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

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

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

Human envenomation caused by bee or wasp stings has been reported to cause acute renal failure (ARF), usually due to acute tubular necrosis (ATN), as a frequent complication. The pathogenetic mechanisms of ATN occurring in these accidents are still unclear. In the present study, female Wistar rats weighing 150-200 g were injected intravenously with Africanized bee venom at a dose of 0.4 microl/100 g body weight and used in functional and light microscopy studies. The animals were divided into two groups: the early group was studied 3-8 h after inoculation, and the late group was studied 24-30 h thereafter. The animals showed ARF characterized by reduction of glomerular filtration rate with increasing levels of plasma creatinine. They also showed increased fractional sodium and potassium excretions, suggesting changes in the proximal portion of the nephron. The water transport through collecting tubules was reduced, with consequent diuresis, indicating functional changes in the distal portion of the nephron. These functional changes were more marked in the early group, with recovery tending to occur after 24 h. Albuminuria was also observed in this group. Light microscopy showed ATN mainly in cortex and outer medulla, with isolated necrosis in cells or small groups of cells and cast formation in the distal and collecting tubules. After 24 h frequent mitotic figures were found in the tubular epithelium. The observed ARF was due to ATN which in turn was probably caused by multiple effects, mainly hemodynamic changes secondary to cardiotoxicity and systemic vasodilation caused by the venom, myohemoglobinuria, and the direct action of the venom on tubular cells.
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PMID:Renal changes induced by envenomation with Africanized bee venom in female Wistar rats. 939 34

We report a 27-year-old Japanese man who developed acute renal failure associated with cold water immersion. The clinical course was consistent with that of acute renal failure attributable to acute tubular necrosis. A renal biopsy specimen showed patchy and focal loss of tubule cells, necrotic epithelium, interstitial edema, and arterial lumina obstructed by diffuse and severe intimal thickening. Endothelin increased more than five times in the early phase of the clinical course. Vasoconstriction and ischemia induced by cold exposure seem to lead to endothelin release. Endothelin may be related to the development of acute renal failure and intimal thickening.
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PMID:Acute renal failure in accidental hypothermia of cold water immersion. 959 Jan 98

Seventeen Sprague-Dawley rats had ischemic nonoliguric acute renal failure (ARF) induced by vascular clamping resulting in their preischemic blood urea nitrogen (BUN) and creatinine levels of 16 +/- 1 and 0.56 +/- 0.05 mg/dl to increase to 162 +/- 4 and 8.17 +/- 0.5 mg/dl, P < 0.001, respectively, at day 4 of postischemia. Vessel dilator, a 37-amino-acid cardiac peptide hormone (0.3 microg x kg(-1) x min(-1) ip), decreased the BUN and creatinine levels to 53 +/- 17 mg/dl and 0.98 +/- 0.12 mg/dl (P < 0.001) in another seven animals where ARF had been established for 2 days. Water excretion doubled with ARF and was further augmented by vessel dilator. Transthoracic echocardiography revealed left ventricular dilation as a probable cause of the increase in vessel dilator in the circulation with ARF, and vessel dilator infusion reversed this dilation. At day 6 of ARF, mortality decreased to 14% with vessel dilator from 88% without vessel dilator. Acute tubular necrosis was <5% in the vessel dilator-treated rats compared with 25% to >75% in the placebo-treated ARF animals. We conclude that vessel dilator improves acute tubular necrosis and renal function in established ARF.
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PMID:Amelioration with vessel dilator of acute tubular necrosis and renal failure established for 2 days. 1077 33

Acute renal failure (ARF) is defined as an abrupt decline in the renal regulation of water, electrolytes, and acid-base balance. It continues to be an important factor contributing to the morbidity and mortality of critically ill infants and children. The frequency of specific diseases that result in ARF differs among different age-groups and geographical areas. The common causes in Indian children include hemolytic uremic syndrome, acute tubular necrosis, glomerulonephritis and urinary tract obstruction. Though the hallmark of renal failure is oliguria, there is increasing recognition of non-oliguric ARF often associated with the use of nephrotoxic drugs. The basic principles of management are avoidance of life-threatening complications, maintenance of fluid and electrolyte balance and nutritional support. Specific management of the underlying disorder is possible only in a minority of cases. All the major dialysis modalities--peritoneal dialysis (PD), hemodialysis (HD) and continuous hemofiltration--can be used to provide equivalent solute clearance and ultrafiltration. Peritoneal dialysis requires minimal equipment and infrastructure, and is easy to perform; this makes it the favoured modality in developing countries where resources for HD or continuous therapies may not be accessible. However, continuous hemofiltration is an excellent alternative to PD in patients with ARF and severe fluid overload. The prognosis of children with renal failure depends on the underlying condition and associated medical complications.
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PMID:Management of acute renal failure. 1079 65

