Nephrocalcinosis Following Roux-en-Y Gastric Bypass Secondary to Suspected Enteric Hyperoxaluria: A Case Report

Nephrocalcinosis refers to the deposition of calcium oxalate or calcium phosphate in the kidney, most commonly within the renal medulla, and is frequently linked with underlying metabolic abnormalities. Roux-en-Y gastric bypass (RYGB) is a well-established risk factor for enteric hyperoxaluria secondary to fat malabsorption, thereby increasing the risk of nephrolithiasis, oxalate nephropathy, and nephrocalcinosis. Despite this association, nephrocalcinosis following RYGB remains an uncommon and underrecognized clinical entity. A 36-year-old male with a history of complicated peptic ulcer disease, multiple prior abdominal surgeries, and previous RYGB presented with acute abdominal pain and distention. Laboratory evaluation revealed an elevated creatinine of 2.27 mg/dL, a suppressed parathyroid hormone level of 6.3 pg/mL, and hypocalcemia with serum calcium of 8.1 mg/dL. Imaging studies revealed bilateral renal medullary calcifications, consistent with nephrocalcinosis. Given the patient’s history of RYGB, chronic pancreatitis, multiple GI surgeries, and evidence of chronic malnutrition, chronic malabsorptive physiology leading to enteric hyperoxaluria was hypothesized to be the most plausible explanation. However, measurements of 24-hour urinary oxalate, calcium, citrate, and vitamin D, as well as a renal biopsy, were not obtained, thereby precluding definitive confirmation of this proposed mechanism. This case highlights the importance of considering metabolic and renal complications in patients with complex GI disease following bariatric surgery and emphasizes the role of comprehensive metabolic evaluation and renal imaging in improving early recognition, diagnostic accuracy, and long-term kidney outcomes.