwent living-donor kidney transplantation in 2014. Following allograft rejection in 2024, she resumed maintenance hemodialysis. She was admitted with fever, weakness, chest pain, and signs of systemic infection. Blood cultures obtained from peripheral blood and the dialysis catheter grew Staphylococcus haemolyticus. Diagnostic evaluation revealed catheter-related sepsis, a fixed right atrial thrombus, bilateral pneumonia, severe anemia, and end-stage kidney disease requiring renal replacement therapy.
The patient received broad-spectrum antimicrobial treatment, anticoagulation, blood transfusions, and extracorporeal support. Two sessions of HA-330 hemoadsorption were performed in combination with hemodiafiltration
A marked reduction in inflammatory biomarkers was observed during treatment. C-reactive protein decreased from 335.1 to 28.7 mg/L (91% reduction), procalcitonin from 98.2 to 1.48 ng/mL (98.5% reduction). Leukocyte count decreased from 18.4×10⁹/L to 8.6×10⁹/L (Table №1). Follow-up echocardiography demonstrated a reduction of the right atrial thrombus from 30×14 mm to 16×11 mm. Repeat blood cultures were sterile, and the patient showed significant clinical improvement with resolution of systemic inflammatory manifestations.
The patient was discharged in stable condition for continuation of maintenance hemodialysis.
Conclusion: This case demonstrates the potential value of HA-330 hemoadsorption as an adjunct to standard therapy in severe catheter-related sepsis among dialysis patients with failed kidney transplants. Combined hemoadsorption and hemodiafiltration may contribute to clinical stabilization and recovery in complex septic conditions, warranting further investigation in larger patient cohorts.

ABSTRACT: Background: The early onset of chronic kidney disease often lacks symptoms, leading to delayed diagnosis and treatment. Regular laboratory testing can detect the disease before it begins, which helps clinicians determine the appropriate treatment for patients. This review sought to assess how ongoing tracking of estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) contributes to understanding the progression of chronic kidney disease (CKD) and determining the risk levels for patients.
Methods: A thorough review of evidence from international clinical practice guidelines, systematic reviews, meta-analyses, and extensive observational cohort studies was conducted. Special attention was given to how eGFR and UACR changed over time and how these changes were linked to the development of advanced CKD, kidney failure, cardiovascular issues, and death. The most recent recommendations from the 2024 KDIGO CKD guideline were included.
Results: Evidence shows that regularly checking eGFR and UACR is essential for effectively monitoring chronic kidney disease. In a group of 91,319 people, a reduction of 30% or more in estimated glomerular filtration rate (eGFR) was linked to a significantly higher risk of developing advanced chronic kidney disease, with a hazard ratio of 7.53 (95% CI, 6.70–8.45).Similarly, an increase of 30% or more in urinary albumin-to-creatinine ratio (UACR) was associated with a hazard ratio of 1.78 (95% CI, 1.59–1.98). At the same time, when both UACR increased and eGFR decreased, the hazard ratio was 15.15 (95% CI, 12.43–18.46) compared to when these values remained stable. KDIGO suggests that patients with chronic kidney disease should have their glomerular filtration rate and albuminuria checked at least once every year.For those at greater risk, more regular check-ups are advised, especially if the results could impact treatment choices. Even though these recommendations were provided, a systematic review of 59 studies that included 3,036,41 patients showed significant shortcomings in standard monitoring practices: the estimated glomerular filtration rate (eGFR) was checked in 81.3% of patients, but testing for albuminuria was done in just 47.4%.
Conclusion: Regular laboratory testing, especially repeated checks of eGFR and UACR, is important for early identification of CKD progression and for assessing individual risk levels. The continued limited use of albuminuria testing highlights a significant gap in care that aligns with established guidelines. Integrating structured laboratory surveillance into routine clinical practice may facilitate timely therapeutic optimization and contribute to delaying kidney failure and reducing cardiorenal complications.

ABSTRACT: Background: IgA nephropathy (IgAN) is an immune complex–mediated glomerular disease characterized by marked clinical and histopathological heterogeneity and a variable risk of progression. The coexistence of IgAN with features of TMA poses a particular diagnostic challenge, as a microangiopathic phenotype may emerge in the setting of severe glomerular injury, endothelial dysfunction, complement activation, and additional external triggers. The clinical consequences of such an interaction may be particularly significant in patients with a solitary functioning kidney.