This review evaluates the various causes and management of acute renal failure (ARF) in children. ARF is defined as an abrupt decline in the renal regulation of water, electrolytes and acid-base balance, and continues to be an important factor contributing to the morbidity and mortality of critically ill infants and children. The common causes of ARF in children include acute tubular necrosis secondary to various causes (including congestive heart failure and sepsis), haemolytic uremic syndrome, and glomerulonephritis and urinary tract obstruction. Ischaemia, toxins (including drugs) as well as primary parenchymal disease, have to be considered and ARF can also be a complication of systemic disease. The basic principles of management are avoidance of life-threatening complications, maintenance of fluid and electrolyte balance, and nutritional support. Only a few patients require specific management of the underlying disorder, although it is important to diagnose these conditions. Knowledge about the use of drugs for the prevention of ARF is scarce. Mannitol, low-dose dopamine, calcium channel antagonists, atrial natriuretic peptide and albumin have been evaluated and, where possible, meta-analyses are cited. Mannitol treatment appears to be warranted prophylactically after paediatric renal transplantation. Albumin infusion can reverse prerenal ARF in children with nephritic syndrome. For treatment of the complications of hyperkalaemia and volume overload, salbutamol, insulin and glucose infusion and diuretics such as furosemide and sodium bicarbonate, are discussed. All of the major dialysis modalities (peritoneal dialysis, haemodialysis and continuous haemofiltration) can be used to provide equivalent solute clearance and ultrafiltration. The indication for, and the choice of the modality depend on the patient requirements and on local resources, and should involve the care of a paediatric nephrologist. Peritoneal dialysis requires minimal equipment and infrastructure, is easy to perform and remains the favoured modality of renal replacement therapy in children. However, continuous haemofiltration is an excellent alternative to peritoneal dialysis in patients with ARF and severe fluid overload. Dialysis remains the most important tool to bridge the time needed for recovery of renal function. There is increasing evidence that more intense use of dialysis may improve the overall prognosis.
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PMID:Acute renal failure in children: aetiology and management. 1173 64

Late structural changes such as interstitial fibrosis in the renal cortex and tubular atrophy have been detected after severe acute tubular necrosis (ATN). The aim of this study was to investigate the expression of fibronectin, alpha-smooth muscle actin and macrophages during the evolution of the ATN induced by glycerol and their relationship with the late structural changes observed in the kidneys of these animals. Forty-nine male Wistar rats were injected with a 50% glycerol solution, 8 mL/kg (4 mL/kg applied i.m. to each hind leg) and 14 with 0.15 m NaCl solution. Before glycerol injection on day 1, water was removed for 17 h. Blood and urine samples were collected 1 day after the injection to quantify sodium and creatinine. The animals were killed 5, 30 and 60 days after the injections and the kidneys removed for histological and immunohistochemical studies. The results of the histological and immunohistochemical studies were scored according to the extent of lesion or staining in the cortical tubulointerstitium, respectively. The percentage of tubulointerstitial lesions was determined by morphometry. Glycerol-injected rats presented a transitory increase in plasma creatinine levels and in fractional sodium excretion. The immunohistochemical studies showed increased fibronectin, alpha-smooth muscle actin (alpha-SM-actin), TGF-beta and ED-1 (macrophages) staining in the renal cortex from rats killed 5, 30 and 60 days after glycerol injection (P < 0.05) compared to control. The animals killed on day 30 and 60 also presented chronic lesions (fibrosis, tubular dilatation and atrophy) in the renal cortex, despite the recovery of renal function. Macrophages, TGF-beta and myofibroblasts may have contributed to the development of renal fibrosis in these rats.
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PMID:Long-term evolution of the acute tubular necrosis (ATN) induced by glycerol: role of myofibroblasts and macrophages. 1248 61

A statistical analysis was made of 2,000 consecutive cases in which prostatic operations were done in the period 1947-1957 at the Southern Pacific General Hospital. The operations included transurethral resections as well as perineal, retropubic and suprapubic prostatectomy. The mortality rates were lowest for transurethral resection and highest for retropubic prostatectomy. Coronary artery disease and pulmonary embolism were the chief causes of death. It was generally felt that preliminary partial vasectomy previous to transurethral resection added very little to successful convalescence. Although distilled water was used routinely for irrigation during transurethral resection, there was no incidence of lower nephron nephrosis. The incidence of recurrence of prostatic obstruction was highest by far after transurethral resection.
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PMID:Prostatectomy: a survey of 2,000 cases. 1383 45

In most severe cases of strychnine poisoning, the patient dies before reaching the hospital. This report describes the treatment and successful outcome of a patient who had taken a dose of strychnine that would normally be fatal. A 28-y-old man was admitted 2 h after ingestion of 1 to 1.5 g of strychnine. He had a Glasgow Coma Score of 14/15 and was severely agitated and in mild respiratory distress; blood pressure was 90/60 mmHg, pulse 110/min, and peripheral pulses weak. He had generalized hyperactive reflexes and had several generalized tonic-clonic convulsions in the emergency department. Treatment consisted of gastric lavage with water, oral administration of activated charcoal and sorbitol solution, continuous intravenous administration of midazolam and then sodium thiopental, furosemide, sodium bicarbonate and hemodialysis for acute renal failure. His clinical course included respiratory distress, agitation, generalized tonic-clonic convulsions, hyperactivity, oliguria and acute tubular necrosis prior to recovery in 23 days. This patient ingested what would normally be a fatal amount of strychnine, had signs and symptoms of severe toxicity and recovered, suggesting that with aggressive supportive care patients may have favorable outcomes.
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PMID:A case of acute strychnine poisoning. 1508 Feb 7


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