Although the basal plasma renin activity in patients with type-2 diabetes was not significantly different from controls, both the renin activity and kallikrein levels increased after furosemide in controls while in diabetics this response was severely blunted, indicating early derangement of the KKS and the RAS as renal hemodynamic mechanisms heralding the onset of nephropathy [37]. The gene discussed is KLK4; the disease is type 2 diabetes mellitus.