Renal Functional Impairment and Sodium Retention in Liver Cirrhosis

Geñtilini, Paolo

doi:10.1159/000199857

Cited by 22 publications

(6 citation statements)

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“…In our opinion the RI is more sensitive and reliable than serum creatinine levels as an indicator of the changes of the functional status of the intrarenal arterial bed in cirrhotic patients both before and after OLT. In fact, it has been clearly shown that normal serum creatinine levels may be associated with a markedly decreased glomerular filtration rate in cirrhosis related kidney dysfunction 3,25 and that more than 50% of patients with end-stage liver disease and increased renal RI who undergo OLT have normal serum creatinine levels. 16 This is probably due to the decreased muscle mass secondary to the poor nutritional state in chronic liver disease.…”

Section: Discussionmentioning

confidence: 99%

“…In this study we evaluated by Doppler ultrasonography the changes of renal vascular resistance occurring during the first month after transplantation. In 16 cirrhotic patients the intrarenal resistive index at the level of interlobar arteries and the blood urea nitrogen and serum creatinine levels were measured before (range, 1 to 34 days) and after transplantation (days 1, 3,7,14,30). Before transplantation the median resistive index value was 0.69 (95% CI, 0.65 to 0.71) and eight of 16 patients showed abnormal values (0.70 or more).…”

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confidence: 99%

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Doppler ultrasonographic evaluation of the early changes in renal resistive index in cirrhotic patients undergoing liver transplantation.

Pompili

Rapaccini

Luca

et al. 1999

Journal of Ultrasound in Medicine

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Renal vasoconstriction commonly occurs in decompensated liver cirrhosis and is entirely reversible after hepatic transplantation. In this study we evaluated by Doppler ultrasonography the changes of renal vascular resistance occurring during the first month after transplantation. In 16 cirrhotic patients the intrarenal resistive index at the level of interlobar arteries and the blood urea nitrogen and serum creatinine levels were measured before (range, 1 to 34 days) and after transplantation (days 1, 3, 7, 14, 30). Before transplantation the median resistive index value was 0.69 (95% CI, 0.65 to 0.71) and eight of 16 patients showed abnormal values (0.70 or more). After transplantation, the median resistive index was significantly decreased on all the evaluation days, and no patient had abnormal values on posttransplantation day 7. No significant correlation was found between resistive index and serum creatinine or blood urea nitrogen levels. Doppler ultrasonography is a simple tool to evaluate the recovery of normal intrarenal arterial resistance levels after liver transplantation. One week appears to be the optimal timing to evaluate the renal resistive index in the posttransplantation period.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Doppler ultrasonographic evaluation of the early changes in renal resistive index in cirrhotic patients undergoing liver transplantation.

Pompili

Rapaccini

Luca

et al. 1999

Journal of Ultrasound in Medicine

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“…The hallmark of HRS is hypo perfusion of the kidney resulting from combined renal vasoconstriction and decreased total renal blood flow 9 . The earliest stages of this apparently functional form of kidney failure often go unrecognized because creatinine elevation occurs late in the hepatorenal syndrome 10 .Duplex ultrasonography is a widely used non-invasive method to assess vascular patency and blood flow in many sites. Duplex Doppler can be used to assess vascular resistance in the small intraparenchymal vessels through simple analysis of Doppler waveform by a parameter termed the resistive index (RI) 11 .…”

Section: Resultsmentioning

confidence: 99%

Study of Resistive Index in Various Stages of Liver Cirrhosis and Its Significance in Calculating the Risk for Hepatorenal Syndrome

