A micropuncture study of renal salt and water retention in chronic bile duct obstruction.

Bank, Norman; Aynedjian, Hagop S.

doi:10.1172/jci108029

Cited by 51 publications

(22 citation statements)

References 28 publications

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“…Micropuncture and lithium clearance studies have also found evidence of increased sodium and water reabsorption in the proximal tubules of animals with cirrhosis and of patients. 30,31 We observed, however, that the urinary excretion of aquaporin-1 was not altered in patients with cirrhosis with or without ascites. By contrast, urinary excretion of aquaporin-1 was extremely reduced in patients with hepatorenal syndrome.…”

Section: Aquaporin-1 Protein In Urinementioning

confidence: 65%

Aquaporin-1 and aquaporin-2 urinary excretion in cirrhosis: Relationship with ascites and hepatorenal syndrome

et al. 2006

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Several experimental models of cirrhosis have shown dysregulation of renal aquaporins in different phases of liver disease. We investigated the urinary excretion of both aquaporin-1 and aquaporin-2 in patients with cirrhosis at different stages of the disease. Twenty-fourhour urine was collected from 11 healthy volunteers, 13 patients with compensated cirrhosis (without ascites), and 20 patients with decompensated cirrhosis (11 with ascites without renal failure and 9 with hepatorenal syndrome). Aquaporin-1 and aquaporin-2 excretion was analyzed by immunoblotting. Urinary aquaporin-2 excretion was reduced in patients with cirrhosis compared to healthy subjects. A progressive decrease in urinary aquaporin-2 excretion was observed as the severity of cirrhosis increased, from compensated cirrhosis to cirrhosis with ascites and hepatorenal syndrome. Patients with hyponatremia had lower urinary aquaporin-2 excretion than patients without hyponatremia. Vasopressin plasma level did not correlate with aquaporin-2 excretion. There were no differences between healthy subjects and patients with cirrhosis with or without ascites in urinary excretion of aquaporin-1, but urinary aquaporin-1 excretion of those with hepatorenal syndrome was extremely low. In conclusion, patients with cirrhosis appear to exhibit a decreased abundance of renal aquaporin-2 and therefore lower water permeability in the collecting tubules. This may represent an adaptive renal response to sodium retention, with expansion of extracellular fluid volume and dilutional hyponatremia observed in those who have cirrhosis with ascites. Finally, aquaporin-1 does not appear to play a role in the progressive dysregulation of extracellular fluid volume in cirrhosis. (HEPATOLOGY 2006;44:1555-1563

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Section: Aquaporin-1 Protein In Urinementioning

confidence: 65%

Aquaporin-1 and aquaporin-2 urinary excretion in cirrhosis: Relationship with ascites and hepatorenal syndrome

et al. 2006

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“…However. Bank and Hagop [3] demonstrated that 10-14 days after bile duct ligation, rats showed positive sodium balance and ascites formation, which resulted from the enhanced sodium and water reabsorption pri marily by cortical nephrons. Yarger et al [2] reported that a decrease in the filtered sodium load and an increase in fractional reabsorption by the superficial nephrons played an impor tant role in the sodium retention observed in the initial stages of ascites formation following bile duct ligation in rats.…”

Section: Discussionmentioning

confidence: 99%

“…The term 'hepato-renal syndrome' was first in troduced to describe the high frequency of postoperative acute renal failure in patients with obstructive jaundice [1]. Similar abnormal renal function were demonstrated in studies of animals after ligation of common bile duct [2,3). The changes in renal function included: re duction in renal hemodynamics; impairment of renal excretion of water and salts; sensitization of the kidney to anoxic damage [4],…”

Section: Introductionmentioning

confidence: 96%

Effects of Rat Bile Infusion on Renal Function in Rats

Shen¹,

Chen²,

Liu³

et al. 1990

Kidney Blood Press Res

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The influence of rat bile infusion on renal function in rats and the possible role of bile-induced hemolysis in these effects were examined. The hemolytic action of rat bile and some bile salts were determined in vitro. After the i.v. infusion of rat bile (70 mg freeze-dried powder/2.55 ml) into pentobarbitone-anesthetized rats, the urine, sodium and potassium excretion rates were reduced more than half, which was due to the decrease of glomerular filtration rate and increase of tubular water and sodium reabsorption. A fall in blood pressure, a rise in hematocrit, and hemolysis were also found. Infusion of hemolysed (30 µl RBC) solution produced by distilled water and then made isotonic caused a short-duration increase in renal excretion and glomerular filtration rate, and the blood pressure was unchanged. Infusion of a rat bile-hemolysed solution after removal of bile acids with cholestyramine increased renal excretions at first with reduction thereafter. Infusion of the rat bile-hemolysed solution treated with barium sulfate produced a renal response very similar to rat bile alone. It is proposed that two factors are involved in the renal response after bile infusion, namely bile acid-induced hemolysis producing diuresis with natriuresis, and bile acid-induced antidiuresis and antinatriuresis, possibly due to a direct renal effect.

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“…There seems to exist a controversy concerning the renal handling of salt and water in hyperbilirubinemic states [1][2][3]11,12,14,19]. Gliedman et al [II] have noticed that the natriuretic response to a saline load is blunted in BDL dogs, though sodium clearance in the control state is not different from that in normal dogs.…”

Section: Discussionmentioning

confidence: 99%

“…There seems to exist a controversy as to the renal handling of salt and water in obstructive jaundice [1][2][3]11,12,14,19], Some investigators have demonstrated sodium retention, ascites formation and urine concentrating defect in jaundiced rats [2,19] and dogs [3,14] 4 days to 7 weeks after the ligation of the common bile duct. Especially rats developed ascites in the early phase of obstructive jaundice [19].…”

Section: Introductionmentioning

confidence: 99%

Renal Handling of Salt and Water in the Early Stage of Obstructive Jaundice in Rabbits

Hishida¹,

Honda²,

Sudo³

et al. 1982

Nephron

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Renal handling of salt and water in the early stage of obstructive jaundice was studied in rabbits 10 days after the ligation of the common bile duct (BDL). Sham-operated (SO) animals served as controls. No sodium retention was found in BDL rabbits, despite reduced renal perfusion and elevated plasma aldosterone level. A redistribution of intrarenal blood flow was not found. The filtration fraction did not change. A saline load resulted in decreases in arterial hematocrit and total serum proteins, and increases in urine output, urinary sodium excretion and osmolal clearance. Blood pressure, glomerular filtration rate (GFR), RPF, the filtration fraction and the intrarenal flow distribution were not significantly affected by the saline load. No significant difference was found in the natriuretic response to the saline load between the BDL and SO groups. After 60 h of water deprivation, there was no significant difference in urine-to-plasma osmolality ratios or renal tissue fluid osmolality between the BDL and SO animals. The findings indicate that renal handling of salt and water was well maintained in the early phase of obstructive jaundice in rabbits. The data also suggest the critical role of the redistribution of intrarenal blood flow rather than of GFR or aldosterone in determining sodium retention in obstructive jaundice.

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A micropuncture study of renal salt and water retention in chronic bile duct obstruction.

Cited by 51 publications

References 28 publications

Aquaporin-1 and aquaporin-2 urinary excretion in cirrhosis: Relationship with ascites and hepatorenal syndrome

Aquaporin-1 and aquaporin-2 urinary excretion in cirrhosis: Relationship with ascites and hepatorenal syndrome

Effects of Rat Bile Infusion on Renal Function in Rats

Renal Handling of Salt and Water in the Early Stage of Obstructive Jaundice in Rabbits

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