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

Incremental ischemic injury was induced in rabbits by transient occlusion of the renal artery. Renal localization of 99mTc-HEDP was quantitated in ischemic and normal kidneys at fixed intervals following restoration of blood flow. Creatinine clearance and microscopic evaluation of renal structure were determined concurrently with scintigraphic studies. There was a sequential reduction in creatinine clearance and an increase in tubular necrosis with prolongation of the ischemic period. 99mTc-HEDP localization in ischemic renal tissue was dependent on the degree of renal injury, ranging from twice normal with minor injury to a nine-fold increase with the most severe ischemic changes. The increased accumulation was demonstrable for longer periods with increasing ischemic injury. Considerable recovery of renal function was apparent in all groups by one week. 99mTc-HEDP may be useful in evaluation of renal failure secondary to ischemic injury.
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PMID:Quantitation of ischemic injury with 99mTc-HEDP in experimental acute tubular necrosis. 677 93

A retrospective analysis has been undertaken of 17 patients among 221 who developed renal failure after aortic and/or iliac reconstructions because of occlusive disease (incidence 8%). In two renal artery occlusion was causing anuria, in the others tubular necrosis was considered to be responsible. This complication is multifactorial and factors of importance may be: operative trauma, haemorrhagic and other postoperative complications with reoperations, age and preoperative angiography. The patients with postoperative renal failure were older, the preoperative serum creatinine slightly higher, operation time longer and intraoperative haemorrhage greater than in patients without postoperative renal failure. Renal insufficiency after aorto-iliac reconstruction is a symptom with poor prognosis, the mortality being significantly higher (35%) than among the 204 patients without renal failure (2.0%). No simple dominating risk factor has been found in this material.
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PMID:Renal failure as a complication to aortoiliac and iliac reconstructive surgery. 683 23

A 16 year old male with a history of recurrent synpharyngitic macroscopic hematuria presented with severe loin pain, macroscopic hematuria and oliguric acute renal failure. Although renal biopsy showed mesangial IgA nephropathy with focal and segmental proliferation with crescents, the extent of glomerular involvement could not explain the severe functional disturbance. Intratubular obstruction and tubular necrosis secondary to the presence of severe glomerular bleeding provide a better explanation. Although renal failure resolved spontaneously, the long-term effects of episodes of this type on structure and function is unknown.
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PMID:Acute renal failure and tubular necrosis associated with hematuria due to glomerulonephritis. 685 Dec 58

Spreading and flattening of glomerular podocyte cell bodies and major processes and an apparent lack of foot processes were observed by scanning electron microscopy in a reversible pedicle-clamping model of acute renal failure in ADH-treated rabbits and in biopsy specimens taken 1 hour after transplantation from patients who later showed clinical signs of "acute tubular necrosis." Glomerular changes were quantified by morphometry in A) normal rabbit kidneys, B) rabbit kidneys obtained 2 hours after 1 hour of left pedicle clamping and right nephrectomy, C) kidneys similar to Group B except that the animals were treated with an agent that reliably lessens the eventual severity of renal failure (clonidine, 30 microgram/kg given intravenously 1/2 hour before unclamping), D) 1-hour-posttransplantation biopsy specimens from human kidneys that functioned well after transplantation (recipient serum creatinine less than 2.5 mg/dl on Day 3), and E) 1-hour-posttransplant biopsy specimens from kidneys that later manifested posttransplantation ischemic acute renal failure (recipient serum creatinine greater than or equal to 2.5 mg/dl on Day 3). The fraction of glomerular capillary surface covered only by podocyte processes smaller than 1 mu (and not by cell bodies and wider processes) was .65 +/- .02 (SEM) in A; .48 +/- .03 in B; .64 +/-.03 in C; .57 +/- .01 in D; and .38 +/- .04 in E (A vs B, P less than .01; B vs C, P less than .02; D vs E, P less than .01). In Groups D and E there was a significant negative correlation between the fraction of glomerular capillary surface covered only by podocyte processes less than 1 mu in width and serum creatinine on the third posttransplantation day (r = --.86, P less than .01 by the Spearman rank test). It is concluded that podocyte changes are seen by scanning electron microscopy early in clinical and experimental postischemic acute renal failure and are more pronounced in those groups that eventually develop more severe renal failure. It is unclear whether these changes reflect a decrease in glomerular hydraulic permeability or an increase in glomerular permeability to protein.
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PMID:Glomerular epithelial cell changes in early postischemic acute renal failure in rabbits and man. 701 70

Thirty-seven guinea-pigs experimentally infected with a virulent strain of L. icterohaemorrhagiae, were submitted to a renal function study as evaluated through the maximal urinary concentration (MUC) test, blood urea nitrogen (BUN) and afterwards had their kidneys examined by light and electron microscopy. Vascular changes were also studied after the administration of colloidal carbon as a marker. Through the MUC test and BUN determination, two groups of tubulo-interstitial lesions can be visualised, one in animals without renal sufficiency, manifested chiefly by cell edema with RE dilation and another, in animals with renal insufficiency, characterised not only by marked cell edema and mitochondrial changes, but also by proximal tubule regenerative aspects without overt tubular necrosis. Interstitial edema and focal nephritis was prominent in both groups, a finding which minimises their role in the pathogenesis of renal failure in experimental leptospirosis. Vascular injury, affecting the vessels of the renal microcirculation chiefly at the cortico-medular junction, was observed in both groups. Its severity and extension ran parallel to the intensity of the tubular injury. This suggests a simultaneous action of a noxious agent liberated by the leptospires over both structures, tubular damage being accentuated by the local circulatory changes.
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PMID:Morpho-functional patterns of kidney injury in the experimental leptospirosis of the guinea-pig (L. icterohaemorrhagiae). 713 Nov 30