Objective: To characterize the clinicopathological features of severe IgAN presenting with a clinical–hematological TMA phenotype in a young woman with a solitary functioning kidney and to explore the potential contribution of local complement activation and recurrent drug exposures as a putative “second hit” to endothelial injury and rapid deterioration of kidney function.
Case presentation: A 22-year-old woman had a solitary functioning right kidney following neonatal left nephrectomy. Kidney function remained preserved for years; however, persistent microscopic hematuria had been documented since 2022, retrospectively suggesting clinically silent glomerular disease. Between 2022 and 2026, she had substantial cumulative exposure to medications and supplements, including recurrent antiviral, antibacterial, and anti-inflammatory therapies, acne-directed treatments, vitamin/mineral preparations, and dietary supplements. These exposures preceded clinical deterioration and were considered potential external triggers in a susceptible renal background rather than evidence of definite drug-induced TMA. In June–July 2026, she developed recurrent massive edema followed by rapidly progressive kidney dysfunction with azotemia, hyperkalemia, active urinary sediment, and proteinuria, ultimately requiring hemodialysis. During hospitalization, microangiopathic hemolytic anemia, severe thrombocytopenia, schistocytosis, reticulocytosis, and elevated lactate dehydrogenase established a clinical–hematological TMA phenotype (Table 1). Preserved ADAMTS13 activity argued against immune-mediated thrombotic thrombocytopenic purpura (TTP), while autoimmune, anti-GBM, antiphospholipid, and infectious investigations were unrevealing. Given rapidly progressive dysfunction of the solitary kidney and an active nephritic syndrome, methylprednisolone and cyclophosphamide were administered before histopathological confirmation. Two sessions of therapeutic plasma exchange were subsequently performed in the setting of the pronounced TMA phenotype. Hematological parameters improved, whereas kidney function did not recover and dialysis dependence persisted. Kidney biopsy demonstrated advanced IgAN with severe chronic kidney damage (Oxford Classification M0E1S1T2C1) and intense mesangial IgA/C3 codeposition despite normal circulating C3. No definitive histopathological evidence of active TMA was identified.
Conclusion: This case demonstrates previously oligosymptomatic IgAN presenting with rapidly progressive kidney dysfunction, dialysis-dependent kidney failure, and a compelling clinical–hematological TMA phenotype. Preserved ADAMTS13 activity and an unrevealing investigation for major secondary causes supported a microangiopathic process distinct from immune-mediated TTP. Marked mesangial IgA/C3 codeposition despite normal circulating C3 raises the possibility that local complement activation may have amplified glomerular inflammation and endothelial injury. However, these findings are insufficient to establish complement-mediated TMA. The absence of active TMA lesions in a biopsy obtained later in the disease course likewise does not establish renal TMA, but cannot exclude a preceding transient or partially resolved microangiopathic process.  A distinctive feature was the substantial cumulative medication and supplement exposure preceding clinical deterioration. In the setting of pre-existing IgAN and a solitary functioning kidney, recurrent drug exposures may have constituted an external “second hit,” potentially promoting immune activation, endothelial stress, and clinical decompensation. The absence of a clear temporal relationship with a single agent, however, precludes attribution to definite drug-induced TMA. Collectively, this case supports a multifactorial, hypothesis-generating model: pre-existing IgAN in a solitary kidney → recurrent external/drug exposures as a potential “second hit” → possible local complement activation and endothelial injury → clinical–hematological TMA phenotype → rapid kidney function deterioration. This proposed sequence should not be interpreted as evidence of direct causality.
Clinical lesson: in patients with IgAN and rapidly deteriorating kidney function, particularly when anemia and thrombocytopenia develop, targeted evaluation for TMA and potential secondary triggers should be considered even when circulating C3 levels are normal.

ABSTRACT: Background: Fabry disease is an X-linked lysosomal storage disorder caused by variants in the GLA gene, leading to progressive multisystem involvement of the kidneys, heart, and central nervous system. Marked phenotypic variability among female carriers is attributed to random X-chromosome inactivation, but pronounced discordance in organ predominance across multiple branches of a single family sharing an identical genotype is rarely documented. We describe such a family carrying the GLA variant c.137A>G (p.His46Arg).
