Acute oxalate nephropathy: A potential cause of acute kidney injury in diabetes mellitus—A case series from a single center

Abstract

BackgroundAcute oxalate nephropathy (AON) is an uncommon condition that causes acute kidney injury (AKI), characterized by the massive deposition of calcium oxalate crystals in the renal parenchyma. In previous studies, urinary oxalate excretion has been found to be increased in patients with diabetes mellitus (DM). Here, we report a case series of diabetic patients with AKI with biopsy-proven AON, aiming to alert physicians to the potential of AON as a trigger of AKI in diabetic patients in clinical practice.Materials and methodsCases with pathological diagnosis of AON who presented with AKI clinically and had DM between January 2016 and December 2020 were retrospectively enrolled. Their clinical and pathological manifestations, treatment, and prognosis were collected.ResultsSix male patients with biopsy-proven AON out of a total of 5,883 native kidney biopsies were identified, aged 58.3 ± 9.1 years at the time of kidney biopsy. Only one patient who had received Roux-en-Y gastric bypass surgery took oxalate-rich food before the onset of the disease. None of them had clinical features of enteric malabsorption. Three patients were currently on renin-angiotensin system inhibitor treatment for hypertension, and 5 of them received non-steroidal anti-inflammatory drugs. Three patients presented with oliguria and 4 patients needed dialysis at the beginning with none requiring dialysis at discharge. Four patients received a course of corticosteroid treatment empirically. Among them, two patients had estimated glomerular filtration rate (eGFR) recovered to over 60 ml/min/1.73 m2, while the other two patients remained with kidney dysfunction at the last follow-up. In two patients without corticosteroid treatment, one patient fully recovered with eGFR over 90 ml/min/1.73 m2 and the other patient remained with kidney dysfunction at the last follow-up.ConclusionAON might be a rare but potentially trigger of AKI in patients with DM. A kidney biopsy could help physicians to make the correct diagnosis. The proper treatment to alleviate oxalate-induced injury needs to be further studied.

Oxalate Nephropathy and the Mechanism of Oxalate-Induced Kidney Injury

“…Treatment of oxalate nephropathy remains largely empirical and should be initiated immediately including high fluid intake, a low-oxalate and low-fat diet, and supplements that could improve the solubility of oxalate, such as calcium, citrate, and sodium bicarbonate, aiming to decrease both plasma and urine oxalate concentration [12, 72, 73]. Pancreatic enzyme therapy, intensive therapy of inflammatory bowel disease, and avoiding abuse of orlistat could be considered depending on the underlying causes [5].…”

“…Using in vitro models, Taguchi et al [ 70 ] showed that M2 macrophages have a significant ability to phagocytose CaOx monohydrate crystals and prevent crystal adherence to renal tubular cells, whereas M1 macrophages facilitated renal crystal formation. Kusmartsev et al [ 71 ] demonstrated that human macrophages in vitro are capable of phagocytizing and degrading calcium oxalate crystals produced naturally in the kidney. Kidneys developing CaOx crystals express several pro-inflammatory cytokines, crystal-related molecules, including osteopontin, CD44, and MCP-1, and adhesion-related genes, such as C3, FN , and Vcam1 .…”

“…Four patients showed improvement in kidney function after active therapy including hydration, oral citrate supplements, and alkalization. Four of the patients with severely elevated serum creatinine levels were administered a course of corticosteroid treatment; however, the rate of kidney function recovery was equal between patients with and without corticosteroid treatment, indicating uncertain efficacy of the steroid therapy [ 73 ]. Overall, the prognosis for oxalate nephropathy is poor and 40–50% of patients reach kidney failure or are dialysis dependent at their last follow-up [ 2 , 5 , 20 ].…”