Abstract
BackgroundCalcium oxalate (CaOx) deposition in the kidney may lead to loss of native renal function but little is known about the prevalence and role of CaOx deposition in transplanted kidneys.MethodsIn patients transplanted in 2014 and 2015, all for-cause renal allograft biopsies obtained within 3 months post-transplantation were retrospectively investigated for CaOx deposition. Additionally, all preimplantation renal biopsies obtained in 2000 and 2001 were studied.ResultsIn 2014 and 2015, 388 patients were transplanted, of whom 149 had at least one for-cause renal biopsy. Twenty-six (17%) patients had CaOx deposition. In the population with CaOx deposition: Patients had significantly more often been treated with dialysis before transplantation (89 vs. 64%; p = 0.011); delayed graft function occurred more frequently (42 vs. 23%; p = 0.038); and the eGFR at the time of first biopsy was significantly worse (21 vs. 29 ml/min/1.73m2; p = 0.037). In a multivariate logistic regression analysis, eGFR at the time of first biopsy (OR 0.958, 95%-Cl: 0.924–0.993, p = 0.019), dialysis before transplantation (OR 4.868, 95%-Cl: 1.128–21.003, p = 0.034) and the time of first biopsy after transplantation (OR 1.037, 95%-Cl: 1.013–1.062, p = 0.002) were independently associated with CaOx deposition. Graft survival censored for death was significantly worse in patients with CaOx deposition (p = 0.018). In only 1 of 106 preimplantation biopsies CaOx deposition was found (0.94%).ConclusionCaOx deposition appears to be primarily recipient-derived and is frequently observed in for-cause renal allograft biopsies obtained within 3 months post-transplantation. It is associated with inferior renal function at the time of biopsy and worse graft survival.
Highlights
Oxalic acid is a small decarboxylate ion (C2O4) and is the end-product of many metabolic pathways
In the population with Calcium oxalate (CaOx) deposition: Patients had significantly more often been treated with dialysis before transplantation (89 vs. 64%; p = 0.011); delayed graft function occurred more frequently (42 vs. 23%; p = 0.038); and the estimated GFR (eGFR) at the time of first biopsy was significantly worse (21 vs. 29 ml/ min/1.73m2; p = 0.037)
In a multivariate logistic regression analysis, eGFR at the time of first biopsy, dialysis before transplantation and the time of first biopsy after transplantation were independently associated with CaOx deposition
Summary
Oxalic acid is a small decarboxylate ion (C2O4) and is the end-product of many metabolic pathways. The plasma concentration of oxalic acid is determined by the balance between dietary intake, intestinal absorption, endogenous production and renal excretion [2]. Hyperoxaluria, defined as an excessive urinary excretion of oxalic acid, can be classified as primary or secondary hyperoxaluria. Primary hyperoxaluria is caused by rare autosomal recessive disorders which cause an excessive production of oxalic acid [5,6,7]. Persistently elevated plasma oxalic acid concentrations cause CaOx deposition in the kidney which leads to permanent loss of renal function. Calcium oxalate (CaOx) deposition in the kidney may lead to loss of native renal function but little is known about the prevalence and role of CaOx deposition in transplanted kidneys
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