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Kidney Week

Abstract: FR-PO230

Oxalate Nephropathy: A Studded Case of AKI

Session Information

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms

Authors

  • Davis, Sissmol, JJM Medical College, Davangere, Karnataka, India
  • Phachu, Deep, Central Mass Nephrology, Worcester, Massachusetts, United States
  • Hata, Jessica Lynn, Brigham and Women's Hospital, Boston, Massachusetts, United States
  • Weins, Astrid, Brigham and Women's Hospital, Boston, Massachusetts, United States
  • Verma, Ashish, Central Mass Nephrology, Worcester, Massachusetts, United States
  • Magoo, Hemant, Central Mass Nephrology, Worcester, Massachusetts, United States
Introduction

Oxalate nephropathy (ON) is a rare manifestation of hyperoxaluria which can present as acute kidney
injury (AKI) with the possibility of rapid progression to end stage kidney disease. We present a case of
AKI with ON on biopsy.

Case Description

A 64-year-old male with obesity, type 2 diabetes mellitus and hypertension presented with nausea and
unsteady gait. He has AKI with a serum creatinine (Cr) of 9.4 mg/dL on admission with a baseline Cr
of 0.8 mg/dL 3 months prior. Clinical history did not reveal a cause for AKI. Urine studies showed the
occasional granular cast but no dysmorphic RBCs, proteinuria or pyuria. Serological workup including
antinuclear antibody, anti-neutrophilic cytoplasmic antibody, and serum monoclonal testing were
unremarkable. He underwent kidney biopsy due to inadequate improvement of renal function with
intravenous fluids.
Kidney biopsy (Figure 1) showed widespread calcium oxalate deposition in the tubules (renal
oxalosis) with associated mild acute tubular injury and mild interstitial nephritis. Genetic testing did
not show a known mutation associated with Primary Hyperoxaluria.

Discussion

Primary Hyperoxaluria is due to a genetic defect leading to abnormal oxalate handling. Secondary
Hyperoxaluria (SH) occurs due to excessive dietary oxalate intake and/or gastrointestinal disorders
that increase absorption of oxalate or oxalate precursors, such as inflammatory bowel disease. Both
diabetes mellitus (DM) and obesity have also been associated with increased urinary oxalate excretion.
We assume that our patient suffered from SH with both obesity and DM playing a role.
Although significantly less common than other causes of acute kidney injury, ON should be included in
the differential for AKI of unclear etiology, especially in patients with concurrent DM and obesity.

Figure 1: Widespread calcium oxalate deposition within the renal tubules under polarized light (arrows).