Sikarwar¹,

Muchhoria²,

Singh³

et al. 2014

jemds

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To evaluate resistive index in various stages of liver cirrhosis and to determine its significance in developing hepatorenal syndrome. METHODS: Study included 60 cirrhotic patients divided into 4 groups (15 patients each): compensated liver cirrhosis (group A), diuretic responsive ascites (group B), refractory ascites (group C), hepatorenal syndrome (group D) and ten healthy persons as control group (E). All patients subjected to detailed history taking and clinical examination. Laboratory investigations included simple urine analysis, complete blood picture, liver function tests, blood urea and serum creatinine, serum sodium and serum potassium, and protein concentration. Ultrasonographic examination and renal duplex Doppler were under taken to assess the Resistive index. RESULTS: The RI of interlobar and arcuate arteries were significantly higher in all patient groups than in control group (p <0.05), the RI was significantly higher in patients with refractory ascites than in patients with diuretic responsive ascites, and also in patient of diuretic responsible ascites than in patients with compensated cirrhosis (p < 0.05), in patient with hepatorenal syndrome than in patient with diuretic responsive ascites and patients with compensated cirrhosis (p<0.05). Also Creatinine levels & blood urea levels in patients with the hepatorenal syndrome was significantly higher than that of other different groups (p<0.05) but there was no significant change in creatinine levels between patients with compensated cirrhosis and control group. While creatinine levels in patient with diuretic responsive ascites was significantly higher than that in patient with compensated cirrhosis (p<0.05) there was no significant change between patient with diuretic responsive ascites and patient with refractory ascites. CONCLUSION: Resistive index increases with degree of hepatic decompensation. Renal duplex ultrasound is a noninvasive, simple and easy method to study intrarenal hemodynamics in patients with liver cirrhosis may predict patients at risk of hepatorenal impairment.

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“…2) [22, [73][74][75]. Bed-rest and restricted sodium intake (<40 mmol/day) may induce complete recov ery from ascites in 10-20% of patients [76], depending on good compliance, whether pre vious episodes of ascites have occurred, the severity of liver dysfunction and the function al state of the kidney [77,78]. For patients who do not respond to bed-rest and a lowsodium diet, an aldosterone antagonist should be added due to the increased plasma aldoste rone concentration and higher sensitivity of the renal tubules to aldosterone [79,80], Even though the aldosterone antagonists are less [73].…”

Section: Tailored Therapymentioning

confidence: 99%

Pathogenesis and Treatment of Ascites in Hepatic Cirrhosis

Geñtilini

Villa²,

Romanelli³

et al. 1994

Cardiology

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In cirrhosis of the liver structural distortion of the sinusoidal vessels is the major factor responsible for the increase in portal venous pressure and the development of abdominal ascites. The mechanisms by which advanced cirrhosis of the liver leads to widespread changes in the systemic circulation including vasodilatation, increased cardiac output and expanded plasma volume, together with activation of a range of antina-triuretic and natriuretic factors, are unclear. Several hypotheses have been proposed to explain these pathophysiological consequences, including underfilling of the systemic arterial system, overflow and peripheral vasodilatation, with a decrease in effective arterial blood volume. The evidence for and against these hypotheses is critically examined. In patients with hepatic cirrhosis complicated by ascites, increased intra-renal release of vasodilating prostaglandins may assist in sustaining renal blood flow and glomerular filtration rate by counteracting the vasoconstrictor effects of noradrenaline and angiotensin II. In advanced stages of the syndrome, cirrhotic ascites may become refractory to medical treatment. In this situation renal function becomes progressively impaired and eventually acute renal failure, so-called hepatorenal syndrome, supervenes due to intense renal vasoconstriction and opening of intrarenal arteriovenous shunts. The progressive renal vasoconstriction may also be accentuated by the reduced synthesis of renal vasodilating prostaglandins. The medical treatment of ascites is based on bed-rest, a low-sodium diet and administration of aldosterone antagonists and loop diuretics. Patients who are refractory to such therapy may be further treated by paracentesis or by the LeVeen shunt, though the long-term results of these physical therapies are unsatisfactory.

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Renal Functional Impairment and Sodium Retention in Liver Cirrhosis

Cited by 22 publications

References 21 publications

Doppler ultrasonographic evaluation of the early changes in renal resistive index in cirrhotic patients undergoing liver transplantation.

Doppler ultrasonographic evaluation of the early changes in renal resistive index in cirrhotic patients undergoing liver transplantation.

Study of Resistive Index in Various Stages of Liver Cirrhosis and Its Significance in Calculating the Risk for Hepatorenal Syndrome

Pathogenesis and Treatment of Ascites in Hepatic Cirrhosis

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