Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0920646 (renal ischemia)
 2,515 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In addition to their role as highly potent antihypertensive drugs, calcium antagonists may also play an important future role in the area of tissue protection and preservation. Calcium antagonists exert favorable effects on renal hemodynamics related to their reversal of renal vasoconstrictors. Calcium antagonists are also capable of blocking intracellular calcium overload induced by various types of ischemic or toxic stimuli. Features such as these may be of substantial value in ameliorating acute renal insufficiency secondary to renal ischemia, iodinated radiographic contrast agents, 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. Calcium antagonists may also play a beneficial role in preventing progressive renal disease. Data from a number of studies conducted in experimental animals, as well as information from clinical trials, support such a view. Although the mechanisms of action of calcium antagonists in the setting of chronic renal failure are not yet fully established, their beneficial effects may be related to protective actions such as the reduction in renal hypertrophy, modulation of mesangial cell uptake of macromolecules, changes in permselectivity of the glomerulus, and a decreased free radical formation. These various aspects will be the topic in this review.
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PMID:Renal protection with the calcium antagonists. 172 49

Vesicoureteral reflux (VUR) is mainly a primary phenomenon due to incompetence of the ureterovesical junction, mostly affecting a pediatric population. During micturition cystourethrography (MCU) reflux into the kidney--intrarenal reflux (IRR)--is occasionally seen. In areas with IRR the kidney surface may subsequently be depressed and the papillae retracted (reflux nephropathy (RN]. VUR may lead to hypertension and/or end-stage renal failure. Most commonly, VUR is discovered during evaluation for urinary tract infection, but it may also be present in patients with hypertension, toxemia of pregnancy, chronic renal failure and proteinuria, and it may be found in siblings of patients with VUR. For the time being VUR is demonstrated at radiographic MCU, whereas RN is diagnosed by demonstration of focal scars and of abnormal parenchymal thickness at urography. In children with VUR and no abnormalities of calyces or parenchymal defects standardized measurement of the parenchymal thickness at three sites may identify kidneys which are likely to develop focal scars. Quantitation of focal scarring should be performed in connection with a measure of the overall kidney size. The occurrence of IRR is dependent of the papillary morphology, intrapelvic pressure and urine flow. There may be an important relationship between renal ischemia and IRR in producing a 'vicious circle of deleterious effects' which, combined with parenchymal extravasation, may lead to RN. Treatment of VUR includes medical and surgical management. Since renal scarring may occur in infancy, prevention should focus on infants and young children. Infants and young children with severe VUR may have normal urograms. Therefore a MCU should also be performed, preferably with the recommended standardized technique.
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PMID:Vesicoureteral reflux and reflux nephropathy. 388 98

3-alpha-Phenyl-propyl-5-beta-diethylaminoethyl-1,2,3-oxadiazole (proxazole), a spasmolytic papaverine-like agent, was i.v. administered to 13 patients with chronic renal failure (mean creatinine clearance 46.4 ml/min/1.73 m2), but did not improve renal plasma flow (p-aminohippurate clearance) or glomerular filtration rate (inulin clearance), nor did this agent prevent or modify nor-adrenaline induced renal ischemia. The oral administration of 400 mg proxazole (5.2--6.5 mg/kg/day) for a period of at least 90 days did not improve renal function in 11 patients with chronic renal failure. It is concluded that both i.v. and p.o. administration of proxazole in the dosages used is ineffective in improving renal function in patients with chronic renal failure.
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PMID:The effects of proxazole on renal function in chronic renal failure. 719 77

