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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fluid retention and ascites are rarely seen in patients with primary biliary cirrhosis (PBC). This contrasts with the conspicuous tendency of patients with Laennec's cirrhosis to retain salt and water. In an attempt to clarify this clinical observation, renal handling of sodium was studied during extracellular volume expansion (ECVE) and maximal suppression of antidiuretic hormone in five patients with PBC. These PBC patients were compared with two control populations: five edema-free patients with Laennec's cirrhosis and nine healthy volunteers. The natriuretic and diuretic response to ECVE was significantly greater in the patients with PBC as compared with the two control groups. CH2O for given rates of urine flow were similar in PBC patients as compared with normal subjects. The data suggest that a supranormal rejection of sodium at the proximal tubule in response to ECVE underlies the exaggerated natriuresis of PBC. The augmented elimination of salt during ECVE in patients with PBC may explain the rarity of ascites and edema in this variety of cirrhosis.
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PMID:Exaggerated natriuretic response to volume expansion in patients with primary biliary cirrhosis. 60 57

Tubular handling of sodium and phosphate were studied in 4 patients with cirrhosis and ascites. The control group consisted of 5 patients with cirrhosis without sodium retention. The degree of phosphaturia was assumed to reflect proximal tubular reabsorption. Whereas fractional excretion of phosphate was comparable in both groups, fractional excretion of sodium was strikingly diminished in the patients with ascites. This observation suggests that sodium retention in these patients occurs beyond the proximal tubule. This interpretation is in accord with our previous observation, based on clearance data, that the proximal tubular reabsorption of sodium in cirrhosis may be normal even in the face of edema formation.
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PMID:Tubular handling of sodium and phosphate in cirrhosis with salt retention. 62 15

Since the reabsorption of lithium occurs almost exclusively in the proximal tubule and is associated with that of sodium, the fractional excretion of lithium (FELit) ws examined in 18 patients with cirrhosis in order to examine the reabsorption rate of sodium at the proximal tubule. As expected, the fractional excretion of sodium (FENa) was significantly lower in cirrhotic patients with ascites (0.43 +/- 0.10%, mean +/- SEM) than in cirrhotic patients without ascites (0.75 +/- 0.14%, P less than 0.05) and healthy controls (0.82 +/- 0.17%, P less than 0.05). By contrast, there was no significant difference in FELit among cirrhotic patients with ascites (16.7 +/- 2.0%), cirrhotic patients without ascites (15.4 +/- 2.0%) and controls (17.4 +/- 1.5%). It is unlikely, therefore, that in cirrhotic patients with ascites, the impaired sodium excretion is solely caused by the abnormal sodium reabsorption capacity of the proximal tubule.
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PMID:A lithium clearance study of sodium reabsorption at the proximal tubule in liver cirrhosis with ascites. 280 32

Increased levels of octopamine in adrenergic nerve terminals and plasma have been implicated in the circulatory and renal disturbances of chronic hepatic failure. Little is known about its renal actions in normal animals. In the present study, DL-octopamine was administered both i.v. and into one renal artery of anaesthetized dogs in doses ranging between 25-200 micrograms/min (1.6-20 micrograms/kg/min). Octopamine was hypertensive in doses of 100 micrograms/min and more and this change was associated with a significant decrement in GFR and renal perfusion. This amine also exerted a direct tubular effect since decreased excretion of sodium and water occurred in the absence of blood pressure or renal perfusional changes when given i.v. When given into one renal artery octopamine produced only an ipsilateral antidiuresis and antinatriuresis, in the absence of any change to GFR or renal perfusion. Lithium clearances suggest that octopamine acts beyond the proximal tubule in altering the tubular reabsorption of salt and water. Because octopamine was found to increase blood pressure in the presence of a hypertensive infusion of noradrenaline, it is likely that this amine exerts a primary pharmacological effect rather than liberating noradrenaline from nerve terminals. Saline expansion (7% body weight), acute biliary obstruction, chronic cirrhosis with ascites, and chronic thoracic caval constriction with the production of ascites all abolish the effect of octopamine when administered at 100 micrograms/min. Though octopamine may directly influence renal perfusion, its possible role in liver disease remains uncertain.
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PMID:Effects of octopamine on renal function in anaesthetized dogs. 314 28

