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Journal of Nephropathology 2017-Jul

Chronic dietary oxalate nephropathy after intensive dietary weight loss regimen.

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Gebran Khneizer
Ahmad Al-Taee
Meher S Mallick
Bahar Bastani

Sleutelwoorden

Abstract

BACKGROUND

Hyperoxaluria has been associated with nephrolithiasis as well as acute and chronic kidney disease. We present a case of end stage renal failure caused by excessive dietary oxalate intake in a dietary weight loss regimen.

METHODS

A 51-year-old Caucasian male with the past medical history of type 2 diabetes mellitus, gout, hypertension and morbid obesity was referred to the primary care clinic after being found pale and easily fatigued. The patient had lost 36 kg over a 7-month period by implementing exercise and intense dietary measures that included 6 meals of spinach, kale, berries, and nuts. Physical examination revealed a blood pressure of 188/93 mm Hg with sunken eyes and dry mucus membranes. Laboratory workup was notable for blood urea nitrogen of 122 mg/dL, creatinine of 12 mg/dL, and estimated glomerular filtration rate (eGFR) of 4.4 mL/min/1.73m2. Patient denied any history of renal disease or renal stones, or taking herbal products, non-steroidal anti-inflammatory drugs, antifreeze (ethylene glycol), or any type of "diet pills." Family history was unremarkable for any renal diseases. After failing intravenous fluid resuscitation, patient was started on maintenance hemodialysis. Abdominal imaging was consistent with chronic renal parenchymal disease with no evidence of nephrolithiasis. Renal biopsy revealed numerous polarized oxalate crystal deposition and diabetic nephropathy class IIA. At this point the patient was instructed to adopt a low oxalate diet. A 24-hour urine collection was remarkable for pH 4.7, citrate <50 mg, and oxalate 46 mg. Importantly, serum oxalate level was undetectable. Repeat renal biopsy 5 months later while patient was still on maintenance hemodialysis revealed persistence of extensive oxalate crystal deposition. Patient has been referred for evaluation for renal transplantation.

CONCLUSIONS

Clinicians need to maintain a high index of suspicion for dietary hyperoxaluria as a potential etiology for acute or chronic kidney failure, particularly in patients pursuing intensive dietary weight loss intervention.

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