PubMed · 8298416
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
D G Williams. 1994-01-08. IgA nephropathy.. https://doi.org/10.1136/bmj.308.6921.74
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Explore the source record for details and available documents.
Recurrence of the original disease is now the third most frequent cause of allograft loss at 10 years after transplantation in patients with underlying glomerulonephritis. IgA nephropathy (IgAN), the most common type of glomerulonephritis, histologically recurs in up to 60% of the patients. Initially considered to be a relatively benign phenomenon, several studies, which included a total of almost 1200 patients with underlying IgAN, have now established that after a mean follow up of 5 years, approximately 13% of the patients will exhibit some recurrence-related renal graft dysfunction and approximately 5% will have lost their graft as a result of recurrent IgAN. The only established predictor of graft loss is the time elapsed since renal transplantation. The risk of recurrence-associated graft loss increases to approximately 25% if a prior graft has already been lost as a result of recurrent IgAN. Whether living, related donor kidneys are at higher risk for recurrence is controversial. Despite all these issues, graft survival in patients with underlying IgAN compared with patients with other renal diseases is excellent. In patients with recurrent IgAN, no specific therapy other than optimal supportive care has been established.
Immunoglobulin A (IgA) nephropathy is a worldwide disease that causes end-stage kidney disease (ESRD) in up to 15-20% of affected patients within 10 years from the apparent onset of disease and in up to 30-40% of individuals within 20 years from diagnosis. No specific treatment has been established and there is wide variation in current practice. This systematic review evaluates the use of immunosuppressive agents to treat patients with IgA nephropathy. The Cochrane Renal Group Specialized Register, Cochrane Controlled Trial Registry, MEDLINE, EMBASE and article reference lists were searched for randomized or quasi randomized trials. Two independent reviewers assessed studies for inclusion criteria (biopsy proven IgA nephropathy, randomized trial, use of immunosuppressive agents) and extracted data regarding the effects of immunosuppressive agents on ESRD, doubling of serum creatinine, glomerular filtration rate, urinary protein excretion and side-effects. Data were analysed with a random effects model. The published trials were few (13 trials, 623 patients) and were generally of poor quality. Compared with placebo, steroids were associated with a lower risk of progression to ESRD (six trials, 341 patients, RR 0.44, 95% CI 0.25-0.80) and lower end-of-trial proteinuria (six trials, 263 patients, weighted mean difference (WMD) -0.49 g/day, 95% CI -0.25 to -0.72). Treatment with alkylating agents significantly reduced end of treatment proteinuria (two trials, 122 patients, WMD -0.94, 95% CI -0.46 to -1.43). Although the optimal management of patients with IgA nephropathy remains uncertain because of limitations with the existing published data, immunosuppressive agents are a promising strategy and should be investigated further.