For patients with IgA nephropathy, a type of kidney disease, steroid treatment can prevent or delay loss of kidney function, according to a study appearing in an upcoming issue of the Journal of the American Society of Nephrology (JASN). IgA nephropathy is an autoimmune disease that affects the kidneys and a major cause of end-stage kidney failure in younger people.

“Our study shows that corticosteroids are very useful in patients with IgA nephropathy, and that the addition of an immunosuppressant drug, such as azathioprine, doesn’t increase their benefit,” comments Claudio Pozzi, MD (Ospedale E. Bassini, Milan).

Patients with IgA nephropathy develop deposits of the protein IgA in the kidneys. The abnormal IgA deposits damage the glomeruli (the filtering units of the kidney), leading to blood and protein in the urine. Previous studies have shown that steroids can reduce urine protein levels and help protect kidney function. However, some patients develop progressive kidney disease, despite steroid treatment.

For the new study, 207 patients with IgA nephropathy were randomly assigned to receive steroids, alone or with the immunosuppressant drug azathioprine. The researchers wanted to see if a more aggressive treatment approach using azathioprine—most commonly used to prevent rejection after organ transplantation—could produce better outcomes.

However, there were no major differences in the results with steroids alone or steroids plus azathioprine. After 5 years’ follow-up, nearly 90 percent of patients in both groups were alive without progressive kidney disease. In contrast, patients receiving azathioprine had more complications and side effects.

The study is the largest clinical trial of IgA nephropathy to date and provides important confirmation that steroids can halt or slow the progression toward advanced kidney disease. “The number of enrolled patients and the length of follow-up make the results very strong,” Pozzi says.

All patients in the study had normal or only slightly reduced kidney function. “However, IgA nephropathy is frequently a silent disease that is not diagnosed until kidney function is already damaged,” Pozzi adds. “We want to verify if this treatment could be useful to slow down the progression of kidney disease in patients with severe renal insufficiency.”

The study did not address the role of drugs called renin-angiotensin system (RAS) blockers. At the time the study began, RAS blockers were sometimes used in patients with kidney disease causing protein in the urine, but not always. “In the following years, RAS blockade has become more frequent in everyday clinical practice,” Pozzi says. “Nearly 40 percent of the patients in our study started these drugs during follow-up.” However, the preservation of kidney function may reflect more the effect of steroids, the researchers believe. Two recent studies found that steroids combined with RAS blockers are more effective than RAS blockers alone.

The authors report no financial disclosures.

Study co-authors were Simeone Andrulli, Lucia Del Vecchio, Francesco Locatelli (Ospedale di Lecco), Antonello Pani (Ospedale di Cagliari), Patrizia Scaini (Ospedale di Brescia), Giambattista Fogazzi (Ospedale Maggiore di Milano), Bruno Vogt (Inselspital di Berna), Vincenzo De Cristofaro (Ospedale di Sondrio), Landino Allegri (Ospedale di Parma), Lino Cirami (Ospedale di Firenze), and Aldo Deni Procaccini (Ospedale di Foggia).

The article, entitled “Addition of Azathioprine to Corticosteroids Does Not Benefit Patients with IgA Nephropathy,” will appear online at http://jasn.asnjournals.org/ on July 15, 2010, doi 10.1681/ASN.2010010117.

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Source:  American Society of Nephrology (ASN)