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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute, usually reversible, renal failure has been observed in patients with normal or minimally altered glomeruli on renal biopsy. This review aims to examine the clinical features of acute renal failure in these patients and to evaluate factors that may contribute to the reduction in glomerular filtration rate (GFR). In an analysis of 79 cases affecting 75 patients reported in the English literature since 1966, with acute renal failure associated with minimal change disease or mild histopathological changes in glomeruli, the average age was 58 +/- 2 years (mean +/- 5 SEM), urine protein excretion 11.6 +/- 0.6 g/d, and serum albumin level 19 +/- 1 g/L (1.9 +/- 0.1 g/dL). Acute renal failure was documented an average of 29 +/- 5 days after onset of nephrotic syndrome, and persisted for 7 weeks in 62 episodes in the 58 patients in whom recovery of renal function occurred. Fourteen patients died of uremia or required chronic dialysis, and 3 were lost to follow-up. Although plasma volume depletion was sometimes cited as the cause of renal failure, objective signs of hypovolemia were not documented and most patients did not improve after treatment designed to correct volume deficits. In contrast, histopathological changes consistent with acute tubular necrosis (ATN) were observed in at least 60% of cases. Since the pathogenesis of acute renal failure in minimal change nephrotic syndrome is unknown, we evaluated hemodynamic determinants of GFR in patients with minimal change disease with normal or near-normal renal function, and in relevant animal models, to obtain insights into the effect of nephrotic syndrome on GFR. Although acute renal failure is uncommon, GFR is reduced concurrently with nephrotic syndrome in approximately 30% of children and adults. Absolute and effective blood volume and renal plasma flow are relatively well preserved. However, clinical and experimental observations suggest that the glomerular ultrafiltration coefficient may be reduced by as much as 50%. These findings, together with renal biopsy changes in cases with acute renal failure, suggest that severe reductions in GFR in some patients with minimal change nephrotic syndrome may result from an interaction between acute ischemic tissue injury and preexisting intrinsic renal abnormalities.
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PMID:Reversible renal failure in the nephrotic syndrome. 155 65

The roles of growth factors in the pathogenesis of various forms of acute and chronic renal disease are largely putative. Nevertheless, there is a growing body of information that links specific growth factors to particular forms of renal injury. In all instances, it is supposed that such associations are not necessarily unique and that multiple cytokines probably interact to determine the pattern of injury or the regenerative response to such injury. Regeneration of tubular epithelium after acute tubular necrosis involves upregulation of the epidermal growth factor (EGF) receptor. Early studies of exogenously administered EGF indicate that the severity and duration of renal failure may be attenuated by this growth factor. Thus far, the observed responses have been limited and the role of EGF as a therapeutic agent requires more study. The mechanism of generation of tubulointerstitial injury in most forms of renal disease is difficult to understand. Early in vitro studies of growth factor production by tubular cells (in the absence of any infiltrating cells) indicate that platelet-derived growth factor produced by the medullary collecting duct is mitogenic for renal medullary fibroblasts, suggesting a paracrine growth system in this region of the kidney. Insulin-like growth factor I has also been shown to be produced by collecting duct cells. Its production is increased by EGF, and its association with certain forms of renal hypertrophy, i.e., diabetes and hypersomatotrophic states, implies its participation in the hypertrophic growth response. Platelet-derived growth factor is a potent mitogen for glomerular mesangial cells, and its production is regulated by a variety of cytokines.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evolving role of growth factors in the renal response to acute and chronic disease. 159 57

Acute stomach, kidney, and bladder toxicity was evaluated in F344 rats after gastric gavage of tetraethylorthosilicate (TES) at daily doses of 0, 0.111, 0.223, and 0.333 g. Five rats of each sex at each dose were sacrificed after 1, 2, and 4 days. In TES-treated groups, silicate accumulated in the stomach glands and the muscle layer of the forestomach and glandular stomach. Serum chemistries demonstrated acute onset of renal failure. In the kidneys, acute tubular necrosis, accumulation of silicates, and superficial necrotizing papillitis were observed. In the renal pelvis and bladder, there was urothelial simple hyperplasia, focal erosion of the mucosa, edema, and inflammation. These acute toxic changes were dose and time dependent, but significant sex differences were not observed. The microscopic changes in the urothelium were similar to those observed following administration of high doses of sodium saccharin to male rats in which urinary silicate precipitate and crystals form.
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PMID:Acute urinary tract toxicity of tetraethylorthosilicate in rats. 159 67

