Angiotensin II type 1 (AT(1)) receptor antagonists in the treatment of hypertension after renal transplantation

Citation
R. Holgado et al., Angiotensin II type 1 (AT(1)) receptor antagonists in the treatment of hypertension after renal transplantation, NEPH DIAL T, 16, 2001, pp. 117-120
Citations number
32
Categorie Soggetti
Urology & Nephrology
Journal title
NEPHROLOGY DIALYSIS TRANSPLANTATION
ISSN journal
09310509 → ACNP
Volume
16
Year of publication
2001
Supplement
1
Pages
117 - 120
Database
ISI
SICI code
0931-0509(2001)16:<117:AIT1(R>2.0.ZU;2-D
Abstract
Hypertension is highly prevalent after renal transplantation and has been a ssociated with lower graft survival. Optimum management of post-transplant hypertension remains to be defined. Losartan, a potent, orally active and s elective non-peptide blocker of the angiotensin subtype I receptor, could r epresent a useful drug for treating post-transplant hypertension. Recently, a prospective study of 12 weeks treatment with losartan has showed a satis factory control of arterial hypertension associated with a decrease in prot einuria in this highrisk group of renal transplant patients. A retrospectiv e study was performed to review the role of losartan as a renoprotective ag ent (evaluating blood pressure and proteinuria) in renal transplant recipie nts in a longterm follow-up. A total of 150 transplant recipients were incl uded in the study. None of the patients had a serum creatinine >3 mg/dl, or suspected renal artery stenosis, or other severe concomitant diseases. The indication for losartan therapy was hypertension, proteinuria and/or post- transplant erythrocytosis. The values of blood pressure, results of fasting haematology, blood chemistry and total proteinuria in 24-h urine samples w ere recorded at the time of initiation of losartan therapy, 6 and 3 months before the start, and at 3, 6, 12, 18 and 24 months thereafter. A tendency analysis by linear regression comparing two slopes before and after treatme nt was realized. A decrease in mean blood pressure and proteinuria, from 10 6.7 +/- 0.9 to 98.2 +/- 2.1 mmHg and from 1253.9+/-188 to 91.2+/-33.7 mg/24 h, P < 0.05, respectively, was observed after introduction of losartan. A progressive increase in creatinine clearance was observed after the third m onth of losartan treatment. No significant changes were seen in haematocrit or serum potassium levels. We can conclude that a progressive decrease in mean arterial pressure associated with a decrease in proteinuria was observ ed during long-term follow-up. Based on the capacity of losartan to improve renal function, this drug could be decisive for the treatment and preventi on of chronic allograft nephropathy.