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

The morphological consequences of acute or chronic renal ischemia may consist of an anemic kidney infarction, bilateral cortical necrosis, acute tubular lesions in circulatory renal failure, so-called subinfarction, as well as arteriosclerotic endstage kidney. In renal biopsies obtained from patients with acute renal failure, renal dysfunction can be morphologically explained by acute intra- and extracapillary necrotizing glomerulonephritis in 50% of cases, and by solely acute tubular lesions in 30% of cases. It is suggested that the development of acute tubular lesions during circulatory insufficiency might be favoured by an angiotensin II-dependent vas efferens constriction, leading to a reduction of peritubular blood flow in the presence of preserved glomerular filtration. The balance between demand and supply of oxygen within the tubular epithelial cells might thereby be critically disturbed.
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PMID:[Pathology of renal ischemia and acute renal failure]. 332 71

To assess the diagnostic value of indices measured on a first-pass curve, we performed 72 radionuclide renal first-pass studies (RFP) in 21 patients during the early weeks following renal allograft transplantation. The diagnosis was based on standard clinical and biochemical data and on fine needle aspiration biopsy (FNAB) of the transplant. Aortic and renal first-pass curves were filtered using a true low-pass filter and five different indices of renal perfusion were computed, using formulae from the literature. Statistical analysis performed on the aortic and renal indices indicated excellent reproducibility of the isotopic study. Although renal indices presented a rather large scatter, they all discriminated well between normal and rejection. Three indices have a particularly good diagnostic value. In the discrimination between rejection and Acute Tubular Necrosis (ATN), only one index gave satisfying results. The indices, however, indicate that there are probably ATN with an alternation of renal perfusion and rejection episodes where perfusion is almost intact. We conclude that radionuclide first-pass study allows accurate and reproducible quantitation of renal allograft perfusion. The measured parameters are helpful to followup the course of a post-transplantation renal failure episode and to gain more insight into renal ischemia following transplantation.
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PMID:Evaluation of allograft perfusion by radionuclide first-pass study in renal failure following renal transplantation. 352 71

Experiments were performed on rats subjected to renal ischemia and various treatment procedures to determine the origin and functional consequences of vascular obstruction. To this end, its occurrence and severity was assessed qualitatively and quantitatively in the outer medulla, where it is particularly prominent. The incidence of medullary hyperemia was not influenced by inhibiting thrombocyte aggregation with 5 or 70 mg/kg of acetyl salicylic acid or preventing fibrin deposition with 100 IE/kg of heparin before ischemia, and these substances produced no improvement renal function. The incidence and degree of hyperemia, however, could be substantially reduced or completely eliminated by acutely raising blood pressure after ischemia or by decreasing the number of circulating erythrocytes before ischemia. These procedures were effective in raising filtration rate and tubular reabsorption from 20% to 60% of normal, in restoring renal blood flow and vascular resistance to completely normal, and in diminishing epithelial damage both three and 18 hours after ischemia. The following conclusions are drawn: first, vascular obstruction, which is not lessened by inhibiting thrombus formation but is easily reversed or prevented by raising perfusion pressure or decreasing hematocrit, is probably caused by erythrocyte aggregation during ischemia. Second, vascular obstruction, which appears to raise renal vascular resistance and lower blood flow and filtration rate, cannot be limited to the medulla but must also be present in the cortex. Finally, reversing or preventing vascular obstruction can fully restore renal perfusion, partially restore glomerular and tubular function, greatly reduce tubular necrosis and thus prevent renal failure.
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PMID:The contribution of vascular obstruction to the functional defect that follows renal ischemia. 356 Jun 46

To evaluate the mechanisms for a low fractional excretion of Na (FENa less than or equal to 1.0) in acute renal failure (ARF) of a sustained nature, causes were determined independent of FENa in 41 patients without volume depletion, obstruction, vasculitis or glomerulonephritis. The 16 patients (39%) with low FENa had lower incidence of preexisting azotemia, lower peak serum creatinine, but higher incidence of renal ischemia and earlier testing (by 1.7 days). Seven of ten such patients converted to high FENa on repeat, whereas FENa remained high in 15 of 17 patients with initially high values. The initial FENa was a direct function of time from the onset of ARF. Low FENa in acute but sustained renal failure is therefore best explained by milder insults; earlier determinations, and/or super-imposed renal ischemia.
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PMID:Low fractional excretion of sodium in acute renal failure: role of timing of the test and ischemia. 356 2

In a restrospective study of 220 patients with melioidosis admitted to the hospital over a period of 3.5 years, acute renal failure was noted in 77 patients. Interesting clinical features included hypercatabolism, hypoalbuminemia, hyponatremia, jaundice and multisystem involvement. Prognosis was poor especially when associated with jaundice, lung involvement and the presence of underlying diseases. Mortality rate was 89.6%. Renal failure is believed to the due to renal ischemia from multiple nonspecific factors. In a limited pathological study renal changes consisted of tubular necrosis, microabscesses, interstitial nephritis and mild tubular degeneration.
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PMID:Renal failure in melioidosis. 360 Sep 25