We observed 3 patients with a severe falciparum malaria infection. Although the patients appeared not to be seriously ill on admission, severe complications occurred. Renal impairment was a prominent feature and haemodialysis was sometimes necessary. Many hypotheses have been proposed regarding the aetiology of renal failure in Plasmodium falciparum but cannot yet be fully substantiated. Whatever the aetiology of renal failure might be, we believe that treatment should not differ essentially from that of acute tubular necrosis after circulatory shock and early diagnosis and treatment is imperative in spite of an initially ostensibly good clinical condition.
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PMID:Acute renal failure in severe chloroquine resistant falciparum malaria. 164 68

Hemorrhagic fever with renal syndrome (HFRS) is an acute viral disease that occurs over wide areas of Europe and Asia. Hantaviruses are the cause of this syndrome. The hallmark of HFRS is the triad of fever, hemorrhage, and renal failure. In its severe form it is associated with significant mortality. The syndrome evolves through five phases: febrile, hypotensive, oliguric, diuretic, and convalescent. The central physiologic derangement in HFRS is vascular dysfunction, manifested by impaired vascular tone and increased vascular permeability. The systemic effects of this dysfunction account for the occurrence of hypotension and shock, while local effects are probably important in the development of renal failure. Shock in HFRS has distributive and oligemic features, while renal failure has features of acute tubular necrosis. Hemorrhage is a consequence of vascular injury and a deficit of functional platelets. Vascular and platelet dysfunction are both compounded by uremia. Disseminated intravascular coagulation contributes to hemorrhage in some patients. Although hantaviruses are infectious for endothelial cells and may cause direct injury, a large body of evidence suggests that immune mechanisms play an important role in the pathogenesis of HFRS.
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PMID:Mechanisms of disease in Hantavirus infection: pathophysiology of hemorrhagic fever with renal syndrome. 167 61

There have been recent reports of rhabdomyolysis associated with cocaine abuse. The pathologic findings from these cases have not been described. Pathologic abnormalities in two fatalities with cocaine-associated rhabdomyolysis, including one with hyperpyrexia, acute renal failure, and disseminated intravascular coagulation, are discussed in detail. Skeletal muscle in both cases showed necrosis without evidence of vasculitis, polarizable foreign crystals, or other specific lesions. The individual with renal failure showed acute tubular necrosis with granular myoglobin casts in tubules. The mechanism of cocaine-associated rhabdomyolysis is unclear, but potentially includes ischemia due to vasoconstriction, direct toxicity, hyperpyrexia, and increased muscle activity from agitation or seizure. Adulterants may also play a role. In unexplained cases of rhabdomyolysis, toxicologic evidence of cocaine should be sought. In those cases of rhabdomyolysis associated with acute renal failure, the presence of cocaine in blood may be prolonged because of impaired renal clearance.
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PMID:Rhabdomyolysis associated with cocaine abuse. 174 98

During the last 6 years, 7 healthy individuals who were reasonably well acclimatised to physical exertion came under observation with acute renal failure due to exercise induced myoglobinuria. Their mean age was 20 years, and renal failure resulted after cross country run of 10-15 km in 6 cases and long route march of 90 km in 3 days in one case. There was no evidence of effects of heat, dehydration or hypotension. Apart from myoglobinuria and significant urinary sediments, serum aldolase (mean 69.0 SL u/ml) and serum creatinine phosphokinase (mean 120.0 Sigma u/ml) were also elevated. Maximum blood urea and creatinine were 224 mg/dl and 13.9 mg/dl respectively. Hypocalcaemia was noticed in 3 cases, hyperkalaemia in 4 cases and hyperuricaemia in one case during the oliguric phase. One case had features of non-oliguric acute renal failure. All cases recovered though 4 cases required dialysis support. Kidney biopsy in 3 cases showed recovering acute tubular necrosis with eosinophilic material in tubules. Lactate studies in the convalescent period revealed normal response and repeat physical exertion of same severity after 6 months did not reproduce the syndrome. It is concluded that exertional rhabdomyolysis unassociated with heat stress is a rare entity, and with prompt diagnosis and energic management results are rewarding.
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PMID:Acute renal failure in severe exertional rhabdomyolysis. 824 Apr 94

