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

The clinical patterns of acute renal failure have changed in the past 10 to 15 years. Nonoliguric acute tubular necrosis has become more common, as has nephrotoxic acute tubular necrosis. Other syndromes that have increased in incidence are acute tubular necrosis secondary to rhabdomyolysis and acute renal failure secondary to nonsteroidal anti-inflammatory drugs. Calculation of the fractional sodium excretion or the renal failure index helps distinguish between prerenal azotemia and acute tubular necrosis. In a significant number of patients with acute renal failure, a kidney biopsy may be necessary to establish the correct diagnosis and initiate the appropriate therapy.
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PMID:New concepts in acute renal failure. 351 96

Adult male Sprague-Dawley rats maintained on a low sodium diet were administered 100 mg of cyclosporine per kg b.wt. per day s.c. for 4 to 10 days. Serum urea nitrogen was significantly elevated by day 4 and continued to rise, whereas serum creatinine was not elevated above control until day 10. Morphologic examination of perfusion-fixed kidneys from cyclosporine-treated rats revealed focal areas of tubular atrophy and interstitial fibrosis in the outer cortex and a generalized increase in interstitial cells in the outer medulla. No areas of acute tubular necrosis were identified. The effect of this dose of cyclosporine on renal hemodynamics was examined in conscious restrained rats. Renal blood flow, measured by microsphere injection, was 70% of control after four daily doses and remained near this level after eight daily doses. The glomerular filtration rate, measured by iodothalamate clearance, was 70% of control after four doses but fell to 34% of control after eight doses. [3H]Thymidine incorporation into renal DNA was used as a sensitive index of renal cell proliferation after cyclosporine administration (100 mg/kg/day). [3H]Thymidine incorporation was increased over control 3-fold in the outer cortex, 7-fold in the inner cortex and 11-fold in the medullary-papillary regions of the kidney after eight daily doses of cyclosporine. Histoautoradiographic examination of renal sections revealed an increase in the number of labeled nuclei in all three regions of the kidney from rats treated with cyclosporine. Morphometric analysis demonstrated that the majority of proliferating cells were located in the interstitium and not in renal tubules.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alterations in renal structure and function in a rat model of cyclosporine nephrotoxicity. 361 60

In male Wistar rats, renal adenosine triphosphate (ATP), inorganic phosphate (Pi) and intracellular pH were measured by 31phosphorus nuclear magnetic resonance (31P NMR) and correlated with renal function before, during, and for one hour after a period of 30 to 40 minutes hemorrhagic hypotension. In animals which suffered no change in these metabolites during hypotension, retransfusion immediately restored normal renal function. When metabolite changes were observed during hypotension, they occurred suddenly with severe ATP depletion, Pi accumulation, and intracellular acidosis occurring almost concurrently. Metabolic changes of this magnitude were always associated with renal dysfunction in the post-hypotensive period, which occurred even when the period of biochemical change was only 10 to 15 minutes. The abnormalities in post-hypotensive renal function resemble the pattern of change seen in human acute tubular necrosis (ATN): depressed glomerular filtration rate (GFR), urine output varying from polyuria to oliguria, decreased urine to plasma inulin ratio, increased urinary sodium concentration, increased fractional excretion of sodium, and increased fractional excretion of potassium. It is postulated that changes in renal cellular energy status during hemorrhagic hypotension distinguish pre-renal failure from early or incipient ATN.
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PMID:Acute renal failure in hemorrhagic hypotension: cellular energetics and renal function. 378 80

Four patients are presented aged over 65 years in whom a state of cardiogenic shock was present due to myocardial infarction of the following localization: anterior in two and posterior in two. According to the parameters all patients satisfied the criteria of cardiogenic shock. Of the four patients three died. In all patients parameters of renal lesion were analyzed after establishment of diureses: sodium in urine, creatinine quotient in urine and plasma, osmolality of urine, osmolality quotient of urine and plasma, the renal failure index and the excretional fraction of filtered sodium. The parameters quoted were analyzed the day after diuresis was established. All parameters, apart from sodium in urine, indicated functional oliguria. In corroboration of this were the values of creatinine clearance which were determined the day after establishing diuresis, amounting in all patients to more than 20 ml/min./1.73 m2, i.e. ranging from 20.6 to 59.0 ml/min./1.73 m2. Of the cases which ended fatally all had fibroses and myocardial scars, apart from recent infarction of the myocardium, generalized atherosclerosis particularly of the coronary arteries, and in all patients hypertrophy of the left ventricle and dilatation of the whole heart. In one patient anaemic infarction of one kidney was found and in another acute tubular necrosis (with the renal failure index of 0.3 and the excretional fraction of filtered sodium of 0.2), while in third patient no renal changes were found.
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PMID:The characteristics of acute renal failure in cardiogenic shock in the elderly. 378 19

