TGF-β antagonism, either by 1D11 [26] or other means, such as the natural TGF-β -binding agent, decorin [15], or TβRII Fc [21, 22], ameliorates uremia and pathological changes in non-proteinuric nephritis models such as Thy1 rat nephritis that mainly involves mesangial proliferation and mesangolysis with minimal proteinuria [51], and the 5/6 nephrectomy rat model [27] that presents only a modest degree of proteinuria [52]. The gene discussed is TGFB1; the disease is uremia.