Atrial natriuretic factor (ANF) ameliorates renal damage in animal models of acute ischemic renal failure. Consequently, ANF could blunt acute tubular necrosis related to ischemia that occurs frequently in cadaveric renal transplants. Ten pairs of cadaveric kidneys were transplanted into 20 recipients. Paired recipients received either alpha-human ANF (hANF) or vehicle alone in a prospective, double-blind protocol. Upon revascularization of the allograft, either hANF or vehicle was administered intravenously as a 50-micrograms bolus, followed by a 4-h infusion (0.1 microgram/kg/min). Glomerular filtration rate ([125I]iothalamate clearance) was measured between 4 and 7 days posttransplant and again between 14 and 21 days posttransplant. Serum creatinine was measured daily when patients were in the hospital, then twice weekly as patients were examined in the outpatient clinic. Between the groups, there was no significant difference in age of the recipients or donors, cold ischemia time, or histocompatibility leukocyte antigen match. Infusion of hANF had no adverse effects. When subjects receiving hANF were compared with those treated with vehicle alone, there were no significant differences in serum creatinine or glomerular filtration rate. Three hANF and four vehicle recipients required dialysis postoperatively. At 1 month posttransplant, 19 of 20 patients had functioning allografts; an allograft from one hANF recipient never functioned. It was concluded that hANF, when given by the protocol of this study, had no beneficial effect on the outcome of cadaveric renal transplantation in humans.
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PMID:Atrial natriuretic factor does not improve the outcome of cadaveric renal transplantation. 183 82

An outbreak of food poisoning resulting in 13 deaths in children occurred in Malaysia during the Chinese Festival of the Nine-Emperor Gods in 1988. The offending food was a Chinese noodle called 'Loh See Fun' (LSF). The source was traced to a factory where a banned food preservative was added to make the LSF. The food poisoning was attributable to aflatoxins and boric acid. The clinical features included vomiting, pyrexia, diarrhoea, abdominal pain, anorexia, giddiness, seizures, and eventual coma. Initially, many presented with a Reye-like syndrome. Eleven post-mortem examinations were performed. The pathological findings included extensive coagulative necrosis of the liver with proliferative 'ductal/ductular metaplasia of the hepatocytes'. Giant cell formation, central vein sclerosis, bile stasis, and steatosis were also noted. There was presence of acute tubular necrosis, superficial upper gastrointestinal erosions, and ensuing encephalopathy. The eventual cause of death is acute hepatic and renal failure.
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PMID:An outbreak of aflatoxicosis and boric acid poisoning in Malaysia: a clinicopathological study. 189 May 47

Three patients treated with intravenous immunoglobulin developed respiratory difficulty and decreased renal function. Previously reported adverse reactions to this class of drugs have included pulmonary toxicity but not, to the best of our knowledge, renal toxicity. Renal dysfunction was mild in one patient but severe in two patients, one of whom required temporary hemodialysis. In all three patients, renal function returned to the pretreatment level after stopping the drug. Urinalysis and urine sodium concentration at the onset of renal failure were consistent with pre renal azotemia although renal biopsy performed later in one patient showed acute tubular necrosis. The exact mechanism of toxicity is unknown, but the fact that all three cases occurred with a particular immunoglobulin preparation would suggest that a contaminant, possibly aggregated IgG might be responsible.
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PMID:Pulmonary and renal toxicity of intravenous immunoglobulin. 158 64


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