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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 effect of transient renal ischemia on renal concentration and distribution of 99mTc-HEDP, 99mTc-DMSA, and 99mTc-DTPA was compared in rabbits with acute tubular necrosis. Scintigrams were obtained after injection in normal rabbits or ones with unilateral or bilateral ischemia. 99mTc-HEDP concentration in ischemic tissue was 8 to 18 times normal 1--4 hours after injection, and the resulting images delineated the morphological changes in the ischemic kidneys more accurately than those obtained with DMSA or DTPA. Calcium concentration in the ischemic kidneys increased sixfold. 99mTc-HEDP may be useful in evaluation of renal failure secondary to tubular injury.
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PMID:Renal hyperconcentration of 99mTc-HEDP in experimental acute tubular necrosis. 22 Jun 70

In cirrhosis and fulminant hepatic failure acute renal failure may occur both without ("functional renal failure") and with tubular necrosis, the two probably being the ends of a spectrum. The underlying pathophysiological change is an intense renal and intra-renal vasoconstriction. Evidence is presented that this is due to systemic endotoxaemia resulting from failure of the liver to filter endotoxins absorbed from the gastrointestinal tract. Acute renal failure complicating obstructive jaundic has also been related to endotoxaemia, but in contrast to cirrhosis and fulminant hepatic failure this is usually due to an associated gram-negative infection and the renal failure almost invariably has the features of acute tubular necrosis. Endotoxins have two major effects on the kidney: (i) renal vasoconstriction, and (ii) glomerular and peritubular fibrin deposition. The nature of the renal failure depends on the balance between these variables which may be profoundly altered by the underlying liver disease.
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PMID:[Renal failure during liver disease--The significance of endotoxins (author's transl)]. 33 83

A case is reported of Fanconi syndrome and nonliquric renal failure, following a brief course of cephalothin and gentamicin, in a patient with diffuse histiocytic lymphoma. These drugs, especially when used in combination, have been associated with nephrotoxicity manifested as acute tubular necrosis and altered proximal tubular function, but biochemical evidence for generalized proximal tubular dysfunction has not been accurately defined. Thus far, only two other antibiotics, degraded tetracycline and streptozotocin, have been implicated in producing an acquired Fanconi syndrome.
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PMID:Fanconi syndrome associated with cephalothin and gentamicin therapy. 34 14

An ivestigation was made of the effect of the duration of posttransplant renal failure on the late prognosis of graft as well as patient survival and on the frequency of complications in 102 patients who had a functioning graft at three months after transplantation. A direct correlation was found between duration of acute tubular necrosis (ATN) and the late prognosis of the graft. The creatinine clearance was significantly higher and the frequency of complications was lower in the group with immediate resumption of renal function. The mortality rate increased with the duration of ATN.
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PMID:Late prognosis in acute posttransplant renal failure in 102 patients. 37 68

The clinical manifestations of drug-induced renal disease may include all the manifestations attributed to natural or spontaneous renal diseases such as acute renal failure, chronic renal failure, acute nephritic syndrome, renal colic, haematuria, selective tubular defects, obstructive nephropathy, etc. It is therefore vital in any patient with renal disease whatever the clinical manifestations might be, to obtain a meticulous drug and toxin inventory. Withdrawal of the offending drug may result in amelioration or cure of the renal disorder although in the case of severe renal failure it may be necessary to utilise haemodialysis or peritoneal dialysis to tide the patient over the period of acute renal failure. Analgesic nephropathy is an important cause of terminal chronic renal failure and it is therefore vital to make the diagnosis as early as possible. The pathogenesis of some drug-induced renal disorders appears to be immunologically mediated. There are many other pathogenetic mechanisms involved in drug-induced renal disorders and some drugs may under appropriate circumstances be responsible for a variety of different nephrotoxic effects. For example, the sulphonamides have been incriminated in examples of crystalluria, acute interstitial nephritis, acute tubular necrosis, generalised hypersensitivity reactions, polyarteritis nodosa and drug-induced lupus erythematosus.
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PMID:Drug-induced renal disease. 38 1

