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

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

The aim of this study was to evaluate the prevalence of renal artery stenosis in patients with clinical signs of peripheral vascular disease and hypertension. One hundred patients, mean age 69 years (range 45-88) with symptoms and clinical signs of severe peripheral ischemia, underwent aortography to determine the degree of peripheral vascular disease and possible renal artery stenosis. History of claudication, and measurement of systolic distal blood pressure (BP) and calculation of the Ankle Brachial Index was used to define the severity of peripheral vascular disease. A total of 31% had renal artery stenosis (14% greater than 50% reduction in luminal diameter). In a subgroup of patients with hypertension and peripheral vascular disease (n = 74), 34% had renal artery stenosis. In the subgroup of patients with renal artery stenosis, 81% have hypertension. Patients with renal artery stenosis and lumen reduction of more than 50%, 93% have hypertension (P < or = 0.001). In conclusion this study shows that the combination of peripheral vascular disease and hypertension is an important clinical clue for renovascular disease. Examination for reno-vascular disease in this population should be considered, since the prevalence of the condition is high. Furthermore examination for renal vascular disease in this population is mandatory, before treatment with angiotensin converting enzyme (ACE) inhibitors is initiated, since treatment might lead to serious renal function impairment.
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PMID:Prevalence of renal artery stenosis in patients with peripheral vascular disease and hypertension. 886 60

Over the past decade, ischemic nephropathy has gained recognition as a distinct and treatable clinical entity. Atherosclerotic renal artery stenosis is the leading cause of ischemic renal disease. Among the aging population entering renal replacement programs, both renal artery and systemic atherosclerosis are common. Over recent years, patients with ischemic renal disease are presenting later and have diffuse atherosclerosis and other comorbid conditions. Improved screening techniques, patient selection, and interventional approaches have resulted in better outcomes in most centers. Percutaneous transluminal renal angioplasty has emerged as the treatment of choice in some centers for nonostial renal artery stenosis. Both percutaneous transluminal renal angioplasty and surgical repair have proven beneficial for renal function salvage. Many studies have elegantly demonstrated the pathophysiologic consequences of acute ischemia to the kidney. The concepts derived from acute studies have served as a springboard for considering the adaptive and maladaptive renal responses to chronic ischemia.
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PMID:Atherosclerotic ischemic renal disease. 901 87

Vascular nephropathies are a steadily increasing cause of end-stage renal failure. Arterionephrosclerosis and arteriolonephrosclerosis are common features in the hypertensive patient. This is especially true for blacks of African descent, in whom hypertension and nephrovasculopathies are a major cause of renal insufficiency. That primary hypertension leads to renal vascular lesions, glomerular obsolescence and interstitial fibrosis has long been established. It should not, however, obscure the fact that renal vascular lesions can be observed in animal models as well as in some humans, especially young blacks, in the absence of, or anticipating the onset of hypertension. This leads to considering the hypothesis that nephroangiosclerosis might stem from a genetic defect in the renal vascular bed and that this defect is strongly associated with the hypertensive trait. Atherosclerotic renal disease is a major, potentially treatable cause of chronic renal disease is a major, potentially treatable cause of chronic renal failure, especially in whites. It leads to renal atrophy, but the ischemic kidney retains a vigorous potential for tubular cell regeneration, which pleads for early recognition and treatment. Recent data suggest that renal ischemia, be it due to renal artery stenosis or to cholesterol crystal embolism, ranks among the multiple causes of secondary focal segmental glomerulosclerosis. Irrespective of its initial mechanism, ischemia induces renal fibrosis, the pathophysiology of which is centered on increased generation of angiotensin II. Finally, renal vascular lesions are commonly observed in the course of various nephropathies, even in the absence of hypertension, and the relationship between these lesions and the unfavorable prognosis of glomerulopathies, especially primary focal-segmental glomerulosclerosis, membranous glomerulopathy and IgA glomerulonephritis, remains to be elucidated. Expanding knowledge of the spectrum of nephrovasculopathies opens perspectives for investigating, understanding and treating a major mechanism of progressive renal insufficiency.
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PMID:Ischemic renal diseases: new insights into old entities. 964 58

Coarctation of the thoracic or abdominal aorta often is associated with reduced perfusion of one or both kidneys, resulting in severe renovascular hypertension, which significantly influences the spontaneous course of these patients. Fourteen of 15 patients who were operated upon between 1983 and 1996 suffered from arterial hypertension. Thirteen patients had ischemia of one or both kidneys resulting from renal artery stenosis or stenosis of the descending or visceral aorta. Because of a hemodynamically significant stenosis the aorta was reconstructed in 11 patients by interposition graft, bypass, or patchplasty. Concerned renal or visceral arteries were reconstructed by bypass/interposition graft, patchplasty, or reimplantation. One patient died, presumably from septic bleeding, 3 weeks post operatively. There was a cure of hypertension in 3 and an improvement in 6 patients. In the individual patient hypertension could be cured more often if the diagnosis of coarctation were established early.
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PMID:[Coarctation of the thoracoabdominal aorta]. 973 21

