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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 renal failure usually occurs during hospitalization, but may also be present on admission to the hospital. To define the causes and outcomes of community-acquired acute renal failure, we undertook a prospective study of patients admitted to the hospital with acute elevations in serum creatinine concentrations. Over a 17-month period, all admission serum creatinine determinations were screened for patients with values greater than 177 mumol/L (2 mg/dL). These values were compared with baseline creatinines to select patients with an acute elevation in serum creatinine occurring outside the hospital. One hundred patients were entered into the study, with an overall incidence of 1% of hospital admissions. Seventy percent of the patients had prerenal azotemia, 11% had intrinsic acute renal failure, 17% had obstruction, and 2% could not be classified. Mean peak serum creatinine (318 +/- 18 mumol/L [3.6 +/- 0.2 mg/dL]) and mortality (7%) was lowest in the group with prerenal azotemia. In this group, volume contraction due to vomiting, decreased fluid intake, diarrhea, fever, glucosuria, or diuretics was the most common underlying cause. The group with intrinsic acute renal failure had the most severe renal failure and the highest mortality (55%). Although ischemic acute tubular necrosis is the most common cause of hospital-acquired intrinsic acute renal failure, this etiology was seen in only one patient. Drug-induced nephrotoxicity and infection-related causes were the most common underlying etiologies of intrinsic acute renal failure. Obstructive renal failure had a mortality of 24% and was most commonly due to benign prostatic hypertrophy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Community-acquired acute renal failure. 199 62

It is generally assumed that acute tubular necrosis is the etiology of renal failure that can occur during the course of Rocky Mountain spotted fever (RMSF). However, histologic examination of kidneys has been mainly limited to autopsy cases of fulminant infections. Acute glomerulonephritis due to glomerular immune complex deposition has not been reported in RMSF. We describe a case of acute oliguric renal failure that developed more than 2 weeks following the onset of RMSF. Renal biopsy showed acute glomerulonephritis with inflammatory cell infiltration and subendothelial immune deposits. Thus, acute glomerulonephritis should be in the differential diagnosis of acute renal failure that occurs in RMSF.
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PMID:Acute glomerulonephritis in a patient with Rocky Mountain spotted fever. 199 79

Ultrasonography (US) of the native kidneys is commonly requested for acute renal failure (ARF), although in most cases the examination results are negative. To detect changes in the Doppler waveform associated with ARF and determine whether Doppler US can provide significant diagnostic information not available with standard US, 91 patients with ARF were studied to determine a mean resistive index (RI) for each patient. Forty-six patients had acute tubular necrosis (ATN) with a mean RI +/- 1 standard deviation of .85 +/- .06, which was significantly higher than the mean RI of .67 +/- .09 in 30 patients with prerenal ARF (P less than .01). Fifteen patients had ARF due to non-ATN intrinsic renal disease (mean RI, .74 +/- .13). An elevated RI (greater than or equal to .75) occurred in 91% of patients with ATN versus only 20% of patients with prerenal azotemia. Patients with severe liver disease (hepatorenal syndrome) are a subset of those with prerenal ARF that accounted for most of the elevated RIs in this group. The study demonstrates that intrarenal Doppler US allows detection of changes associated with ARF far more often than standard US. More important, Doppler US may be helpful in distinguishing ATN from prerenal azotemia.
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PMID:Acute renal failure: possible role of duplex Doppler US in distinction between acute prerenal failure and acute tubular necrosis. 201 84

There is a growing number of hospitalised patients who develop a drug-induced renal problem because increasing numbers of potent drugs have been added to the therapeutic arsenal in recent years. The 3 clinical syndromes that can be recognised in drug-induced nephropathy are acute renal failure, chronic interstitial nephritis and the nephrotic syndrome. The first can be caused by prerenal problems, acute interstitial nephritis, acute tubular necrosis and intratubular obstruction. The most important drugs that cause prerenal failure are NSAIDs, captopril and cyclosporin. NSAIDs inhibit the synthesis of prostaglandins, and consequently vasoconstriction of the afferent arteriole leads to lowering of the glomerular filtration rate (GFR); captopril blocks the formation of angiotensin II (which also leads to a lower GFR), and should be used with caution in patients with stenotic renal arteries; cyclosporin causes vasoconstriction of the afferent arteriole, which is probably mediated by the sympathetic system. Combinations of these drugs result in increased nephrotoxicity. The drugs most likely to cause acute interstitial nephritis are antibiotics and NSAIDs. Normally, signs of an allergic reaction are also present. Acute interstitial nephritis is usually self-limiting, but in some studies it is claimed that steroids may promote recovery. Four important causal agents of acute tubular necrosis are aminoglycosides, amphotericin B, radiocontrast agents and cyclosporin. Approximately half of the cases of drug-induced renal failure are related to the use of aminoglycosides: generally, 10 days after start of treatment a nonoliguric renal failure develops, with recovery after withdrawal of the drug in almost all cases. The aminoglycosides are particularly nephrotoxic when combined with other nephrotoxic drugs. 80% of amphotericin B-treated patients develop renal insufficiency, a percentage that increases as the cumulative dose exceeds 5g. It is because of its unique antifungal properties that there are still some indications for the use of this highly nephrotoxic drug; the high percentage of nephrotoxicity can probably be prevented in part by sodium loading. The nephrotoxicity of radiocontrast agents is largely dependent on renal function: from 0.6% in patients with normal renal function to 100% in patients with a serum creatinine above 400 mumol/L. Diabetes mellitus does not add greatly to the risk of radiocontrast nephrotoxicity. The nephrotoxicity of cyclosporin is dose-dependent and reversible, although there are some reports of irreversibility after long term use. Cyclosporin can also result in nephrotoxicity in combination therapy.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Drug-induced nephrotoxicity. Aetiology, clinical features and management. 204 84

