The clinical features associated with worse outcomes include persistent proteinuria (>1 g/day), elevated serum creatinine concentration at diagnosis, and poorly controlled hypertension.

The pathologic features associated with worse outcomes include moderate to severe mesangial hypercellularity, the presence of endocapillary hypercellularity, segmental sclerosis, and tubular atrophy/interstitial fibrosis affecting more than 25% of the cortical area. Similarly, the presence of extensive cellular crescent formation portends worse outcomes.

Although IgA deposition recurs in up to 50% of renal allograft recipients, this is usually an isolated immunohistochemical finding, without significant glomerular hypercellularity or clinical signs of disease (e.g., hematuria and proteinuria). Graft loss from recurrent IgAN is rare.

Compared with primary IgAN, secondary IgAN appears to have a lower rate of progression to end-stage renal disease. In most cases, the clinical course is dominated by the underlying disease (e.g., alcoholic cirrhosis).