Keyword: Acute Kidney

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: 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: 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: 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: 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).