Abstract

Aim. The aim of this study was to compare urinary alpha 1 microglobulin (A1MG) in healthy individuals with and without family burden for Balkan endemic nephropathy (BEN) in an endemic village. Methods. Otherwise healthy inhabitants with microalbuminuria or proteinuria were divided into two groups: with (n = 24) and without (n = 32) family BEN burden and screened for urinary A1MG and A1MG/urine creatinine ratio. Results. Average value of urinary A1MG was 10.35 ± 7.01 mg/L in group with and 10.79 ± 8.27 mg/L in group without family history for BEN (NS, P = 0.87). A1MG was higher than 10 mg/L in eight (33.33%) inhabitants with family history and in 12 (37.5%) without (NS, P = 0.187). Average values of urinary A1MG/creatinine ratio were 1.30 ± 1.59 and 0.94 ± 0.78 in group with and group without family BEN history (NS, P = 0.39, resp.). Elevated values of this ratio were found in 13 (54.17%) inhabitants with and 14 (43.75%) without family history for BEN (NS, P = 0.415). Conclusion. We did not find statistically significant difference in the examined markers between healthy individuals with and without family burden for BEN. We concluded that these markers are not predictive of risk for BEN.

Highlights

  • Balkan endemic nephropathy (BEN) is chronic irreversible tubulointerstitial nephritis that is diagnosed in agrarian regions of the Balkan (Bosnia and Herzegovina, Bulgaria, Croatia, Romania, and Serbia)

  • Hematuria was found in eight examinees (33.33%) in group with family burden for BEN and in five examinees (15.63%) in group without family burden for BEN

  • alpha 1 microglobulin (A1MG) was elevated in eight (33.33%) inhabitants with family burden and 12 (37.5%) examinees without family burden for BEN (Fisher’s exact test, P = 0.187)

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Summary

Introduction

Balkan endemic nephropathy (BEN) is chronic irreversible tubulointerstitial nephritis that is diagnosed in agrarian regions of the Balkan (Bosnia and Herzegovina, Bulgaria, Croatia, Romania, and Serbia). During the past half century, numerous dilemmas and conflicting opinions regarding BEN aetiology have been proposed and the theory that BEN is caused by chronic poisoning with aristolochic acid ingested by food in people with genetic predisposition has gained credence [3]. Based on these reports, BEN is proposed to be categorized as a toxic tubulointerstitial nephropathy, with clinical picture and disease progression not different from other tubulointerstitial nephropathies, but with BEN having an insidious and gradual progression to end stage renal disease. In accordance with our former studies [4], recent studies of cadmium nephropathy in Japan [5] and in BEN [6], it seemed that alpha 1 microglobulin (A1MG) could be good

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