Glomerular hyperfiltration in patients with well-compensated alcoholic cirrhosis

Wong, Florence; Massie, Denise; Colman, John; Dudley, F. J.

doi:10.1016/0016-5085(93)91026-e

Cited by 49 publications

(37 citation statements)

References 23 publications

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“…It has been shown that chronic aldosterone-receptor blockade prevents sodium retention in rats with cirrhosis induced by CCl 4 22 or common bile duct ligation. 8 However, the present study, as well as studies by others [4][5][6][7][8]23,24 shows that plasma levels of aldosterone are normal during early sodium retention in cirrhosis. This argues against hyperaldosteronism and increased collecting-duct sodium reabsorption as a major factor in early sodium retention.…”

Section: Renal Function During Early Sodium Retention In Cirrhosissupporting

confidence: 40%

Increased natriuretic efficiency of furosemide in rats with carbon tetrachloride-induced cirrhosis

et al. 2000

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The authors examined the natriuretic efficiency of furosemide in rats with cirrhosis induced by carbon tetrachloride (CCl 4 ). Rats were treated for 17 weeks with intraperitoneal injections of CCl 4 in groundnut oil twice a week throughout the study. Control rats were treated with vehicle (groundnut oil). Studies in metabolic cages showed that sodium retention was present from week 14. Renal clearance experiments were performed in chronically, instrumented conscious rats at the end of week 14 and at the termination of the study (end week 16) when ascites and hyponatremia were present. After 14 weeks, cirrhotic rats had sodium retention along with increased renal plasma flow, normal GFR, normal renal lithium handling, and a significantly increased diuretic (؉41% vs. control) and natriuretic (؉56% vs. control) response to a test dose furosemide (7.5 mg/kg b.w., intravenously). The natriuretic efficiency of furosemide, i.e., the natriuresis expressed relative to the furosemide excretion rate (⌬U Na V/U FUR V) was increased by 51% versus control. After 17 weeks, ascites and hyponatremia had developed, and significant decreases in renal plasma flow (؊33%), GFR (؊30%), and fractional lithium excretion (؊44%) were observed. At this stage urinary recovery of furosemide was significantly decreased and the diuretic (؊27% vs. Control) and natriuretic (؊38% vs. control) responses to furosemide were significantly impaired. However, the increased natriuretic efficiency of furosemide was still present (؉34% vs. control). Together these results suggest that increased sodium reabsoprtion in the thick ascending limb of Henle's loop is involved in the renal sodium retention in cirrhosis in rats that eventually results in decompensation with the

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Section: Renal Function During Early Sodium Retention In Cirrhosissupporting

confidence: 40%

Increased natriuretic efficiency of furosemide in rats with carbon tetrachloride-induced cirrhosis

et al. 2000

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“…However, other investigators have reported higher average GFR values in cirrhotic well as the urinary excretion values are summarized in table 2. The cirrhotic patients showed higher NO 3 plasma patients [2,12,23]. The discrepancy could be due to different patient populations or a different study design.…”

Section: Metabolites Of Nitric Oxidementioning

confidence: 83%

Renal Function in Compensated Hepatic Cirrhosis: Effects of an Amino Acid Infusion and Relationship with Nitric Acid

