The aim of this study is to localize and study the presence of clotting proteins and platelet antigens in various renal conditions. I have studied 30 surgical specimens and 22 post mortem specimens constituting 12 transplant nephrectomies, 16 biopsies of glomerulonephritis and 2 of morphologically normal kidneys. Of the post mortem renal tissue, 8 patients died of septicaemia, 6 cases of disseminated intravascular coagulation, one of eclampsia and a further 6 cases of glomerulonephritis. A follow-up study of 20 cases of kidney transplants was carried out. There were 11 cases of vascular rejection and 9 cases of cellular rejection, the study included early, mid and final biopsies or nephrectomies. The control specimens used used were antemortem and surgical thrombi, in vitro blood clot, fibrinogen precipitate, fibrin clot and platelet pellet. All specimens were formalin fixed and paraffin embedded. They were stained using the immunoperoxide technique with a panel of antisera. These were AFbg, AFNT, AFXII, AFXIII, AFXIII-A, ATC, AVIII-RA, APF4 and ABTG. Both parts of the study were assessed according to presence or absence of positive staining. The follow-up cases were also assesssed and scored on a semiquantative, blind basis according to the extent of the reaction. Statistical analysis of scores using Mann Whitney U test, Wilcoxon sign rank test and Spearmans rank correlation were carried out. The results showed that intrinsic coagulation is a mechanism of blood clotting important in cases of KTX and GN, in the latter it can be continued to the venous site. In glomerulonephritis, the capillary wall and crescents are sites for Fbg, FNT, FXIII and PF4 localization. The mesangium localizes some coagulation proteins as a response to the underlying pathology and the presence of Fbg is only significant when associated with other coagulation proteins. In KTX there are signs of tubular and vascular injury more than in the glomeruli though they show depressed reactivity to FVIII-RA in the capillary walls. In follow-up cases maximum reactivity to antiocoagulation and platelet proteins occurs in late vascular rejection. However examination of earlier biopsies could prove valuable in early detection of the vascular rejection process.