J Nephropathol. 2017;6(3): 126-129.
doi: 10.15171/jnp.2017.21
PMID: 28975090
PMCID: PMC5607971
Scopus ID: 85019853058
  Abstract View: 4324
  PDF Download: 2385

Case Report

Chronic dietary oxalate nephropathy after intensive dietary weight loss regimen

Gebran Khneizer 1, Ahmad Al-Taee 1, Meher S Mallick 2, Bahar Bastani 1

1 Department of Internal Medicine, Saint Louis University School of Medicine, Saint Louis, Missouri, USA
2 Saint Louis Nephrology Associates, Saint Louis, Missouri, USA
*Corresponding Author:


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.

Case Presentation: 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

Implication for health policy/practice/research/medical education:

Clinicians need to be familiar with dietary oxalate nephropathy in the setting of growing use of dietary weight loss regimens with high oxalate content.

Please cite this paper as: Khneizer G, Al-Taee A, Mallick MS, Bastani B. Chronic dietary oxalate nephropathy after intensive dietary weight loss regimen. J Nephropathol. 2017;6(3):126-129. DOI: 10.15171/jnp.2017.21.

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ePublished: 05 Feb 2017
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