Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In liver cirrhosis, renin-angiotensin system (RAS) activation sustains renal sodium retention and hepatic fibrogenesis. New information has recently enlivened the traditional concept of RAS. For instance, renin and prorenin bind their ubiquitous receptors, resulting in the local production of angiotensin (Ang) II; increased serum calcium and calcimimetic agents, through stimulation of extracellular calcium-sensing receptors (CaSR), blunt renin production and lead to natriuretic effects in human and experimental cirrhosis. Alongside systemic production, there is Ang II tissue production within various organs through RAS enzymes different from angiotensin-converting enzyme (ACE), that is chymase, tissue plasminogen activator and several cathepsins. In experimental cirrhosis, inhibition of chymase leads to natriuretic and hepatic antifibrotic effects, without changes in systemic haemodynamics. In the kidney, local RAS coordinates proximal and distal tubular sodium reabsorption. However, renalase, whose plasma and tissue levels are severely altered in experimental cirrhosis, degrades systemic and renal tubule catecholamines, antagonizing the effects of renal RAS. Angiotensinogen-derived natriuretic and vasodilating peptides (Ang1-9, Ang1-7, Ang3-8) and their receptors have been described. Receptor agonists or antagonists are available to affect portal hypertension and sodium retention in cirrhosis. ACE2-dependent generation of Ang1-7 may inhibit experimental liver fibrosis. inhibition of Ang1-7 clearance by means of neprilysin blockade has portal hypotensive and natriuretic effects. Ang1-12, whose production renin does not regulate, is converted to several different angiotensin peptides via chymase. Finally, Ang II behaves as either an antinatriuretic or a natriuretic agent, based on the tissue content of AT1 R and AT2 R receptors, their ratio being prone to pharmacological modulation.
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PMID:Pathways of hepatic and renal damage through non-classical activation of the renin-angiotensin system in chronic liver disease. 3158 May 14

Urinary biomarkers such as neutrophil gelatinase-associated lipocalin (NGAL) and renalase were recently studied for their potential role in the early detection of acute kidney injury (AKI) in patients with cirrhosis. Our study was conducted on 50 patients with end-stage liver disease undergoing living donor liver transplantation. The patients were divided into two groups: Group I contained 23 patients with AKI who had undergone liver transplantation and Group II included 27 non-AKI patients who had undergone liver transplantation. Serum renalase and NGAL levels were measured by ELISA; renalase was measured on day 1, day 7, and three months after liver transplantation. NGAL was measured on day 1 postliver transplantation. There was an improvement in liver function, kidney functions, hemoglobin level, platelet count, and C- reactive protein levels in patients at three months posttransplantation when compared to day 1, day 3, and day 7 (P < 0.01). Comparison of the renalase level at day 1, day 7, and three months showed that there was a highly significant decline at three months in the AKI group compared to the non-AKI group (P < 0.01). Regarding the NGAL level at day 1, there was no significant difference between the AKI and non-AKI groups (P > 0.05). The receiver operating characteristic curve for the renalase biomarker showed a borderline significant change between the AKI and non-AKI groups at day 1 [area under the curve (AUC): 0.54, P = 0.08], day 7 (AUC: 0.605, P = 0.08), and three months (AUC: 0.605, P = 0.08). However, the NGAL biomarker level was not significantly different between the AKI and non-AKI groups. Our study suggests that renalase showed a better predictive value and a higher accuracy in identifying postliver transplantation patients with AKI than NGAL.
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PMID:Novel biomarkers of acute kidney injury following living donor liver transplantation. 3239 8