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

There are very limited data on overall epidemiology of ARF. It is crucial to know the incidence, etiology and clinical feature of ARF to promote prevention strategies and to implement adequate resources for the management of this entity. During a nine month period, a collaborative prospective protocol with 98 variables was developed to assess all ARF episodes encountered in the 13 tertiary-care hospitals in Madrid, Spain (covering 4.2 million people of over 14 years of age). ARF was considered when a sudden rise in serum creatinine concentration (SCr) to more than 177 mumol/liter was found in patients with normal renal function, or when the sudden rise (50% or more) was observed in patients with previous mild-to-moderate chronic renal failure (SCr < 264 mumol/liter). Of the 748 cases of ARF studied, 665 episodes presented in inhabitants from the Madrid area. This gives an overall incidence of ARF of 209 cases per million population (p.m.p.; 95% CJ 195 to 223). The incidence of acute tubular necrosis (ATN) was 88 cases p.m.p. (95% CI 79 to 97), prerenal ARF 46 p.m.p (95% CI 40 to 52), acute-onset chronic ARF 29 p.m.p. (95% CI 24 to 34), and obstructive ARF 23 p.m.p. (95% CI 19 to 27). The mean age was 63 +/- 17 years. The most frequent causes of ARF were ATN (45%), prerenal (21%), acute-onset chronic renal failure (12.7%) and obstructive ARF (10%). Renal function was normal at admission in 48% of patients who later developed ARF. Mortality (45%) was much higher than that of the other patients admitted (5.4%, P < 0.001). This real outcome correlated extremely well with the expected outcome calculated through out the severity index of ARF (SI) 0.433 +/- 0.246 (mean +/- SD). In 187 cases, mortality was attributed to underlying disease, thus corrected mortality due to ARF was 26.7%. Dialysis was required in 36% of patients, and was associated with a significantly higher SI of ARF (0.57 +/- 0.23 vs. 0.35 +/- 0.19, P < 0.001) and mortality (65.9 vs. 33.2%, P < 0.001). Mortality in patients hemodialyzed with biocompatible synthetic membranes (N = 50) was similar to that observed with cellulosic ones (N = 84; 66% vs. 59.5%, NS). Mortality was higher in patients with coma, assisted respiration, hypotension, jaundice (all P < 0.001) and oliguria (P < 0.02). This study gives, for the first time, the incidence of all forms of ARF in a developed country. ARF is iatrogenically induced at a high rate by modern medicine. Prevention strategies, particularly in the perioperative period, are needed to decrease its impact.
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PMID:Epidemiology of acute renal failure: a prospective, multicenter, community-based study. Madrid Acute Renal Failure Study Group. 887 55

Renal changes that occur with aging mainly consist of impairment in the ability to concentrate urine and to conserve sodium and water. These physiological changes increase the risk of volume depletion and the prerenal type of acute renal failure (ARF) in elderly people. Bladder outlet obstruction caused by benign prostatic hypertrophy is a common cause of ARF in elderly men. Another frequent cause of ARF in the elderly is drug-induced nephropathy. Nonsteroidal anti-inflammatory drugs (NSAIDs) and antibiotics are most often implicated in the development of ARF in the elderly. However, considering the high usage of these drugs, the incidence of drug-induced nephropathy is relatively small. NSAIDs are more likely to cause ARF in patients with congestive heart failure, chronic renal disease (including diabetic nephropathy) or chronic liver disease than in otherwise healthy individuals. NSAID-induced ARF is often of the prerenal type, but may be caused by acute interstitial nephritis (AIN). The presence of heavy proteinuria or nephrotic syndrome differentiates NSAID-induced AIN from AIN caused by other drugs. Antibiotics, especially semisynthetic penicillins, more commonly give rise to AIN associated with peripheral blood eosinophilia and eosinophiluria than NSAIDs. Ciprofloxacin is increasingly reported to cause AIN. Fever commonly accompanies AIN, especially when induced by antibiotics. Aminoglycosides produce ARF by inducing acute tubular necrosis (ATN), which results from the excessive accumulation of myeloid bodies in the tubules. In all cases of ARF it is essential to obtain a good history, to perform a through physical examination, with particular attention to skin turgor, and to measure blood pressure, pulse rate (supine and upright), urinary electrolyte and creatinine levels. Fractional excretion of sodium and the urine:plasma creatinine ratio are reliable indices that distinguish prerenal ARF from ATN. A prompt response to fluid challenge, with an increase in urine output and urinary sodium excretion, and a rapid decrease in blood urea nitrogen, constitutes strong evidence for prerenal ARF. However, these indices are unreliable when prerenal ARF has progressed to ATN or when ARF has an obstructive pattern to begin with. In all cases of ARF, especially in elderly men, urinary tract obstruction should be suspected unless the history is otherwise clear cut. Ultrasound of the kidneys and bladder is a simple, non-invasive and meaningful test that can be used to rule out obstructive causes of ARF. If obstruction is the cause of ARF, ultrasound will be positive; in contrast, urinary obstruction is very unlikely if ultrasound findings are normal in a patient who has been oliguric or anuric for 48 hours or more. Similarly, acute glomerulonephritis, including rapidly progressive glomerulonephritis, should be suspected when ARF is associated with heavy proteinuria. In such instances, percutaneous renal biopsy is essential to document the diagnosis. It is of utmost importance to establish whether ARF is of prerenal or postrenal type, both of which are potentially fully reversible. In contrast, patients with ATN or rapidly progressive glomerulonephritis may not recover, or may only partially recover, their renal function. Haemodialysis and nutritional support are common measures for patients with severe ATN and a highly catabolic state. Corticosteroids and immunosuppressive therapy should be instituted for rapidly progressive glomerulonephritis, in addition to haemodialysis. haemodiafiltration instead of haemodialysis is recommended for patients who are haemodynamically unstable [i.e., with a persistently low blood pressure (systolic < or = 100 mm Hg)]. Haemodiafiltration has been shown to improve acid-base balance and uraemia better than standard haemodialysis. However, despite dialysis, mortality in patients with ARF associated with ischaemic ATN remains high.
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PMID:Management of acute renal failure in the elderly. Treatment options. 889 22

