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

To estimate the renal ischemia-protective effect of saralasin, model studies were performed on rats and dogs. Acute ischemic renal failure was induced in rats by clamping off the vascular pedicle for 90 minutes. When the drug was prophylactically administered before the ischemia episode, a premature increase in post-ischemic plasma urea level and a shortening of survival time of the animals were observed compared with the untreated control. Following auto-transplantation of 24-hour cold-stored dog kidneys, the infusion of saralasin failed to improve renal blood flow (MRBF), glomerular filtration rate (KrCl) and fractional sodium excretion (FENa). On the other hand, the angiotensin blockade with captopril led to an increase in MRBF which was associated, however, with significant decreases in KrCl and FENa. This discrepancy was suggested to be due to a predominant postglomerular vasodilation. The results show that the application of saralasin before renal ischemia may aggravate the loss of renal function whilst the post-ischemic administration of the drug has no substantial effect on the acute failure of transplanted kidneys.
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PMID:[Experimental studies on the modifiability of ischemic acute renal failure by saralasin]. 391 17

Histological studies have been performed on experimental acute renal failure induced by intravenous injection of hemoglobin in rats. These have been correlated with alterations in renal excretory function, assessed by the measurement of inulin clearance, at various stages of the lesion. The most prominent morphological changes during the first 24 hr after hemoglobin injection, when inulin clearance is most markedly suppressed, are: the presence of hemoglobin within the lumen of small intrarenal vessels, particularly the vasa recta; hemoglobin cast formation involving predominantly the thick ascending limbs of the loops of Henle; and evidence of injury of the epithelium of the proximal tubules and thick ascending limbs. Notably absent during this stage of the lesion are marked tubular dilatation, interstitial edema, and cast formation in the distal collecting ducts. The considerable recovery of function which occurs at 72 hr is accompanied by a marked reduction in involvement of the vasa recta. Standard sections and microdissection reveal many markedly dilated proximal tubules at this stage of the lesion, suggesting obstruction of filtering nephrons. These data have led to a tentative hypothesis regarding the pathogenesis of renal failure in this experimental lesion. It is suggested that renal ischemia and failure of glomerular filtration are the primary factors responsible for the early and severe impairment of renal function, and that these are related to intravascular aggregation of hemoglobin pigment. As this defect recedes, tubular obstruction by hemoglobin casts prevents restitution of excretory function in a variable fraction of the nephrons. The latter accounts for the relatively prolonged, moderate reduction in inulin clearance associated with the late stages of this lesion. These hypotheses form the basis for a continuing study of this renal lesion.
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PMID:The renal lesion associated with hemoglobinemia. II. Its structural characteristics in the rat. 593 61

The role of renal ischemia in the pathogenesis of the renal failure produced by hemoglobin injection in the rat is evaluated. The data indicate that in the initial hours of this lesion renal blood flow is consistently reduced and that during its subsequent evolution blood flow rises towards normal levels, in some animals, while inulin clearance remains severely depressed. Volume expansion during the initial stage of the lesion may effect a rise in renal blood flow to normal levels with little effect on inulin clearance rate, further demonstrating the relative lack of dependence of the excretory defect on concomitant renal ischemia. These observations indicate that renal ischemia is probably a necessary factor in the initial production of the lesion; that it persists during its initial phase, up to 24 hours in most rats; and that, although it may contribute to the observed excretory defect, it is not the predominant etiologic factor. Other functional data indicate that renal blood is perfusing nephrons in which the excretory capacity is impaired but which retain the ability to extract Diodrast from the peritubular capillaries. This functional pattern indicates an excretory defect secondary either to intratubular obstruction or to a primary reduction of glomerular filtration rate of undefined etiology. The morphological findings of numerous dense intratubular hemoglobin casts and, in the well-perfused kidney, dilatation of proximal tubules, are suggestive of an obstructive lesion. However, the data do not conclusively distinguish between these two pathogenetic mechanisms.
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PMID:The renal lesion associated with hemoglobinemia: a study of the pathogenesis of the excretory defect in the rat. 602 73

