Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
 ...
PMID:[Renal failure during liver disease--The significance of endotoxins (author's transl)]. 33 83

Twelve patients with otherwise uncomplicated acute viral hepatitis (two were HBsAg-positive) developed renal failure. Apart from dehydration due to repeated vomiting in one patient, no factor responsible for precipitating renal failure could be identified. The clinical course was characterised by renal failure with plasma urea concentrations reaching maximum values of 26-69 mmol/l (175-416 mg/100 ml). Ten patients needed dialysis for up to two weeks. Seven patients recovered completely, while the other five died from sepsis. The types of renal failure were similar to those described in fulminant hepatic failure and cirrhosis--namely, functional renal failure in five patients and acute tubular necrosis in seven. Two of the patients with functional renal failure later developed tubular necrosis. The mechanism responsible for renal failure in acute viral hepatitis is uncertain, though endotoxaemia may contribute.
 ...
PMID:Renal failure in otherwise uncomplicated acute viral hepatitis. 68 5

Magnesium deficiency can occur in congestive heart failure, after diuresis with furoxemide, ethacrynic acid and mercurials, and with digitalis intoxication, diabetic acidosis, acute and chronic alcoholism, delerium tremens, cirrhosis, malabsorption syndromes, protracted postoperative cases, open heart surgery, the diuretic phase of acute tubular necrosis, and with hypoparathyroidism, primary aldosteronism, juxta-glomerular hyperplasia and pancreatitis. Two cases of serious ventricular arrhythmias associated with magnesium depletion are described. Clinical manifestations are vague but center around neurologic symptoms such as weakness, tremors, stupor, coma, nausea, vomiting and anorexia. Serious cardiac arrhythmias also occur with magnesium depletion. Magnesium appears to be very useful in hypomagnesemic or digitalis-toxic tachyarrhythmias. Magnesium may also be valuable in normomagnesemic tachyarrhythmias. Ten to fifteen milliliters of a 20 percent magnesium sulfate solution, given intravenously over 1 minute, followed by a slow 4 to 6 hour infusion of 500 ml of 2 per cent magnesium sulfate in 5 per cent dextrose in water is recommended. Recurrence of arrhythmias is common and a second infusion of magnesium sulfate may be necessary. Hypermagnesemia occurs frequently in renal insufficiency, and magnesium therapy may then be contraindicated. Serum levels above 5.5 meq/liter should be avoided. Loss of deep tendon reflexes and a decrease in respiratory rate can be used as guides to magnesium therapy. A plea is made for frequent analysis of serum magnesium so that more knowledge can be gained regarding this important biologic element in cardiovascular disorders.
 ...
PMID:Magnesium deficiency and cardiac disorders. 80 29

The hepatorenal syndrome following right hemiphepatectomy is reported in a previously healthy patient who sustained a shotgun wound in the abdomen. In spite of the development of severe oliguric renal insufficiency and the administration of massive amounts of volume expanders and furosemide, the urine sodium concentration remained very low, therby excluding the diagnosis of acute tubular necrosis. Although severe hyperbilirubinemia developed, the prothrombin time was only slightly abnormal and the liver doubled in size in the 2 weeks after surgery. The study of functional renal failure in patients with liver disease other than decompensated cirrhosis and with significant preservation of hepatic function may suggest that factors other than a circulating toxin participate in mediating the hepatorenal syndrome.
 ...
PMID:Hepatorenal syndrome following hemihepatectomy. 126 Nov 3

Retinol binding protein (RBP) was analyzed in the sera and urines of 5 patients with hepato-renal syndrome (HRS), 4 with acute tubular necrosis (ATN), 20 liver cirrhosis patients with normal kidney function (NKF), 14 chronic renal failure (CRF) patients, and 19 healthy adults. All renal failure patients had high mean urine RBP (URBP): HRS, 8 mg/L; ATN, 11 mg/L; CRF, 8 mg/L respectively; p less than 0.001 vs the rest. Those with ATN and CRF had high mean serum RPB (SRBP): 146 and 149 mg/L, respectively, p less than 0.001 compared to the other groups. In HRS, in spite of renal failure, SRBP was very low (mean = 12 mg/L). The cirrhotics with NKF averaged less than 50% of the SRBP values of the healthy controls (16 vs 41 mg/L RBP, p less than 0.001); their RBP excretion was normal (mean URBP of 0.1 vs 0.06 mg/L in the control group). RBP analyses before and during HRS in two patients showed a marked increase in urine RBP during HRS (35- and 600-fold respectively) with practically unchanged serum levels. Impaired hepatic production and/or release is proposed to explain the low serum RBP in HRS, and a renal tubular injury or dysfunction to account for its high excretion. The RBP urinary loss could further compromise an already abnormal RBP metabolism and its serum levels. This combination (of low serum and high urine RBP), in the context of renal failure occurring in alcoholic liver cirrhosis, could help in the recognition of HRS.
 ...
PMID:Analysis of serum and urinary retinol binding protein in hepato-renal syndrome. 356 46

