Spectrum of renal tubular damage in renal failure secondary to cirrhosis and fulminant hepatic failure.

Wilkinson, Stephen; Hirst, D. V.; Day, David W.; Williams, Roger

doi:10.1136/jcp.31.2.101

Cited by 33 publications

(13 citation statements)

References 19 publications

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“…In a study similar in design t,o the present one, Wilkinson et al (6) found increased fractional clearance of lysozyme, a protein metabolized by the kidneys in a manner analogous to B2MG, in a subgroup of patients with HRS. These patients typically had creatinine clearances of <1 ml per min, urine sodium concentrations above 10 mEy per liter, isosthenuria, abnormal urinalyses and evidence of "acute tubular necrosis" on postmortem histological examination of the kidney.…”

Section: Discussionmentioning

confidence: 77%

Tubular dysfunction in the deeply jaundiced patient with hepatorenal syndrome

et al. 1985

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We examined beta 2-microglobulin (B2MG) excretion, an index of tubular function, in patients with hepatorenal syndrome, in whom tubular function is generally regarded as normal. Urine B2MG was significantly higher in these patients than in control patients with normal serum creatinine concentration. Patients with high urine B2MG concentration had markedly higher serum bilirubin than did patients with normal values (31 +/- 3 vs. 10 +/- 8 mg%, p less than 0.001), whereas prothrombin activity, serum albumin and serum B2MG concentration were similar. A "threshold" serum bilirubin concentration of about 23 mg% differentiated patients with normal and high urine B2MG values. Renal morphology at autopsy was unremarkable in both groups. Tubular dysfunction, manifested by increased urinary excretion of B2MG, occurs in patients with hepatorenal syndrome and deep jaundice. This measurement cannot, therefore, be used to make a diagnosis of acute tubular injury, as due to aminoglycosides, in such patients.

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Section: Discussionmentioning

confidence: 77%

Tubular dysfunction in the deeply jaundiced patient with hepatorenal syndrome

et al. 1985

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“…Advanced hepatic disease, such as fulminant hepatitis or terminal liver cirrhosis, is frequently accompanied by renal injury (Epstein et al 1970;Wilkinson et al 1976Wilkinson et al , 1978, although the exact cause of this additional injury is not known. It has been reported that endotoxin, which can enter systemic circulation following substantial liver damage, can lead to renal injury (Wilkinson et al 1974(Wilkinson et al a, 1977.…”

Section: Introductionmentioning

confidence: 99%

Investigation of the renal injury caused by liver ischemia-reperfusion in rats

et al. 1993

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To explain the mechanism of renal injury caused by liver ischemia-reperfusion, we investigated biochemical and morphological changes in the liver and kidney in rats. After reperfusion following 60 min of liver ischemia, numerous changes were found. The level of serum transaminases and lipid peroxide formation in the liver tissue increased significantly. Electron microscopic studies revealed that most of the hepatocytes had swollen mitochondria and clumping of the nuclear chromatin. The sinusoidal endothelium was disrupted and the sinusoidal lumen was filled with numerous erythrocytes. Blood endotoxin concentration, plasma lipid peroxide levels, and serum beta-glucuronidase activities were significantly higher than in the control group. Biochemical and morphological renal injury was also observed. Tissue lipid peroxide levels increased in both the kidney and the liver. Microscopic examination revealed damage to the renal tubules, including interstitial edema, dilatation of the lumen, and granular casts derived from necrotic cells in the proximal convoluted tubule. The levels of urinary N-acetyl-beta-D-glucosaminidase (NAG) in the liver ischemia-reperfusion group were also higher than in the control group. These results suggest that the renal injury was caused by an increase in endotoxin, lipid peroxide, and lysosomal enzymes in the blood following the liver injury induced by the ischemia-reperfusion.

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“…This may be true for both chronic pancreati tis, an inflammatory disease with clinical and biochemi cal relapses, and for pancreatic cancer: the latter is fre quently associated with an inflammatory reaction in the pancreatic tissue surrounding the neoplastic mass. In pancreatic cancer patients, however, the role of liver dysfunction (presence of liver métastasés and extrahepatic cholestasis) appeared to be prominent in determin ing enzymuria, as reported for liver cirrhosis [31,32], and indeed a substantial number of those patients with abnor mal GGT, AGL and RNase urinary excretion had liver métastasés an d /o r jaundice. The primary role of jaun dice in altering tubular cells [33] was confirmed in the present study: jaundice increased GGT and RNase in all patients.…”

Section: Discussionmentioning

confidence: 99%

Renal Tubular Dysfunction in Pancreatic Cancer and Chronic Pancreatitis

Fabris

Basso²,

Favero³

et al. 1989

Nephron

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Urinary excretion of alpha-glucosidase (AGL), gamma-glutamyltransferase (GGT) and ribonuclease (RNase), and serum amylase and immunoreactive trypsin (IRT) were determined in 38 control subjects, 48 patients with pancreatic cancer, 77 with chronic pancreatitis and 47 with extrapancreatic diseases in order to ascertain the presence of a renal tubular damage and to investigate its etiology. A significantly increased frequency of pathological results for all urinary enzymes was documented in the various groups of patients as compared to controls. Significant correlations were detected among AGL, GGT and RNase. Considering the subjects as a whole, GGT and RNase excretions correlated with serum IRT and amylase; the two urinary enzymes were found to be higher when jaundice was present. In chronic pancreatic disease enzymuria was related to increased serum pancreatic enzymes; in extrapancreatic diseases it was associated to hyperbilirubinemia. The vast majority of patients with pancreatic cancer and elevated urinary enzymes presented hepatic metastases and/or jaundice. We can conclude that an anatomical and functional tubular impairment is detectable in some patients with chronic pancreatic and extrapancreatic diseases. Tubular damage seems at least in part to be related to pancreatic inflammation and necrosis in chronic pancreatic disease, while jaundice may be found to play an important role in diseases of the hepatobiliary tract. In pancreatic cancer, liver dysfunction (presence of liver metastases and/or extrahepatic cholestasis) also appears to be involved in altering tubular cells.

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Spectrum of renal tubular damage in renal failure secondary to cirrhosis and fulminant hepatic failure.

Cited by 33 publications

References 19 publications

Tubular dysfunction in the deeply jaundiced patient with hepatorenal syndrome

Tubular dysfunction in the deeply jaundiced patient with hepatorenal syndrome

Investigation of the renal injury caused by liver ischemia-reperfusion in rats

Renal Tubular Dysfunction in Pancreatic Cancer and Chronic Pancreatitis

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