The current nonsurgical therapeutic options for patients with peripheral vascular disease are rapidly expanding. No longer is conservative management the only alternative for patients with significantly symptomatic but noncritical limb ischemia. Certainly for vascular disease above the inguinal ligament interventional procedures especially with adjunctive stent placement have excellent success and long term patency. Femoropopliteal vascular disease of relatively limited nature also is well-treated with interventional procedures. Infrapopliteal vascular disease treated with a surgical venous bypass appears to have superior results than intervention. However, for poor surgical risk patients or in patients without the necessary venous conduit, limb salvage is still good with a percutaneous approach. Renal artery stenosis appears now to be well treated with interventional techniques. Early data with up to one year follow-up shows that even ostial stenoses respond well when vascular stents are utilized. Extending the life of failing hemodialysis grafts is another area where interventional techniques are of benefit. In the future, more extensive vascular disease and other vascular disease entities such as cerebrovascular disease and abdominal aortic aneurysm may be successfully treated by a percutaneous approach.
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PMID:Current status of percutaneous vascular procedures. 1015 68

Disseminated cholesterol crystal embolism (CCE) is a devastating complication of atherosclerosis that is often considered beyond therapeutic resources. We designed and implemented a treatment protocol based on an analysis of the main causes of death in disseminated CCE with renal involvement. From 1985 to 1996, we applied this protocol in 67 consecutive atherosclerotic patients admitted to our renal intensive care unit for acute renal failure (serum creatinine level, 6 +/- 2.5 mg/dL) accompanied by signs and symptoms of CCE. The other principal clinical features in these patients were cardiac failure with pulmonary edema (61%), gastrointestinal ischemia (33%), cutaneous ischemia (90%), and retinal cholesterol embolism (22%). Disseminated CCE followed one or several precipitating factors, including angiographic procedure(s) (85%), anticoagulant treatment (76%), and cardiovascular surgery (33%). Our treatment schedule systematically addressed the identified causes of death in these patients. (1) To avoid CCE recurrence, any form of anticoagulant treatment was withdrawn, and aortic catheterization and surgery were proscribed. (2) To treat or prevent cardiac failure, a high-dose vasodilator regimen was instituted, including angiotensin-converting enzyme (ACE) inhibitors. In case of cardiac failure refractory to vasodilators, loop diuretics were added and, if necessary, overhydration was corrected by ultrafiltration/hemodialysis (11 patients). (3) To avoid cachexia, severe metabolic disorders were treated by hemodialysis (41 patients), and special attention was given to providing enteral or parenteral nutritional support. Patients with declining general status and laboratory evidence of inflammation, as well as those with new episodes of CCE, were treated with corticosteroids. Statistical analysis found a significant correlation between the requirement for hemodialysis and previous anticoagulation, degree of renal insufficiency, and severity of cardiac failure. Conversely, there was no correlation between requirement for hemodialysis and ACE inhibitor treatment or presence of atherosclerotic renal artery stenosis/thrombosis. The inhospital mortality rate was 16%. There were no clinical or laboratory elements found on admission that were predictive of inhospital mortality. Among survivors, 32% had to remain on maintenance hemodialysis therapy for irreversible chronic renal failure. Including initial hospitalization, the 1-year survival rate was 87%, which compares favorably with reports in the literature indicating a first-year mortality rate of 64% to 81%. Overall follow-up was 19 +/- 20 months, ranging from 1 to 74 months. The 4-year survival rate was 52%. We conclude that an intensive-care, specific-treatment schedule reduces mortality in multivisceral cholesterol embolism.
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PMID:Supportive treatment improves survival in multivisceral cholesterol crystal embolism. 1067 43