Nutritional therapy can be impaired if imbalances in water and electrolyte status have led to gross disorders of the cardiovascular, pulmonary, renal, metabolic, and central nervous systems. Restauration and maintenance of the functional extracellular fluid volume is the primary therapeutic goal in water and electrolyte resuscitation. Hyper- and hypoosmolar disturbances are automatically corrected by intrinsic regulatory mechanisms. Potassium deficiency or overload, or potassium disequilibrium between the intracellular and extracellular space can lead to dangerous cardiac arrhythmias. Hyper- and hypokalemia usually develop within days or even weeks and should not be corrected within a few hours. If life threatening hyperkalemia develops during acute renal failure, 20 ml 10% calcium gluconate solution can be given intravenously in order to avoid ventricular fibrillation or cardiac arrest. The discrimination between prerenal disease, acute tubular necrosis and other causes of acute renal failure is based on special investigations, such as urinary osmolality, urinary sodium concentration, clearance of creatinine, osmolar solutes, free water, and fractional sodium excretion. The clinical examination of a patient should be the basis of assessing his water and electrolyte state. Laboratory findings which are in disagreement with the clinical state have to be repeated, critically interpreted, but not completely rejected. Third space losses make fluid balance difficult.
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PMID:[Imbalances of the water and electrolyte status]. 393 12

Determining the cause of acutely deteriorating renal function is a common problem in clinical nephrology. The fractional excretion of filtered sodium (FENa) has been demonstrated to be a reliably discriminating test between prerenal azotemia and acute tubular necrosis. However, with increasing clinical use of the FENa, numerous reports of low FENa (less than 1%) have appeared. The clinical settings of these reports include oliguric and nonoliguric acute tubular necrosis, urinary tract obstruction, acute glomerulonephritis, hepatorenal syndrome, renal allograft rejection, sepsis, and drug-related alterations in renal hemodynamics. One particular urinary index cannot be expected to reliably discriminate between prerenal azotemia and acute renal failure in all cases. The utility of the FENa test in the differential diagnosis of acute renal failure must be interpreted in conjunction with the patient's clinical course and the use of additional urinary and serum tests.
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PMID:Fractional excretion of sodium. Exceptions to its diagnostic value. 397 Jun 21

Fractional excretion of filtered sodium (FENa) is typically elevated (greater than 3%) in acute tubular necrosis and decreased (less than 1%) with volume depletion. We describe a patient who developed acute tubular necrosis with a FENa of 13%. Four weeks later, he was still oliguric but had also become volume-depleted. FENa was 0.4% to 0.8%, considerably lower than FENa's measured in eight nonvolume-depleted patients in acute renal failure. Vigorous intravenous fluid therapy in this patient produced a prompt increase in urine volume and improvement in renal function. We conclude the following: (1) a marked decrease in FENa in a patient with acute tubular necrosis should suggest the development of a superimposed sodium-retaining state such as volume depletion, and (2) severe volume depletion may delay or mask recovery from acute tubular necrosis.
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PMID:Fractional excretion of sodium as a guide to volume depletion during recovery from acute renal failure. 402 24

A patient with acute decompensated chronic liver disease developed acute tubular necrosis after an episode of hypotension. Renal failure was managed by hemodialysis for 11 weeks during which period hepatic function improved. Despite persistently severe oliguria, tubular function recovered as judged by a fall in urine sodium content and a rise in specific gravity, suggesting the development of the hepato-renal syndrome. Therefore, a peritoneovenous shunt was inserted. This was followed by a prompt diuresis; further dialysis was not required. This case suggests potential roles for hemodialysis and peritoneovenous shunting in patients with advanced, but potentially reversible hepatic and renal failure and draws attention to the need for formal evaluation of such a possibility.
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PMID:Hepatorenal syndrome managed with hemodialysis, then reversed by peritoneovenous shunting. 404 79

Of 48 patients with fulminant hepatic failure who progressed to grade III or IV encephalopathy 38 showed evidence of renal impairment. In 32 of these patients the underlying cause could be placed initially into one of three categories-prerenal uraemia (4 patients), acute tubular necrosis (16), and "functional renal failure" (12). The latter differed in several respects from that seen with liver failure secondary to cirrhosis. The frequency and type of renal impairment was the same in those patients in whom the fulminant hepatic failure had resulted from an overdose of paracetamol as in the other aetiological groups.Abnormalities in plasma electrolytes were common-in particular hypernatraemia occurred in 11 patients from an osmotic diuresis precipitated by hypertonic dextrose or fructose given intravenously, and from the sodium in the fresh frozen plasma used to correct the coagulation disturbance when renal excretion of this ion was inappropriately low.
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PMID:Frequency and type of renal and electrolyte disorders in fulminant hepatic failure. 481 48

The urine/plasma creatinine ratio (U/P Cr), the urine sodium concentration (UNa), and the diuretic response to mannitol infusion in 23 patients were reviewed in an attempt to differentiate functional renal failure (FRF) from acute tubular necrosis (ATN). FRF was diagnosed if the plasma urea nitrogen (PUN) or serum creatinine stabilized within 72 hours. When renal failure persisted longer, patients had ATN. Subjects dying within 72 hours were excluded. Ten patients had ATN and five survived. The minimum duration of renal failure among survivors was 10 days. None responded to mannitol. Of 13 patients with FRF, 11 survived. Seven of 12 who received mannitol responded with a diuresis. The mean UNa in the patients with ATN was 51.4 mEq./1. +/- 9.48 (SE). The mean U/P Cr was 11.2 +/- 1.12. In patients with FRF, the mean UNa was 14.0 mEq./1. +/- 4.2 and the mean U/P Cr was 42.5 +/- 11.5. A significant overlap was present between the two groups. When UNa was factored by the U/P Cr, the resultant ratio was significantly different for the two groups of patients (P < 0.01), and this proved to be a useful clinical index with which to distinguish FRF from established ATN.
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PMID:Diagnostic indices in acute renal failure. 601 69


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