Literature DB >> 25586405

Microscopic nephrocalcinosis in chronic kidney disease patients.

Pieter Evenepoel1, Kristien Daenen1, Bert Bammens1, Kathleen Claes1, Björn Meijers1, Maarten Naesens1, Ben Sprangers1, Dirk Kuypers1, Eveline Lerut2.   

Abstract

BACKGROUND: Experimental data indicate that microscopic calcium phosphate deposition in the kidney (nephrocalcinosis) may accelerate progression of chronic kidney disease (CKD). Data on the prevalence, risk factors and implications of nephrocalcinosis in CKD patients are scarce. A mineral metabolism disorder could play an important pathogenetic role, as suggested by recent protocol biopsy findings in incident renal transplant recipients.
METHODS: Kidney biopsy cylinders of CKD patients, collected between January 1989 and December 2007, were screened for the presence of nephrocalcinosis. Only patients with ≥1 parathyroid hormone (PTH) level available within 180 days of the biopsy were eligible for inclusion (n = 211). Demographics and mineral metabolism parameters were retrieved from medical files. Data on renal death (up to December 2012) were obtained from the Flemish ESRD registry. Baseline biopsies from 110 deceased kidney transplant donors served as controls.
RESULTS: The prevalence of nephrocalcinosis in kidney donors and patients with CKD 1-2, CKD 3-4 and CKD 5-5D was 4.6, 14.3, 20.2 and 54.0%, respectively (P < 0.0001). Among CKD patients, patients with nephrocalcinosis were characterized by lower estimated GFR, lower serum bicarbonate level and higher serum PTH and calcium level. In multivariate regression analysis, high serum PTH, calcium and creatinine level, and low serum bicarbonate level were all significantly and independently associated with nephrocalcinosis. Serum phosphorus level, but not nephrocalcinosis predicted renal death, independent of renal function.
CONCLUSIONS: Our data demonstrate that prevalence rates of nephrocalcinosis increase with increasing CKD stage to reach more than 50% in end-stage renal disease patients and suggest that acid-base and mineral metabolism disturbances are implicated in its pathogenesis.
© The Author 2015. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.

Entities:  

Keywords:  CKD-MBD; nephrocalcinosis

Mesh:

Substances:

Year:  2015        PMID: 25586405     DOI: 10.1093/ndt/gfu400

Source DB:  PubMed          Journal:  Nephrol Dial Transplant        ISSN: 0931-0509            Impact factor:   5.992


  5 in total

Review 1.  Dietary Phosphorus Intake and the Kidney.

Authors:  Alex R Chang; Cheryl Anderson
Journal:  Annu Rev Nutr       Date:  2017-06-14       Impact factor: 11.848

2.  Osteopontin protects against high phosphate-induced nephrocalcinosis and vascular calcification.

Authors:  Neil J Paloian; Elizabeth M Leaf; Cecilia M Giachelli
Journal:  Kidney Int       Date:  2016-03-09       Impact factor: 10.612

3.  Renal matrix Gla protein expression increases progressively with CKD and predicts renal outcome.

Authors:  Kana N Miyata; Cynthia C Nast; Tiane Dai; Ramanath Dukkipati; Janine A LaPage; Jonathan P Troost; Leon J Schurgers; Matthias Kretzler; Sharon G Adler
Journal:  Exp Mol Pathol       Date:  2018-07-06       Impact factor: 3.362

4.  Malabsorption syndrome as a rare cause of nephrocalcinosis.

Authors:  Rui Abreu; Cláudia Bento; Luís Oliveira; Teresa Morgado
Journal:  Clin Cases Miner Bone Metab       Date:  2017-02-10

5.  Risk factors and implications associated with renal mineralization in chronic kidney disease in cats.

Authors:  Pak-Kan Tang; Rosanne E Jepson; Yu-Mei Chang; Rebecca F Geddes; Mark Hopkinson; Jonathan Elliott
Journal:  J Vet Intern Med       Date:  2022-01-19       Impact factor: 3.333

  5 in total

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