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

Some chronic renal failure patients maintained on dialysis have uncontrollable hypertension. Those with elevated renin levels require bilateral nephrectomies prior to kidney transplant to avoid nephrosclerosis. The morbidity and mortality from surgical nephrectomies are high. In 2 such patients we embolized the renal arteries with gelfoam and successfully occluded all the major vessels. One patient became normotensive. The second remained hypertensive and had increased renin levels, probably on the basis of ischemia. Subsequent surgical nephrectomies demonstrated completely occluded segmental branches but only focal areas of infarction. Collateral blood supply determines the success of the procedure.
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PMID:Gelfoam embolization of the kidneys for treatment of malignant hypertension. 66 23

The term nephrosclerosis is customarily used to designate a pathological entity that tends to characterize subjects with high blood pressure; it refers to a condition of diffuse fibrous replacement of renal substance secondary to ischemia from hypertension-related vascular injury. The features of parenchymal fibrosis can be distinguished from those of vasculopathies in tissue sections, parenchymal fibrosis being measured by assessing the degree of interstitial fibrosis and by counting obsolete glomeruli, while vasculopathies are measured by determining arterial intimal fibroplasia and by counting hyalinized arterioles. A series of 166 autopsies in subjects aged 25 to 92 years, selected because ample documentation of blood pressure was available, was assessed. One form of vasculopathy, arterial fibroplasia, is a better correlate of high blood pressure than is parenchymal fibrosis in this body of data. Cases with much vasculopathy and little parenchymal fibrosis occurred frequently, and these subjects were usually hypertensive. Cases with little vasculopathy and much parenchymal fibrosis were also encountered, but these subjects were usually not hypertensive. The suggested conclusion is that blood pressure relates less to the renoprival state of nephron loss than it does to renal ischemia in patients with nephrosclerosis.
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PMID:Blood pressure related separately to parenchymal fibrosis and vasculopathy of the kidney. 149 64

To ascertain whether or not vascular lesions lead to renoparenchymal damage through ischemia and to a deterioration of renal function in patients with essential hypertension, correlations among morphometrical findings and renal function were examined in 36 renal biopsies from Japanese patients with a benign nephrosclerosis. The following histological parameters were investigated; glomerular sclerotic index (GS), interstitial volume (IV), measured by the point-counting method, index of arteriolar hyaline change (HC) and intimal thickening (IT), determined by morphometry. Arteries were divided into two groups; those with less than 3 layers of medial smooth muscle cells (SMC less than 3) and those with more than 3 cell layers (SMC greater than or equal to 3). The mean of IT in each size was calculated. IT (SMC less than 3) showed a significant correlation with GS and IV. IT (SMC less than 3), GS and IV significantly correlated with Ccr. On the other hand, IT (SMC greater than or equal to 3) and HC showed no correlation with GS nor Ccr. IT (SMC less than 3) and HC correlated with both blood pressure and the duration of hypertension, and here, IT (SMC greater than or equal to 3) showed no correlation. These data suggest that hyaline change and intimal thickening of small arteries and arterioles (SMC less than 3) are closely related to high blood pressure and that intimal thickening of small arteries rather than hyaline change causes renoparenchymal damage through ischemia and leads to a deterioration of renal function, in those with a benign nephrosclerosis.
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PMID:Morphometrical and functional correlations in benign nephrosclerosis. 342 33

Renal arterial disease-induced tubulo-interstitial lesions described in this chapter include benign arterio- and/or arteriolo-sclerotic and malignant nephrosclerosis, renal infarction and renal cortical necrosis. In these conditions renal glomeruli as well as tubules are always involved, and consequent loss of nephrons, or renal parenchyma results in interstitial fibrotic changes. The parenchymal lesions have a spectrum from slowly progressive atrophy and loss to necrosis of abrupt onset and disappearance of glomeruli and tubules. As for glomerular reactions to the ischemia, the intermediate type consisted of mesangial degeneration and epithelial cell proliferation described as "alterative glomerulitis" is noteworthy. Briefly, in renal arterial diseases, glomeruli are rather variably involved than tubules and loss of the parenchyma results in interstitial fibrosis.
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PMID:[Renal arterial disease-induced tubulo-interstitial lesions]. 756 46

