The most effective treatment option for patients with IgA nephropathy (IgAN) who develop end-stage kidney disease (ESKD) is kidney transplant. Our featured experts discuss transplant outcomes, including the risk of recurrence and what might be done to mitigate the risk.

Kidney transplant is certainly the best treatment option for ESKD. Dialysis is a tough burden for patients, requiring numerous hours, and it is associated with low quality of life. Kidney transplant has much better outcomes, and patients with IgAN typically do very well after the procedure. It is thought that up to 40% of those with IgAN will need or be eligible for a kidney transplant within 20 years. For patients presenting with more proteinuria or lower kidney function, however, this might occur within just 3 to 5 years.

The vast majority of patients with IgAN will have the opportunity to receive a kidney transplant, but wait times can be long and difficult for some patients. Not everyone has the option of receiving a kidney transplant from a living and related donor, so many patients often have to spend at least some time on dialysis.

A significant issue for patients who receive kidney transplants is that IgAN is a systemic disease, and a person’s genetics predisposes them to produce galactose-deficient IgA and to make autoantibodies against it. Therefore, a brand-new kidney may be damaged by circulating immune complexes, and the patient may be at risk for progressive kidney dysfunction. It looks like up to 50% of patients are eventually affected by recurrent IgAN (as seen on biopsy). Hopefully, we will soon have data on whether some of the medications that we now use or will soon employ for IgAN are effective when the disease recurs post transplant.

As Dr Lafayette said, a general rule of thumb is that 20% to 40% of patients with IgAN approach ESKD within 20 years of diagnosis, but there are absolutely patients who approach end-stage disease very quickly and have crescentic glomerulonephritis. The length of time really depends on how aggressive the patient’s disease is. I think that all of us in the glomerular disease world have had patients who developed ESKD much sooner than within 10 years. For instance, I had a pediatric patient whose IgAN progressed to ESKD within 2 years of diagnosis. So, it definitely can happen.

The younger a patient is, the more we hope to do a preemptive kidney transplant to avoid dialysis. But, for patients who are unable to receive a kidney transplant preemptively, we try to get them to transplant as soon as we possibly can. However, even with a kidney transplant, there is still a risk for IgAN recurrence, and that is something that the transplant team needs to be aware of.

The quoted number for IgAN clinical recurrence at 10 years after kidney transplant is approximately 10%. If you were to perform protocol biopsies in the transplanted kidneys at 1, 2, 5, or 10 years after transplant, you would commonly see IgA deposition that is not causing disease. So, approximately 10% or maybe 20% of patients would experience proteinuria and worsening kidney function from IgAN at the end of 10 years. The people at highest risk for IgAN recurrence are those whose IgAN progresses very rapidly to ESKD and those who are younger. There are other factors, but these, in my mind, are the 2 most important factors to predict IgAN recurrence after kidney transplant.

One of the best protective factors against IgAN recurrence after kidney transplant is the use of immunosuppression to prevent graft rejection. Once recurrent IgAN is diagnosed, we do not have evidence-based data on what the best course of treatment is. We may change the immunosuppressive protocol, and we really need to be cognizant of the role of blood pressure and supportive care in such patients. It is unlikely that there will ever be a randomized controlled trial focusing on how best to treat IgAN recurrence after transplant, but, with modern therapies, I am sure that we can find a combination of treatment strategies to help our patients.