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Enalapril Renoprotective in Chronic Allograft Nephropathy Show Comments PDF Print E-mail
Thursday, 12 June 2003
BERLIN (Reuters Health) - The progression of renal failure in kidney transplant patients with chronic nephropathy is slowed when they are treated with the ACE inhibitor enalapril, a researcher said at the World Congress of Nephrology.

BERLIN (Reuters Health) - The progression of renal failure in kidney transplant patients with chronic nephropathy is slowed when they are treated with the ACE inhibitor enalapril, a researcher said at the World Congress of Nephrology.

"This is the first study to show that an ACE inhibitor can reduce proteinuria and blood pressure in these patients," Dr. Anna R. Bagdasaryan, a staff nephrologist at the Research Institute of Transplantology and Artificial Organs in Moscow, told Reuters Health.

"We found less efficacy, though, in patients with high levels of proteinuria than in those with more moderate levels. We found that it is safe after transplantation."

Considering the limited data about the renoprotective efficacy of ACE inhibitors in chronic allograft nephropathy, Dr. Bagdasaryan and her co-investigators wanted to know the effect of enalapril in these patients. In a retrospective study, they reviewed the records of 207 patients who had received cadaveric kidneys.

The patients were divided into two groups. One consisted of 110 patients who had never been given ACE inhibitors. The second group, consisting of 97 patients, had been treated with 5 mg to 10 mg of enalapril daily.

All patients received cyclosporine-based immunosuppression and received calcium-channel blockers, beta-blockers, or both for hypertension. They were followed-up for an average of 29 months.

The investigators further divided the patients into two subgroups based on whether their baseline proteinuria levels were more or less than 0.5 g/d. In the subgroup with no ACE inhibitor and high baseline proteinuria levels, moderate hypertension remained stable during the follow-up period, at a mean arterial blood pressure of 113 mm Hg. Their proteinuria increased from a mean of 0.12 g/d to 0.3 g/d (p<0.001).

In the subgroup with high proteinuria that was treated with enalapril, the blood pressure decreased from a mean of 113 mm Hg to 107 mm Hg (p<0.005). Their proteinuria was not significantly changed, from a mean baseline of 0.12 g/d to 0.08 g/d.

The rate of 48-month serum creatinine doubling in this subgroup was 17%; in the subgroup with high proteinuria but no ACE inhibition treatment it reached 40% (p<0.01).

In patients with moderate proteinuria and no ACE inhibition therapy, mean blood pressure remained stable at 117 mmHg. However, in the subgroup with moderate proteinuria and enalapril treatment, blood pressure decreased from 120 mm Hg to 109 mm Hg (p<0.0001). Proteinuria decreased in 51% of these patients, while in the subgroup with moderate proteinuria and no ACE inhibition, proteinuria increased in 38% of patients (p<0.01).

In the subgroup with moderate proteinuria, the rate of serum creatinine doubling was 50% with enalapril treatment, but 86% without ACE inhibition (p<0.001).

"Our findings show the renoprotective efficacy of enalapril in chronic allograft nephropathy independently of its effect on proteinuria," Dr. Bagdasaryan said. "Its effects are associated mainly with its action as an antihypertensive."


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