Rodriquez¹,

Martín²,

Oterino³

et al. 1999

Dig Dis

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Aims: In order to assess the possible participation of nitric oxide (NO) in renal function during compensated hepatic cirrhosis, we studied renal function, the plasma and urinary levels of cGMP and the concentration of nitrates and nitrites, as markers of NO synthesis in blood and urine, in 10 patients with Child A hepatic cirrhosis as compared with 10 control subjects, both under basal conditions and during stimulation (amino acid-induced glomerular hyperfiltration). Methods: To study renal function, the glomerular filtration rate (GFR), effective renal plasma flow (ERPF), renal functional reserve (RFR), renal venous resistance (RVR) and the filtration fraction (FF) were measured. Renin and aldosterone levels were determined to assess the possible involvement of these compounds in the renin-angiotensin-aldosterone axis. Results: GFR and ERPF were significantly lower in the patients with cirrhosis than in the controls (mean GFR: 82±12.3 vs. 105±15 ml/min, p = 0.01; ERPF 452±86 vs. 543±56 ml/min, p = 0.002). The RFR value was similar in both groups. In the basal situation cGMP levels were higher in plasma and urine in patients with cirrhosis than in the controls (plasma cGMP in cirrhosis 8.4±2.4 vs. 4.2±3.5 pmol/ml; urine cGMP in cirrhosis 1.2±2.1 vs. 0.68±0.1 pmol/ml). The NO levels were also higher in plasma and urine in patients with cirrhosis vs. controls (plasma NO in cirrhosis 45.5±9.2 vs. 30.3±1.2 μmol/l; urinary NO in cirrhosis 6.2±1.3 vs. 3.1±2.3 μmol/ml). In both groups the amino acid perfusion increased GFR, ERPF, cGMP and NO levels in plasma and urine. In the patients with cirrhosis the RVR decreased significantly during perfusion and no noteworthy changes in FF were observed. The GFR values observed during amino acid perfusion were similar in patients with cirrhosis and portal hypertension to those observed in the controls (27.2±12 vs. 25.3±16%). However, the changes induced the ERPF were more marked in patients with cirrhosis (cirrhosis 35.3±15 vs. 22.2±13%, p = 0.02). Conclusions: The present findings point to certain alterations in renal function in patients with hepatic cirrhosis and portal hypertension without ascitis, a clear difference being visible between the ERPF and GFR following amino acid-induced stimulation. The significant elevation in cGMP and NO levels in plasma and urine implies a maintained vasodilatory action that may at least partly compensate the vasoconstrictor effects of angiotensin II.

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“…The significance of urinary LCN2 with respect to renal dysfunction has not yet been studied in liver cirrhosis. Although renal function is believed to be relatively well preserved in compensated cirrhosis (Wong et al 1993;Woitas et al 1997), further studies are warranted to elucidate the possible correlation between urine LCN2 and the glomerular filtration rate in patients with HCV-associated liver cirrhosis.…”

Section: Discussionmentioning

confidence: 99%

Increased Urinary Lipocalin-2 Reflects Matrix Metalloproteinase-9 Activity in Chronic Hepatitis C with Hepatic Fibrosis

Kim

Lee

Jeong

et al. 2010

Tohoku J. Exp. Med.

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Hepatic fibrosis is characterized by excessive accumulation of extracellular matrix. Matrix metalloproteinases (MMPs) play an important role in the remodeling of the extracellular matrix during hepatic fibrosis. Lipocalin-2 (LCN2) forms complexes with MMP-9 and can be detected in the urine of patients with several types of cancers. The objective of this study was to examine the relationship between urinary LCN2 levels and MMP-9 activity with respect to the stage of liver fibrosis in patients with chronic hepatitis C (CHC), and to assess the utility of urine LCN2 as a non-invasive marker of hepatic fibrosis. Fresh spot urine samples were prospectively collected from forty-two interferon-naive CHC patients who underwent liver biopsy. The stage of hepatic fibrosis was assessed according to the METAVIR fibrosis score; 18 patients had no or mild fibrosis (stages F0 and F1) and 24 patients showed significant fibrosis (stages F2-F4). Immunoblot analyses demonstrated co-migration of urine LCN2 and MMP-9. Gelatin zymography showed that urinary MMP-9/MMP-2 activity ratios were higher in patients with significant fibrosis (F2-F4) than in patients no or mild fibrosis (F0-F1). Urine LCN2 levels which were normalized to urine creatinine concentration (urine LCN2-to-creatinine ratio; ULCR) were higher in F2-F4 patients compared to F0-F1 patients. There was a positive correlation between ULCR and urine MMP-9/MMP-2 activity ratios (r = 0.735). ULCR and AST-to-platelet ratio index were independent predictors of significant fibrosis by multivariate analysis. The present study suggests that urinary LCN2 is a novel marker of hepatic fibrosis by reflecting urine MMP-9 activity in CHC.

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Glomerular hyperfiltration in patients with well-compensated alcoholic cirrhosis

Cited by 49 publications

References 23 publications

Increased natriuretic efficiency of furosemide in rats with carbon tetrachloride-induced cirrhosis

Increased natriuretic efficiency of furosemide in rats with carbon tetrachloride-induced cirrhosis

Renal Function in Compensated Hepatic Cirrhosis: Effects of an Amino Acid Infusion and Relationship with Nitric Acid

Increased Urinary Lipocalin-2 Reflects Matrix Metalloproteinase-9 Activity in Chronic Hepatitis C with Hepatic Fibrosis

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