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Early renal and vascular changes in ADPKD patients with low-grade albumin excretion and normal renal function
Background. Autosomal dominant polycystic kidney disease (ADPKD) shows an increase in both urine monocyte chemoattractant protein-1 (MCP-1) and carotid intima–media thickness (CIMT) before changes in serum creatinine concentration. Although microalbuminuria is an index of disease progression, data o...
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Published in: | Nephrology, dialysis, transplantation dialysis, transplantation, 2009-08, Vol.24 (8), p.2458-2463 |
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Main Authors: | , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
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Online Access: | Get full text |
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Summary: | Background. Autosomal dominant polycystic kidney disease (ADPKD) shows an increase in both urine monocyte chemoattractant protein-1 (MCP-1) and carotid intima–media thickness (CIMT) before changes in serum creatinine concentration. Although microalbuminuria is an index of disease progression, data on whether renal alterations and vascular remodelling are already present at normal or minimally increased levels of urine albumin excretion in early stages of the disease are lacking. Methods. Forty-eight ADPKD patients (24.8 ± 0.8 years) with normal renal function (MDRD 108.1 ± 3.1 ml/min) and 21 age-matched controls were studied in a cross-sectional study. The urine albumin/creatinine ratio (UACR) above the upper range of controls (6.8 mg/g) was taken as the predictor of renal alterations and vascular remodelling. Urine MCP-1, MCP-1 fractional excretion (FEMCP-1), endothelial-dependent vascular relaxation (EDVR), aortic pulse-wave velocity (Ao-PWV) and CIMT were chosen as biological markers. Results. No differences between ADPKD with UACR ≤6.8 mg/g and controls were observed in urine MCP-1 (77.7 ± 13.9 versus 57.8 ± 6.3 ng/g), FEMCP-1 (91 ± 19 versus 74 ± 8%) and CIMT (0.47 ± 0.06 versus 0.44 ± 0.07 mm), respectively. Conversely, ADPKD with UACR >6.8 mg/g showed values that were different from the two other groups. In addition, patients with UACR >6.8 and |
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ISSN: | 0931-0509 1460-2385 |
DOI: | 10.1093/ndt/gfp136 |