Keyword: Kidney

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

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: 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: 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: 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: 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: 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: 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: 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: Rapid identification of patients at risk of contrast-associated acute kidney injury (AKI) is essential in acute settings such as acute myocardial infarction and ischemic stroke. Point-of-care (POC) creatinine testing provides immediate assessment of kidney function; however, its reliability for clinical risk stratification relative to standard laboratory measurements remains uncertain. This study evaluated the agreement between laboratory- and POC creatinine-based risk stratification and their association with subsequent AKI after contrast angiography.
Methods: In this prospective observational study, 295 adults undergoing contrast-enhanced angiography for acute myocardial infarction or acute ischemic stroke were enrolled. Serum creatinine was measured using both standard laboratory methods and a POC device before contrast administration. Estimated glomerular filtration rate (eGFR) was calculated using the CKD-EPI 2021 equation, and predicted risk of post-contrast AKI was assessed using the Mehran risk score. AKI was defined according to KDIGO criteria (≥1.5-fold increase from baseline or ≥26.5 µmol/L increase within 7 days). Agreement between laboratory- and POC-derived risk categories was evaluated using weighted Cohen’s kappa.
Results: The median age was 64 years (interquartile range 57–70), and 66.8% of participants were male. Based on laboratory measurements obtained in the hospital central laboratory, categories were low in 8.8%, moderate in 37.3%, high in 25.4%, and very high in 28.5% of patients. Among patients with available follow-up creatinine measurements (n = 127), CA-AKI occurred in 11.0% (14/127). Agreement between laboratory- and POC-based risk classifications was near-perfect (κ = 0.97, 95% CI 0.95–0.98). The correlation between laboratory and POC creatinine values was moderate (r = 0.63, p < 0.001).
Conclusion: POC creatinine–based Mehran risk stratification shows excellent diagnostic agreement with laboratory-based assessment for identifying patients at risk of post-contrast AKI. POC testing may facilitate rapid bedside risk assessment in patients undergoing angiography for acute myocardial infarction or ischemic stroke without compromising risk classification reliability.

ABSTRACT: Background: To evaluate diabetic kidney disease (DKD) knowledge, attitudes, and practices (KAP) among adults with type 2 diabetes (T2D) in southern Kyrgyzstan.
Methods: A cross-sectional survey assessed DKD KAP among adults with T2D recruited from public healthcare facilities in Osh, Kyrgyzstan. We used a structured questionnaire guided by the Health Belief Model and the Health Locus of Control. We used multiple linear regression models to examine factors associated with KAP scores.
Results: A total of 207 adults participated (mean age 61.0 ± 10.7 years; 61.4% female). Although 91.3% identified healthcare workers as their most trusted information source, only 49.3% reported receiving DKD-related information from a healthcare provider. Only 13.5% recognized that early kidney damage does not cause pain. Despite generally positive attitudes towards kidney protective behaviors, 72.9% of participants reported low personal control over their health outcomes. In adjusted models, prior receipt of provider DKD information was the sole factor consistently associated with higher knowledge (β = 1.25, 95% CI 0.43–2.08, p = 0.003), attitudes (β = 3.11, 95% CI 1.61–4.61, p < 0.001), and practices (β = 3.99, 95% CI 2.26–5.71, p < 0.001).
Conclusion: Adults with T2D in southern Kyrgyzstan experience significant knowledge gaps and misconceptions regarding kidney protection, despite high trust and willingness to learn from healthcare providers. Prior provider-delivered information was associated with better practices, highlighting the need for structured DKD counseling that explicitly addresses misconceptions and aligns health messages with local beliefs to strengthen self-efficacy.

ABSTRACT: Background: The purpose of this study is to evaluate serum creatinine as a marker of estimated glomerular filtration rate (eGFR) in excessive alcohol use people, and to determine correlation between total kidney volume (TKV) and other relevant factors.  
Methods: In this study, 95 people were examined 2025. We measured serum creatinine based GFR using the MDRD formula. Biochemical analysis and serum creatinine were evaluated using a fully automatic analyzer. TKV was determined by ellipsoid method using 2D sonographic transducer.
Result: The mean subject age was 52±10, BMI 25±4 and male female ratio was 4:1. Mean arterial pressure was 108±14 mmHg, eGFR 90±19 ml/min/1.73m².  Age, body mass index (BMI) and mean arterial pressure (MAP) were inversely correlated with eGFR (P<0.01) and no difference between male and female recipients. There is no statistically significant correlation between TKV and eGFR. BMI and arterial pressure was correlated with TKV (P<0.01). Mean eGFR and TKV was calculated into 4 groups of 10-year intervals, that eGFR was decreased significantly with age groups.  
Conclusion: According to our research, one of the optimal methods for assessing kidney function is the creatinine-based calculation method, and long-term excessive alcohol consumption is a risk factor for chronic kidney disease (CKD).

