Chronic dietary oxalate nephropathy after intensive dietary weight loss regimen

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. 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

Chronic Kidney Disease as a Result of Secondary Oxalate Nephropathy From Excess Dietary Intake of Peanut Butter and Coffee

“…At the same time, cryopyrin-null mice were immune to developing end-stage renal disease in response to high oxalate insult, showing that there is likely a significant genetic component to these cases of secondary oxalate nephropathy. More importantly, this and other similar studies have shown a mechanistic connection between oxalate nephropathy and crystal arthropathies such as gout, which may possibly be an underappreciated set of comorbidities, given that our patient and two other patients from similar case reports of secondary oxalate nephropathy all had gout [20][21][22][23][24].…”

Acute oxalate nephropathy: A potential cause of acute kidney injury in diabetes mellitus—A case series from a single center

“…Urinary oxalate is derived either exogenously from dietary oxalate intake and net intestinal absorption or endogenously from oxalate synthesis mainly in the liver ( 10 ). Most reported AON cases in the literature have attributed the cause to either high intakes of oxalate-containing foods or oxalate precursors ( 12 – 15 ) or malabsorption induced by short-bowel syndrome ( 16 ), including celiac disease ( 17 ), gastric surgery (Roux-en-Y gastric bypass) ( 18 ), inflammatory bowel disease ( 19 ), chronic pancreatitis or pancreatic insufficiency, etc. ( 20 , 21 ).…”

Diet-induced oxalate nephropathy from excessive nut and seed consumption

“…Case reports have documented diet-induced ON secondary to spinach, kale, berries, nuts and nut milk, cocoa powder, wheat germ, green smoothies, chagas mushrooms and vitamin C supplements. [9][10][11][12][13][14] The majority followed this diet for presumed health benefits and had partial recovery with restriction of oxalate consumption, increased oral hydration and calcium acetate supplementation to bind gut oxalate.…”