Progressive renal failure is conditioned by a number of factors, including type of renal disease, sex, level of arterial pressure, insulin deficiency and/or hyperglycemia in diabetes mellitus, and dietary protein intake. Elevated arterial pressure may cause a progressive renal disease, hypertensive nephrosclerosis, and accelerate the rate of progression of all other chronic renal disease. Hypertension contributes to progressive renal failure by inducing myointimal hyperplasia of arcuate and afferent arterioles, causing glomerular ischemia, and by increasing pressure in the glomerular capillaries. The latter leads to hyperfiltration of protein, increased mesangial ingestion of protein, and glomerular sclerosis. Increased glomerular pressure may also be induced by protein feeding, insulin deficiency and hyperglycemia, especially in the presence of reduced nephron number. Thus at least one common mechanism underlies the effect of hypertension, protein feeding, and diabetes on the progression of chronic renal disease.
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PMID:Pathophysiology of progressive renal failure. 793 15

Nephrosclerosis is the most typical and widespread renal manifestation of hypertension and can be judged as the pathological hallmark of essential hypertension. Nephrosclerosis is an important and frequent cause of progressive renal disease, however, information in the literature on the risk of developing renal failure in the course of essential hypertension is sparse. Traditionally, nephrosclerosis was thought to result from glomerular ischemia. Alternatively, glomerular sclerosis in hypertension may result from glomerular hyperperfusion or hypertension. Studies in experimental models of renal disease have identified a promising intervention with either Ca antagonists or angiotensin-converting enzyme inhibitors. Application of these therapies to patients with nephrosclerosis should await the results of careful clinical trials.
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PMID:[Nephrosclerosis: current status]. 841 83

Between May 1, 1986 and May 31, 1992 at the University of Minnesota, we interpreted 129 renal allograft biopsy specimens (done in 48 grafts during the first 6 months posttransplant) as showing changes consistent with chronic rejection. For this retrospective analysis, we reexamined these biopsies together with clinical information to determine: (a) whether a diagnosis other than chronic rejection would have been more appropriate, (b) how early posttransplant any chronic rejection changes occurred, and (c) if the diagnosis correlated with outcome. We found that (1) chronic rejection is uncommon in the first 6 months posttransplant; it was documented in only 27 (2.4%) of 1117 renal allografts and was preceded by acute rejection in all but 3 recipients (for these 3, the first biopsy specimen showed both acute and chronic rejection). (2) Chronic vascular rejection was seen in 1 recipient as early as 1 month posttransplant; the incidence increased over time and was associated with an actual graft survival rate of only 35%. (3) The most frequent cause of arterial intimal fibrosis in the first 6 months posttransplant was arteriosclerotic nephrosclerosis (ASNS) of donor origin. Long-term graft function for recipients with ASNS was 67%. (4) Early-onset ischemia or thrombosis was seen in 14 recipients and predicted poor outcome: only 35.7% of these recipients had long-term graft function. (5) Cyclosporine (CsA) toxicity was implicated in only 3 recipients, who had mild diffuse interstitial fibrosis in association with elevated CsA levels. Other variables (including systemic hypertension, urinary tract infection, obstructive uropathy, neurogenic bladder, cobalt therapy, and recurrent disease) were not significantly associated with chronic renal lesions in the first 6 months posttransplant. A significant number of biopsies were originally interpreted as showing chronic rejection, but the diagnosis was changed upon reevaluation in conjunction with clinical data. We conclude that many factors coexist to produce chronic lesions in biopsies during the first 6 months posttransplant, so clinical correlation is needed before establishing a diagnosis of chronic rejection.
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PMID:Chronic renal allograft rejection in the first 6 months posttransplant. 854 66