Experiments were performed on rats to investigate the significance of the medullary hyperemia known to follow renal ischemia. To this end, its frequency was determined, its severity was quantified, and its relation to renal function was examined early (1 to 3 hr) and later (18 hr) after 45 min of warm ischemia. All kidneys were found to have a hyperemic outer medulla early after ischemia, which was shown to develop during the period of ischemia itself, but which was found to be highly variable in its severity. The degree of hyperemia was assessed both subjectively by grading and by histometric determinations of inner stripe capillary volume. One to hours after ischemia, the severity of medullary hyperemia was reflected in all indices of renal function, the least congested kidneys showing the best function. Eighteen hours after ischemia, the degree of medullary hyperemia was reflected in all indices of renal function, except urine flow rate; the non-congested kidneys showed functional recovery and the still-congested kidneys showed worsening function. Glomerular blood flow, known to be preferentially reduced in deep nephrons 1 to 3 hr after ischemia, had normalized 18 hr after ischemia in the non-congested kidneys but was still severely and unevenly depressed in the congested kidneys. It is concluded that congestion of the outer medulla is a key event in ischemic renal failure, its occurrence is coincidental with the reduction in deep nephron perfusion and urinary concentrating power in the early and maintenance phase and its disappearance heralds the restoration of deep nephron perfusion and urinary concentrating ability in the recovery phase.
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PMID:Role of the medullary perfusion defect in the pathogenesis of ischemic renal failure. 651 74

Renal ischemia was produced in rats by clamping of the renal artery for 1 h. Upon termination of the ischemic period a 20% solution of DMSO (5 g kg-1 b.w.) was given intravenously to 33 rats. Eighteen control animals received normal saline. All DMSO-treated animals survived while all control animals died within the subsequent seven days. At 24 h following the experiment, the mean blood urea of the control rats was 254 mg/100 ml and the mean plasma creatinine 7.2 mg/100 ml. By contrast, the DMSO-treated rats had a mean blood urea of 69 mg/100 ml and plasma creatinine of 1.6 mg/100 ml. In 17 animals the kidney was perfused with DMSO prior to the closure of the renal artery. All these rats survived the procedure and showed near normal kidney function at 24 h. The renal artery was clamped for 60 min in ten dogs. Five dogs received DMSO (3 g kg-1 b.w.) and the other five received an equivalent dose of normal saline. Three weeks later a contralateral nephrectomy was performed. Renal function was normal in the DMSO-treated dogs. One control dog died of uremia, in the remaining four a transient renal failure was observed. These experiments in two different animals highlight the protective effect of DMSO on the ischemic kidney when the drug is administered after the ischemic period.
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PMID:Dimethyl sulfoxide in acute ischemia of the kidney. 657 89

Glomerular visceral epithelial cells (podocytes) undergo flattening and spreading of major processes detectable by scanning electron microscopy in early postischemic acute renal failure in both animals and man. The authors examined the kinetics of development of these epithelial cell changes in the renal pedicle-clamping model of ischemic renal failure in the rabbit. They found that these changes develop progressively, increasing with increasing length of ischemia, and occur while the pedicle clamp is still in place. To assess the possible role of angiotensin II and vasopressin in producing the epithelial changes, the authors compared glomerular morphology before and during pedicle clamping in hydrated rabbits and in dehydrated rabbits. Dehydration alone produced changes in glomerular epithelial cells comparable to those seen in the postischemic kidney. The angiotensin-converting enzyme inhibitor captopril did not prevent the podocyte changes in either group. In vitro incubation studies confirmed that both angiotensin II and vasopressin produce glomerular epithelial cell changes with a threshold between 10(-7) M and 10(-8) M, a concentration that may be physiologically significant for angiotensin II, which is synthesized at the glomerulus and may have local paracrine effects. Such local synthesis may not be inhibited by systemic administration of captopril. Angiotensin II may play a role in producing podocyte alterations during renal ischemia, as well as in the dehydrated state.
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PMID:Glomerular epithelial cell changes after ischemia or dehydration. Possible role of angiotensin II. 669 12

