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Query: UMLS:C0920646 (renal ischemia)
 2,515 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The experimental discovery of the pathophysiological relationship between renal artery stenosis and arterial hypertension was historically reported (1934) before the clinical description of the disease in human patients (1950). The experimental model explains the relation between renal ischemia, renal endocrine activation, and morphological alterations of the homo and contralateral kidneys. In particular, the experimental model improves the understanding of the evolution of renovascular disease. In human patients, renal artery stenosis does not always lead to clinical disease. Because of the frequency of arterial hypertension, there is not always a clear relationship between hypertension and renal insufficiency or renal artery stenosis. Therefore a complete diagnosis of renal endocrine and exocrine function is needed to understand this relation before deciding on the therapeutic approach. This diagnosis is made by exploration of the renal renin-angiotensin axis, its pharmacological blockade and the response of the excretory function. This approach corresponds to the clinical description of the evolution of the disease; the peripheral and renal vein renin assays; the pressure and scintigraphic response to converting enzyme inhibition and renal morphological definition by echography and CT scan. This pathological approach permits a rational choice of the therapeutic indication: non-intervention, specific medical treatment, endovascular or surgical revascularization or nephrectomy.
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PMID:[Is in depth diagnosis important in renal artery stenosis?]. 815 92

A growing body of evidence supports the notion that calcium antagonists exert a renal protective effect. Calcium antagonists may play an important future role in renal hemodynamics related to their reversal of renal vasoconstrictors. Calcium antagonists are also capable of blocking intracellular calcium overload induced by various types of ischemia or toxic stimuli. Features such as these may be of substantial value in ameliorating acute renal insufficiency secondary to renal ischemia, iodinated radiographic contrast media, or the administration of various nephrotoxic drugs. The latter includes agents such as the aminoglycoside antibiotics, cyclosporine A, and the cancer chemotherapeutic agent cisplatin. Recent prospective, controlled studies from our group indicate that calcium antagonists protected against postischemic acute renal failure in the setting of cadaveric renal transplantation. Moreover, in a prospective, randomized, controlled clinical trial, we were able to demonstrate that the prophylactic use of nitrendipine reduced the decrease in GFR in patients receiving radiographic contrast agents. Such protection may extend to favorably influencing the course of chronic renal insufficiency, particularly when the latter is complicated by hypertension. Seven putative mechanisms have been proposed by which calcium antagonists may ameliorate the decline in GFR associated with renal insufficiency. These are: (a) reduction in blood pressure per se, (b) reduction in renal hypertrophy, (c) modulation of mesangial traffic of macromolecules, (d) reduction in metabolic activity in remnant renal tissue, (e) amelioration of uremic nephrocalcinosis, (f) reduction of pressure-induced calcium entry into vessel walls, and (g) reduction of free radical formation. Experimental investigations in rats with reduced renal mass, desoxycorticosterone-induced hypertension, or chronic angiotensin II infusion, and in spontaneously hypertensive rats support such a view.
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PMID:Calcium antagonists and renal protection. 851 90

Contrast-media associated nephropathy (CMAN) consists in a sudden impairment of glomerular filtration rate following exposure to radiographic contrast materials. Damage may be limited to an asymptomatic mild increase of blood creatinine, or reach the highest levels of nitrogen retention compatible with acute renal failure. Some preexisting clinical conditions or pathologies may lead to CMAN: not only renal insufficiency, diabetes mellitus, multiple myeloma, congestive heart failure and severe hypertension, but also simple dehydration and a growing series of immunologic diseases are recognized as predisposing condition. The exact mechanism responsible for renal injury is still doubtful but recently animal models have shown substantial ischemic changes that may be added to the traditional presumed pathogenesis of direct tubular toxicity and intra-tubular obstruction. As renal ischemia stimulates both endogenous vasoconstrictor and vasodilator substances, it is now supposed that CMAN acts similarly to non-steroidal anti-inflammatory agents, selectively inhibiting the vasodilatory prostaglandin phase and therefore causing a derangement of the physiologic vasoconstriction/vasodilatation balance of renal circulation. The role of oxygen free radicals to contribute to renal dysfunction is considered. Low osmolality non ionic contrast media when compared to conventional high osmolality ionic contrast media have reduced but not eliminated CMAN. Simple but effective lines of prevention include the previous selection of patients predisposed to CMAN for concomitant pathology, suspension of FANS or any other recognized nephrotoxic substance, the least amount of contrast media compatible with radiologic visualization of the patient's problem, careful hydration of the patient before contrast injection and sustained diuresis afterwards. The usefulness of pre-treatment with Ca-channel blockers or atrial natriuretic factors remains sub judice.
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PMID:[Physiopathology, clinical aspects and prevention of renal insufficiency caused by contrast media]. 917 67