The renal response to a maximal water load was evaluated in eight cirrhotic patients free of ascites and without previous evidence of ascites and in seven controls. Fractional sodium reabsorption in the proximal and diluting segment was estimated by clearance methods during hypotonic diuresis. Since phosphate excretion has been proposed as a proximal marker in liver cirrhosis, sodium reabsorption in the proximal tubule was compared with phosphate fractional excretion. In spite of a normal sodium balance during the pre-study period, non-ascitic cirrhotics showed a blunted proximal natriuretic response to maximal water load. In fact sodium excretion during hypotonic diuresis was reduced (p less than 0.05) and proximal sodium reabsorption increased (p less than 0.005) in cirrhotics. Fractional phosphate excretion was not impaired in our patients, and no correlation was found between phosphate excretion and proximal sodium reabsorption, as evaluated by clearance methods. This study demonstrates that an increased reabsorption of sodium in the proximal tubule is responsible for the impaired response to maximal water load in non-ascitic cirrhotics. Abnormalities in tubular handling of phosphate may account for the dissociation between proximal sodium reabsorption and phosphate excretion during hypotonic diuresis in these patients.
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PMID:Tubular handling of sodium and phosphate in non-ascitic liver cirrhosis. 358 89

The present study was attempted to evaluate sodium and water balance in compensated liver cirrhosis. Renal sodium and water handling was studied in six cirrhotic patients without ascites and/or oedema and in six controls before and after saline loading. Fractional sodium reabsorption at the various nephron sites (proximal, diluting and distal) was evaluated by means of clearance techniques during maximal water diuresis and hypotonic saline infusion. Compensated cirrhotic patients showed a normal baseline sodium and water balance but a blunted natriuretic response when saline loaded (urinary sodium excretion after saline load = 338 +/- 290 compared to 933 +/- 504 mumol min-1 of controls; P less than 0.05). The impaired natriuresis was found to be related to an increased reabsorption of sodium in the proximal tubule (proximal fractional sodium reabsorption = 88.4 +/- 3.8 compared to 81.7 +/- 4.3% of controls; P less than 0.05). These findings confirm the hypothesis that renal sodium handling abnormalities might precede ascites formation. Additional studies, however, are necessary to further define renal factors mediating the increased reabsorption of sodium in compensated liver cirrhosis.
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PMID:Renal water and sodium handling in compensated liver cirrhosis: mechanism of the impaired natriuresis after saline loading. 393 5

In a group of eight patients with cirrhosis the rate of renal excretion of the 18-glucuronide metabolite of aldosterone (U Aldo V) was found to be closely related to the aldosterone secretion rate (ASR). U Aldo V was therefore used as an index of ASR in a further group of fifty patients in order to evaluate the possible importance of factors known to regulate aldosterone secretion. U Aldo V showed statistically significant relationships to both plasma renin activity (PRA) and the plasma sodium concentration (P Na), but not to the plasma potassium concentration (PK) or the renal excretion of cortisol (U Cort V), the latter sued as an index of adrencorticotrophic hormone activity. The plasma aldosterone concentration (P Aldo) was determined in fifty-eight patients and also found to show statistically significant relationships to PRA and P Na. P Aldo showed a weak, though statistically significant, relationship to PK, but not to U Cort V. These findings are in keeping with a role for the renin-angiotensin system in the control of aldosterone secretion in cirrhosis although evidence from other studies suggest other factors to be involved also. Whether P Na was another determinant of ASR, or whether aldosterone was a determinant of P Na through regulating sodium reabsorption by the proximal tubule of the nephron, is uncertain.
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PMID:Factors relating to aldosterone secretion rate, the excretions of aldosterone 18-glucuronide, and the plasma aldosterone concentration in cirrhosis. 702 Oct 11

