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Tubular dysfunction in cirrhotic patients with HEPA torenal syndrome
TuRuIAR DYsPuNcTIow I" CIaRHoTICPATIENTS"ITS HEPA ToRESAI.5INDiwHL!
K.L.nt.W.Druml,G.Grinm,A.W.Lsqqner,Chr.Wadl. B.SchneeweiB Intens.Care Unit, I.Ked.Clinic Univ.Vienna, Austria Progressive impairmentin renal sodiumand water excretion frequentlydevelopsin patientswith advanced hepatic disease. It is associated with renal hypoperPxion, which resultsfrom functional renal vasoconstriction combinedwith systemicvasodilation Although mxphologicalabnormalities of the kidney .I. absent. deterioration in renal blood flow (RBr) might lead to renalmedullary hypopsrfusionwith tubular insufficiency.Therefor2BF and sodium .xcr.tion (NAexcr) were measuredin B normovolemic (cVP>S .mnHg,PCWP>l2smHg) patientswith deccmpensated cirrhosis and sewre impairment in renal (inulincl.S-35 ml/min)and the correlation function betweenRBF and electrolyteexcretionY.S studied. Results: Naexcr.0.66*0.16 mval/h,RSF 2X+55 ml/min Nsconc.15~3mvai,l(u&e), HZ0 Cl. -15.5+3.3ml/h FENao.49:0.12\.There were significantcorrelations p=O.Oll), and between betweenRBF and FENa (r=-0.83, RBF and urine Naconc.(p=-0.73, p-=0.03) indicatingan increase in sodiumexcretionwith decreasing RBF. Conclusion: In decompensated cirrhosis progressive impainwnt in renal blood flow is associated with deteriorationof tubularfunctionwith increasing loweredurine sodiumconcentration and FENa, indicating an intermediate syndromebetweenprerenal failure and acute hypoxictubularnecrosis.
mmpard withthe stu&nl i IW - 2) fof thi group 1 morphom&ic ~a”md”s war. condaM wilh 16 did& vwbbbs. 1, bbbaii
PaoTEcTIVE EFFECT OP HEPATIC FAClORSAGAINST CIRRHOTICALmTION
5UCCESSFUL. TREA’IMENT OF PRIMARY BILIARYCIRRHOSIS Will-lCICLOSPORINS
T.S. Lie. T. Kriiger. J. Vogel, G. Brunner. M. Bach %ctlon of TranSplantatIon. Departmentof Surgery, Institutof Pathology,Universityof Bonn. FRG
T.S. Lie, G. BrunnerSection of Transplantation. Departlnent, University of Bonn, FRG In 35-, 52-, 53- and 62-years-old patientswe diagnosed prinaxy biliary cirrhosis @X1, based on elevated levels of GGT, alkaline phosphatase, inaunonlobulin- and MA-titers. The+ were treated with l& doses of Ciclosporina (CiS)-and 4 mg/d Methylorednisolone. We ordered the dosaae of CiS not &cording to ita blood levels b&t-& the alteration of serum transaminase levels. In our experience Z-2.5 mg/kg/d CiS are optimal as initial dosage&cause of its hepatotoxicity. high doses cause severe elevation of liver enzylses and bilirubin levels in the patient’s se-. We observed in all oatients nut only impmveaent of enzymelevels and sjmtbetic liver functions, but also of general conditions. AMA-titers and lsnmoglobulin levels are strongly decreased. Swnarizad. we would like to say: the treatment of Pw: with low doses of CiS and Methylprednisolona is tbe most effective and ComPlicationless procedure. This therapy. could be applied successfully in the progressed stage of the disease.
Cirrhosis is a maior cmolication of chronic heoatic disease. As I& previbusly reported, the rhsates of cell &rana damaaadrat liver (LF7eshowad a strong inhibitory ability on fibmblaat proliferation in vitro. Such hepatic factors we found in aera of animaIa with acute damagedlivers, but not in sera of animals with chronic hepatitis or cirrhosis. We assuwd, therefore, that deficiency of such hepatic factors results in cirrhotic alteration of chronically damagedlivers. To clarify this hypothesis, we have treated rats 6 waaks with hepatotoxin (Cc141 induced cbmnic liver dauage. with LP to protect cirrhotic alteration. We found in the control group 63% fibrosis with cirrhosis, however. only 26% in LP treated animaIs. Miniual fibrosis was found in 501 of Lp treated rats in contrast to 14\ in the control group. Furthanwxc the LP treated animals presented a very lowar dagrea of fatty degeneration than the control groups. Our results indicate stq anticirrhotic effectof LP. Sunerizad we would rntion that application of such liver factors could protect cirrhotic alteration in the patient with chronic hepatitis.
