Kidney Week

Abstract: SA-PO0327

Severe Oxalate Nephropathy After Gastric Bypass in a Patient with Excess Black Tea Intake

Session Information

• AKI: Case Reports - Drug/Toxin Injury, Crystals, Obstruction, and Unusual Presentations
  October 24, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

• 102 AKI: Clinical, Outcomes, and Trials

Authors

• Bilal, Muhammad, University of Kentucky, Lexington, Kentucky, United States

Muhammad Bilal, MD

• Rudy, Mark Cason, University of Kentucky, Lexington, Kentucky, United States

Mark Cason Rudy, MD

Introduction

Enteric hyperoxaluria is a known complication of Roux-en-Y gastric bypass and predisposes to oxalate nephropathy. Excess dietary oxalate intake can precipitate severe kidney injury.

Case Description

A 70-year-old female with prior Roux-en-Y gastric bypass (2006) and previously normal kidney function (eGFR >90 mL/min/1.73 m²) presented with rapidly progressive kidney injury identified on routine evaluation. She reported fatigue and new-onset hypertension; labs showed eGFR decline to 21 mL/min/1.73 m², further decreasing to 10 mL/min/1.73 m² over 6–8 weeks (peak creatinine 4.6 mg/dL).
Urinalysis showed proteinuria and microscopic hematuria; 24-hour urine protein was 0.48 g/day. Serologic workup (ANA, ANCA, C3, C4, anti-GBM) was negative. Imaging showed increased renal echogenicity without obstruction. Kidney biopsy demonstrated acute oxalate nephropathy with acute tubular injury and abundant calcium oxalate crystal deposition, along with moderate interstitial fibrosis and tubular atrophy (40–50%) and mild global glomerulosclerosis, without immune complex disease.
Further history revealed consumption of ~1 gallon of black tea daily as sole fluid intake for 3 months.
Management included cessation of oxalate intake, hydration, and calcium-based binders. Kidney function stabilized (creatinine ~3.6–3.7 mg/dL, eGFR ~13) without dialysis; she is undergoing transplant evaluation.

Discussion

After Roux-en-Y gastric bypass, fat malabsorption reduces luminal calcium, increasing intestinal oxalate absorption and systemic oxalate burden. Excess oxalate intake (e.g., black tea) exacerbates this process. Calcium oxalate deposition causes tubular obstruction, epithelial injury, and progressive tubulointerstitial damage. Secondary oxalate nephropathy carries a poor renal prognosis, especially with advanced fibrosis. Diagnosis requires high suspicion and often a biopsy, as dietary contributors may be missed without a targeted history.

Calcium oxalate crystals in renal tubules