Paraquat poisoning is very severe. When it is ingested, this herbicide may be responsible for causative lesions of the digestive tract, cytolytic hepatitis, renal tubular necrosis, circulatory failure, and/or pulmonary fibrosis. Since a very low dose (as little as one mouthful) is potentially lethal, it is important to understand why 11 of our 28 patients who entered our department for paraquat poisoning survived. The main prognostic factors appear to be the following: Route of administration. Of four patients who had inhaled paraquat aerosols and/or contaminated their skin with the herbicide, all survived. Ingested amount. Above 50 mg/kg, patients died of circulatory failure within 72 h; between 35 and 50 mg/kg, a progressive pulmonary fibrosis occurred. Delay between ingestion and the last meal. Paraquat is adsorbed and neutralized by foodstuffs. Caustic gastric lesions revealed by early endoscopic examination. The occurrence of an organic renal failure. The plasma paraquat concentrations within the first 24 h. Patients whose plasma concentrations do not exceed 2.0, 0.6, 0.3, 0.16, and 0.1 mg/L at 4, 6, 10, 16, and 24 h, respectively, are likely to survive. The different treatments that have been tested (fuller's earth, forced diarrhea, furosemide, hemodialysis, hemoperfusion, artificial ventilation with hypoxic breathing mixtures) did not modify the initial prognosis. The 11 survivals are only linked to the circumstances of the poisonings (route of administration, ingested amount, delay between ingestion and the last meal, etc.). The treatments did not modify the outcome.
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PMID:Prognosis and treatment of paraquat poisoning: a review of 28 cases. 717 91

2 patients with systemic lupus erythematosus and mild renal functional impairment were treated with ibuprofen, one of the phenylproprionic nonsteroidal anti-inflammatory drugs. Within days after the onset of therapy, both developed renal insufficiency manifested by elevated serum creatinine levels, increased proteinuria, and active urinary sediments; 1 patient was oliguric. Renal biopsies disclosed mesangial proliferative lupus glomerulonephritis and acute tubular necrosis, the latter more pronounced in the oliguric patient. Renal failure resolved following discontinuation of ibuprofen and supportive therapy. It is postulated that altered blood flow, mediated through the well-known prostaglandin synthetase inhibitory effects of ibuprofen, resulted in tubular necrosis. This undesirable complication of ibuprofen therapy may be enhanced in patients with underlying renal disease, and may be a factor governing the limitation of its usage.
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PMID:Ibuprofen-induced acute renal failure with acute tubular necrosis. 718 Sep 1

cis-Diamminedichloroplatinum (CP), an important chemotherapeutic agent, produces acute renal failure by an unknown mechanism. Other heavy metals, such as mercury, are thought to be nephrotoxic by reacting with sulfhydryl (SH) groups. To investigate the mechanism of CP nephrotoxicity, F344 rats were injected once with 6 mg of CP per kg. After 96 hr, the blood urea nitrogen rose to 140 mg/100 ml. The SH concentration in control kidneys was 20.4 +/- 0.1 muml/g wet weight. Total renal SH groups decreased to a maximum of 14% at 120 hr (P less than .01). The fall in SH groups was entirely due to a decrease of protein-bound SH groups. Cell fractionation studies showed that the greatest decline of SH groups occurred in the "mitochondrial" and "cytosol" fractions. These fractions also had the highest Pt concentrations. There was no stoichiometric relationship between Pt accumulation and the change in SH groups. Furthermore, in vitro studies demonstrated that CP does not directly interact with SH groups. To determine if the change in renal SH groups was nonspecific effect of acute injury, renal failure was induced with glycerol (5 g/kg i.m.). Total SH groups per kidney increased after glycerol. These results indicate that the decrease in renal SH groups produced by CP is not due to nonspecific tubular necrosis. The present findings suggest the possibility that the nephrotoxic effects of CP may be related to depletion of SH groups. However, a direct cause-effect relationship has not been established.
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PMID:Mechanism of cis-platinum nephrotoxicity: I. Effects of sulfhydryl groups in rat kidneys. 719 25

There is considerable evidence that the principal functional abnormality in patients with acute reversible renal failure (ARF, or "acute tubular necrosis") is reduced cortical perfusion with diminished glomerular filtration. However, in such patients, high-dose intravenous urograms most commonly show an immediate obvious nephrogram. Since nephrographic density is believed to depend on the filtration of contrast medium into the tubular lumen, it is difficult to reconcile the early development of the nephrogram if glomerular filtration is reduced. Extensive experiments with both mercuric chloride and glycerol rat models of ARF have confirmed rapid intraluminal accumulation of contrast medium, albeit in reduced amounts. Studies using the normally filtered compound sodium nitroprusside and its precipitation as "prussian blue" suggest rapid transtubular diffusion from peritubular capillaries in kidneys with ARF. This, it is suggested, is also the mechanism for the rapid intraluminal ingress of contrast media and explains the early appearance of nephrogram. The less common intravenous urogram finding in ARF of a slowly developing and increasingly dense nephrogram may then represent cases with only slight tubular necrosis with predominant reduction in glomerular filtration.
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PMID:The functional basis for nephrographic patterns in acute tubular necrosis. 720 53

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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