IgA Nephropathy: Are We Doing Enough?

Immunoglobulin A nephropathy (IgAN) was first identified and described as a disease by Berger and Hinglais in 1968. It is the most common primary glomerulopathy worldwide [1], most prevalent in East Asians and Caucasians and rare in black individuals. There are four key elements that contribute to IgAN, which determine the severity, course, and prognosis of the disease: circulating IgA immunocomplexes that favor mesangial deposition, the efficiency of the reticuloendothelial system, mesangial cell affinity and reaction to mesangial accumulation of poorly glycosylated IgA1, and the renal tendency to glomerulosclerosis and interstitial fibrosis. Clinical manifestations among patients with IgAN include hematuria, approximately 40% to 50% of cases present with one or more episodes of hematuria, usually preceded by upper respiratory tract infections. Between 30% and 40% present with hematuria and non-nephrotic range proteinuria that may be associated with arterial hypertension and impaired renal function. The TESTING study reveal a significant decrease in outcomes such as the risk of a 40% decrease in glomerular filtration rate or the need for renal replacement therapy in the group treated with steroids. The decrease in renal function compared to the group treated in the previously mentioned STOP-IgAN trial was 4 times less than in the TESTING study. Are we doing enough? Obviously, more trials are required with the use of adequate nephroprotection measures. We present 3 patients with a diagnosis of IgA nephropathy who attend the follow-up consultation and voluntarily decide to take part in the review.