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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although acute renal failure, caused either by renal ischemia or nephrotoxic agents, is usually characterized by oliguria, a severe fall in glomerular filtration rate, and a fall in renal blood flow, some patients and experimental models display a non-oliguric pattern of renal injury. The present study was designed to evaluate the mechanism of preservation of high urinary flow rate under this condition. Following the administration of the aminoglycoside gentamicin to rats for five days, a decrease in concentrating ability was demonstrated, caused by impaired vasopressin-mediated water transport. Further treatment resulted in a fall in Cin to 15 percent of control, although RBF was reduced to only 67 percent of control, and urine flow rate rose above control levels. Induction of acute and renal failure with dichromate was associated with variable high or low urinary flow rates according to pre-injury intake of sodium. Urine volume correlated directly with cortical blood flow. These data suggest that the non-oliguric pattern of acute renal injury is caused by preservation of cortical perfusion in the setting of severe tubular injury.
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PMID:Studies on the mechanism of non-oliguric experimental acute renal failure. 732 6

Previous reports suggest the value of renal decapsulation in the prevention of renal failure after acute ischemia. It has been suggested that this response is due to a release of "compartmental" pressure resulting in increased blood flow to the decapsulated kidney. Ten dogs were evaluated following 90 minutes of renal ischemia created by occlusion of the suprarenal aorta. Each animal underwent random unilateral decapsulation, with the contralateral kidney acting as control. Labeled 15 micron microspheres (Se85 and Ce141) were injected into the left ventricle at 15 minutes and one hour following decapsulation in six dogs. In the remaining animals the injection was carried out at 15 minutes and 48 hours. No difference in renal blood flow was found between decapsulated and control kidneys in either group. Similarly, using sectioned kidneys no difference in intrarenal distribution of blood flow was found. These data suggest that the effects caused by decapsulation are not due to hemodynamic alterations.
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PMID:Renal blood flow and intrarenal distribution of blood flow after decapsulation in the postischemic kidney. 736 10

Renal tubular cells are involved both in secretion and in reabsorption processes within the kidney. Normally, most xenobiotics are secreted into the urine at the basolateral membrane of the tubular cell, whereas amino acids are reabsorbed quantitatively at the luminal side. Under different pathological or experimental circumstances, these transport steps may be changed, e.g., they may be reduced by renal impairment (reduction of kidney mass, renal ischemia, administration of nephrotoxins) or they may be enhanced after stimulation of transport carriers. Furthermore, a distinct interrelationship exists between excretory functions of the kidney and the liver. That means liver injury can influence renal transport systems also (hepato-renal syndrome). In this review, the following aspects were included: based upon general information concerning different transport pathways for xenobiotics and amino acids within kidney cells and upon a brief characterization of methods for testing impairment of kidney function, the maturation of renal transport and its stimulation are described. Similarities and differences between the postnatal development of kidney function and the increase of renal transport capacity after suitable stimulatory treatment by, for example, various hormones or xenobiotics are reviewed. Especially, renal transport in acute renal failure is described for individuals of different ages. Depending upon the maturity of kidney function, age differences in susceptibility to kidney injury occur: if energy-requiring processes are involved in the transport of the respective substance, then adults, in general, are more susceptible to renal failure than young individuals, because in immature organisms, anaerobic energy production predominates within the kidney. On the other hand, adult animals can better compensate for the loss of renal tissue (partial nephrectomy). With respect to stimulation of renal transport capacity after repeated pretreatment with suitable substances, age differences also exist: most stimulatory schedules are more effective in young, developing individuals than in mature animals. Therefore, the consequences of the stimulation of renal transport can be different in animals of different ages and are discussed in detail. Furthermore, the extent of stimulation is different for the transporters located at the basolateral and at the luminal membranes: obviously the tubular secretion at the contraluminal membrane can be stimulated more effectively than reabsorption processes at the luminal side.
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PMID:Renal handling of drugs and amino acids after impairment of kidney or liver function--influences of maturity and protective treatment. 749 61

Renovascular hypertension is one of the more common causes of secondary hypertension. The true prevalence of this condition is not known, because only a selected few with hypertension are considered for thorough diagnostic work-up. The higher incidence figures come from centers with a special interest in this disease. The ability of a clinician to detect renovascular hypertension has improved substantially, thanks to the advances in radiology. The predominant mechanism of blood pressure elevation from renal ischemia is activation of the renin-angiotensin system. Clinically, the pathological lesions that cause renal artery stenosis are atherosclerosis and fibromuscular dysplasia; the former is typically seen in older men, and the latter is typically found in young women. Suspicion of the presence of renovascular disease should prompt the physician to obtain appropriate screening and confirmatory tests. Once diagnosed, the management of patients with renovascular hypertension requires a carefully planned multidisciplinary approach to offer the patient a best possible therapeutic option, with surgical revascularization or balloon angioplasty, or chronic medical therapy. However, these options are not mutually exclusive. The best long-term results are obtained with surgical therapy. Although balloon angioplasty is being increasingly used perhaps as the preferred initial therapeutic procedure for many patients with renal artery stenosis, long-term results comparable with surgery are not yet available. The ideal rational therapy for patients with renal artery stenosis is reperfusion of the ischemic kidney either by surgical correction or by balloon dilation. The aim is not only to improve the blood pressure control, but also to prevent and at times to reverse renal failure. Although effective antihypertensive drugs have become available, the role of medical management of renovascular hypertension is shrinking and should be limited to patients who have contraindications to or unwilling to undergo corrective procedures to relieve renal ischemia.
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PMID:Renovascular hypertension. 777 25

