Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the effects of renal ischemia with reperfusion on the reactivity of rabbit renal vasculature. The main renal and arcuate arteries were isolated and studied as ring preparations. In the renal artery, concentration-response curves for potassium chloride (KCl), noradrenaline (NA), serotonin (5-HT), angiotensin II (AII), acetylcholine (ACh), A23187 or sodium nitroprusside (SNP) were unaltered after ischemia and reperfusion. Under the same conditions, the relaxation of arcuate arteries elicited by ACh was reduced when vessels were precontracted with methoxamine but not with KCl, whereas SNP-induced responses were unaffected. In anesthetized rabbits, renal blood flow and corresponding renal vascular resistances (RVR) were not modified by ischemia and reperfusion. ACh (1, 3 and 10 micrograms/kg per min) reduced RVR (maximally -24 +/- 8%) and this response was unchanged after ischemia and reperfusion (maximally -25 +/- 10%). These results demonstrate that the rabbit renal vasculature is relatively resistant to an ischemic insult and is probably not involved in the development of postischemic renal failure.
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PMID:Endothelium-dependent control of vascular tone in the rabbit kidney after ischemia and reperfusion. 845 77

A case of thrombotic microangiopathy presenting as a hemolytic uremic syndrome complicated by untreatable hypertension and ultimately requiring bilateral nephrectomy is discussed. Severe hypertension and renal failure may complicate the course of vascular diseases of the kidney, including thrombotic microangiopathy, chronic hypertension, and scleroderma. Toxins, pressure stress, and immune material may trigger the initial injury to vascular endothelium. The malignant course of these renal vascular diseases seems linked to the severity of vascular injury. Endothelial injury manifests with swelling and detachment of endothelial cells from the basement membrane, expansion of the subendothelial space, and newly formed basement membrane-like material. In arterioles, endothelial injury precedes myointimal swelling and proliferation, leading to vascular lumina narrowing or obliteration and secondary glomerular ischemia, with glomerular tuft collapse and garland-like wrinkling and thickening of the capillary wall. Endothelial cell injury is very likely the common determinant of a cascade of events that lead to irreversible renal failure. When the initial insult (toxins, mechanical stress, antibodies) is promptly removed, lesions are self-limiting and the patient usually recovers. However, a severe insult persisting for some time can lead to chronic and irreversible vascular lesions that, through renal ischemia, trigger maximal activation of the renin angiotensin system with a brisk elevation in arterial blood pressure that may combine to further vascular injury and renal ischemia. Moreover, enhanced shear stress in the severely narrowed microcirculation, through abnormal von Willebrand factor processing, can also favor endothelial injury and platelet aggregation, which may further worsen the vascular lesions and sustain the microangiopathic process. Plasma manipulation, arteriolar vasodilators, and angiotensin-converting enzyme inhibitors normally control the vicious circle, but in few severe cases bilateral nephrectomy remains the last chance to save the patient's life.
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PMID:Malignant vascular disease of the kidney: nature of the lesions, mediators of disease progression, and the case for bilateral nephrectomy. 867 55

Thus I would like to conclude by saying that an idiopathic form of obliterative renal arteriopathy account for the rare presentation of severe hypertension and progressive renal failure with or without overt hemolytic anemia and thrombocytopenia in children. It can be labelled as primary malignant nephrosclerosis (NScl) or atypical HUS, based on primary thrombotic angiopathy. This, essentially intimal changes, is seen in diverse conditions and appears to result from primary endothelial injury followed by intimal exudation, thrombosis, and repair by fibrosis. Persistent or recurrence of this process form the basis of progressive obliterative arteriopathy. The result is renal ischemia and renin-angiotensin mediated hypertension. Establishment of a vicious circle would further accelerate HT and lead to end stage renal failure. Early recognition and prompt therapeutic intervention might prove beneficial.
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PMID:Thrombotic microangiopathy with hypertension and acute renal failure in children (a typical hemolytic uremic syndrome). 869 75