Renal failure in aortic surgery is frequently due to the additive effects of multiple subthreshold insults that progressively decrease renal reserve. Prevention of renal failure requires a high index of suspicion concerning the clinical setting in which renal injury may occur. If cardiac hemodynamics and arterial pressure are maintained at optimal levels, especially during periods of maximum hemodynamic stress, ischemic renal injury can be minimized. This requires aggressive monitoring of cardiac hemodynamics using a Swan-Ganz (thermodilution) catheter for measurement of pulmonary artery wedge pressure and cardiac output. Prompt recognition of hemodynamic instability allows rapid intervention to correct the renal ischemia before irreversible renal injury can occur.
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PMID:Renal failure following abdominal aortic reconstruction. 684 81

The effects of calcium blockade with verapamil on postischemic renal failure were tested in dogs. Two experiments were performed. In experiment 1 (n = 7), one kidney in each dog received an infusion of verapamil and the other received saline for 30 minutes prior to induction of 1 hour of ischemia. Inulin clearance (CIN), urine flow, and renal blood flow (RBF) were measured. Infusion of verapamil increased urine flow from 0.99 to 4.29 ml/min (P less than 0.001). CIN and RBF did not change significantly nor did urine flow in the saline-treated kidney. Three hours after ischemia there was no significant difference in CIN, although it was lower in verapamil-treated kidneys. RBF declined in both treatments. In experiment 2 (n = 6) kidneys were treated with verapamil and saline for 50 minutes beginning immediately after 1 hour of ischemia. Urine flow and CIN were significantly higher in verapamil-treated kidneys during the infusion (3.09 +/- 0.44 versus 0.26 +/- 0.12 ml/min, P less than 0.001; 28.6 +/- 7 .4 versus 6.2 +/- 3.1 ml/min, P less than 0.025, respectively). CIN remained elevated in verapamil-treated kidneys at 3 hours, however RBF was depressed in both verapamil- and saline-treated kidneys. These results suggest that verapamil is a potent diuretic and that verapamil can be given after renal ischemia with significant attenuation of postischemic renal failure.
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PMID:Beneficial effects of verapamil on postischemic renal failure. 687 43

Previous studies have shown that adenosine triphosphate-magnesium chloride (ATP-MgCl2) administered after 30 to 60 min of renal ischemia ameliorated the resulting acute renal failure in different species of animals. The purpose of this study was to determine whether addition of ATP-MgCl2 to the perfusate during renal preservation, prior to transplantation, might improve renal function. Dog kidneys were subjected to normothermic ischemia for 35 min, after which they were preserved by pulsatile perfusion for 24 hr at 7 C. The perfusate contained albumin in a balanced electrolyte solution with an without ATP-MgCl2. Following 24 hr of pulsatile perfusion, the kidneys were autotransplanted and renal function was determined 3 days post-transplantation. The results indicated that dog kidneys subjected to ischemia followed by perfusion preservation developed severe oliguric renal failure 3 days after transplantation. However, if ATP-MgCl2 was added to the perfusate, such kidneys demonstrated markedly improved renal function and ATP levels. These results indicate that kidneys which have been subjected to episodes of warm ischemia could be salvaged by addition of ATP-MgCl2 to the perfusate.
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PMID:Improved renal function using adenosine triphosphate-magnesium chloride in preservation of canine kidneys subjected to warm ischemia. 701 14

The high blood flow rate/gram of kidney tissue supplies mainly the renal cortex. The net effect of the interaction of the renin-angiotensin system, the kallikrein-kinin system and prostaglandins is to autoregulate renal blood flow within a narrow range. Drugs and neurogenic factors also influence renal hemodynamics. The renal circulation responds to changes in extracellular fluid volume, and in cardiac output. Renal ischemia occurs readily as these parameters decrease and prompt correction of circulatory dynamics can restore renal blood flow and prevent tubular necrosis. With hypovolemia or heart failure, angiotensin II is a mediator of efferent arteriolar constriction promoting a proportionately greater fall in renal plasma flow than in glomerular filtration rate, thereby augmenting sodium reabsorption. With renal failure, glomerulotubular balance is affected conversely promoting sodium loss. Appreciating these distinctions allows recognition of inappropriate sodium retention or loss. With such data, prognosis can be estimated more accurately and attempts to restore circulatory dynamics can be guided.
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PMID:Pathophysiology of renal hemodynamics. 726 10


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