During experimental renal ischemia and reperfusion in rabbits, morphine as well as naloxone significantly inhibited the increased superoxide anion (O2-) generation by resting and opsonized zymosan-stimulated phagocytes in renal venous blood. Morphine with naloxone in combination inhibited O2- generation to a lesser extent than that observed when these drugs were used separately. Morphine and/or naloxone did not significantly affect erythrocyte superoxide dismutase (SOD-1), glutathione peroxidase (GPx) and catalase activities or malonyldialdehyde (MDA) concentrations in venous blood during renal ischemia. During reperfusion there was a tendency to a slight reduction of erythrocyte catalase activity in morphine-treated animals, and to slight diminutions of erythrocyte SOD-1 and GPx activities and erythrocyte MDA concentrations in rabbits treated with naloxone and morphine in combination. These results indicate that opioid receptor agonists and antagonists modify the response of the kidney to acute injury. These effects may have relevance to the pattern of oxidative stress seen in patients with acute ischemic renal failure.
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PMID:Effect of morphine and naloxone on oxidative metabolism during experimental renal ischemia and reperfusion. 785 38

Infusion (0.46 mumol/kg/min) of the endothelin (ET)-converting-enzyme inhibitor, phosphoramidon (P), protected function and structure after 30 min renal ischemia in rats more than treatment (5 mumol/kg/min) with the ETA receptor antagonist, BMS-182874 (B). The glomerular filtration rate (GFR; 0.7 +/- 0.12 ml/min) and renal plasma flow (RPF) decreased approximately 40% at 2 h reflow versus controls (C: 1.2 +/- 0.12). B weakly protected the GFR (0.8 +/- 0.07 ml/min); P restored it (1.1 +/- 0.05). Both compounds reduced tubular injury at 2 h reflow; P ameliorated glomerular changes. At 24 h the GFR (0.6 +/- 0.06 ml/min) and RPF decreased 67% versus C (1.8 +/- 0.08). B did not protect the GFR and RPF. P partially protected the GFR (0.9 +/- 0.07 ml/min) but not RPF, and reduced tubular injury. The results suggest that both ETA and non-ETA receptors mediate ET-induced changes in ischemic renal failure.
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PMID:Comparison of a novel ETA receptor antagonist and phosphoramidon in renal ischemia. 789 82

The pathophysiology of ischemic acute renal failure is complex, and the role of leukocyte adhesion in this process is not well defined. A monoclonal antibody (mAb) against intracellular adhesion molecule 1 (anti-ICAM-1), administered at the time of bilateral renal ischemia in the rat, prevented both functional impairment and histologic changes of acute renal failure. Plasma creatinine measured (mg/dl) 24 hr after 30 min of ischemia was 0.61 +/- 0.05 in the anti-ICAM-1-treated animals compared with 2.4 +/- 0.14 (P < 0.0001) in the vehicle-treated ischemic group. Forty-eight hours after ischemia, creatinine values were 0.46 +/- 0.05 and 2.03 +/- 0.22 (P < 0.0001) in anti-ICAM-1 and vehicle-treated groups, respectively. A low dose of anti-ICAM-1 that was itself nonprotective, when given with partially protective doses of a mAb against lymphocyte function-associated antigen-1 (anti-LFA-1), acted synergistically to prevent renal failure. Anti-ICAM-1 mAb also protected the kidney when administered 0.5 or 2 hr but not 8 hr after restoration of blood flow and when the ischemic period was extended to 40 min. Ischemia-induced increases in tissue myeloperoxidase, a marker of neutrophil infiltration, were mitigated with anti-ICAM-1 treatment. Thus, anti-ICAM-1 mAb protected the kidney against ischemic renal failure, even when the antibody was administered after the ischemic period. These results suggest a critical role for leukocytes and adhesion molecules in the pathophysiology of ischemic injury and may have important therapeutic implications.
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PMID:Antibody to intercellular adhesion molecule 1 protects the kidney against ischemic injury. 790 59

