Keyword: Renal

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: 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: 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: 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: 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.

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

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: 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: Familial Mediterranean Fever (FMF) is an autosomal recessive autoinflammatory disorder caused by mutations in the MEFV gene. It is most common among populations from the Eastern Mediterranean region, including Turks, Armenians, Arabs, and Sephardic Jews. One of the most serious complications of FMF is AA amyloidosis, which develops as a result of chronic inflammation and the deposition of serum amyloid A protein. AA amyloidosis frequently affects the kidneys, leading to nephrotic syndrome and chronic kidney disease.
We report a case of a 17-year-old Turkish male presenting with recurrent episodes of fever, joint pain, periodic skin rashes, and intermittent hypertension. Laboratory evaluation revealed nephrotic-range proteinuria, hypoalbuminemia, low serum IgG, and elevated inflammatory markers. Renal biopsy confirmed AA amyloidosis with moderate interstitial lymphocytic infiltration and mild fibrosis. Genetic testing identified a homozygous pathogenic variant in exon 10 of the MEFV gene (p.Met694Val), previously reported and strongly associated with FMF.
This case highlights the rarity of such presentations and emphasizes the importance of early diagnosis of FMF complicated by AA amyloidosis. The patient remains on colchicine therapy with careful monitoring for potential complications; corticosteroids were gradually tapered following confirmation of amyloidosis, with supportive and symptomatic management continued.
 

ABSTRACT: A 41-year old female patient who underwent kidney transplantation as an outcome of chronic glomerulonephritis came to the hospital with the signs of acute upper respiratory tract infection. As the patient further developed oliguria, peripheral edema, fever, and an increased BP, she was further relocated to the University Medical Center (UMC). Upon admission to UMC, signs of septic shock were detected, and acute transplant rejection was suspected, to exclude which kidney biopsy was performed and stage 3 chronic kidney disease (CKD) in allograft kidney was detected. Antibacterial treatment as well as pulse therapy were performed as patient had septic shock and tubulointerstitial nephritis (TIN).

ABSTRACT: A 46-year old male was admitted to the University Medical Center (UMC) hospital with the following symptoms of anuria, abdominal fullness, hypotension, exertional dyspnea, and peripheral edema. The purpose of his visit was the insertion of a peritoneal dialysis catheter. He had chronic kidney disease stage 5 as a consequence of diabetic nephropathy, liver cirrhosis due to hepatitis C infection, and HIV. His disease course was further complicated by the presence of a urinary tract infection. As a result of his multiple comorbidities, he underwent a complex treatment regimen which included renal replacement therapy with ultrafiltration, blood transfusions for his anemia, platelet transfusions for his thrombocytopenia, albumin infusion for his hypoalbuminemia, and antibiotic treatment for his concurrent infection. Additionally, he received diuretic treatment for his hypervolemia and anti-hypertensives to control his blood pressure. After peritoneal dialysis (PD) insertion, the patient successfully underwent PD and was discharged home.