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

Recent evidence has implicated proinflammatory mediators such as TNF-alpha in the pathophysiology of ischemia-reperfusion (I/R) injury. Clinically, serum levels of TNF-alpha are increased after myocardial infarction and after cardiopulmonary bypass. Both cardiopulmonary bypass and renal ischemia-reperfusion injury induce a cascade of events leading to cellular damage and organ dysfunction. Tumor necrosis factor (TNF), a potent proinflammatory cytokine, is released from both the heart and the kidney in response to ischemia and reperfusion. TNF released during cardiopulmonary bypass induces glomerular fibrin deposition, cellular infiltration, and vasoconstriction, leading to a reduction in glomerular filtration rate (GFR). The signaling cascade through which renal ischemia-reperfusion induces TNF production is beginning to be elucidated. Oxidants released following reperfusion activate p38 mitogen-activated protein kinase (p38 MAP kinase) and the TNF transcription factor, NFkappaB, leading to subsequent TNF synthesis. In a positive feedback, proinflammatory fashion, binding of TNF to specific TNF membrane receptors can reactivate NFkappaB. This provides a mechanism by which TNF can upregulate its own expression as well as facilitate the expression of other genes pivotal to the inflammatory response. Following its production and release, TNF results in both renal and myocardial apoptosis and dysfunction. An understanding of these mechanisms may allow the adjuvant use of anti-TNF therapeutic strategies in the treatment of renal injury. The purposes of this review are: (1) to evaluate the evidence which indicates that TNF is produced by the heart following cardiopulmonary bypass; (2) to examine the effect of TNF on myocardial performance; (3) to outline the mechanisms by which the kidney produces significant TNF in response to ischemia and reperfusion; (5) to investigate the role of TNF in renal ischemia-reperfusion injury, (6) to describe the mechanisms of TNF-induced renal cell apoptosis, and (7) to suggest potential anti-TNF strategies designed to reduce renal insufficiency following cardiac surgery.
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PMID:Role of TNF in mediating renal insufficiency following cardiac surgery: evidence of a postbypass cardiorenal syndrome. 1042 18

Angiotensin converting enzyme (ACE) inhibition scintirenography was performed to help establish the diagnosis and plan treatment of renovascular hypertension (RVH) in 57 hypertensive pediatric patients, 33 infants and 24 children older than 1 year. In 16 of 33 hypertensive infants, ACE inhibition scintirenography established the diagnosis of RVH from renal ischemia (due to aortic or renal arterial thrombi). Two scintigraphic criteria were used for the diagnosis of RVH: criterion I, ischemic and damaged kidney (a non-functioning kidney on or off ACE inhibition) and criterion II, ischemic but not damaged kidney (ACE inhibition induced deterioration of function of the kidney). When criterion I was present and the contralateral kidney was normal, ACE inhibitors could be used for treatment of hypertension without deterioration of renal function; kidneys satisfying criterion I eventually involuted or manifested growth arrest and frequently caused persistent RVH, even after resolution of the thrombus, requiring nephrectomy. When criterion II was present bilaterally, or it was associated with criterion I contralaterally, the use of antihypertensive drugs other than ACE inhibitors was necessary in order to prevent renal insufficiency or failure from ACE inhibitors. However, kidneys with criterion II showed normal growth and, following retraction or dissolution of the aortic thrombus, hypertension resolved. In 2 of 24 hypertensive children older than 1 year, the test was diagnostic of branch renal artery stenosis; RVH was cured by selective angioplasty. ACE inhibition scintirenography is useful in the evaluation and planning of treatment in children with hypertension and may predict the outcome of therapy and ultimate renal function.
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PMID:ACE inhibition scintigraphy in the management of hypertension in children. 1045 77

