title: Effects of spironolactone on residual renal function and peritoneal function in peritoneal dialysis patients.
abstract: There is increasing evidence that long-term peritoneal dialysis (PD) is associated with structural changes in the peritoneal membrane. Inhibition of the renin-angiotensin system has been demonstrated to lessen peritoneal injury and to slow the decline in residual renal function. Whether spironolactone affects residual renal function in addition to the peritoneal membrane is unknown. We evaluated 23 patients (13 women) with a glomerular filtration rate of 2 mL/min/1.73 m2 or more who were receiving PD. Patients with an active infection or peritonitis episode were excluded. Baseline measurements were obtained for serum high-sensitivity C-reactive protein (hs-CRP), vascular endothelial growth factor (VEGF), transforming growth factor beta (TGF-beta), and connective tissue growth factor (CTGF); for daily ultrafiltration (in milliliters); for end-to-initial dialysate concentration of glucose (4/D0 glucose), Kt/V, and peritoneal transport status; and for dialysate cancer antigen 125 (CA125). Spironolactone therapy (25 mg) was given daily for 6 months, after which all measurements were repeated. Mean age of the patients was 46 +/- 13 years. Duration of PD was 15 +/- 21 months (range: 2-88 months). After spironolactone therapy, mean dialysate CA125 was significantly increased compared with baseline (20.52 +/- 12.06 U/mL vs. 24.44 +/- 13.97 U/mL, p = 0.028). Serum hs-CRP, VEGF, TGF-beta, CTGF, daily ultrafiltration, D/Do glucose, Kt/V and peritoneal transport status were similar at both times. At the end of the study period, residual glomerular filtration rate in the patients was lower. In PD patients, treatment with spironolactone seems to slow the decline of peritoneal function, suppress the elevation of profibrotic markers, and increase mesothelial cell mass.
authors.forename: Berna
authors.initials: B
authors.lastname: Yelken
authors.forename: Numan
authors.initials: N
authors.lastname: Gorgulu
authors.forename: Meltem
authors.initials: M
authors.lastname: Gursu
authors.forename: Halil
authors.initials: H
authors.lastname: Yazici
authors.forename: Yasar
authors.initials: Y
authors.lastname: Caliskan
authors.forename: Aysegul
authors.initials: A
authors.lastname: Telci
authors.forename: Savas
authors.initials: S
authors.lastname: Ozturk
authors.forename: Rumeyza
authors.initials: R
authors.lastname: Kazancioglu
authors.forename: Tevfik
authors.initials: T
authors.lastname: Ecder
authors.forename: Semra
authors.initials: S
authors.lastname: Bozfakioglu
mesh_terms: D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000378:metabolism; D018394:CA-125 Antigen / Q000378:metabolism; D055513:Connective Tissue Growth Factor / Q000097:blood; D004232:Diuretics / Q000494:pharmacology*; D005260:Female; D005919:Glomerular Filtration Rate; D006801:Humans; D007676:Kidney Failure, Chronic / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy*; D008297:Male; D008875:Middle Aged; D010530:Peritoneal Dialysis; D010537:Peritoneum / Q000187:drug effects*; D013148:Spironolactone / Q000494:pharmacology*; D016212:Transforming Growth Factor beta / Q000097:blood; D042461:Vascular Endothelial Growth Factor A / Q000097:blood; D055815:Young Adult
chemical_list: D015415:Biomarkers; D018394:CA-125 Antigen; D004232:Diuretics; D016212:Transforming Growth Factor beta; D042461:Vascular Endothelial Growth Factor A; D055513:Connective Tissue Growth Factor; D013148:Spironolactone