Previous experimental and human data suggests a detrimental effect on the course of acute renal failure related to exposure of blood to artificial dialysis membranes of poor biocompatibility. We performed a 2.5-year prospective randomized trial to compare the clinical course of acute renal failure (post-operative ischemic acute tubular necrosis, ATN) in patients receiving a cadaveric renal transplant requiring supportive hemodialysis in the immediate post-transplant setting. Patients were randomized to either a cuprophane or polymethylmethacrylate (PMMA) conventional hollow fiber dialyzer. All patients received a standard immunosuppressive regimen which included induction therapy with either horse anti-thymocyte gamma globulin (ATGAM) or the murine anti-CD3 monoclonal antibody (OKT3). Of 53 patients randomized, 17 were excluded (2 for intervening biopsy-proven rejection prior to recovery from ATN, 10 for primary graft nonfunction and 5 for other reasons), leaving 36 evaluable cases of uncomplicated ATN, 18 in each group. There was no difference by age, race, gender, cause of ESRD, immunosuppressive regimen, cold or warm ischemia time, use of pre-transplant dialysis, percent oliguria or the incidence of intra-dialytic hypotension between the 2 groups. There was no difference in the mean time to recovery from ATN posttransplant (8.9 days in the cuprophane group vs 9.5 days in the PMMA group, p = NS) or in the average number of hemodialysis treatments required (3.6 in both groups, p = NS). There was also no difference in long term allograft outcome in terms of the nadir serum creatinine, the number of episodes of subsequent acute rejection or in the development of chronic rejection. An intent-to-treat analysis of all 53 originally randomized patients similarly yielded no significant differences. A subsequent, non-randomized study using a membrane of intermediate biocompatibility (Hemophan) also showed no difference in recovery time from ATN. Bioincompatible membranes do not seem to have a significant clinical impact on the course of recovery of this form of acute renal failure. The striking benefits of biocompatibility in the course of ARF seen in other human trials may relate more to the non-renal systemic toxic effects of bioincompatibility.
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PMID:Biocompatible dialysis membranes and acute renal failure: a study in post-operative acute tubular necrosis in cadaveric renal transplant recipients. 898 57