Nephrovasculopathies are an increasing cause of end-stage renal failure. Nephrosclerosis is a common finding in the hypertensive patient. However, genetic factors play a prominent role in its incidence. Nephrosclerosis is a common cause of early renal failure in blacks of African ancestry, as opposed to white Europeans, in whom hypertensive nephrosclerosis rarely and slowly leads to uremia. That primary hypertension is accompanied by arterionephrosclerosis and arteriolonephrosclerosis, by focal and segmental glomerulosclerosis leading to glomerular obsolescence and by interstitial fibrosis has been established for nearly a century. However, renal vascular lesions can be observed in animal models as well as in some humans, especially blacks, in the absence of, or preceding the onset of hypertension. This suggests that nephroangiosclerosis might stem from a genetic defect in the renal vascular bed, a defect closely associated with the hypertensive trait. Atherosclerotic renal artery stenosis is a major, potentially remediable cause of chronic renal failure, especially in whites. Its prevalence in the atherosclerotic population is in the order of 15 percent. This figure has obvious bearing in terms of health cost. Early diagnosis and treatment by angioplasty or surgery can preclude development to end-stage renal disease and maintenance hemodialysis, as renal atrophy due to chronic ischemia resulting from renal artery stenosis can be halted or partially reversed by revascularization before extensive fibrosis sets in. Finally, renal vascular lesions are commonly observed in the course of various nephropathies, even in the absence of hypertension. The relationship between fibrogenesis and these vascular lesions, which develop along with interstitial fibrosis and entail an unfavorable prognosis in various glomerulopathies, remains to be elucidated. This is especially the case for focal-segmental glomerulosclerosis, membranous glomerulopathy and IgA glomerulonephritis. The pathophysiology of renal fibrosis induced by ischemia is centered on increased generation of angiotensin II that is fibrogenic owing to interaction with endothelin 1, PDGF-BB and TGF-beta. These notions open perspectives toward pharmacologic means to retard or even prevent the development of such various ischemic conditions to end-stage renal failure.
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PMID:[Vascular mechanisms of renal fibrosis. Vasculonephropathies and arterial hypertension]. 1037 63

Computed tomography (CT) plays an important role in evaluation and management of primary renovascular disease. Nonenhanced CT is useful for demonstrating renal hemorrhage, renal parenchymal or vascular calcifications, and masses. Contrast material-enhanced CT is essential to identify global or regional nephrographic abnormalities resulting from the vascular process (eg, renal infarcts, ischemia secondary to renal artery stenosis, arteriovenous communications). In addition, renal manifestations of a systemic disease (eg, vasculitis, thromboembolic disease) can be seen at CT. In trauma, occlusion of the main renal artery can be accurately diagnosed with contrast-enhanced CT. In cases of spontaneous renal hemorrhage without an apparent cause (eg, vasculitis, coagulopathy), a careful CT study should be performed to exclude renal cell carcinoma. The presence of fat in a hemorrhagic renal mass larger than 4 cm in diameter is characteristic of angiomyolipoma complicated by hemorrhage. Acute renal vein thrombosis appears as a clot in a distended renal vein, whereas renal vein retraction with collateral vessels is highly indicative of chronic thrombosis. Helical CT, especially with multiplanar two-dimensional and three-dimensional reconstruction following an intravenous injection of iodinated contrast material, has greatly improved our ability to directly image the proximal renal arteries and detect vascular lesions.
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PMID:CT evaluation of renovascular disease. 1099 21

In ischemia, nitric oxide (NO) production is increased, possibly to preserve flow. The role of NO was investigated in hypertensive patients with or without renal artery stenosis (RAS). Fifty-five hypertensive patients scheduled to undergo diagnostic renal angiography underwent mean renal blood flow (MRBF) measurements before and after an intrarenal injection of the NO synthase blocker N(g)-monomethyl-L-arginine (L-NMMA) at 0.03 microg/kg, before angiography. A dose-response study indicated that this dose of L-NMMA significantly blocked NO synthesis. MRBF was measured at baseline and 1, 5, 10, and 20 min after L-NMMA treatment. On the basis of the angiographic results, patients were divided into three diagnostic categories, i.e., essential hypertension (n = 26), unilateral RAS (n = 16), or bilateral RAS (n = 8). In essential hypertension, MRBF was decreased by 18 +/- 4% at 20 min. In unilateral RAS, L-NMMA did not affect MRBF in the stenotic kidney but reduced MRBF in the nonstenotic kidney by 40 +/- 9% at 20 min. In bilateral RAS, L-NMMA reduced flow by 32 +/- 14% at 20 min. In the nonstenotic kidney in unilateral RAS, a positive correlation was observed between the effect of NO blockade on MRBF and arterial renin levels (P = 0.009). In the stenotic kidney, in contrast, this correlation was inverse (P = 0.007). In conclusion, MRBF depends on NO in hypertensive patients, except in the stenotic kidney in unilateral RAS. In the nonstenotic kidney in unilateral RAS, NO bioavailability is increased. It is suggested that a compensatory mechanism, regulated by NO and possibly angiotensin II, may preserve renal function.
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PMID:Nitric oxide dependence of renal blood flow in patients with renal artery stenosis. 1151 76


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