ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on Twitter

Kidney Week

Abstract: FR-PO103

Unusual Consequences of Dietary Supplements in a Patient Presenting With AKI

Session Information

Category: Acute Kidney Injury

  • 101 AKI: Epidemiology‚ Risk Factors‚ and Prevention

Authors

  • Badra, Sherif, University of Florida, Gainesville, Florida, United States
  • Chamarthi, Gajapathiraju, University of Florida, Gainesville, Florida, United States
  • Ortiz Espinal, Ramon, University of Florida, Gainesville, Florida, United States
  • Clapp, William L., University of Florida, Gainesville, Florida, United States
  • Ruchi, Rupam, University of Florida, Gainesville, Florida, United States
Introduction

Oxalate nephropathy is a rare disorder that can lead to acute kidney injury (AKI). Hereby, we report a case of secondary oxalate nephropathy with biopsy proven oxalate crystalline deposits.

Case Description

A 26-year-old male was referred for hospital admission after blood work showed worsening of creatinine (cr) from baseline 1.1 to 3.2 mg/dl. Past medical history was significant for polyglandular autoimmune syndrome and pancreatic insufficiency treated with pancreatic enzyme replacement therapy. The patient reported single episode of nephrolithiasis 7 years ago. Ultrasound showed no hydronephrosis or stones. Acute interstitial nephritis was suspected based on recent use of antibiotics for skin lesions consistent with sweet syndrome. Kidney biopsy was performed and showed tubulopathy with calcium oxalate deposits (Figure 1).

Upon further evaluation in our stone clinic, patient reported taking daily Vitamin C and high oxalate supplements (turmeric). Genetic testing for primary hyperoxaluria was negative, and serum oxalate was normal. Patient was advised to maintain low oxalate diet and discontinue the supplements. Subsequent 24-hour urine showed an oxalate of 51 mg/d. Although there was partial recovery of renal function on follow up, with cr improving to 1.6 mg/dl, he developed chronic kidney disease (CKD) stage 3a secondary to oxalate nephropathy.

Discussion

Detailed history of high oxalate supplements is crucial for diagnosis of secondary hyperoxaluria. Renal biopsy can be useful in cases of oxalate nephropathy when etiology of AKI is unclear.

Physicians should be aware about that condition that can lead to kidney failure. Our case shows the importance of kidney biopsy to diagnose oxalate nephropathy.