Following acute tubular necrosis (ATN), kidney plasma membrane insulin-like growth factor-I (IGF-I) receptor number increases markedly, although IGF-I receptor mRNA levels do not change. To determine whether this increase could represent a redistribution of intracellular receptors and whether receptor function is intact in acute uremia, rats with ATN of 2 days duration and pair-fed controls were studied. Skeletal muscle receptor binding was unchanged. In contrast, binding to receptors in solubilized cortex and isolated cortical plasma membranes increased significantly due to an increase in receptor number. However, the increase in membrane binding was threefold greater than the increase in solubilized cortex binding. This indicates that the increase in total cellular IGF-I receptors can only account for a minor portion of the increase in abundance of plasma membrane receptors number and is consistent with a redistribution of receptors from an intracellular to a membrane location as the major mechanism. Autophosphorylation and receptor kinase activity were unaffected by the uremia (blood urea nitrogen of approximately 198 mg/dl). Since these early steps of IGF-I receptor signaling are intact early in acute uremia, it is likely that at this time in the course of the disease the increase in receptor number will heighten the sensitivity to IGF-I and may thus favor its participation in renal repair.
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PMID:IGF-I receptor binding, autophosphorylation, and kinase activity in kidney and muscle of acutely uremic rats. 908 75

The incidence of ARF in pediatric population varies according to the definition of the syndrome. If the diagnosis is based on a decrease of glomerular filtration rate (GFR), possibly accompanied by a decrease of urinary output and the sudden change of renal function indexes, then the number of patients which can be considered affected by ARF in hospital practice is high, as it comprises all the cases with functional impairment of renal function. The availability of tables with normal values of serum creatinine for different gender and age and the knowledge of the minimal urine output compatible with the normality allows a precise diagnosis of ARF. The differential diagnosis of ARF must take into account prerenal, renal and postrenal causes. Prerenal and renal ARF may be sometimes difficult to differentiate. Indexes such as sodium fractional excretion, utilizing urinary to plasma ratios of sodium and creatinine, can be helpful: values less than 1 indicate prerenal ARF, more than 2 renal ARF. The management of ARF is dependent on the causes of ARF. Prerenal ARF is normally treated by measures of volume expansion and/or removal of the underlying cause. Renal ARF requires an accurate control of water and electrolyte balance and of nutritional status and the prevention or treatment of numerous complications, which may worsen the course of the syndrome. Indications to dialysis must be evaluated every day and an assessment of nutritional status performed. All the factors which may cause hypercatabolism, such as infections, hemorrhage, low calorie intake, must be recognized and treated. This approach allows a better control of serum urea, potassium, phosphate and acidosis. Nutrition must be implemented and an adequate protein and calorie intake must be obtained, through spontaneous oral route and, whenever required, enteral and parenteral nutrition. In conclusion, patients with mild-degree, mostly of prerenal origin, ARF represent a common finding in hospital practice. Identification and prompt treatment of the underlying cause is the best prevention of acute tubular necrosis. Patients with ARF of renal origin require, in particular, daily nutritional assessment and dietary treatment to delay the onset of dialysis.
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PMID:[Management of acute renal failure in hospital practice]. 928 Sep 5

NSAID use is pervasive in our society. Existing NSAIDs pose little risk to patients who tolerate them early during their administration. Among persons with normal renal function who have no other risk factors (dehydration) for an acute hemodynamic effect, there is no risk. However, NSAID administration to susceptible persons may cause decrements in renal plasma flow and glomerular filtration rate within hours. This acute hemodynamic effect is the most common renal syndrome caused by NSAIDs. With careful monitoring, this effect is readily detected with routine clinical laboratory tests (serum creatinine and/or blood urea nitrogen concentrations). However, patients who continue administration of NSAIDs in this setting risk acute tubular necrosis and permanent damage to the kidney. Newer NSAIDs that selectively inhibit cyclooxygenase-2: cyclooxygenase-1 ratio may provide a more favorable risk profile for patients who cannot tolerate existing drugs.
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PMID:Effects of NSAIDs on the kidney. 938 87

Here, we report a 35-year-old man with non-fulminant acute non A, non B, non C hepatitis which developed into acute renal failure. The patient was admitted to hospital with the chief complaints of general fatigue, nausea and a high-grade fever of 40 degrees C. Laboratory examination revealed severe liver dysfunction and renal insufficiency on admission: his serum glutamic oxaloacetic transaminase was 3.203 IU/ml, serum glutamic pyruvic transaminase was 3.825 IU/ml, lactic dehydrogenase was 2.840 IU/ml, blood urea nitrogen was 65 mg/dl, and creatinine was 7.6 mg/dl. Hemodialysis was conducted during the initial 19-day period after admission because anuria was manifested on admission. On the 36th day after onset, renal functions returned to normal and the patient was negative for IgM-HA antibody. HBs antigen, IgM-HBC antibody, HCV antibody, cytomegalovirus antibody, and Epstein-Barr virus antibody. However, liver biopsy for histological examination on the 44th day after onset revealed no specific findings except the healing stage of acute hepatitis. Renal biopsy on the 49th day showed the healing stage of acute tubular necrosis without any glomerular change. It has been infrequently reported that acute renal failure develops following a non-fulminant acute state without hepatitis A, B or C virus infection. It is necessary to take acute renal failure into account in the clinical course of non-fulminant non A, non B, non C hepatitis.
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PMID:[Acute renal failure in non-fulminant acute hepatitis without hepatitis A, B or C virus infection]. 951 78

