Secondary oxalosis induced acute kidney injury in allograft kidneys

Abstract

Secondary oxalosis causing acute kidney injury (AKI) has been widely reported in native kidneys but its occurrence in allograft kidneys is relatively uncommon. We present three patients with acute kidney allograft dysfunction secondary to tubular oxalate microcrystal deposits confirmed on allograft biopsy in the setting of acute gastrointestinal dysfunction. These three patients presented with AKI that was preceded by episodes of ongoing diarrhea ranging from 10 to 90 days. All patients were on vitamin C and/or multivitamin supplementation. Two of the three patients needed long-term renal replacement therapy with the third patient recovering his kidney function after 2 months. The risks versus benefits of vitamin C supplementation in renal transplant patients should be carefully evaluated especially in the setting of gastrointestinal dysfunction.

Vitamin C-induced oxalate nephropathy in a renal transplant patient related to excessive ingestion of cashew pseudofruit (Anacardium occidentale L.): a case report

“…Recently, some reports of patients with renal allografts developing oxalate nephropathy and worsening of renal function with vitamin C ingestion have been reported [ 20 , 21 ]. Getting JE et al [ 20 ] described 65 patients with biopsy proven calcium oxalate crystals.…”

“…Among these patients, five patients showed oxalate nephropathy associated with high intake of vitamin C, including two patients status post kidney transplant and three patients with chronic kidney diseaseysli. Suneja M et al [ 21 ] described three patients, two with a history of kidney transplant and one with a history of pancreas-kidney transplant. All three patients had history of vitamin C ingestion.…”

Crystalline nephropathy in renal transplant: A series of 4 cases

“…Oxalate is a metabolic end product that is excreted essentially unchanged in the urine after absorption in the gastrointestinal tract. [6] Hyperoxaluria is a rare metabolic disorder characterized by CaOx deposition in different tissues. The kidney primarily excretes the excess oxalate.…”

“…[7] Urinary oxalate is largely derived from the endogenous metabolism of glycine, glycolate, hydroxyproline, and Vitamin C. Hyperoxalosis from any cause converges on a common final pathophysiological pathway of supersaturation of the renal tubular fluid leading to the precipitation of oxalate crystals in the renal interstitium creating an interstitial nephritis, macrophage recruitment and surge in inflammatory mediators ultimately leading to tubular atrophy and acute kidney injury (AKI). [6]…”

Calcium oxalate crystal deposition in the kidney: identification, causes and consequences

“…Failure to diagnose PH prior to transplantation may result in early graft failure [79,80]. Likewise for secondary hyperoxalurias, failure to recognise may lead to acute kidney injury [81] or even graft failure. There have been graft failure case reports for enteric hyperoxaluria [82,83] and excessive vitamin C intake [84].…”