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.


CONCLUSIONS
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.
Casal
J Antonio
JA
Central Laboratory, Hospital Clinico Universitario, Santiago de Compostela, Spain.
Hermida
Jesús
J
Lens
Xosé M
XM
Tutor
J Carlos
JC
D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000419:Albuminuria / Q000097:blood / Q000175:diagnosis* / Q000652:urine; D015415:Biomarkers / Q000097:blood / Q000652:urine; D003401:Creatine / Q000097:blood; D055316:Cystatin C; D015891:Cystatins / Q000097:blood; D005260:Female; D005919:Glomerular Filtration Rate; D005979:Glutathione Peroxidase / Q000097:blood; D054819:Hexosaminidase B; D006801:Humans; D006977:Hypertension, Renal / Q000097:blood / Q000175:diagnosis* / Q000652:urine; D007527:Isoenzymes / Q000652:urine; D008297:Male; D008875:Middle Aged; D016891:Polycystic Kidney, Autosomal Dominant / Q000097:blood / Q000175:diagnosis* / Q000652:urine; D014508:Urea / Q000097:blood; D001619:beta-N-Acetylhexosaminidases / Q000652:urine
D015415:Biomarkers; C525030:CST3 protein, human; D055316:Cystatin C; D015891:Cystatins; D007527:Isoenzymes; D014508:Urea; D005979:Glutathione Peroxidase; D054819:Hexosaminidase B; D001619:beta-N-Acetylhexosaminidases; D003401:Creatine