Interleukin-1 (IL-1) is a central component of many acute inflammatory processes. Blocking IL-1 receptor (IL-1R) with IL-1R antagonist (IL-1Ra) has attenuated ischemic reperfusion injury in brain, heart, and liver models. However, the role of IL-1 in renal ischemic reperfusion injury (IRI) is not known. Therefore, the role of IL-1 in renal IRI was evaluated using the complementary approaches of IL-1R blockade in wild-type mice in addition to the study of renal IRI in IL-1R knockout (KO) mice. Ischemia was induced by bilateral renal pedicle clamping for 30 min. IL-1Ra was administered at 10 mg/kg every 4 h, high doses that have been protective in previous organ injury models in mice. IL-1R KO animals, previously characterized as insensitive to IL-1, had the absence of IL-1R1 confirmed by DNA blots. IL-1Ra, IL-1R KO, and control groups had similar elevations of blood urea nitrogen (114 +/- 13, 133 +/- 11, and 120 +/- 11 mg/dl) and serum creatinine (1.7 +/- 0.3, 2.1 +/- 0.2, and 1.6 +/- 0.3 mg/dl) 24 h after ischemia. Furthermore, acute tubular necrosis scores were also similar in IL-1Ra-treated mice (3.0 +/- 0.3), IL-1R KO mice (2.7 +/- 0.3), and control mice (3.1 +/- 0.2). However, both IL-1Ra and IL-1R KO groups, compared with control animals, developed significantly less infiltration of polymorphonuclear leukocytes per 10 high-power fields in postischemic renal tissue (1111 +/- 228 and 967 +/- 198 versus 1820 +/- 190, P < 0.05). In contrast to the comparable renal functions at 24 h, recovery of renal function was significantly accelerated in the IL-1R KO group compared with control at both 48 (P < 0.05) and 72 (P < 0.05) h. Recovery in the IL-1Ra group was similar to that in the control animals. These data demonstrate that IL-1 is unlikely to be beneficial in the recovery of renal function after ischemia and may play a deleterious role.
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PMID:Role of IL-1 in renal ischemic reperfusion injury. 955 64

Gliclazide, a sulfonlyurea class molecule, is used to control glycaemic levels in non-insulin-dependent diabetes mellitus. Acute and chronic toxicity studies, conducted in various animal species, have demonstrated a very low toxicity. We report a patient who developed acute renal failure due to acute tubular necrosis following a massive ingestion of gliclazide in an suicide attempt. The patient ingested 28 grams of gliclazide; the normal dose of gliclazide is 80 mg one or twice a day. At admission the patient was hypoglycaemia and in a few days became oliguric with an increase in the serum creatinine concentration, but with a normal blood urea nitrogen level. He underwent dialysis and ten days after ingestion of gliclazide, his renal function improved rapidly.
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PMID:Acute renal failure after massive ingestion of gliclazide in a suicide attempt. 960 41

To examine the mechanisms involved in the progression of mercury chloride (HgCl2)-induced acute tubular necrosis (ATN), we investigated the histopathological changes and the expression of inducible nitric oxide synthase (iNOS) mRNA and protein in renal cortices of rats at 20 hours after exposure to HgCl2. The expression of iNOS mRNA was significantly augmented in renal cortices of rats with HgCl2-induced acute renal failure (ARF). Likewise, the induction of iNOS protein was observed in damaged proximal tubule epithelial cells of rats with HgCl2-induced ARF. Pretreatment of rats with iNOS inhibitor aminoguanidine, however, suppressed the development of proximal tubule epithelial cell injury and prevented an increase in blood urea nitrogen and serum creatinine as well as resulting in a marked fall in iNOS mRNA and protein in rats with HgCl2-induced ARF. These observations indicate that the induction of iNOS may play a role in the progression of HgCl2-induced ATN through the exacerbation of proximal tubule epithelial cell damage.
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PMID:Inducible nitric oxide synthase expression in mercury chloride-induced acute tubular necrosis. 981 Jan 45


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