Oxalate-Induced Nephropathy Causes Rare AKI

Introduction: Oxalate nephropathy, linked to dietary, genetic, and metabolic factors, rarely causes severe acute kidney injury (AKI). Calcium oxalate crystal-induced AKI often goes unrecognized in clinical practice due to nonspecific signs and lack of biomarkers, impairing kidney function. The definite diagnosis of calcium oxalate-induced AKI is challenging and requires a kidney biopsy. Case Description: We present a case of a 66-year-old male with hypertension, hyperlipidemia, type 2 diabetes mellitus, and CKD IIIA, hospitalized in July 2024 with AKI and a rise in serum creatinine to 7.4 mg/dL from 4.3 in May 2024, and a baseline of 1.7–2.2. Urine sediment showed a few crystals and RBCs, with no RBC or granular casts. Extensive AKI work-up—including CPK, dsDNA Ab, ANA, C3, C4, ANCA, ethylene glycol, and infectious panel—was negative, except for a mildly elevated K/L ratio of 2.04 (0.22–1.74), attributed to underlying CKD. Kidney US showed no obstruction or stones. Doppler was negative for renal artery stenosis. Withholding losartan and giving IV fluids did not significantly improve renal function. Urgent renal biopsy confirmed acute tubular injury with multifocal intratubular calcium oxalate deposition (Figure 1). Dietary review revealed excessive intake of spinach and dry nuts as part of a health regimen. The spot urine oxalate/creatinine ratio was 33 mg/g (normal <30 mg/g). The patient was counseled on dietary modifications, particularly oxalate restriction. He was advised to increase oral fluid and calcium intake, and stop vitamin D supplements. At nine-month follow-up, renal function improved without dialysis, serum creatinine stabilized around 3.0 mg/dL, and no new urinary crystals were observed. Discussion: This case highlights the contribution of excessive dietary oxalate intake, particularly spinach and dry nuts consumption, to calcium oxalate-induced nephropathy and acute kidney injury in susceptible individuals. Prompt recognition, diagnosis, and management of oxalate crystal-induced nephropathy may delay, and even reverse the progression of kidney disease.Multifocal intratubular calcium oxalate crystal deposition