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.
 ...
PMID:Frequency and type of renal and electrolyte disorders in fulminant hepatic failure. 481 48

Forty patients with terminal cirrhosis and 40 patients with fulminant hepatic failure-all consecutively admitted-were studied with regard to incidence, types, and prognosis of complicating renal insufficiency. Renal failure was considered present when the serum creatinine was greater than 0.20 mmol/l. Of the patients with cirrhosis 26 (65%) developed renal failure. In 15 the type was functional, in three due to acute tubular necrosis, and in eight indeterminable. Of the patients with fulminant hepatic failure 22 (55%) had renal insufficiency; of these 13 had functional renal failure, five acute tubular necrosis, and in four the type was indeterminable. In both categories of patients, renal failure was equally frequent among patients with or without gastrointestinal bleeding and with or without ascites or diuretic therapy. The biochemical tests of liver function were similar in patients with or without renal failure in both categories. The mean renal blood flow in seven unselected patients with fulminant hepatic failure was reduced in the same order as previously observed in patients with cirrhosis. In terminal cirrhosis the mortality rate was 88% in the presence of renal failure, 71% in its absence (p greater than 0.05), while the same figures in fulminant hepatic failure were 100% and 67% (p less than 0.05). The incidence, relative frequency, and prognosis of renal failure were not different in the two conditions, indicating identical pathophysiological circumstances.
 ...
PMID:Renal failure in fulminant hepatic failure and terminal cirrhosis: a comparison between incidence, types, and prognosis. 726 32

Acute renal failure in liver disease includes prerenal renal failure, acute tubular necrosis (ATN) and hepatorenal syndrome (HRS). Patients with liver cirrhosis are susceptible to prerenal renal failure because of gastrointestinal bleeding, diuretics and paracentesis etc. ATN is more common in patients with obstructive jaundice but it also develops as a result of prolonged prerenal renal failure. HRS is a functional form of oliguric acute renal failure, occurring in patients with advanced liver disease in the absence of known cause of renal failure. Intrarenal vasoconstriction, attributable to a decrease in effective arterial blood volume, induced by peripheral arterial vasodilation, is proposed to play a causative role. Central hemodynamic monitoring is useful to distinguish HRS from other reversible conditions with renal failure in liver disease.
 ...
PMID:[Renal damage in liver cirrhosis: pathophysiology and management]. 811 86

In order to clarify the role of endotoxin in acute tubular necrosis in liver cirrhosis, lipopolysaccharide (LPS) was injected to rats with liver injury with exposure to carbon tetrachloride (CCl4) inhalation. Rats showed liver cirrhosis with ascites retention after 10 weeks' CCl4 treatment and liver fibrosis after 6 weeks' CCl4 treatment. Histopathological grading of kidney injuries after LPS treatment was more severe either in cirrhotic rats or in liver fibrotic rats than in normal rats. All cirrhotic rats had severe acute tubular necrosis after either dose of LPS, but only small necrotic foci of tubuli were seen in a few normal and liver fibrotic rats. The results indicate that endotoxin, which overflows due to disturbance of inactivation in the cirrhotic liver, may contribute to acute tubular necrosis. This effect of endotoxin is supposed to be a direct hemodynamic damage.
 ...
PMID:Endotoxin-induced acute tubular necrosis in cirrhotic rats. 815 14

There are conflicting reports on the ability of aspirin as a single agent to cause acute or chronic renal failure in experimental animals. Chronic administration of aspirin alone over 18 to 68 weeks in doses of 120 to 500 mg/kg/d has been reported to cause renal papillary necrosis in rats. However, some investigators have been unable to produce renal papillary necrosis in other species or in rats given lower divided doses comparable to therapeutic doses used in humans. In a variety of rat strains, aspirin administered as a single high dose intravenously or by oral gavage produces acute tubular necrosis of proximal tubules, rarely accompanied by renal papillary necrosis in susceptible strains. Several human studies have addressed the chronic nephrotoxicity of aspirin alone or relative risk of end-stage renal disease in association with aspirin use after correction for other analgesics. With the exception of one case control study demonstrating a low, but statistically significant risk of end-stage renal disease in association with aspirin use, all other case control studies and several prospective studies have been unable to identify a significant risk of chronic renal failure in patients using aspirin alone in therapeutic doses. In healthy adults, short-term aspirin administration in therapeutic doses has no effect on creatinine clearance, urine volume, osmolar clearance, or sodium and potassium excretion. However, in predisposed individuals with glomerulonephritis, cirrhosis, and chronic renal insufficiency, and in children with congestive heart failure, short-term aspirin use in therapeutic doses may precipitate reversible acute renal failure. Acute aspirin intoxication (>300 mg/kg) frequently causes acute renal failure and doses of 500 mg/kg may be lethal. Chronic salicylate intoxication has been reported to cause reversible or irreversible acute renal failure in association with a pseudosepsis syndrome.
 ...
PMID:Does aspirin cause acute or chronic renal failure in experimental animals and in humans? 866 25


1 2 3 4 5 Next >>