Case presentation: The proband, a 47-year-old woman, presented with recurrent ischemic strokes (four episodes since 2004) and a spinal cord infarction, initially misdiagnosed as multiple sclerosis for over a decade until molecular testing in 2018 confirmed Fabry disease (α-galactosidase A activity 3.4; lyso-Gb3 5.4). She developed a fixed pyramidal tetrasyndrome with neuropathic pain, started enzyme replacement therapy, and recently experienced a sixth cerebrovascular event accompanied by new-onset oliguria suggestive of emerging renal involvement. Her mother had died of renal failure at age 31 (not genetically confirmed). Her 26-year-old daughter, despite abnormal biochemistry (enzyme 0.3; lyso-Gb3 46.2), remains largely asymptomatic, while her 16-year-old son does not carry the variant. The proband's maternal aunt (73 years), a confirmed carrier, required pacemaker implantation for cardiac conduction impairment; her three sons displayed a strikingly different, predominantly renal phenotype: one died young of acute kidney injury, one has required hemodialysis since 2013 and shows lacunar cerebral infarcts on MRI with left ventricular hypertrophy on ECG, and one has nephrotic syndrome but declined further evaluation. A second maternal aunt, also genetically confirmed, remains asymptomatic; her two mutation-positive sons have refused testing and treatment. All affected relatives share the identical GLA variant.
Conclusion: This three-generation family illustrates striking intrafamilial phenotypic heterogeneity - cerebrovascular, cardiac, and renal - despite a shared GLA genotype, underscoring the limited predictive value of genotype-phenotype correlation in Fabry disease. The decade-long misdiagnosis as multiple sclerosis highlights the need to consider Fabry disease in unexplained recurrent stroke. Cascade family screening should be offered to all at-risk relatives regardless of sex, age, or symptom status, since disease severity and target-organ involvement in one member do not predict outcomes in others.

ABSTRACT: Background: Renal involvement may be the first and only manifestation of systemic autoimmune disease, including ANCA-associated vasculitis (AAV) and systemic lupus erythematosus (SLE). In some cases the diagnosis is established only at stage 5 chronic kidney disease (CKD), once renal replacement therapy (RRT) becomes unavoidable, substantially worsening prognosis. Early recognition of autoimmune etiology is particularly important in patients urgently starting maintenance hemodialysis, since timely immunosuppressive therapy may, in selected cases, restore renal function and allow RRT discontinuation. This study aimed to characterize detection of autoimmune etiology of renal injury among patients with newly diagnosed stage 5 CKD urgently initiating maintenance hemodialysis.
Methods: We conducted a retrospective observational study of patients admitted to BBNURA LLP (Astana, Kazakhstan) with newly diagnosed stage 5 CKD requiring urgent hemodialysis initiation. Urgent admissions accounted for 98 of 330 patients in 2023, 89 of 363 in 2024, 70 of 424 in 2025, and 85 from January through September 2026 (342 total). From this cohort, 70 patients with clinical evidence of multisystem involvement (≥2 extrarenal systems affected, or unexplained systemic symptoms at admission) were selected for diagnostic work-up, assessing the ENT organs, lungs, skin, nervous system, eyes, gastrointestinal tract, musculoskeletal system, and cardiovascular system. Immunological markers (ANCA, anti-dsDNA antibodies, complement components) were evaluated, and diagnoses were confirmed using clinical, laboratory, and, where indicated, histopathological data.
Results: Systemic autoimmune markers were identified in 17 of 342 patients (5.0%) overall, and in 17 of 70 (24.3%) among those selected for screening (10 women, 7 men). AAV was diagnosed in 11 patients, confirmed by renal biopsy in 2 cases. SLE with renal, cutaneous, articular, and vascular involvement was diagnosed in 6 patients. Within the first 3 months, 3 patients died from complications of autoimmune disease, and 14 remained on maintenance hemodialysis. One patient with biopsy-confirmed AAV achieved complete remission, with recovery of kidney function and discontinuation of hemodialysis, following immunosuppressive therapy.
Conclusion: Autoimmune etiology of renal injury is clinically significant among patients with newly diagnosed stage 5 CKD urgently initiating hemodialysis, and targeted clinical screening substantially increased detection yield (5.0% overall vs. 24.3% among selected patients), predominantly identifying AAV and SLE. These findings support active screening for systemic autoimmune disease in newly diagnosed end-stage renal disease and warrant prospective, unselected screening to determine true population prevalence. Timely diagnosis and early therapy may restore renal function, reduce reliance on long-term RRT, and decrease mortality associated with disease complications.