Acute expansion of extracellular fluid volume during maximal water diuresis was induced in 8 chronic liver disease patients without clinical evidence of fluid retention, and in 8 controls. Fractional reabsorption of sodium was inferred in the proximal tubule, in the ascending limb of Henle's loop, and in the more distal site of the tubule. The results indicate that the significantly reduced increment of sodium excretion in cirrhotic patients was due to its augmented reabsorption in the proximal tubule. To establish whether there was a reduced activity of a natriuretic factor, a biologic assay was performed in 16 albino Wistar rats by using urine samples collected immediately after completion of a saline load and processed with gel filtration. The infusion of this fraction resulted in a significant lowering of the increment of urine output, and absolute and fractional sodium excretion only in the rats infused with urine extracts from cirrhotic patients. The results of this study raise the possibility that a reduced production of a natriuretic factor may play some role in the pathogenesis of sodium retention, which is observed in patients with cirrhosis of the liver.
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PMID:Renal handling of sodium and water in early chronic liver disease. Evidence for a reduced natriuretic activity of the cirrhotic urinary extracts in rats. 723 29

The functions of the different nephron segments follow changes in the effective arterial blood volume and the extracellular fluid volume. In syndromes with reduced effective arterial blood volume, for example congestive heart failure, decompensated hepatic cirrhosis and nephrotic syndrome, hyperreabsorption of sodium in the proximal tubule reduces the sodium load in the more distal segments of the nephron. As this is a major site of sodium excretion, reduction in the response to a diuretic may be predicted by a reduced fractional excretion of sodium (< 0.2%). Such diuretic resistance may be overcome with acetazolamide, which increases delivery of sodium to the distal tubule. In syndromes with increased extracellular fluid volume, such as chronic renal failure, distal tubular rejection of sodium leads to a progressive increase in its fractional excretion as the glomerular filtration rate is reduced. The remaining intact nephrons exhibit a relatively increased response to diuretics. The efficacy of loop diuretics in renal failure can be optimized by combination with thiazides. The latter prevent early distal tubular hyperreabsorption following diuretic-induced blockade of sodium transport in the loop of Henle. For these reasons, low-dose combinations of different diuretics induce 'segmental nephron blockade' and are, therefore, potentially more clinically effective and safer than high doses of single compounds.
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PMID:Functional state of the nephron and diuretic dose-response--rationale for low-dose combination therapy. 795 41

Proximal and distal sodium reabsorption values were calculated from lithium clearance in 63 patients with renal diseases, 13 cirrhotic patients with ascites and 12 control subjects. In the patients with renal diseases, fractional excretion of lithium (FELi) and fractional proximal reabsorption of sodium (FPRNa) were not changed in patients whose glomerular filtration rate (GFR), was over 30 mL/min, but FELi was increased and FPRNa was decreased when the GFR was lower than 30 mL/min. Moreover, fractional distal reabsorption of sodium (FDRNa) was decreased in patients whose GFR was under 40 mL/min. These results indicate that proximal tubular function is well adapted to the degree of renal function even if the etiologies of renal diseases are different. Five patients with nephrotic syndrome (minimal change type) were subjected to lithium clearance method before and after steroid treatment. FPRNa in nephrotic patients was reduced after the treatment, though there was no significant difference in FDRNa. In cirrhotic patients, FELi, FPRNa and FDRNa did not differ from the values in the control subjects, which were not influenced by the decrease in GFR. Thus, the reduction of FPRNa with GFR which was observed in renal disease, was absent in liver cirrhosis. In conclusion, these data indicate that renal adjustment of sodium excretion in chronic renal disease at first takes place in the distal parts of the nephron and later in the proximal tubule, and in addition, that in appropriate reabsorption of sodium from the proximal tubule probably plays a role in ascites formation in cirrhotic patients.
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PMID:[Clinical assessment of renal proximal tubular function using lithium clearance method]. 870 17


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