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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Severe essential hypertension in a subset of American black subjects is associated with marked stenosis of interlobular arteries and arterioles of the kidneys, observed by renal biopsy and binephrectomy specimens. The interlobular arterial stenosis is caused by marked thickening of the intima due mainly to the presence of smooth muscle cells, basement membrane material, and acid mucopolysaccharide. Because of this makeup, we propose the term "musculo-mucoid intimal hyperplasia" for this lesion. The media of these arteries appears maximally dilated, and by electron microscope displays degenerative changes of the smooth muscle cells. The arterioles are thickened, due mainly to hyalinization, but also due to the musculo-mucoid change (onionskin effect). The smooth muscle cells are degenerated and atrophic. These patients do not exhibit fibrinoid necrosis of the arteries, arterioles, and glomeruli, presumably because of the rapidity of the development of the arterial stenotic lesion. Accordingly, the glomeruli are destroyed by ischemia, and there is no evidence of glomerulitis (no "Kombinations" form of Fahr). A unifying hypothesis concerning renal hypertensive arterial disease is suggested by these studies. This hypothesis places the main emphasis for all the morphological expressions of the intrinsic visceral vasculature on changes involving the main functional unit of the vessel wall, the medical smooth muscle.
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PMID:Malignant hypertension due to musculo-mucoid intimal hyperplasia of intrarenal arteries. Absence of renal fibrinoid necrosis. 4 31

During the 1970s renal biopsies were obtained after blood pressure had been controlled in 41 black patients in Memphis who had severe hypertension plus excretory renal failure. An additional 13 binephrectomy specimens were also studied. This material yielded significant information on the state of the renal arteries--arterioles under these circumstances. Fibrinoid necrosis of the afferent glomerular arteriole and proliferative glomerulitis were not noted. Rather, the vascular lesion characterized by the accumulation of smooth muscle cells and mucopolysaccharide in the intima attended by a marked narrowing of the lumen was dominant. This lesion caused pronounced ischemia associated with obsolescence of glomeruli, atrophy, and fibrosis (end-stage kidney). This lesion has been renamed musculomucoid intimal hyperplasia as a result of changes revealed by electron microscopic and histochemical studies. Since this study the incidence of this severe vascular disease of the kidney in the same geographic area has been markedly reduced. There are a number of possible reasons for this change in incidence, but a major one appears to be improved treatment of hypertension and better compliance with antihypertensive therapy. Why such extreme changes occur in a subset of hypertensive blacks is not known. It is apparent that without improved antihypertensive treatment, this type of end-stage renal disease due to severe vascular damage will continue to be encountered.
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PMID:Histopathology of severe renal vascular damage in blacks. 262 Apr 72

The renal allograft is host to a number of injuries and all its structural components are prone to damage. The glomeruli respond to these varied stimuli in many ways. The fibrinoid necrosis, thrombosis, and polymorphonuclear cell exudation that accompany hyperacute or accelerated rejection are well-recognized. The transplant may also be afflicted by forms of de novo or recurrent glomerulonephritis. Apart from these, there are other patterns of reaction. The mesangium is often the site of a rapidly reversible change; it expands readily. Arterial changes initiate ischemia and collapse of glomerular capillary spaces. Glomerulitis accompanies cases of acute rejection, but when seen as a predominant feature, usually antedates chronic rejection. Heavy proteinuria may be associated with profound alterations in the peripheral capillary basal lamina including irregular thickening, interposition of mesangial cell cytoplasm, and lamellation. Allografts with these glomerular changes eventually fail.
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PMID:Glomerular changes in renal allografts. 351 May 33

Transplant glomerulopathy (TG) is traditionally considered to be a chronic entity. However, in our practice we observed patients who presented with features of TG as early as 14 days posttransplantation. We investigated the clinicopathological features of these cases. During a 4-year period, all patients with acute rejection were identified. Charts were reviewed to identify patients with antibody-mediated rejection and biopsy features of TG within 6 months posttransplantation. Three patients met the above-mentioned criteria. All of them had diffuse margination of inflammatory cells in peritubular capillaries in the setting of acute renal failure or delayed graft function. Monocyte (CD68-positive) margination in peritubular capillaries was a common feature. All 3 patients had donor-specific antibodies and features suggestive of antibody-mediated rejection. C4d stain in peritubular capillaries was focal and mild or absent in serial biopsies. Occlusive endothelial swelling of glomerular capillary loops (endotheliosis) preceded TG. None of the patients had evidence for other causes of similar glomerular changes in a transplant, such as calcineurin inhibitor toxicity, ischemia, hepatitis C, or immune complex glomerulonephritis. They did not have other biopsy features of chronicity when TG appeared and as it progressed. TG can occur as an acute phenomenon. We propose that endotheliosis is a more accurate and specific precursor of TG than mere glomerulitis. These cases of acute TG may represent a form of antibody-mediated rejection associated with proteinuria and poor response to treatment.
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PMID:Acute transplant glomerulopathy is associated with antibody-mediated rejection and poor graft outcome. 2109 5