An outline is given of the pathophysiology of IgA nephropathy (IgA) in order to emphasize the role of eicosanoids, angiotensin II, and reactive oxygen species. ACE inhibitors and early corticosteroid usage are prime therapies. Tonsillectomy is to be considered, certainly for individual cases. It is logical that other components of a cocktail could be (i) thromboxane antagonists, (ii) leukotriene antagonists, or (iii) PAF antagonist. In theory there should be benefit from antioxidants. Fish oils have not come up to expectation. PDGF aptamers look promising for the prevention of mesangial cell proliferation. Heparins are not used in the way that they could be. Various other agents could help reduce decline.