Kidney Week

Abstract: PUB045

Renal Oxalosis from Excess Dietary Intake: A Guide to Improve Kidney Function

Session Information

• Publication Only

Category: Acute Kidney Injury

• 102 AKI: Clinical, Outcomes, and Trials

Authors

• Khalfan, Muhammed, NYU Langone Hospital - Long Island, Mineola, New York, United States

Muhammed Khalfan, DO

• Yang, Hong, NYU Langone Hospital - Long Island, Mineola, New York, United States

Hong Yang, MD, PhD

• Silverio De Castro, Yinelka G., NYU Langone Hospital - Long Island, Mineola, New York, United States

Yinelka G. Silverio De Castro, MD

• Karingattil, Jerin, NYU Langone Hospital - Long Island, Mineola, New York, United States

Jerin Karingattil, MD

• Drakakis, James, NYU Langone Hospital - Long Island, Mineola, New York, United States

James Drakakis, DO

Introduction

Hyperoxaluria may be due to hereditary defects of key enzymes of oxalate metabolism or from excess intake or increased enteric absorption. High dietary intake is related to ingestion of vitamin C, spinach, rhubarb, or beets. Acute kidney injury (AKI) is due to calcium oxalate crystals desposited within tubules causing acute tubular injury. Renal recovery is possible with correction of the underlying cause. However, the insult may also be severe enough to require dialysis and can even lead to end stage renal disease. We present a case of oxalate nephropathy (intake related) whereby kidney function improved significantly with strict dietary oxalate restriction.

Case Description

69 year old female with no past history was found with serum creatinine 2.4 mg/dL. Baseline one year prior 0.9 mg/dL. UA without blood or RBC and urine protein quantification 144 mg/g. Renal ultrasound with increased echogenicity and non obstructing kidney stones. Kidney biopsy showed acute tubular injury with multifocal tubular oxalate crystal deposition (renal oxalosis); 30% tubular atrophy and interstitial fibrosis. This was not primary oxalosis related to inherited enzyme defect (genetic testing negative). Nor prior surgeries or predisposing conditions to suggest enteric form. History was elucidated that she was on a diet rich in oxalate. With very tight restriction of 50-100 mg oxalate per day (ingesting foods <5 mg oxalate per serving), creatinine improved to 1.26 mg/dL (10 months after initial diagnosis).

Discussion

The prognosis of acute oxalate nephropathy is variable, with insult severe enough to warrant renal replacement in at least one half of paitents. Treatment depends on underlying cause but generally includes hydration, oral calcium supplementation, correction of hyperoxalauria causing conditions and as in our case, low oxalate diet. Literature review reveals most patients do not make a complete recovery in terms of renal function. Our patient bolstered her urine output to upward of 3 liters per day, and lowered oxalate intake to <100 mg per day. Serum creatinine improved in less than 1 year from diagnnosis to 1.26 from 2.4 mg/dL. This cause illustrates the importance of dietary modification in renal oxalosis from excess intake and the potential for significant renal recovery, otherwise described as being unlikely.