Rats within the early maintenance phase of post-ischemic acute renal failure (ARF) can resist additional ischemic insults. This study assessed whether this protection exists directly at the tubular cell level, and if so, whether it is a consequence of prior cell injury (for example, due to heat-shock protein synthesis; HSP), or if it arises in response to reductions in functional renal mass and/or the uremic environment. Rats were subjected to either 15 or 35 minutes of unilateral or bilateral renal ischemia, and after 15 minutes to 24 hours of reflow, proximal tubular segments (PTS) were isolated for study. Their viability following oxygenation and hypoxic/reoxygenation injury (H/R) was tested (LDH release). The influence of uremia/reduced renal mass was determined by studying PTS extracted 24 hours after 1 1/2 nephrectomy, and by determining whether PTS exposure to a "uremic milieu" (urine addition) blocks H/R damage. HSP effects were gauged by correlating renal cortical HSP-70 expression with degrees of in vitro protection, and by ascertaining whether in vivo hyperthermia (42 degrees C; 15 min) mitigates subsequent PTS H/R damage. Results were compared with those obtained from normal PTS. The in vivo experimental protocols did not substantially alter PTS isolation or their viability during oxygenation. Fifteen minutes of ischemia induced neither azotemia nor PTS cytoprotection. In contrast, 35 minutes of ischemia conferred marked protection against subsequent H/R, but only when azotemia was permitted to develop (protection seen after 24 hr, but not at 4 hr of reflow; protection abrogated by retention of 1 normal kidney). Renal failure in the absence of tubular necrosis (1 1/2 uninephrectomy) protected PTS from H/R damage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Post-ischemic acute renal failure protects proximal tubules from O2 deprivation injury, possibly by inducing uremia. 793 24

Increased intraabdominal pressure (IAP) has been demonstrated to cause intestinal and renal ischemia in both animals and humans. Neonates undergoing closure of anterior abdominal wall defects are at risk for these complications from markedly increased IAP, which are putatively responsible for a 13% to 20% mortality. In an effort to decrease morbidity and mortality we performed a 4-year prospective clinical study to determine if monitoring IAP using bladder pressure (BdP) measurements would significantly improve perioperative care in infants with abdominal wall defects. Forty-two consecutive infants with gastroschisis (28) and omphalocele (14) were prospectively studied. Intraoperative and serial postoperative measurements of BdP were obtained from an indwelling bladder catheter using a standard pressure transducer. Methods of initial closure, as well as manipulations in sedation, paralysis, and silo reduction, were selected to keep BdP < 20 mm Hg. Bladder pressure monitoring significantly altered the management of 64% of our patients, particularly those with gastroschisis (74%). Thirteen patients with gastroschisis underwent staged closure; in 7 (54%) this decision was based on high BdP even though bowel reduction was mechanically possible. Elevated BdP influenced the closure method and timing of silo reductions in 5 of 14 (42%) infants with omphalocele. There were no episodes of renal failure or refractory oliguria. There were three patients in a single cluster who developed uncomplicated, nonsurgical necrotizing enterocolitis late in their respective courses. One patient whose bowel was placed in a silo had severe hypotension associated with group B streptococcal sepsis and subsequently developed necrotic bowel despite low BdP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bladder pressure monitoring significantly enhances care of infants with abdominal wall defects: a prospective clinical study. 826 3

Iron-dependent free radical reactions and renal ischemia are believed to be critical mediators of myohemoglobinuric acute renal failure. Thus, this study assessed whether catalytic iron exacerbates O2 deprivation-induced proximal tubular injury, thereby providing an insight into this form of renal failure. Isolated rat proximal tubular segments (PTS) were subjected to either hypoxia/reoxygenation (H/R: 27:15 min), "chemical anoxia" (antimycin A; 7.5 microM x 45 min), or continuous oxygenated incubation +/- ferrous (Fe2+) or ferric (Fe3+) iron addition. Cell injury (% lactic dehydrogenase [LDH] release), lipid peroxidation (malondialdehyde, [MDA]), and ATP depletion were assessed. Under oxygenated conditions, Fe2+ and Fe3+ each raised MDA (approximately 7-10x) and decreased ATP (approximately 25%). Fe2+, but not Fe3+, caused LDH release (31 +/- 2%). During hypoxia, Fe2+ and Fe3+ worsened ATP depletion; however, each decreased LDH release (approximately 31 to approximately 22%; P < 0.01). Fe(2+)-mediated protection was negated during reoxygenation because Fe2+ exerted its intrinsic cytotoxic effect (LDH release: Fe2+ alone, 31 +/- 2%; H/R 36 +/- 2%; H/R + Fe2+, 41 +/- 2%). However, Fe(3+)-mediated protection persisted throughout reoxygenation because it induced no direct cytotoxicity (H/R, 39 +/- 2%; H/R + Fe3+, 25 +/- 2%; P < 0.002). Fe3+ also decreased antimycin toxicity (41 +/- 4 vs. 25 +/- 3%; P < 0.001) despite inducing marked lipid peroxidation and without affecting ATP. These results indicate that catalytic iron can mitigate, rather than exacerbate, O2 deprivation/reoxygenation PTS injury.
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PMID:Inorganic iron effects on in vitro hypoxic proximal renal tubular cell injury. 843 70


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