Oxalate Nephropathy Associated with Chronic Pancreatitis

Abstract

SummaryBackground and objectives Enteric overabsorption of oxalate may lead to hyperoxaluria and subsequent acute oxalate nephritis (AON). AON related to chronic pancreatitis is a rare and poorly described condition precluding early recognition and treatment.Design, setting, participants, & measurements We collected the clinical characteristics, treatment, and renal outcome of 12 patients with chronic pancreatitis-associated AON followed in four French renal units.Results Before AON, mild to moderate chronic kidney disease was present in all patients, diabetes mellitus in eight (insulin [n ϭ 6]; oral antidiabetic drugs [n ϭ 2]), and known chronic pancreatitis in only eight. At presentation, pancreas imaging showed gland atrophy/heterogeneity, Wirsung duct dilation, calcification, or pseudocyst. Renal findings consisted of rapidly progressive renal failure with tubulointerstitial profile. Acute modification of glomerular filtration preceded the AON (i.e., diarrhea and diuretics). Increase in urinary oxalate excretion was found in all tested patients and hypocalcemia in nine (Ͻ1.5 mmol/L in four patients). Renal biopsy showed diffuse crystal deposits, highly suggestive of oxalate crystals, with tubular necrosis and interstitial inflammatory cell infiltrates. Treatment consisted of pancreatic enzyme supplementation, oral calcium intake, and an oxalate-free diet in all patients and renal replacement therapy in five patients. After a median follow-up of 7 months, three of 12 patients reached end-stage renal disease.Conclusion AON is an under-recognized severe crystal-induced renal disease with features of tubulointerstitial nephritis that may occur in patients with a long history of chronic pancreatitis or reveal the pancreatic disease. Extrinsic triggering factors should be prevented.

Weight loss at a high cost: Orlistat-induced late-onset severe kidney disease

“…Steatorrhoea can lead to undigested fatty acids that compete with oxalate for intraluminal calcium, leading to insoluble calcium 'soap' synthesis and increased colonic permeability to oxalate. This can cause acquired hyperoxalaemia, with subsequent deposition of calcium oxalate crystals in renal tubules [6]. Enteric hyperoxaluria with secondary oxalate nephropathy has been reported with inflammatory bowel disease, coeliac disease, jejunoileal bypass, bariatric surgery and chronic pancreatitis [6][7][8].…”

Enteric Oxalate Nephropathy in the Renal Allograft: An Underrecognized Complication of Bariatric Surgery

“…Oxalate nephropathy is a rare cause of acute and chronic renal failure (1)(2)(3)(4). Oxalate accumulation in renal allografts may arise de novo, or as "recurrence" of native kidney disease if underlying hyperoxalosis remains uncorrected.…”

“…Secondary hyperoxaluria can arise from a variety of different processes (Table 1), including iatrogenic causes. Gastrointestinal surgery is a known cause of hyperoxaluria, most notably in situations of fat malabsorption and diarrhea (1)(2)(3)(4).…”

Primary Hyperoxaluria: A Case Report and Review of the Literature

“…By light microscopy, calcium oxalate crystals are graywhite, speculated and are birefringent under polarized light, whereas calcium phosphate crystals do not polarize (5,7). Few or isolated tubular oxalate crystals are not rare in normal or failing kidneys, and in transplanted kidneys; their presence does not imply renal damage.…”

“…Few or isolated tubular oxalate crystals are not rare in normal or failing kidneys, and in transplanted kidneys; their presence does not imply renal damage. On the contrary, abundant tubular or interstitial calcium oxalate deposits are highly suggestive of a hyperoxaluric condition (7).…”