with high risk of worsening kidney function. however, these results have not been reproduced by other study groups and in two subsequent meta-analyses. however, fish oil therapy does not have the drawbacks of immunosuppressive therapy. also, apart from its unpleasant taste and abdominal discomfort, it is relatively safe to consume. the events that tend to progressive kidney failure are not unique to iga nephropathy and non-specific measures to reduce the same would be equally useful. these include a low-protein diet and optimal control of blood pressure. the choice of the antihypertensive agent is open as long as the blood pressure is controlled to desired level. however, angiotensin converting enzyme inhibitors and angiotensin ii receptor antagonists are favoured due to their anti-proteinuric effect. in december 2021, budesonide (tarpeyo) was approved for medical use in the us to reduce proteinuria in adults with primary iga nephropathy at risk of rapid disease progression. prognosis male sex, proteinuria (especially > 2 g/day), hypertension, smoking, hyperlipidemia, older age, familial disease and elevated creatinine concentrations are markers of a poor outcome. frank hematuria has shown discordant results with most studies showing a better prognosis, perhaps related to the early diagnosis, except for one group which reported a poorer prognosis. proteinuria and hypertension are the most powerful prognostic factors in this group. there are certain other features on kidney biopsy such as interstitial scarring which are associated with a poor prognosis. ace gene polymorphism has been recently shown to have an impact with the dd genotype associated more commonly with progression to kidney failure. epidemiology men are affected three times as often as women. there is also marked geographic variation in the prevalence of iga nephropathy throughout the world. it is the most common glomerular disease in the far east and southeast asia, accounting for almost half of all the patients with glomerular disease. however, it accounts for only about 25% of the proportion in europeans and about 10% among north americans, with african–americans having a very low prevalence of about 2%. a confounding factor in this analysis is the existing policy of screening and use of kidney biopsy as an investigative tool. school children in japan undergo routine urinalysis (as do army recruits in singapore) and any suspicious abnormality is pursued with a kidney biopsy, which might partly explain the high observed incidence of iga nephropathy in those countries. genetics though various associations have been described, no consistent pattern pointing to a single susceptible gene has been identified to date. associations described include those with c4 null allele, factor b bf alleles, mhc antigens and iga isotypes. ace gene polymorphism (d allele) is associated with progression of kidney failure, similar to its association with other causes of chronic kidney failure. however, more than 90% of cases of iga nephropathy are sporadic, with a few large pedigrees described from kentucky and italy (online mendelian inheritance in man (omim): 161950). history dr jean berger william heberden, the elder, first described the disease in 1801 in a 5-year-old child with abdominal pain, hematuria, hematochezia, and purpura of the legs. in 1837, johann lukas schönlein described a syndrome of purpura associated with joint pain and urinary precipitates in children. eduard heinrich henoch, a student of schönlein's, further associated abdominal pain and renal involvement with the syndrome. in 1968, jean berger (1930–2011), a pioneering french nephrologist, with co-author, the electron microscopist nicole hinglais, was the first to describe iga deposition in this form of glomerulonephritis and therefore it is sometimes called berger's disease.