In the European cooperative study 66 children and young adults with early-stage IgA nephropathy (IgAN) were randomly assigned to treatment with the angiotensin-converting enzyme (ACE) inhibitor benazepril or an inactive placebo. IgA nephropathy is caused by deposits of the protein IgA—an immune system antibody—within the filtering units of the kidney (glomeruli). The abnormal IgA deposits damage the glomeruli, leading to blood and protein in the urine. The disease can progress over time, eventually requiring dialysis or transplantation to replace lost kidney function.
The patients in the study all had relatively mild disease, with normal or near-normal kidney function and only mildly elevated levels of protein in the urine. "Our trial focused on a subset of patients with a sort of 'pure' IgAN, without the confounding effects of aging or environmental toxic exposures, including smoking and alcohol, and without severe high blood pressure," says Dr. Rosanna Coppo of Regina Margherita Hospital in Turin, Italy, lead author of the new study.
After a median three years of treatment, the rate of decreased kidney function was just three percent for patients treated with the ACE inhibitor, compared to fifteen percent in the placebo group. The combined risk of decreased kidney function or rising level of protein in the urine was also lower in the ACE inhibitor group: three percent versus 26 percent.
Overall, the urine protein level remained stable and below the level considered harmful in about 40 percent of patients taking benazepril, compared to nine percent of the placebo group. Recent studies have shown that ACE inhibitors are helpful for patients with various kidney diseases. Some studies have found ACE inhibitors beneficial in IgAN, but these have had important limitations.
MEDICA.de; Source: American Society of Nephrology