Abstract: SA-PO0085
Oxalate Nephropathy from Excessive Cashew Consumption
Session Information
- AKI: Clinical Diagnostics and Biomarkers
November 08, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Ramrattan, Amit, The University of Tennessee Health Science Center College of Medicine, Memphis, Tennessee, United States
- Showkat, Arif, The University of Tennessee Health Science Center College of Medicine, Memphis, Tennessee, United States
- Vo, Hieu Q., The University of Tennessee Health Science Center College of Medicine, Memphis, Tennessee, United States
- Shafiq, Ihtesham, The University of Tennessee Health Science Center College of Medicine, Memphis, Tennessee, United States
- Shah, Syed Muhammad Obaida M, The University of Tennessee Health Science Center College of Medicine, Memphis, Tennessee, United States
Introduction
Oxalate is either derived from our diet or can be produced endogenously in our liver, all of which is excreted in the urine. Hyperoxaluria increases the risk of nephrolithiasis or crystalline nephropathy. We present a rare case of oxalate nephropathy from excessive cashew nut consumption.
Case Description
A 78-year-old male with a history of chronic kidney disease (CKD) secondary to diabetes mellitus and hypertension was seen in the emergency room for an acute rise in serum creatinine level of 6.0 mg/dl. His baseline serum creatinine level was 2.05 mg/dl. On presentation, his physical examination and urinalysis were unremarkable. Laboratory investigations showed serum sodium 142 mmol/L, potassium 4 mmol/L, bicarbonate 15 mmol/L, calcium 8.8 mg/dl, albumin 3.4 g/dl, and BUN 99 mg/dl. Renal ultrasound failed to show any obstructive uropathy. A renal biopsy showed diffuse acute tubular injury frequently associated with calcium oxalate crystal deposition within the tubular lumens (yellow arrow) and moderate interstitial fibrosis and tubular atrophy (Figure 1). Crystals were birefringent under polarized light (Figure 2). A dietary history revealed that over the last year, he consumed 3-4 oz of cashew nuts daily, equivalent to 222 to 300 mg of oxalate daily, far above the average daily consumption of 100 -150 mg. The patient did not require renal replacement therapy. Two months later, his serum creatinine level was 3.74 mg/dl during a follow-up visit.
Discussion
Dietary oxalate nephropathy should be considered in patients with AKI or progressive CKD with an unclear etiology. A low threshold for kidney biopsy in the setting of unexplained AKI could help diagnose more cases of oxalate nephropathy. Nephrologists must consider a proper dietary history in cases of rapid renal function decline in CKD patients and not just fault the progression of the original disease as the cause. As this case illustrates, early dietary intervention in a patient with advanced CKD could have been a valuable protective measure against renal function decline.