We examined the effect of temporary renal ischemia (30 min or 60 min) and reperfusion (1 day or 5 days) on the expression of renal aquaporins (AQPs) and urinary concentration in rats with bilateral ischemia-induced acute renal failure (ARF). Next, we tested whether reducing ischemia/reperfusion (I/R) injury by treatment with alpha-melanocyte stimulating hormone (alpha-MSH) affects the expression of AQPs and urine output. Rats with ARF showed significant renal insufficiency, and urinary concentration was markedly impaired. In rats with mild ischemic injury (30 min), urine output increased significantly to a maximum at 48 h, and then nearly normalized within 5 days. Consistent with this, semiquantitative immunoblotting revealed that kidney AQP1 and AQP2 abundance was significantly decreased after 24 h to 30 +/- 5% and 40 +/- 11% (n = 8) of controls (n = 9), respectively (P < 0.05). Five days after ischemia, AQP2 abundance was not significantly decreased and urine output was normalized. In contrast, severe ischemic injury (60 min) resulted in a marked reduction in urine output at 24 h, despite a significant decrease in urine osmolality and solute-free water reabsorption, T(c)H(2)O. AQP1 and AQP2 abundance was markedly decreased to 51 +/- 5% and 31 +/- 9% (n = 10) of controls (n = 8) at 24 h (P < 0.05). After 5 days, the rats developed gradually severe polyuria and had very low AQP2 and AQP1 levels [11 +/- 4% and 6 +/- 2% (n = 5) of controls (n = 8), respectively; P < 0.05]. A similar reduction was observed for AQP3. The reduction in AQP expression in the proximal tubule and inner medullary collecting duct was confirmed by immunocytochemistry. Next, we found that intravenous alpha-MSH treatment of rats with ARF significantly reduced the ischemia-induced downregulation of renal AQPs and reduced the polyuria. In conclusion, the I/R injury is associated with markedly reduced expression of the collecting duct and proximal tubule AQPs, in association with an impairment of urinary concentration. Moreover, alpha-MSH treatment significantly prevented the reduction in expression of AQPs and renal functional defects. Thus decreased AQP expression is likely to contribute to the impairment in urinary concentration in the postischemic period.
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PMID:Reduced abundance of aquaporins in rats with bilateral ischemia-induced acute renal failure: prevention by alpha-MSH. 1048 25

Chronic renal ischemia caused by renal artery stenosis (RAS) elicits a complex biologic response. Although the traditional pathophysiologic pathways underlying renal ischemia have been well studied, there is emerging evidence that additional mechanisms may be responsible for producing many of the hemodynamic alterations and end-organ injury seen in patients with RAS, including persistent hypertension, renal insufficiency, and cardiac disturbance syndromes. A better understanding of these mechanisms may allow earlier identification of RAS, provide markers to predict the response to revascularization, or allow unique therapeutic targets for drug development. This and a subsequent article will explore the pathophysiologic and clinical implications of chronic renal ischemia.
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PMID:Chronic renal ischemia: pathophysiologic mechanisms of cardiovascular and renal disease. 1242 6

In an effort to identify preoperative and perioperative factors impacting outcome in repair of juxtarenal abdominal aortic aneurysm (JRAAA), hospital records and CT scans (for calcification, intraluminal thrombus, and aortic diameter) of all patients undergoing JRAAA repair over the past 10 years were reviewed. The 87 men and 25 women had a mean age of 72, and a mean maximal aortic diameter of 6.2 cm. Renal artery stenosis (RAS) and iliac disease were present in 13 (11%) and 40 patients (35%), respectively. Comorbidities included coronary artery disease (n = 49, 44%), COPD (n = 28, 25%), diabetes mellitus (n = 10, 9%), and preoperative renal insufficiency (PRI; Cr >1.4 mg/dL; n = 14, 12%). A midline incision was used in most of the patients (n = 98, 88%). The proximal aortic clamp was placed in the supraceliac (SC) position in 92 (82%) patients, and directly above one or both renal arteries in 20 (18%) patients. The overall mortality was 6% (n = 7). Cardiac complications occurred in 26 patients (23%); pulmonary, in 22 (20%); renal, in 14 (12%); and gastrointestinal, in 10 (9%). No patient experienced mesenteric ischemia. Mean elevation in creatinine was greater in patients with PRI (1.8 mg/dL vs. 0.13 mg/dL, p = 0.04). Mean blood loss (EBL) was 2701 +/- 189 cc, and mean LOS was 16.1 +/- 1.7 days. Age >70 was associated with increased length of stay (LOS) (12.1 days vs. 18.6 days, p = 0.05) and higher mortality (0 vs. 10%, p = 0.02); otherwise there were no significant relationships between pre- and perioperative parameters and any of the measured outcomes including death, postoperative RI, and LOS. Preferential SC clamping may substantially reduce complications of JRAAA repair (such as mesenteric and renal ischemia) related to proximal cuff disease, but cannot overcome the deleterious affects of advanced age and PRI.
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PMID:Optimal operative strategies in repair of juxtarenal abdominal aortic aneurysms. 1252

We report the case of a 71-year-old male, submitted to percutaneous transluminal renal angioplasty (PTA) plus stent implantation following the confirmation, at intravascular ultrasound, of severe unilateral renal artery stenosis in the setting of a single functional kidney and of evidence of renal insufficiency (serum creatinine value 300 mumol/l). At 6 months of follow-up the serum creatinine levels had returned to normal (98 mumol/l). This case shows the role of direct PTA on the overall renal function in a case of global renal ischemia.
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PMID:Effect of renal artery stenting on the progression of renovascular renal failure: a case of intravascular ultrasound-confirmed renovascular disease. 1261 Nov 27


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