Oxalate nephropathy presenting in exocrine pancreatic insufficiency
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.