S.E. Deurvorst, J. Alberga, A. van Tellingen
Woensdag 20 april 2016
15:20 - 15:30u in Zaal 0.5
Parallel sessie: Parallelsessie 4: Case reports/research
A sixty-nine year old Caucasian male with a history of late-onset diabetes mellitus type I was found to have rapid progressive kidney failure on routine diabetes follow up. Except for a loss of appetite no other clinical signs or symptoms were present and physical examination was normal. The urine sediment was inactive.
CT scan of the abdomen revealed no abnormalities of the kidneys nor the collecting systems, but did show extensive pancreatic calcifications due to chronic pancreatitis. Low fecal elastase level corresponded with severe pancreatic insufficiency. Laboratory and imaging studies could however not elucidate the cause of the pancreatitis.
Kidney biopsy revealed tubulointerstital nephritis with an excessive amount of oxalate crystals in the tubuli. Treatment with high dose prednisone and a fat- and oxalate poor diet could not prevent the need for kidney replacement therapy.
Pancreatic insufficiency causes more fatty acids to be present in the colon which increases intestinal permeability to oxalate. Secondly calcium binds to these fatty acids instead of binding to oxalate. The unbound oxalate will be absorbed in the colon which causes hyperoxaluria and oxalate nephropathy. The chronic pancreatitis in our patient can explain both the acute oxalate nephropathy and the late-onset diabetes mellitus. Other causes of enteral hyperoxaluria are among others gastrointestinal surgery and inflammatory bowel disease which have similar pathophysiologic mechanisms.
Diagnosing oxalate nephropathy is challenging. Using this case report we show pancreatic insufficiency is a rare cause of hyperoxaluria and raise clinical suspicion for other identified causes which contribute in developing oxalate nephropathy.