Oxalate nephropathy presenting in exocrine pancreatic insufficiency

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Oxalate nephropathy represents formation of tubular oxalate crystals with progressive renal dysfunction.1 A 66 year old Caucasian male presented with a 3 month history of malaise, nausea, lethargy and polyuria associated with steatorrhoea on a background of prior extensive alcohol intake. He had acute on chronic kidney disease with his plasma creatinine peaking at 568 µmol/L. Urine examination and ultrasound imaging were unhelpful beyond dilatation of the pancreatic duct. A renal biopsy demonstrated birefringent tubular crystals with interstitial inflammatory infiltrate and interstitial fibrosis with background hypertensive change (Fig. 1). The appearances were consistent with oxalate nephropathy. Magnetic resonance cholangiopancreatography demonstrated fatty replacement of the pancreas, and exocrine pancreatic deficiency was confirmed (faecal elastase <15 mg/g). An endoscopic retrograde cholangiopancreatogram was unsuccessful. Endoscopic ultrasound did not show an obstructing lesion. Pancreatic enzyme replacement, oral potassium citrate and low oxalate diet was commenced. Renal function stabilized with a creatinine of 320–350 µmol/L (eGFR 18 mL/min/1.73 m2) after 4 months.
Exocrine pancreatic insufficiency is failure of the pancreas to secrete an appropriate amount of digestive enzymes, presenting with steatorrhoea and weight loss. Impaired enzyme secretion causes maldigestion of fats with an increased intestinal fatty acid load, which binds calcium leaving oxalate uncomplexed.1 The increased solute gradient with resultant increased paracellular permeability (large intestine) causes passive hyperabsorption of oxalate and hyperoxalaemia with hyperoxaluria. Oxalate nephropathy can present as acute tubulointerstitial nephritis because of calcium oxalate tubular deposition, confirmed on biopsy with birefringent crystals under polarized light.1 The incidence of oxalate nephropathy is unknown. In a case series,1 40% progressed to end‐stage kidney disease within 2 years. Early therapeutic measures to replace pancreatic enzymes and alkalinize the urine may help delay or prevent the progression of the kidney injury. We report a rare case of rapidly progressive renal insufficiency as a result of biopsy confirmed oxalate nephropathy in the setting of pancreatic insufficiency due to chronic pancreatitis. Manipulation of the oxalate handling by the gut and measures to alter the solubility of oxalate crystals appear to have resulted in a degree of recovery/stabilization of kidney function in this case.
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