Faculty Opinions recommendation of Comparison of the novel hydroxyethylstarch 130/0.4 and hydroxyethylstarch 200/0.6 in brain-dead donor resuscitation on renal function after transplantation.

2008 ◽  
Author(s):  
Michael James
Keyword(s):  
Renal Function ◽  
The Novel ◽  
Brain Dead ◽  
Brain Dead Donor

scholarly journals Comparison of the novel hydroxyethylstarch 130/0.4 and hydroxyethylstarch 200/0.6 in brain-dead donor resuscitation on renal function after transplantation

2008 ◽  
Vol 100 (4) ◽  
pp. 504-508 ◽  
Author(s):  
V. Blasco ◽  
M. Leone ◽  
F. Antonini ◽  
A. Geissler ◽  
J. Albanèse ◽  
...  
Keyword(s):  
Renal Function ◽  
The Novel ◽  
Brain Dead ◽  
Brain Dead Donor

scholarly journals Vagal stimulation in brain dead donor rats decreases chronic allograft nephropathy in recipients

2013 ◽  
Vol 29 (3) ◽  
pp. 544-549 ◽  
Author(s):  
S. Hoeger ◽  
J. Fontana ◽  
J. Jarczyk ◽  
J. Selhorst ◽  
R. Waldherr ◽  
...  
Keyword(s):  
Vagal Stimulation ◽  
Chronic Allograft Nephropathy ◽  
Brain Dead ◽  
Brain Dead Donor

Significant reduction of proinflammatory cytokines by treatment of the brain-dead donor

2005 ◽  
Vol 37 (1) ◽  
pp. 387-388 ◽  
Author(s):  
O. Kuecuek ◽  
L. Mantouvalou ◽  
R. Klemz ◽  
K. Kotsch ◽  
H.D. Volk ◽  
...  
Keyword(s):  
Proinflammatory Cytokines ◽  
Brain Dead ◽  
The Brain ◽  
Brain Dead Donor

Administration of desmopressin in brain-dead donors and renal function in kidney recipients

The Lancet ◽  
1998 ◽  
Vol 352 (9135) ◽  
pp. 1178-1181 ◽  
Author(s):  
Richard Guesde ◽  
Benoît Barrou ◽  
Isabelle Leblanc ◽  
Saïda Ourahma ◽  
Jean-Pierre Goarin ◽  
...  
Keyword(s):  
Renal Function ◽  
Kidney Recipients ◽  
Brain Dead

COLD PRESERVATION INDUCES A STRONG ADDITIONAL DAMAGE IN GRAFTS FROM BRAIN-DEAD DONOR RATS

2008 ◽  
Vol 86 (Supplement) ◽  
pp. 377
Author(s):  
B Yard ◽  
S Hoeger ◽  
K Petrov ◽  
A Reisenbuechler ◽  
R Waldherr ◽  
...  
Keyword(s):  
Cold Preservation ◽  
Brain Dead ◽  
Brain Dead Donor

Increased Potency and Decreased Elimination of Lamifiban, a GPIIb-IIIa Antagonist, in Patients with Severe Renal Dysfunction

1998 ◽  
Vol 79 (06) ◽  
pp. 1119-1125 ◽  
Author(s):  
Knut Nordal ◽  
Karsten Midtvedt ◽  
Timothy Goggin ◽  
Frank Brosstad ◽  
Gustav Lehne
Keyword(s):  
Renal Function ◽  
Renal Impairment ◽  
Ex Vivo ◽  
Severe Renal Impairment ◽  
Thrombus Formation ◽  
Drug Dosage ◽  
The Novel ◽  
Platelet Membrane Receptor ◽  
Group 3 ◽  
Group 2

SummaryActivation of the platelet membrane receptor glycoprotein (GP) IIb-IIIa is essential for thrombus formation. The novel nonpeptide GPIIb-IIIa antagonist, lamifiban, represents a promising approach for antiplatelet therapy in patients with cardiovascular disease. Since renal impairment frequently occurs in these patients, we designed a phase I study to assess the tolerability, pharmacodynamics and pharmacokinetics of lamifiban in patients with renal impairment. Four healthy volunteers (Group 1) with creatinine clearance (CLCR) >75 ml/min, eight patients (Group 2) with mild to moderately impaired renal function (CLCR 30-74 ml/min) and eight patients (Group 3) with severe renal impairment (CLCR 10-29 ml/min) were studied. They received stepwise increased doses of lamifiban intravenously (IV). There was a linear relationship between the systemic clearance of the drug and renal function (R2 = 0.86). The mean plasma concentration required for half-maximal inhibition of thrombin-receptor agonist peptide (TRAP) induced platelet aggregation (EC50) ex vivo was 21, 28 and 11 ng/ml in Groups 1, 2 and 3. The patients in Group 3 were sensitized to the anti-platelet effect allowing an 18-fold dosage reduction without compromising the pharmacodynamics. In conclusion, the decreased clearance of lamifiban may act in concert with increased potency of the drug in patients with severe renal impairment, and the drug dosage should be reduced accordingly.

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