An unusual cause of acute kidney injury due to oxalate nephropathy in systemic scleroderma

Abstract

Oxalate nephropathy is an uncommon cause of acute kidney injury. Far rarer is its association with scleroderma, with only one other published case report in the literature. We report a case of a 75-year-old African-American female with a history of systemic scleroderma manifested by chronic pseudo-obstruction and small intestinal bacterial overgrowth (SIBO) treated with rifaximin, who presented with acute kidney injury with normal blood pressure. A renal biopsy demonstrated extensive acute tubular injury with numerous intratubular birefringent crystals, consistent with oxalate nephropathy. We hypothesize that her recent treatment with rifaximin for SIBO and decreased intestinal transit time in pseudo-obstruction may have significantly increased intestinal oxalate absorption, leading to acute kidney injury. Oxalate nephropathy should be considered in the differential diagnosis of acute kidney injury in scleroderma with normotension, and subsequent evaluation should be focused on bowel function to include alterations in gut flora due to antibiotic administration.

Oxalate nephropathy in systemic sclerosis: Case series and review of the literature

“…Nevertheless, even when some reversibility in renal injury is present and histology does not clearly demonstrate associated inflammation, renal oxalosis remains a predictor of poor transplant outcome, and it consistently denotes a poor prognosis in enteric oxaluria [22, 39, 57]. In a series of post-Roux-en-Y enteric nephropathy patients for example, 8 of 11 cases progressed to renal failure, similar to the poor recovery reported in the two systemic sclerosis cases to date[22, 26, 27]. Determination of whether oxalate nephropathy on renal biopsy remains a negative prognosticator even among the subset of patients with systemic sclerosis, kidney injury, and severe bowel disease, will require more cases and a more systematic identification of renal calcium oxalate deposition.…”

“…Enteric hyperoxaluria is a well-described consequence of malabsorptive states, including Crohn’s disease [25], Roux-en-Y gastric bypass [28], chronic pancreatitis [29, 30], and two cases of systemic sclerosis bowel disease [26, 27]. [19–24, 31–33][25][28][29, 30][26, 27] The common pathophysiology requires chronic malabsorption of dietary fats in the small intestine, with relatively preserved colonic absorption.…”

“…[19–24, 31–33][25][28][29, 30][26, 27] The common pathophysiology requires chronic malabsorption of dietary fats in the small intestine, with relatively preserved colonic absorption. The increased luminal fatty acids in the small intestine displace calcium from oxalate, which in turn is more readily absorbed in the colon in its unbound form [13].…”

“…Two case reports of acute kidney injury secondary to oxalate nephropathy have been reported in patients with systemic sclerosis and small intestinal involvement causing decreased motility and steatorrhea [26, 27]. We now report a case series of systemic sclerosis-related oxalate nephropathy among patients followed in the Johns Hopkins Scleroderma Center.…”

Acute Oxalate Nephropathy Associated With Orlistat

“…Physical exam was non-contributory, with a weight of 71 kg, height 1.55 m and blood pressure of 144/61 mm Hg. Her body mass index calculated at 29.5 kg/ m 2 . Urinalysis with microscopy was unremarkable, except for 5 WBCs/high power fields with no crystals or cast formation.…”