alexa Nephropathy by Oxalate Deposits: Not Only a Tubular Dysfunction
ISSN: 2165-7920

Journal of Clinical Case Reports
Open Access

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Case Report

Nephropathy by Oxalate Deposits: Not Only a Tubular Dysfunction

Muraro E1, Gianesello L1, Priante G1, Comacchio A1, Carraro G2, Naso A2, Anglani F1, Valente M3 and Del Prete D1*
1Department of Medicine, Nephrology Unit University of Padua, Italy
2Nephrology and Dialysis Unit Padua Hospital, Italy
3Department of Medical-Diagnostic Sciences and Special Therapies, University of Padua Medical School, Padua, Italy
*Corresponding Author : Dorella Del Prete
Department of Medicine, Nephrology
Unit University of Padua, Italy
Tel: +39 049 8217887
Fax: +39 049 8212151
E-mail: [email protected]
Received December 28, 2015; Accepted February 19, 2016; Published February 23, 2016
Citation: Muraro E, Gianesello L, Priante G, Comacchio A, Carraro G, et al. (2016) Nephropathy by Oxalate Deposits: Not Only a Tubular Dysfunction. J Clin Case Rep 6:713. doi:10.4172/2165-7920.1000713
Copyright: © 2016 Muraro E, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
 

Abstract

Background: Hyperoxaluria may be either inherited or acquired. Primary Hyperoxaluria (PH) is a rare autosomal recessive disease characterized by increased endogenous oxalate production and accumulation in renal and extrarenal tissues. The excess oxalate is excreted in the urine and frequently patients with PH present signs or symptoms related to kidney stones and progressive nephrocalcinosis. Here we present a case of a young man with an unexplained progressive renal failure, without symptoms of nephrolithiasis or nephrocalcinosis. Renal biopsy examination was performed to clarify renal dysfunction. Kidney biopsy showed a glomerular and tubulo-interstitial nephropathy by oxalate deposits. Genetic testing was used to confirm histopathological evaluation, demonstrating the c.731T>C mutation at exon 7 of AGTX gene. Conclusions: This case of PH type 1 was peculiar for the clinical presentation (renal failure without evidence of urolithiasis or nephrocalcinosis) and for the glomerular histopathological aspect of oxalate deposition. To our knowledge, this is the first demonstration of CaOx deposition in the glomeruli to be reported in the literature. The histopathological diagnosis enable us to study in deep the bio-humoral profile of the patient and to reach an accurate diagnosis.

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