The delayed onset of anuria/oliguria in acute tubular necrosis has been theorized to represent a complicating compartment syndrome, i.e., parenchymal swelling within an unyielding capsule. To test this proposition, 12 monkeys had suprarenal aortic cross-clamping, followed by unilateral renal decapsulation to create an experimental as well as a control kidney unit in the same animal. Histologic examination uniformly confirmed tubular necrosis at death or sacrifice. Subsequent split renal function studies (creatinine, urea, and free water clearances) indicated significantly greater maintenance of renal function by the decapsulated kidney than by its paired control. Clinical evaluation in 21 hemorrhagic shock patients, with the capsule of one kidney stripped, revealed on follow-up that 15 developed a renal failure consistent with acute tubular necrosis. Although three patients with polyuric failure died before split studies could be run and two others have been too recent for computer analysis to have been completed, nine of the remaining ten had significantly greater renal plasma flows (194 versus 121 ml/min M(2), p < .01) and significantly greater urine flows (.99 versus .18 ml/min M(2), p < .01) on the decapsulated side than on the control, as determined by differential renal scans. No significant difference in these same lateralized renal functions was noted in the tenth patient with renal failure and in the six survivors without renal failure. Renal decapsulation as prophylaxis reduced the anticipated incidence of oliguria/anuria from an expected 75% to 7% (p < .01) in these 21 shock patients. Such data suggest that delayed renal ischemia, possibly based on a compartment syndrome, may be the cause for a progression of acute tubular necrosis from polyuria to oliguria and then to anuria.
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PMID:Renal decapsulation in the prevention of post-ischemic oliguria. 40 54

The course of nonoliguric acute renal failure (ARF) in 11 patients was analyzed. The possible etiology of the renal failure was multiple in all cases and did not differ from that seen in oliguric acute tubular necrosis (ATN). Other than the urine volume, which ranged from 510 to 2,325 ml/day, there was no major clinical or biochemical difference between these cases of nonliguric ARF and those described for oliguric ATN. Creatinine clearance, however, was higher than anticipated in oliguric ATN and ranged from 2.8 to 15.0 ml/min. There was a direct relationship between creatinine clearance and daily urine volume. The essential difference between oliguric and nonoliguric renal failure appears to be the lesser degree of renal damage in the nonoliguric form.
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PMID:Nonoliguric acute renal failure. 42 44

Five patients with severe jaundice resulting from amoebic liver abscess are described. All had features of hepatic parenchymal damage and cholestasis, and 1 patient developed hepatic coma. In addition, acute tubular necrosis and renal failure occurred in 3 patients. Four patients in the series survived. The importance of early recognition and treatment of amoebic liver abscess in patients presenting with jaundice is emphasized, so that the serious and often fatal complications of hepatic and renal failure can be prevented.
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PMID:Amoebic liver abscess in patients presenting with jaundice. A report of 5 cases. 42 69

In one case of fulminant hepatic failure by acute alcoholic hepatitis, renal failure seemed to be related to active renal vasoconstriction by systemic endotoxemia due to impaired hepatic clearance of toxins, associated with or complicated by a located intravascular coagulation with acute tubular necrosis. The associated thiamin deficiency may have accentuated this renal vasoconstriction.
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PMID:[Acute tubular necrosis in acute alcoholic hepatitis with cardiac beriberi (author's transl)]. 55 56

Although acute renal artery obstruction causes cessation of kidney function, the viability of the nephron is often maintained by collateral circulation. When renal artery blood flow is restored, filtration is resumed and the resulting acute tubular necrosis is gradually resolved as renal tubular cells regenerate. We have observed several different mechanisms of acute renal artery obstruction resulting in anuric renal failure: temporary suprarenal placement of an aortic clamp during absominal aneurysmectomy, resulting in bilateral renal artery occlusion; embolus, presumably of cardiac origin, to a solitary kidney; and thrombosis of the distal aorta extending to a level proximal to the renal arteries. There is no correlation between the duration of renal artery occlusion and the viability of kidney parenchyma. Viability of the kidney can only be determined by visual inspection at operation and response to revascularization. When vascular obstruction is a possible cause of acute anuric renal failure, immediate angiography is indicated. If a correctable vascular lesion is identified, operative intervention is mandatory.
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PMID:Revascularization of the ischemic kidney. 62 86


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