Chronic ischemia may cause end stage renal disease, especially in older patients with atherosclerotic renal artery stenosis. Examining the pathology of the ischemic kidney is a fundamental first step toward understanding the mechanisms of this injury. In experimental renal hypoperfusion, there is evidence of a mixture of adaptive responses, tubular and endothelial cell damage and repair events. These processes are reflected in a wide spectrum of morphological changes that include atrophy, focal necrosis, epithelial regeneration, apoptosis, inflammation, interstitial fibrosis, and thrombosis. The most severe damage is seen in the outer medulla, a region with marginal oxygenation even in normal circumstances. In the usual clinical case, the effects of aging, pre-existent hypertension, and the process of atherosclerosis further complicate the pathological picture. Lesions related to these factors include arteriosclerosis, athero-emboli, various types of glomerulosclerosis, and severe tubulointerstitial damage leading to "atubular glomeruli" and regional cortical scarring (nephrosclerosis). In this article, some mechanisms determining the varied and complex pathological findings that may be observed in individual cases are outlined.
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PMID:The pathology of chronic renal ischemia. 872 83

How an increase in blood pressure, in and of itself, induces hypertensive nephrosclerosis is unclear. In an earlier study we found that leukocyte infiltration, proximal tubular cell proliferation, matrix deposition and interstitial fibrosis occur in the unclipped kidney of 2 K 1 C Goldblatt hypertensive rats. In this study we tested the hypothesis that the cell surface adhesion molecule ICAM-1 is expressed on the vascular endothelium and tubular epithelium of unclipped kidneys at 4 weeks. As a positive control, we examined the clipped kidney as well. We found that systolic blood pressure was significantly elevated in renovascular hypertensive rats compared to sham-operated controls after 4 weeks (198 +/- 5 mmHg vs 121 +/- 2 mmHg, P < 0.001). Furthermore, quantitative (densitometry) measurements showed that ICAM-1 expression on vascular endothelium and on tubular cells was significantly increased in unclipped kidneys compared to controls (P < 0.05). The same was true for monocyte and granulocyte infiltration (P < 0.05). These same variables were even more prominent in the clipped kidneys, compared to unclipped and control kidneys (P < 0.05). Our data show that ICAM-1 is expressed in unclipped kidneys exposed to hypertension as well as in clipped kidneys exposed to ischemia. We suggest that mechanical injury induced by increased blood pressure is responsible for an inflammatory adhesion molecule-mediated response and concomitant renal injury.
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PMID:Leukocyte infiltration and ICAM-1 expression in two-kidney one-clip hypertension. 917 41

Prostatic atrophy (PA) is one of the most frequent mimics of prostatic adenocarcinoma. It occurs almost exclusively in the peripheral zone of the gland and gained importance with the increasing use of needle biopsies for the detection of prostatic carcinoma The etiopathogenesis is unknown, and there is controversy related to the potential of PA as a precancerous lesion. The frequency increases with age. Compressions caused by hyperplastic nodules, inflammation, hormones, nutritional deficiency, or systemic or local ischemia, are all possible factors in the pathogenesis of PA. The peripheral zone of the prostate was step-sectioned and totally embedded from the bodies of 100 consecutively autopsied men more than 40 years of age. The fragments were microscopically studied for presence of PA, latent (histologic) carcinoma, high-grade prostatic intraepithelial neoplasia, local arteriosclerosis, and prostatitis. The prostates were macroscopically examined for the presence of nodular prostatic hyperplasia. The autopsy reports provided information concerning the presence of generalized atherosclerosis and benign or malignant nephrosclerosis. PA was seen in 85 of the 100 prostates examined and histologically was subtyped into simple, hyperplastic, and sclerotic atrophy. In 65 (76.47%) of 85 cases, the histologic subtypes were combined. In 33 (50.76%) of these 65 cases, the three subtypes were seen concomitantly, favoring the hypothesis that they represent a morphologic continuum of only one lesion. Fibrosis of the stroma may or may not be present in simple and hyperplastic atrophy. Hyperplastic atrophy associated with fibrosis of the stroma is the histologic subtype that most frequently mimics adenocarcinoma Sclerotic atrophy always presents fibrosis of the stroma. PA increases with age, and, in our study, ischemia caused by local intense arteriosclerosis seems to be a potential factor for its etiopathogenesis. Because there was no relation to latent (histologic) carcinoma or high-grade prostatic intraepithelial neoplasia, PA is probably not a premalignant lesion.
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PMID:Prostatic atrophy: an autopsy study of a histologic mimic of adenocarcinoma. 955 22


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