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Abstract: FR-PO202

Oxalate Nephropathy: An Insidious Cause of Renal Insufficiency

Session Information

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms


  • Tarabochia, Alex D., Dartmouth Health, Lebanon, New Hampshire, United States
  • Pettus, Jason R., Dartmouth Health, Lebanon, New Hampshire, United States
  • Rajan, Roy, Dartmouth Health, Lebanon, New Hampshire, United States

Oxalate nephropathy is caused by urinary super saturation of calcium oxalate, crystal formation with obstruction of tubules and deposition into the renal parenchyma.

Case Description

Patient is a 73-year-old male with Crohn’s disease, distant history of oxalate renal stones 5 years ago, and hypertension referred for chronic kidney disease (CKD) with baseline serum creatinine (Cr) of 1.6 with stable Cr for more than a year, which increased to 2 over the period of six months. Blood pressure (BP) was at goal and he had not had a Crohn’s flare in four years.

Renal ultrasound (US) was negative for obstruction but did show small, non-obstructing (8mm on the left, 7mm on the right) renal stones in the bilateral lower renal poles. Specific gravity was 1.015, calcium was 8.5, protein: creatine (UPC) ratio was 0.1, and urine sediment was unremarkable with light microscopy.

Routine labs were obtained one month later and serum Cr was 6.5. His symptoms were remarkable for fatigue and confusion. Pertinent medical history and repeat renal imaging were unremarkable. Specific gravity was 1.014 on urinalysis; calcium, UPC and light microscopy were unremarkable. The lack of obvious findings and lack of improvement with IV hydration prompted renal biopsy which showed tubular atrophy (15%) with diffuse calcium oxalate deposition and minimal acute tubular injury. Twenty-four-hour urine collection showed low urine citrate (113mg/day) and high urine oxalate (92 mg/day). He was started on potassium citrate and was instructed to increase fluid intake after which Cr improved to 2.5 over a period of two months.


This case illustrates the insidious nature of oxalate nephropathy where the ongoing, mild super saturation leads to CKD and an acute super saturation leads to AKI. Risk factors include dehydration, high oxalate diet, and disorders with malabsorption of fat including Crohn's disease which leads to saponification and increased oxalate absorption. The case highlights the importance of biopsy to distinguish this from other forms of AKI and 24-hour urine studies to manage stone formation.