s97
K.L.nt.W.Druml,G.Grinm,A.W.Lsqqner,Chr.Wadl. B.SchneeweiB Intens.Care Unit, I.Ked.Clinic Univ.Vienna, Austria Progressive impairmentin renal sodiumand water excretion frequentlydevelopsin patientswith advanced hepatic disease. It is associated with renal hypoperPxion, which resultsfrom functional renal vasoconstriction combinedwith systemicvasodilation Although mxphologicalabnormalities of the kidney .I. absent. deterioration in renal blood flow (RBr) might lead to renalmedullary hypopsrfusionwith tubular insufficiency.Therefor2BF and sodium .xcr.tion (NAexcr) were measuredin B normovolemic (cVP>S .mnHg,PCWP>l2smHg) patientswith deccmpensated cirrhosis and sewre impairment in renal (inulincl.S-35 ml/min)and the correlation function betweenRBF and electrolyteexcretionY.S studied. Results: Naexcr.0.66*0.16 mval/h,RSF 2X+55 ml/min Nsconc.15~3mvai,l(u&e), HZ0 Cl. -15.5+3.3ml/h FENao.49:0.12\.There were significantcorrelations p=O.Oll), and between betweenRBF and FENa (r=-0.83, RBF and urine Naconc.(p=-0.73, p-=0.03) indicatingan increase in sodiumexcretionwith decreasing RBF. Conclusion: In decompensated cirrhosis progressive impainwnt in renal blood flow is associated with deteriorationof tubularfunctionwith increasing loweredurine sodiumconcentration and FENa, indicating an intermediate syndromebetweenprerenal failure and acute hypoxictubularnecrosis.
mmpard withthe stu&nl i IW - 2) fof thi group 1 morphom&ic ~a”md”s war. condaM wilh 16 did& vwbbbs. 1, bbbaii
PaoTEcTIVE EFFECT OP HEPATIC FAClORSAGAINST CIRRHOTICALmTION
5UCCESSFUL. TREA’IMENT OF PRIMARY BILIARYCIRRHOSIS Will-lCICLOSPORINS
T.S. Lie. T. Kriiger. J. Vogel, G. Brunner. M. Bach %ctlon of TranSplantatIon. Departmentof Surgery, Institutof Pathology,Universityof Bonn. FRG
T.S. Lie, G. BrunnerSection of Transplantation. Departlnent, University of Bonn, FRG In 35-, 52-, 53- and 62-years-old patientswe diagnosed prinaxy biliary cirrhosis @X1, based on elevated levels of GGT, alkaline phosphatase, inaunonlobulin- and MA-titers. The+ were treated with l& doses of Ciclosporina (CiS)-and 4 mg/d Methylorednisolone. We ordered the dosaae of CiS not &cording to ita blood levels b&t-& the alteration of serum transaminase levels. In our experience Z-2.5 mg/kg/d CiS are optimal as initial dosage&cause of its hepatotoxicity. high doses cause severe elevation of liver enzylses and bilirubin levels in the patient’s se-. We observed in all oatients nut only impmveaent of enzymelevels and sjmtbetic liver functions, but also of general conditions. AMA-titers and lsnmoglobulin levels are strongly decreased. Swnarizad. we would like to say: the treatment of Pw: with low doses of CiS and Methylprednisolona is tbe most effective and ComPlicationless procedure. This therapy. could be applied successfully in the progressed stage of the disease.
Cirrhosis is a maior cmolication of chronic heoatic disease. As I& previbusly reported, the rhsates of cell &rana damaaadrat liver (LF7eshowad a strong inhibitory ability on fibmblaat proliferation in vitro. Such hepatic factors we found in aera of animaIa with acute damagedlivers, but not in sera of animals with chronic hepatitis or cirrhosis. We assuwd, therefore, that deficiency of such hepatic factors results in cirrhotic alteration of chronically damagedlivers. To clarify this hypothesis, we have treated rats 6 waaks with hepatotoxin (Cc141 induced cbmnic liver dauage. with LP to protect cirrhotic alteration. We found in the control group 63% fibrosis with cirrhosis, however. only 26% in LP treated animaIs. Miniual fibrosis was found in 501 of Lp treated rats in contrast to 14\ in the control group. Furthanwxc the LP treated animals presented a very lowar dagrea of fatty degeneration than the control groups. Our results indicate stq anticirrhotic effectof LP. Sunerizad we would rntion that application of such liver factors could protect cirrhotic alteration in the patient with chronic hepatitis.
s97