Endothelin is an important modulator of renal function via its binding to abundant receptors in renal tissue and by the ability of renal endothelial and epithelial cells to synthesize and release endothelin. In the kidney, endothelin may function as a paracrine-autocrine factor in the regulation of renal blood flow, glomerular hemodynamics, and sodium and water homeostasis. Recent evidence suggests that circulating endothelin may play an important role in renal regulation in cardiorenal states of endothelin activation. Endothelin is a potent renal vasconstrictor that has dual actions on glomerular filtration rate due to its ability to preferentially constrict efferent arterioles preserving glomerular filtration. Furthermore, endothelin modulates sodium excretion and water balance at the level of the proximal tubule and medullary collecting ducts, respectively, by mechanisms that are still unclear. In addition, endothelin stimulates the renin-angiotensin-aldosterone system and atrial natriuretic peptide release and inhibits arginine vasopressin-mediated water reabsorption in the inner medullary collecting duct. Recent studies using specific receptor antagonists have demonstrated a pathophysiologic role for endothelin during renal ischemia, cyclosporine-induced toxicity, and chronic renal failure. This review highlights recent research that supports an important role for endothelin as a locally produced vasoactive and natriuretic peptide in the regulation of renal hemodynamic and excretory functions.
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PMID:Physiologic and pathophysiologic roles of endothelin in the kidney. 785 Apr 14

Ischemic renal disease (IRD) is defined as a clinically important reduction in glomerular filtration rate or loss of renal parenchyma caused by hemodynamically significant renal artery stenosis. IRD is a common and often overlooked clinical entity that presents itself in the setting of extrarenal arteriosclerotic vascular disease in older individuals with azotemia. Eleven to 14% of end-stage renal disease (ESRD) cases are attributable to chronic IRD. A high percentage of patients entering ESRD programs are hypertensive. Many patients with a presumed diagnosis of hypertensive nephrosclerosis actually have undiagnosed ischemic nephropathy as the etiology of their ESRD. It is important for the clinician to identify IRD, because IRD is a potentially reversible cause of chronic renal failure in a hypertensive patient. Atherosclerotic renal artery disease is common among patients with coronary artery disease and aortic and peripheral vascular disease. Atherosclerotic renal artery disease is a progressive disorder, and its progression is associated with loss of renal mass and functioning. A decrease in glomerular filtration rate sufficient to cause an elevation of the serum creatinine concentration requires injury to both kidneys. Consequently, IRD can arise from one of two main clinical situations: bilateral hemodynamically significant renal artery stenosis leading to bilateral renal ischemia; and hemodynamically significant renal artery stenosis in a solitary functioning kidney, or in a kidney that is providing the majority of a patient's glomerular filtration. The primary reason for establishing the diagnosis of IRD is the hope that correction of a renal artery stenosis will lead to improvement of renal function, or a delay in progression to ESRD. There are six major clinical settings in which the clinician could suspect IRD: acute renal failure caused by the treatment of hypertension, especially with angiotensin converting enzyme inhibitors; progressive azotemia in a patient with known renovascular hypertension; acute pulmonary edema superimposed upon poorly controlled hypertension and renal failure; progressive azotemia in an elderly patient with refractory or severe hypertension; progressive azotemia in an elderly patient with evidence of atherosclerotic disease; and unexplained progressive azotemia in an elderly patient. Noninvasive testing modalities that have been used recently include the angiotensin converting enzyme inhibitor renal scan, duplex Doppler sonography, magnetic resonance angiography, and the spiral computed tomography. Treatment methods include percutaneous transluminal angioplasty, endovascular stenting, and surgical revascularization. The results of treatment for preservation of renal function have been encouraging, with stabilization or improvement in renal function observed in a significant proportion of cases.
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PMID:Ischemic renal disease: an emerging cause of chronic renal failure and end-stage renal disease. 943 40

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

Non-steroid anti-inflammatory drugs are easily available and commonly used. Mechanism of their action is based on inhibiting prostaglandin synthesis. Prostaglandins are arachidonic acid derivatives that are responsible, among others, for regulation of renal blood flow. In some kidney disorders as well as in hemodynamic disturbances, their increased release aims at balancing substances causing kidney ischemia. Blocking prostaglandin synthesis in such conditions may result in development of nephrotoxic effect, manifesting in water-electrolyte imbalance, acute tubulo-interstitial nephropathy, nephrotic syndrome, acute and chronic renal papillary necrosis as well as acute or chronic renal failure. Analgesic nephropathy with papillary necrosis is a particular form of the nephrotoxic effect of non-steroid anti-inflammatory drugs. Development of this complication has been described in patients abusing phenacetin or other analgesic drugs and especially their combination.
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PMID:[Nonsteroidal anti-inflammatory drugs--nephrotoxic mechanism of action]. 1037 54