ABSTRACT: A 68-year-old asian man was admitted with decompensated chronic heart failure with a left ventricular ejection fraction of 20%, permanent arterial fibrillation, and chronic kidney disease. Sacubitril/Valsartan (Uperio) was prescribed. This review details the initiation of sacubitril/valsartan in an Asian patient with heart failure with low ejection fraction (20%) and comorbidities. The paper highlights the pharmacodynamic and pharmacokinetic profiles of Sacubitril/Valsartan. The focus is on a thorough review of clinical trials to assess the therapeutic efficacy and potential adverse events associated with Sacubitril/Valsartan administration in this specific patient group.
Since 2014, sacubitril/valsartan has been widely prescribed for heart failure. Nevertheless, the coexistence of additional diseases such as arthritis, renal insufficiency, diabetes mellitus, or chronic lung disease with the heart failure syndrome should logically require a modification of treatment, outcome assessment, or follow-up care.

ABSTRACT: Background: Chronic kidney disease (CKD) is an increasing global health concern and a major contributor to cardiovascular morbidity and mortality. Although its global prevalence is estimated at about 13%, data from Central Asia are limited.
Objective: To assess the prevalence, structure, and key determinants of CKD among adults in the Kyrgyz Republic.
Methods: A population-based cross-sectional study was conducted among adults aged ≥18 years across different regions. CKD was defined according to Kidney Disease: Improving Global Outcomes (KDIGO) criteria as an estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m² and/or a urinary albumin-to-creatinine ratio (UACR) ≥30 mg/g. Disease severity was staged by eGFR and albuminuria categories. Logistic regression identified independent predictors of CKD.
Results: The overall CKD prevalence was 10.8%, comparable to global estimates. Prevalence increased with age, reaching 25.0% among participants ≥70 years, of whom 64.3% had reduced kidney function. CKD was more common in women than in men (p<0.001). Major etiologic factors included diabetes mellitus (29%), chronic glomerulonephritis (23%), chronic pyelonephritis (17%), and hypertension (10%). In multivariable analysis, diabetes, hypertension, dyslipidemia, obesity (BMI ≥30), and rural residence were independent predictors of CKD (p<0.05).
Conclusion: CKD is highly prevalent among adults in the Kyrgyz Republic. Risk factors align with international data, but regional patterns show higher rates of chronic glomerulonephritis and pyelonephritis. Strengthening early detection, integrating CKD screening into national health programs, and focusing on high-risk groups—older adults, women, and rural populations—are crucial to reducing the CKD burden in Kyrgyzstan.

ABSTRACT: Background: Chronic kidney disease (CKD) is a major global health challenge, yet population-based data from Central Asia are scarce. We conducted a population-based screening study to assess kidney function distribution and associated risk factors in Astana, Kazakhstan.
Methods: In March 2024, 636 adults were screened through convenience sampling at four major institutions in Astana. After excluding incomplete data, 569 participants were analyzed. Demographic, lifestyle, and clinical information were collected, and serum creatinine was used to estimate glomerular filtration rate (eGFR). Reduced renal function was defined as eGFR <90 mL/min/1.73 m². Group comparisons and logistic regression analyses were performed to identify risk factors for reduced renal function.
Results: The median age of participants was 46 years (IQR 33–55), and 79.8% were women. Median eGFR was 92.8 (IQR 79.8–111.3) mL/min/1.73 m²; 54.1% had eGFR ≥90, 42.4% had eGFR 60–89, and 3.5% had eGFR 45–59. Reduced renal function was more common among older adults, females and those with hypertension and heart failure. In multivariable analysis, older age and female sex were independent predictors of reduced renal function. Awareness was low: only 15.0% of individuals with eGFR 45–59 reported having CKD.
Conclusion: This study provides the population-based evidence on kidney function in Astana, Kazakhstan. Reduced renal function was common, particularly among older adults. Findings highlight the importance of population-based screening and targeted prevention strategies to address kidney health in Kazakhstan.

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.