ABSTRACT: Background & Objective: Acute tubulointerstitial nephritis (ATIN) is a potentially reversible cause of acute kidney injury (AKI). However, when presenting with rapid loss of renal function and fever of unknown origin, ATIN frequently mimics rapidly progressive glomerulonephritis (RPGN). In Kazakhstan, patients presenting with severe renal dysfunction (eGFR <10 mL/min/1.73m²) are frequently denied or delayed from undergoing diagnostic kidney biopsy due to institutional safety concerns, procedural hesitation, and a regional deficit in subspecialized nephropathology services. This abstract demonstrates the critical diagnostic value of renal biopsy in advanced AKI with clinicopathological dissociation and highlights systemic diagnostic barriers in Central Asia.
Case Presentation: A 41-year-old female with no prior history of kidney disease presented in June 2026 with an unexplained persistent fever (37.0–38.0°C). Despite empirical antibacterial therapy ('ex juvantibus'), her fever persisted. Over 8 weeks, serial laboratory testing revealed a dramatic, rapidly progressive decline in kidney function (Table 1): serum creatinine escalated from a baseline of 70 µmol/L (eGFR 96 mL/min/1.73m²) in June 2026 to 130 µmol/L (09.07.2026), 381 µmol/L (31.07.2026), 441 µmol/L (06.08.2026), and peaked at 524 µmol/L (20.08.2026, eGFR 8.6 mL/min/1.73m²). Remarkably, diuresis remained fully preserved, and urinary abnormalities were strikingly mild (proteinuria 0.13–0.60 g/L, absence of active urinary sediment/hematuria). Immunological evaluation showed positive immunoblot reactivity to SS-B, RP11, and Mi-2α; however, classic systemic connective tissue disease criteria were not met, and ANCA, anti-GBM, and C3/C4 levels were unremarkable. Due to severe renal failure (eGFR <10 mL/min), local clinical evaluation in Kazakhstan hesitated to perform a kidney biopsy, categorizing the condition as RPGN vs. ESRD (CKD Stage 5). The patient subsequently traveled to Turkiye (Istanbul) for an urgent ultrasound-guided renal biopsy on August 20, 2026. Light microscopy (22 glomeruli) revealed intact glomeruli without crescents or necrosis, but severe active interstitial inflammation (mononuclear and neutrophilic infiltrate, tubulitis, leukocyte casts) and acute tubular injury, alongside early chronic tubulointerstitial changes. Direct immunofluorescence was negative. Immediate high-dose corticosteroid therapy (IV Methylprednisolone pulse 80 mg followed by oral Prednisolone 32 mg/day with gradual taper) was initiated. Renal function responded dramatically: serum creatinine dropped from 524 µmol/L to 294.1 µmol/L within 7 days (27.08.2026), 218.9 µmol/L (02.09.2026), and reached 148.2 µmol/L (10.09.2026, eGFR 39.0 mL/min/1.73m²), with complete normalization of inflammatory markers (CRP 1.1 mg/L). Hemodialysis was completely avoided.
Conclusions & Policy Implications: Discrepancy between profound renal failure and mild urinary sediment (clinicopathological dissociation) strongly points toward acute tubulointerstitial disease rather than RPGN. Severe reduction in eGFR should not be considered an absolute contraindication to diagnostic kidney biopsy. Without biopsy, this patient would likely have been mislabeled as end-stage renal disease (ESRD) and initiated on lifelong maintenance dialysis. There is an urgent health policy imperative in Kazakhstan to modernize nephrobiopsy protocols, invest in state-of-the-art biopsy technology, and establish dedicated nephropathology training to prevent irreversible progression of treatable renal diseases.

ABSTRACT: Background: Acute kidney injury (AKI) is a major contributor to morbidity and mortality in critically ill children, and rhabdomyolysis is an important yet underrecognized trigger of severe AKI after major trauma. Continuous veno-venous hemodiafiltration (CVVHDF) allows simultaneous correction of fluid, electrolyte and acid–base disturbances together with clearance of myoglobin and inflammatory mediators in hemodynamically unstable patients. Data on adequately dosed, prolonged CVVHDF in adolescents with combined trauma-induced rhabdomyolysis and septic acute kidney injury remain limited. We report a case of severe RIFLE-Failure AKI in a polytrauma adolescent successfully managed with 15 days of continuous renal replacement therapy.
Case Presentation: A 13-year-old boy (weight 85–90 kg) was admitted to the pediatric intensive care unit after severe polytrauma sustained in a road traffic accident and underwent intramedullary osteosynthesis of long-bone fractures. On postoperative day 3 he developed a hardware-associated abscess with systemic inflammatory response and sepsis, complicated by traumatic rhabdomyolysis and severe AKI, RIFLE-Failure stage: anuria, metabolic acidosis, hyperkalemia and rising azotemia. Baseline values were creatinine 567 µmol/L, potassium 6.16 mmol/L, pH 7.28, AST 7001 U/L and ALT 5591 U/L.