Atherosclerotic narrowing of the renal arteries may result in severe consequences including chronic renal ischemia, renal artery atheroembolism and renal vascular hypertension. Ischemic renal disease is increasingly recognised as a potentially treatable cause of chronic renal failure. Its precise prevalence is still poorly determined as there is no population based studies. The patients with ARD, particularly those with high grade stenosis and systolic hypertension are at very high risk for renal atrophy and renal failure. Angiogram is usually required to confirm the diagnosis. However, the diagnosis is likely in the elderly patient with systemic atherosclerosis and hypertension in whom a rapid rise in serum creatinine concentration is associated with decreased renal length. Disease is associated with high mortality when treated medically. In contrast, clinical improvement is reported after renal revascularisation. Therefore, consider the diagnosis in the patients at risk, because revascularisation (surgical or endovascular) can successfully preserve renal function in selected patients.
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PMID:Ischemic nephropathy. 1086 22

The role of EGF in the evolution of renal lesions after injury is still controversial. To determine whether the EGF expression is beneficial or detrimental, we generated transgenic mice expressing a COOH-terminal-truncated EGF-R under the control of the kidney-specific type 1 gamma-glutamyl transpeptidase promoter. As expected, the transgene was expressed exclusively at the basolateral membrane of proximal tubular cells. Under basal conditions, transgenic mice showed normal renal morphology and function. Infusion of EGF to transgenic animals revealed that the mutant receptor behaved in a dominant-negative manner and prevented EGF-signaled EGF-R autophosphorylation. We next evaluated the impact of transgene expression on the development of renal lesions in two models of renal injury. After 75% reduction of renal mass, tubular dilations were less severe in transgenic mice than in wild-type animals. After prolonged renal ischemia, tubular atrophy and interstitial fibrosis were reduced in transgenic mice as compared with wild-type mice. The beneficial effect of the transgene included a reduction of tubular cell proliferation, interstitial collagen accumulation, and mononuclear cell infiltration. In conclusion, functional inactivation of the EGF-R in renal proximal tubular cells reduced tubulo-interstitial lesions after renal injury. These data suggest that blocking the EGF pathway may be a therapeutic strategy to reduce the progression of chronic renal failure.
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PMID:Targeted expression of a dominant-negative EGF-R in the kidney reduces tubulo-interstitial lesions after renal injury. 1090 38

The present study examined the long-term consequences of warm renal ischemia (WRI) with or without renal ablation. Male Sprague-Dawley rats (250-300 g) were subjected to 60 min of complete WRI by pedicle clamping and then followed for 52 wk. Animals were organized into four groups: rats in which both kidneys were subjected to warm ischemia (2WIK); rats with left WRI and right nephrectomy (1WIK); uninephrectomized rats with a left nonischemic kidney (1NK); and sham-operated rats (2NK). Additional animals were studied at 24 h, 7 days, and 16 and 32 wk. In the first week after WRI, rats from the 2WIK and 1WIK groups displayed a similar degree of acute renal damage. After recovering from acute renal failure, 1WIK rats developed progressive and severe proteinuria, whereas it was mild in the 2WIK group, as well as in the 1NK and 2NK groups. Only animals from the 1WIK group developed severe chronic renal failure, glomerulosclerosis, interstitial fibrosis, and upregulation of transforming growth factor-beta(1) (TGF-beta(1)) gene, which was associated with increased TGF-beta(1) protein expression in tubular epithelial cells, arterioles, and in areas of mononuclear interstitial cell infiltrate. On the contrary, long-term renal TGF-beta(1) expression, function, and histology were similar in 2WIK and 2NK rats. The present study shows that prolonged bilateral WRI, when both kidneys are retained in place, induces very mild long-term renal lesions as opposed to the severe renal scarring observed when WRI is combined with contralateral nephrectomy.
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PMID:Influence of nephron mass in development of chronic renal failure after prolonged warm renal ischemia. 1091 44


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