A comparative study of three kidney biomarker tests in autosomal-dominant polycystic kidney disease

被引:12
作者
Casal, JA
Hermida, J
Lens, XM
Tutor, JC [1 ]
机构
[1] Univ Santiago de Compostela, Hosp Clin, Cent Lab, Santiago De Compostela 15706, Spain
[2] Univ Santiago de Compostela, Hosp Clin, Hereditary Renal Dis Unit, Santiago De Compostela, Spain
关键词
autosomal-dominant polycystic kidney disease; albuminuria; beta-N-acetylhexosaminidase isoenzymes; glutathione peroxidase; cystatin C; ultrasound score;
D O I
10.1111/j.1523-1755.2005.00488.x
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
A comparative study of three kidney biomarker tests in autosomal-dominant polycystic kidney disease. Background. The relationship between the progress of tubular damage and renal insufficiency in autosomal-dominant polycystic kidney disease (ADPKD) is a subject of doubtless interest, and is the object of this present work. Methods. A total of 92 adult ADPKD patients of both genders were studied, none of which presented end-stage renal disease (ESRD), and classified according to an ultrasound score based on kidney size and number of cysts. Urinary albumin and beta-N-acetylhexosaminidase (Hex) and its isoenzymes were determined, together with serum glutathione peroxidase, cystatin C, creatinine, and urea. Results. A frequent elevation of the urinary Hex was found and an alteration of its isoenzymatic profile, with 31% of the normotensive patients with normoalbuminuria already presenting an increased proportion of Hex B isoenzyme. Keeping age constant, a partial significant correlation was found between the ultrasound score and the proportion of Hex B (r= 0.352, P < 0.05), but not with albuminuria or cystatin C. In 42 patients the different biochemical variables were again determined after 1 year, finding that in the 13 normotensive patients with normoalbuminuria there had been a significant decrease in the concentration of cystatin C (P < 0.05), and a significant increase in the urinary excretion of albumin and Hex B isoenzyme (P < 0.05). By the other hand, in the other 29 patients with micro- or macroalbuminuria and hypertension, no significant differences were found. Conclusion. The results point toward an important participation of tubular damage in the pathogenesis of this disease. It may also be suggested that in normotensive and normoalbuminuric ADPKD patients, a gradual increase of glomerular filtration would be produced. After the start of hypertension and microalbuminuria, the glomerular filtration rate (GFR) would decrease progressively, although more slowly.
引用
收藏
页码:948 / 954
页数:7
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