This report was designed to assess response of the renal nerve activity (RNA) during and after renal ischemia in chronic hypoxic rats. Hypoxia was induced by placing the female Wistar rats in an altitude chamber set at 5500 m for 4 weeks. Simultaneous recordings of left renal efferent (RENA) and afferent (RANA) nerve activity were performed in each pentobarbital-anesthetized rat throughout the experiment. Ischemic renal failure was induced by complete occlusion of the left renal artery for 45 min. During renal arterial occlusion (RAO), RENA gradually decreased while RANA enhanced initially and then this decreased gradually in both sea level (SL) controls and chronic hypoxic (high-altitude; HA) rats. During 45 min of reperfusion, RENA depressed more in comparison with RANA in both groups of animals. In addition, RANA returned to baseline level in SL rats, while it remained elevated in HA rats. In the second experiment, six groups of renal ischemic rats were challenged by rapid intravenous infusion of 10 ml of saline, and urine was collected for 90 min from the left ureter. Baseline RENA was low in rats 4 h after RAO of SL (4SL) and of HA (4HA) groups. The effects of saline loading on RENA and RANA were different in HA and SL rats. Saline loading significantly decreased RENA but increased RANA more in SL rats. Following saline loading, RENA in 4SL and 4HA rats, as well as animals 24 h after RAO of SL (24SL) and HA (24HA) were comparable to their respective SL or HA animals. In 4SL rats, RANA was significantly enhanced, and remained elevated during saline loading and the recovery period. In 4HA, 24HA and 24SL rats, RANA reduced significantly during saline loading, then its activity returned to the baseline value. The insulted kidneys showed increased renal excretion of water and sodium in 4SL and 4HA rats. Urinary excretion reduced significantly in 24SL rats but was almost normal in 24HA rats. These results indicate that a decrease in RENA may play a protective role in response to renal ischemia in both SL and HA rats. In response to renal ischemia and saline loading, different alterations of RANA in SL and HA rats may reflect a beneficial mechanism located in the hypoxia-pretreated kidney.
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PMID:Renal neural response to ischemic renal failure in chronic hypoxic rats. 874 Jun 54

Acute renal failure caused by radiocontrast agents remains a severe problem, particularly in patients with risk factors. There is debate concerning the pathophysiology of contrast media-induced acute renal failure, including, but not limited to, renal ischemia or tubular damage. Vascular ischemia is considered a major contributor because consistent changes in renal hemodynamics have been recorded experimentally. We describe a patient who has a typical course of contrast-associated renal failure manifested by severe renal vasoconstriction and backflow of the contrast agent during renal angiography performed after 6 days of an intravenous urography. Such degree of renal vasoconstriction is noteworthy in that this particular case might serve as a model in delineation of the pathogenetic mechanisms of acute renal failure after contrast media administration.
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PMID:Severe renal vasoconstriction and anuria after intravenous urography in a patient with renal impairment. 880 47

The leukocyte adhesion molecule ICAM-1 is implicated in ischemic renal reperfusion injury. We tested the utility of an ICAM-1 antisense oligodeoxyribonucleotide (ODN) with lipofectin, six hours prior to 30 minutes of bilateral renal ischemia in the rat. We measured ICAM-1 expression by immunohistochemistry and Western blot. Our antisense ODN showed a specific ICAM-1 surface expression inhibition in vitro. We then assessed ICAM-1 expression, leukocyte infiltration, serum creatinine, serum urea concentration, and renal histology in rats subjected to renal ischemia and controls. Serum creatinine and urea concentrations 12 and 24 hours post-ischemia were increased in saline treated and reverse ODN treated rats, compared to antisense ODN treated or sham operated rats (P < 0.05). Western blotting showed decreased ICAM-1 protein in antisense ODN-treated kidneys, compared to reverse ODN treated and saline treated ischemic controls (P < 0.05). Antisense ODN also ameliorated the ischemia-induced infiltration of granulocytes and macrophages (P < 0.05), and resulted in less cortical renal damage as assessed by a quantitative pathological grading scale (P < 0.05), compared to reverse ODN or saline treatment. Thus, antisense ODN for ICAM-1 protected the kidney against ischemic renal failure. The clinical applicability of these findings extends beyond ischemic acute renal failure.
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PMID:Antisense oligonucleotides for ICAM-1 attenuate reperfusion injury and renal failure in the rat. 884 Feb 75