CVVHDF was initiated on postoperative day 3 via an internal jugular venous catheter, using a MultiFiltrate® platform (Fresenius Medical Care): blood flow 200 mL/min, dialysate and replacement fluid each 1500 mL/h, ultrafiltration 100 mL/h, corresponding to an effluent dose of approximately 34–36 mL/kg/h. Anticoagulation was maintained with unfractionated heparin 1250 U/h under laboratory monitoring. Therapy continued for 15 days without catheter- or circuit-related complications. Progressive correction of acidosis, hyperkalemia, azotemia and cytolysis markers was achieved (Table 1), and diuresis recovered to 1150 mL/day by day 15, allowing discontinuation of extracorporeal support; the patient was transferred from the intensive care unit to a specialized ward.
Conclusion: This case demonstrates that adequately dosed, prolonged CVVHDF (≈35 mL/kg/h) can safely and effectively reverse life-threatening metabolic derangements and achieve complete renal recovery in an adolescent with trauma-induced rhabdomyolysis and septic RIFLE-Failure acute kidney injury. Early initiation on postoperative day 3, uncomplicated vascular access and close monitoring supported an uneventful 15-day course. The case underscores the role of timely, adequately dosed continuous renal replacement therapy as a bridge to renal recovery in pediatric trauma patients with combined rhabdomyolysis and sepsis-associated acute kidney injury.

ABSTRACT: Background: Urolithiasis presenting in early childhood requires evaluation for hereditary and metabolic causes, including primary hyperoxaluria. Particular attention is warranted in children with recurrent bilateral nephrolithiasis and a predominantly oxalate stone composition. We report a case of hyperoxaluria in a young child in whom evaluation for primary hyperoxaluria did not confirm an inherited disorder, while further metabolic assessment revealed severe hypomagnesemia.
Case Presentation: A 2-year-10-month-old boy with no family history of urolithiasis first developed nephrolithiasis in June 2025, at approximately 18 months of age. Computed tomography demonstrated bilateral renal calculi and pyelectasis. In July 2025, he underwent left ureteral stent placement, right-sided lumbotomy, and pyelolithotomy. Assessment of kidney function showed an estimated glomerular filtration rate (eGFR) of 75.8 mL/min/1.73 m². In April 2026, nephrolithotomy, left-sided lumbotomy, and pyelolithotomy were performed. Infrared spectroscopy of the extracted stone demonstrated 65% oxalates and 35% phosphates. Metabolic evaluation also confirmed hyperoxaluria.
Given the early age at onset, bilateral stone formation, reduced kidney filtration, and hyperoxaluria, primary hyperoxaluria was considered and molecular genetic testing was performed. Whole-exome sequencing by next-generation sequencing (NGS) detected no pathogenic variants, likely pathogenic variants, or variants of uncertain clinical significance meeting the search criteria for hereditary kidney or metabolic disorders.
In September 2026, severe hypomagnesemia was identified for the first time, with a serum magnesium concentration of 0.18 mmol/L. In view of this finding and the negative genetic evaluation, the hyperoxaluria was considered secondary and associated with magnesium deficiency. Kidney function subsequently improved, with a serum creatinine level of 34.33 µmol/L and an estimated GFR of 92.5 mL/min/1.73 m². Follow-up imaging with ultrasonography and computed tomography demonstrated reduced size of the right kidney and no calculi in the kidneys or urinary collecting system. Management included optimization of fluid intake, dietary recommendations, and magnesium supplementation.
Conclusion: Early-onset oxalate nephrolithiasis in children warrants investigation for primary hereditary causes. A negative molecular genetic result does not eliminate the need for an extended metabolic evaluation. Magnesium deficiency may alter glyoxylate metabolism in the liver and kidneys, promoting accumulation of glyoxylate, a precursor of oxalate, and may also increase intestinal oxalate absorption, thereby increasing oxalate load. This case highlights the importance of assessing not only genetic causes of pediatric hyperoxaluria but also performing a comprehensive metabolic evaluation, including assessment of magnesium status.

