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      Kidney allograft failure due to acute phosphate nephropathy associated with severe secondary hyperparathyroidism

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          Abstract

          Intratubular calcification is a common finding in renal allografts. However, possible harmful effect of this calcification is not well recognized, and allograft failure purely due to this condition has not been reported. We report a kidney transplant recipient who suffered from severe secondary hyperparathyroidism and unexplained early allograft failure. A diagnosis of acute phosphate nephropathy was made subsequently based on serial allograft biopsy findings. This case calls for a high index of suspicion to look for this rare cause of allograft dysfunction among high-risk patients. It also highlights the importance of good calcium–phosphate control before renal transplantation.

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          Most cited references10

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          Early calcification of renal allografts detected by protocol biopsies: causes and clinical implications.

          Interstitial calcification has been described in renal allografts, however, the etiology and significance of this finding for the graft are unclear. The aim of this study was to examine calcification in serial protocol biopsies, to test the hypothesis that calcification is related to parameters of calcium homeostasis in these patients and to analyze a possible relation between calcification and graft function at 1 year. We studied 213 patients with 586 protocol biopsies obtained 6 weeks, 3 and 6 months after transplantation. Calcifications increased over time, from 6.1% at 6 weeks to 17.8% at 6 months. Out of the 213 patients, 56 had calcification in one or more biopsies. Patients age and gender, underlying renal disease, dialysis mode and duration, previous transplantations, donor type, age and gender, HLA matches and ischemia time had no influence on calcification. Calcification was not related to rejection episodes, acute tubular lesions, calcineurin inhibitor toxicity or tubulointerstitial fibrosis and tubular atrophy. Patients with calcification had significantly higher serum parathormone and calcium levels. In patients with calcification, high PTH levels correlated with an inferior outcome of graft function at 1 year after transplantation (p<0.05). Therefore, treatment of hyperparathyroidism should be considered earlier and more often in these patients.
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            Nephrocalcinosis: new insights into mechanisms and consequences

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              Calcium levels as a risk factor for delayed graft function.

              Delayed graft function (DGF) occurs in up to 50% of renal transplants. Hypercalcemia and hyperparathyroidism are associated with impaired renal function. Little is known on the effects of serum calcium levels on DGF. This issue was addressed in the current study. Patients receiving a cadaveric renal transplant between 1986 and 1996 were studied. Data on calcium metabolism and histologic characteristics of nephrocalcinosis, acute tubular necrosis (ATN), and acute rejection in biopsies taken within the first week were related to the occurrence of DGF. The incidence of DGF in a cohort of 585 cadaveric transplants was 31%. DGF correlated independently with serum calcium levels (odds ratio [OR] 1.14 [95% confidence interval (CI) 1.04-1.26] per 0.1 mmol/L). The use of calcium channel blockers before transplantation protected against DGF (OR 0.5 [95% CI 0.29- 0.87]). In this selected group, we found an association with histologic signs of ATN and DGF. However, most of the biopsies also had features of acute rejection or nephrocalcinosis. Nephrocalcinosis was found in 12 of 71 biopsies and was not associated with serum calcium levels or the occurrence of DGF. In this study, serum calcium levels were independently associated with DGF. This could not be explained by the presence of microscopic nephrocalcinosis. Therefore, DGF is attributed to high intracellular calcium levels. Because calcium supplementation and vitamin D analogues are commonly used in dialysis practice, hypercalcemia influences long-term graft outcome by its effect on DGF. The pretransplant use of calcium channel blockers has a protective effect on the occurrence of DGF.
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                Author and article information

                Journal
                NDT Plus
                NDT Plus
                ndtplus
                ckj
                NDT Plus
                Oxford University Press
                1753-0784
                1753-0792
                October 2011
                15 July 2011
                15 July 2011
                : 4
                : 5
                : 324-326
                Affiliations
                [1 ]Renal Unit, Department of Medicine & Geriatrics, Kwong Wah Hospital, Hong Kong SAR, China
                [2 ]Department of Pathology, Kwong Wah Hospital, Hong Kong SAR, China
                Author notes
                Correspondence and offprint requests to: Ping-Nam Wong; E-mail: apnwong@ 123456yahoo.com
                Article
                10.1093/ndtplus/sfr078
                4421720
                25984179
                eeb5d4b0-139d-48fa-b9d9-5aaf9c281ec4
                © The Author 2011. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

                History
                : 07 April 2011
                : 31 May 2011
                Categories
                II. Clinical Reports
                Case Reports

                Nephrology
                acute phosphate nephropathy,hyperparathyroidism,nephrocalcinosis,tubular injury
                Nephrology
                acute phosphate nephropathy, hyperparathyroidism, nephrocalcinosis, tubular injury

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