This report concerns two boys with minimal change nephrotic syndrome progressed to renal failure. The first case aged 17 being a steroid sensitive infrequent relapse developed acute renal failure at his third relapse and recovered soon after the treatment with diuretics and corticosteroids. The second case aged 15 being a steroid dependent frequent relapse became steroid resistant at his 11th relapse and progressed to renal failure seven months later. As the causes of renal failure, acute tubular necrosis and tubular obstruction by casts were suspected in the former. Renal vein thrombosis, morphological transition of renal histology, hemodynamic change and change in glomerular permeability might be occurred in the latter. Renal failure is a rare complication of minimal change nephrotic syndrome and the cause is variable. Precise diagnosis and prompt treatment should be needed to improve the prognosis.
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PMID:[Rapid deterioration of renal function in minimal change nephrotic syndrome]. 205 45

The actions of L-channel calcium antagonists on the kidney are the result of direct and indirect effects. The direct effects are characterized by vasodilation, especially when the renal vascular resistance was enhanced beforehand. The increase in glomerular filtration rate is small and transient in most of the clinical trials with chronic administration. An important direct effect of calcium channel antagonists on renal function is the increase of sodium and water excretion by a tubular action that occurs in the absence of hemodynamic changes. The mechanism of the tubular effects of calcium channel antagonists is not understood at present. An indirect effect of calcium channel antagonists on the kidney is the inhibition of the aldosterone secretion by the adrenals. A sodium and water loss due to inhibition of tubular reabsorption leads to an increase in renin activity and aldosterone concentration in the plasma as seen typically with diuretics. The dissociation of renin- and aldosterone increase by calcium channel antagonists is a new finding and contributes favorably to the anti-hypertensive efficacy of calcium channel antagonists. In experimental acute renal failure mainly diltiazem and verapamil improved recovery of kidney function. In kidney transplantation, diltiazem reduced posttransplant acute tubular necrosis and improved primary graft function. It remains to be seen whether other calcium channel antagonists have a similar beneficial therapeutic effect in pathological states of renal function.
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PMID:Renal actions of calcium channel antagonists. 207 37

The objectives of this study were first to develop a reproducible and reversible model of acute renal failure following contrast medium infusion in the rat; second to use that method to compare the nephrotoxicity of low- and high-osmolar contrast agents. Contrast media or saline were perfused in the aorta while a clamp was applied on the aorta just above the renal artery. Three minutes of renal ischemia with or without infusion of isotonic saline induced no change in serum creatinine and a slight and transient decrease in creatinine clearance at 24 h. Urinary N-acetyl glucosaminidase (NAG) excretion was not modified in this control group. All 17 kidneys which were examined were normal. 2,100 mosm/kg hypertonic saline induced a significant increase in serum creatinine and a significant decrease in creatinine clearance (from 1.8 +/- 0.1 to 0.8 +/- 0.1 and 1.0 +/- 0.2 ml/min at 24 and 48 h, respectively). Urinary NAG excretion increased from 23 +/- 18 to 48 +/- 20 and 8 +/- 4 mumol h-1/mmol creatinine at 24 and 48 h, respectively (p less than 0.05). Histologic analysis of 5 kidneys revealed acute tubular necrosis (n = 3) and no histologic abnormalities (n = 2). Diatrizoate induced an acute and reversible renal failure. Creatinine clearance decreased from 1.6 +/- 0.1 to 0.4 +/- 0.1 and 0.8 +/- 0.1 ml/min at 24 and 48 h, respectively (p less than 0.01). Urinary NAG excretion increased also significantly from 43 +/- 9 to 352 +/- 79 and 64 +/- 23 mumol h-1/mmol creatinine at 24 and 48 h, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal effects of radiocontrast agents in rats: a new model of acute renal failure. 207 9

Failure to visualize a kidney on radionuclide scanning using technetium-99m (99mTc) chelates and other renal radiopharmaceuticals such as iodine-131 hippuran has been described as potentially misleading in patients who have acute renal failure due to acute tubular necrosis and urinary tract obstruction. Such failure has not been described in a single kidney nor following angioplasty. The authors report a patient in whom a kidney was not visualized on 99mTc diethylenetriamine penta-acetic acid dynamic and serial scanning 3 days after renal angioplasty. The kidney was believed to be infarcted. Three months later there was almost complete recovery of renal function.
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PMID:Spontaneous return of renal flow and function on technetium-99m scan in a patient with renal artery thrombosis following angioplasty. 214 69

Reported was an aged woman (80-year-old) of minimal change nephrotic syndrome which was complicated with reversible oliguric acute renal failure. The patient presented massive proteinuria, anasarca, and severe azotemia. She recovered conservatively from the acute renal failure and subsequently remitted from the nephrotic syndrome after the treatment which comprised albumin infusion, diuretics, adrenocorticosteroid hormones (including the pulse therapy), antiplatelet drug, and anticoagulants. The histopathologic findings of renal biopsy were compatible with minor glomerular abnormalities and acute tubular necrosis with many tubular casts. The previously reported cases older than 80-year-old which remitted from minimal change nephrotic syndrome complicated with reversible acute renal failure, were very rare. The present case was the second case among the literatures.
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PMID:[An aged woman with minimal change nephrotic syndrome complicated with reversible acute renal failure]. 219 Nov 62

The term acute tubular necrosis refers to those forms of acute renal failure that occur in association with ischemic or hypoxic injury or exposure to nephrotoxic substances. This article discusses the various alternative classifications that are based solely on the clinical setting in which the acute renal failure occurs, and the types of therapies used in the management of them.
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PMID:Diagnosis and management of acute tubular necrosis. 219 59


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