To evaluate the combined effects of a brief ischemic insult and cyclosporine, four groups of male Munich Wistar rats were given: a) parenteral cyclosporine (60 mg/kg i.p.) for 4 days following 20 minutes of bilateral renal ischemia, b) the castor oil cyclosporine vehicle in a comparable volume and the same ischemic insult, c) saline in the same volume and ischemia, or d) saline and sham surgery. The cyclosporine animals ate and drank poorly, and therefore the other groups were pair-fed and watered with them. The cyclosporine-ischemia group developed significant renal failure. The other groups exhibited only a mild rise in blood urea nitrogen. Tubular vacuolization was a prominent feature in the cyclosporine and vehicle groups, but not in the saline groups. Vacuolization was correlated with severity of renal impairment. Lipid stains showed that many of the vacuoles contained lipid. Eosinophilic cytoplasmic inclusions were seen only in the cyclosporine or vehicle- (castor oil) treated animals. These findings emphasize the probable functional importance of tubular lesions in cyclosporine-induced acute renal failure, and suggest that the castor oil vehicle of parenteral cyclosporine may have renal effects of its own.
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PMID:Acute renal failure produced by combining cyclosporine and brief renal ischemia in the Munich Wistar rat. 370 29

The mechanism of clinical cyclosporine nephrotoxicity has remained unclear. We have established an animal model of cyclosporine-induced acute renal failure in the male Munich-Wistar rat by giving four daily doses of parenteral cyclosporine 60 mg/kg intraperitoneally (IP). In this model, 20 minutes of bilateral renal ischemia preceding the first cyclosporine dose did not significantly increase the renal failure, but did increase mortality (65% v 17%), which was due in part to the CNS effect of cyclosporine. Pair-fed and pair-watered vehicle and saline controls were used. The renal morphologic changes induced by the castor oil vehicle of the commercial parenteral cyclosporine solution were quantitatively similar to those induced by cyclosporine, although the severity of the changes by light microscopy was considerably less in the vehicle-treated groups. However, by electron microscopy, pale lipid vacuoles were seen only in the cyclosporine-treated groups, whereas dense alterations in lysosomes and dilated endoplasmic reticulum were also seen in other groups. Renal blood flow determined by electromagnetic flow probe showed a significant decline during 2 hours after a single IP injection of cyclosporine (6.6 +/- 0.4 to 5.0 +/- 0.6 mL/min). A similar decline was seen following injection of the castor oil vehicle of the commercial cyclosporine parenteral preparation (6.6 +/- 0.5 to 5.1 +/- 0.5 mL/min), but not after an injection of a similar volume of mineral oil (6.7 +/- 0.3 to 6.3 +/- 0.2 mL/min). These studies suggest that brief renal ischemia does not increase cyclosporine nephrotoxicity significantly in this rat model.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal blood flow, glomerular filtration rate, and renal morphology in cyclosporine-induced acute renal failure in Munich-Wistar rats. 378 71

It has been difficult to produce a good animal model for cyclosporine nephrotoxicity. It has been suggested that by following 20 minutes of renal ischemia with four daily doses of cyclosporine 60 mg/kg intraperitoneally, one can create a model of reproducible renal failure. We observed excessive mortality (65%), due in part to cyclosporine's CNS effects, with these combined insults in the Munich Wistar rat. In contrast, cyclosporine alone in this dosage produced only 17% mortality and resulted in a similar degree of renal failure. Pair-fed and pair-watered vehicle and saline controls were used. The morphologic changes brought about by the castor oil vehicle of the parenteral cyclosporine solution were qualitatively similar to those brought about by cyclosporine by light microscopy, although the severity of the changes was considerably less in the vehicle-treated groups. However, by electron microscopy, pale lipid vacuoles were seen only in the cyclosporine-treated groups, whereas dense alterations in lysosomes and dilated endoplasmic reticulum also were seen in other groups. Urine sodium determined by flame photometry and urine chloride determined by Saltex reagent strips tended to be high in the initiation phase of cyclosporine-induced acute renal failure and low in the maintenance phase. In animals that developed acute renal failure following the combination of ischemia and cyclosporine, the initial urine sodium and chloride were significantly correlated with the eventual degree of renal failure. The use of Saltex urine chloride sticks in clinical urine samples showed that the readings correlated well with urine sodium and chloride determined by conventional methods, suggesting that these strips may be useful in making a quick diagnosis in the setting of acute renal failure.
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PMID:Renal morphology and function and urine electrolytes in experimental acute renal failure produced by cyclosporine and ischemia. 384 27

Symptomatic juxtarenal aortic atherosclerosis is a rare and threatening form of aortic disease. The formidable implications of complex aortic reconstruction, the high operative mortality and morbidity rate and the uncertainties regarding the beneficial effects of operation combined to foster highly conservative attitude regarding management. Our reported experience and a brief review which has been highlighted in this report, support an aggressive use of combined aortic and renal branch repair rather than a staged repair or medical management. Operative mortality was higher only in the patients with the most extensive patterns of atherosclerosis. This should caution careful preoperative assessment in order to plan optimum technique and extent of the reconstruction for these higher risk patients. The renal revascularization had a significant beneficial effect on hypertension and excretory function observed both early and late following operation. Furthermore a lower than expected late mortality supports our contention that combined aortic and renal reconstruction increases survival of the patients by preventing the complications of progressive renal ischemia, accelerated hypertension, and renal failure.
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PMID:Operative treatment of juxtarenal aortic atherosclerosis. 386 7

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


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