ABSTRACT: Background: Intradialytic hypotension (IDH) is one of the most common complications of hemodialysis and may manifest as weakness, dizziness, syncope, and poor tolerance of treatment. The risk is increased in elderly patients and those with diabetes mellitus or cardiovascular disease. A key mechanism is an imbalance between ultrafiltration rate and plasma refilling of the intravascular compartment. We present a case of recurrent IDH in a high-risk patient with stage 5 chronic kidney disease (CKD), type 2 diabetes mellitus, and hypertensive heart and kidney disease.Case Presentation
A female patient, born in 1952, had stage 5 CKD (N18.5), extracorporeal dialysis (Z49.1), anemia in chronic disease (D63.8), type 2 diabetes mellitus (E11), and hypertensive heart and kidney disease (I13). Diabetes mellitus had been diagnosed in 2010, with longstanding arterial hypertension.
On December 15, 2022, following a fall and osteosynthesis of the right femur, serum creatinine was 481 μmol/L and blood urea 29.1 mmol/L. Repeat testing showed creatinine 505 μmol/L and urea 32 mmol/L. A double-lumen catheter was placed and renal replacement therapy initiated. On February 27, 2023, an arteriovenous fistula was created. The patient subsequently continued maintenance hemodialysis at Fresenius Medical Care Kazakhstan LLP, Talgar.
Baseline blood pressure was 160/90 mmHg. During every hemodialysis session, approximately 30 minutes after initiation, blood pressure decreased to 80/50 mmHg without adjustment of dialysis parameters.
Management included individualized dialysis prescription. Dry weight was assessed by bioimpedance spectroscopy (BCM), with adjustment of ultrafiltration volume and rate. Dialysate temperature was reduced to 35.5–36.5°C. Dialysate sodium, potassium, and calcium concentrations were 138, 3, and 1.5 mmol/L, respectively. Ultrafiltration profiling was used when fluid overload exceeded 3% of body weight. During hypotensive episodes, the patient was placed in the Trendelenburg position with elevated lower extremities, and ultrafiltration and dialysis parameters were adjusted. AF81 dialysate was used.
Following optimization, intradialytic blood pressure remained approximately 100/60–120/70 mmHg without significant hypotensive episodes. Post-dialysis blood pressure was 130/80 mmHg. Treatment tolerance improved, with clinical observations indicating improved quality of life.
Conclusion: Individualized hemodialysis prescription, including accurate dry-weight assessment, optimized ultrafiltration, reduced dialysate temperature, appropriate dialysate composition, ultrafiltration profiling, timely Trendelenburg positioning, and regular blood pressure monitoring, contributed to improved hemodynamic stability and reduced IDH severity in this high-risk patient.

ABSTRACT: Background: Chronic kidney disease (CKD) is characterized by progressive loss of kidney function associated with intraglomerular hypertension, hyperfiltration, podocyte injury, tubular damage, and tubulointerstitial fibrosis. Sodium–glucose cotransporter 2 (SGLT2) inhibitors have demonstrated nephroprotective effects beyond glycemic control. This study aimed to quantitatively assess the effect of SGLT2 inhibitors on CKD progression and to summarize the morphological mechanisms underlying their nephroprotective effects.
Methods: A systematic review and quantitative meta-analysis of randomized controlled trials (RCTs) evaluating SGLT2 inhibitors and renal outcomes was performed. The primary quantitative analysis included the CREDENCE, DAPA-CKD, and EMPA-KIDNEY trials. Pooled hazard ratios (HRs) with 95% confidence intervals (CIs) were calculated using a random-effects model. Statistical heterogeneity was assessed using the I² statistic and Cochran’s Q test. Published evidence on morphological and structural renal changes associated with SGLT2 inhibition was additionally analyzed.
Results: SGLT2 inhibitors reduced the risk of the primary renal composite endpoint in CREDENCE (HR 0.70; 95% CI 0.59–0.82), DAPA-CKD (HR 0.61; 95% CI 0.51–0.72), and EMPA-KIDNEY (HR 0.72; 95% CI 0.64–0.82). The pooled analysis demonstrated a significant reduction in the risk of CKD progression (HR 0.68; 95% CI 0.62–0.75), corresponding to an approximately 32% relative risk reduction. Heterogeneity between studies was low (I²=17.5%). Morphological evidence demonstrated attenuation of glomerular hyperfiltration, preservation of podocytes and the glomerular filtration barrier, reduction of tubular injury, and attenuation of tubulointerstitial fibrosis.
Conclusion: SGLT2 inhibitors are associated with a significant reduction in the risk of CKD progression. Their nephroprotective effects appear to involve complementary hemodynamic, glomerular, tubular, and tubulointerstitial mechanisms. The consistency between clinical trial findings and morphological evidence supports a multifactorial basis for SGLT2 inhibitor-mediated nephroprotection.