To clarify the development of tubular necrosis and its healing process in ischemic renal failure observing degeneration, necrosis, cell proliferation and the involvement of apoptosis in the renal tubular epithelial cells before and after renal ischemia in rats through morphological examination. Eight week-old male rats were used for this study. The model for acute renal failure was by obstruction of bilateral renal arteries and veins for 45 minutes in several intervals (0 hr, 1 hr, 3 hr, 6 hr, 12 hr, 24hr, 48 hr, 96 hr, 1 week, 2 weeks and 4 weeks) each following reperfusion. Urinary beta 2-microglobulin (BMG) levels were measured to evaluate renal tubular function. In evaluating tubular necrosis and cell proliferation, observations of renal tubular tissue were made serially by use of light microscopy and immunological staining of proliferating cell nuclear antigen (PCNA) and bromodeoxyuridine (BrdU), respectively. The number of nuclei in the proximal tubular epithelium/circumference of the basement membrane (n/BM index) was calculated using a tissue measuring device. Transmission electron microscopy and the TdT-mediated dUTP-biotin nick end labeling (TUNEL) methods were used as indices of apoptosis. Maximal BMG values were obtained 24 hours after ischemia when injury in the proximal tubular epithelium was most prominent. The maximal number of PCNA and BrdU-positive cells were obtained 24 hours after ischemia and thereafter gradually decreased. The n/BM index in the disorder group was significantly increased 96 hours and 1 week after ischemia (p < 0.001). Electron microscopy revealed nuclear fragmentation and apoptosis in the tubular area indicating that there were significant differences. The number of positive cells for in situ nick end labelling increased 24 hours and 2 weeks after ischemia, exhibiting a two peak curve. However, the number of positive cells significantly decreased 4 weeks after ischemia. In the proximal kidney tubules damaged by reperfusion after ischemia, epithelial hyperplasia developed 3 to 6 days after the most active period of S-phase cells was noted. Thereafter, a decreasing number of epithelial cells was observed. It seemed that the decreasing number of these cells had been produced by apoptosis detected 2 weeks after ischemia.
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PMID:[A pathomorphological study on damage and repair process of tubuli after renal ischemia]. 895 3

Acute renal failure (ARF) is a frequent complication in hospitalized patients and is strongly related to increase in mortality. In order to analyze the clinical outcome and the prognostic factors in hospital-acquired ARF, a prospective study was performed. Data from 200 patients with established ARF during the period of January 1987 through July 1990 were collected. The incidence of ARF was 4.9/1000 admissions. Renal ischemia (50%) and nephrotoxic drugs (21%) were the main etiologic factors. The histologic study done in 43 patients showed: acute tubular necrosis (53%), tubular hydropic degeneration (16%), glomerulopathies (16%), and other lesions (15%). Dialysis therapy was performed in 101 patients. The mortality rate was 46.5% and the most important causes of death were: sepsis (38%), respiratory failure (19%), and multiple organ failure (11%). Higher mortality was observed in oliguric patients (62.9%) than nonoliguric (34.5%) (p < 0.05) and in ischemic renal failure (56.7%) when compared to nephrotoxic renal failure (14.7%) (p < 0.05). As primary cause of death was not associated to the acute renal failure, we conclude that acute renal failure is an important marker of the gravity of the underlying disease and not the cause of death.
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PMID:Acute renal failure: clinical outcome and causes of death. 910

We examined the influence of renal ischemia in rats with diabetes mellitus (DM). Male Wistar rats were rendered diabetic by streptozotocin treatment. Two weeks later, 30 minutes of complete ischemia was induced in the left kidney of DM and non-DM animals. Both groups were evaluated functionally and morphologically four or eight weeks post-ischemia. In non-DM animals renal function and morphology showed almost complete recovery. In the DM animals, however, this comparatively short period of ischemia caused a substantial loss of renal function. Four weeks post-ischemia inulin clearance in the DM kidneys rendered ischemic was only 20% of that in the corresponding non-DM kidneys, and after eight weeks the DM kidneys were completely anuric. Extensive inflammation and tubulointerstitial fibrosis were evident in DM kidneys four weeks after ischemia and seemed to increase over time. After eight weeks, tubular atrophy was found in the ischemic DM kidneys, resulting in a substantial loss of kidney mass. We conclude that in diabetic rats renal ischemia causes rapidly progressive kidney damage that in several respects resembles diabetic nephropathy in humans. Since advanced renal lesions similar to those seen in human diabetic nephropathy never develop in the rat solely as a result of DM, the present study may provide an experimental model for further studies on renal failure in diabetes mellitus.
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PMID:Ischemia causes rapidly progressive nephropathy in the diabetic rat. 932 37

In the vast population of patients with established hypertension, there is a small group in whom the blood pressure elevation is caused by renal ischemia. These patients have renovascular hypertension, which can presently be diagnosed with greater precision than in the past. The exact prevalence of renovascular hypertension is not known and the diagnosis is probably missed in many patients. It is important to recognize this condition in clinical practice, because it is a correctable from of secondary hypertension and because it is a reversible cause of renal failure in some patients. Clinical identification of patients with renovascular hypertension has been so imprecise and complex that the very diagnostic quest for this condition has been questioned. However, it is well recognized that renovascular disease is a progressive disorder with serious sequelae if appropriate therapy is not rendered.
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PMID:Renovascular hypertension. 937 73


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