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Table of Contents
Vol. 26, No. 1, 2006
Issue release date: April 2006
Section title: In-Depth Topic Review
Am J Nephrol 2006;26:1–11
(DOI:10.1159/000090705)

Etiology of Balkan Endemic Nephropathy and Associated Urothelial Cancer

Stefanovic V.a · Toncheva D.b · Atanasova S.c · Polenakovic M.d
aInstitute of Nephrology and Hemodialysis, Faculty of Medicine, Niš, Serbia; bDepartment of Medical Genetics, Medical University, Sofia, Bulgaria; cDepartment of Clinical Chemistry, Georg August University, Göttingen, Germany, and dMacedonian Academy of Sciences and Arts, Skopje, Macedonia

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Article / Publication Details

First-Page Preview
Abstract of In-Depth Topic Review

Received: September 29, 2005
Accepted: November 30, 2005
Published online: April 05, 2006
Issue release date: April 2006

Number of Print Pages: 11
Number of Figures: 0
Number of Tables: 4

ISSN: 0250-8095 (Print)
eISSN: 1421-9670 (Online)

For additional information: http://www.karger.com/AJN

Abstract

Balkan endemic nephropathy (BEN) is a familial chronic tubulointerstitial disease with insidious onset and slow progression to terminal renal failure. Evidence has accumulated that BEN is an environmentally induced disease. There are three actual theories attempting to explain the environmental cause of this disease: (1) the aristolochic acid hypothesis, which considers that the disease is produced by chronic intoxication with Aristolochia, (2) the mycotoxin hypothesis, which considers that BEN is produced by ochratoxin A, and (3) the Pliocene lignite hypothesis, which proposes that the disease is caused by long-term exposure to polycyclic aromatic hydrocarbons and other toxic organic compounds leaching into the well drinking water from low-rank coals in the vicinity to the endemic settlements. Moreover, it was suggested that BEN risk is influenced by inherited susceptibility. Therefore, it has been expected that molecular biological investigations will discover genetic markers of BEN and associated urothelial cancer, permitting early identification of susceptible individuals who may be at risk of exposure to the environmental agents. Since kidney pathophysiology is complex, gene expression analysis and highly throughput proteomic technology can identify candidate genes, proteins and molecule networks that eventually could play a role in BEN development. Investigation of gene-gene and gene-environment interactions could be the content of further studies determining the precise risk for BEN.

© 2006 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of In-Depth Topic Review

Received: September 29, 2005
Accepted: November 30, 2005
Published online: April 05, 2006
Issue release date: April 2006

Number of Print Pages: 11
Number of Figures: 0
Number of Tables: 4

ISSN: 0250-8095 (Print)
eISSN: 1421-9670 (Online)

For additional information: http://www.karger.com/AJN


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