Keyword: Kidney Biopsy

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: 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: 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).