Protein Binding of Diphenylhydantoin and Desmethylimipramine in Plasma from Patients with Poor Renal Function

Plasma protein binding of valproic acid in healthy subjects and in patients with renal disease.

“…Significant difference in albumin and total protein concentrations were not seen between the groups of this study, so that definite conclusions on the effect of a reduced albumin or total protein concentration on the binding of VPA cannot be drawn, although the dilution experiment suggested such relationship. A similar correlation between binding of phenytoin and both, serum creatinine and serum blood urea nitrogen, has been described by Reidenberg and associates (1971) and Hooper et al, (1974), but a correlation between binding and albumin concentration could only be established in one of the studies (Reidenberg et al, 1971). Our findings show that the binding of VPA is altered in renal insufficiency eiven with normal total plasma protein or plasma albumin concentration.…”

“…Hypoalbuminemia may be found in newborns (Rane, Lunde, Jailing, Yaffe & Sjoqvist, 1971), in renal failure (Reidenberg et al, 1971;Odar-Cederlof & Borg&, 1974), in chronic hepatic disease (Affrime & Reidenberg, 1975;Olsen, Bennet & Porter, 1975), but in particular in the nephrotic syndrome , Gugler & Azarnoff, 1976 The reduction of VPA protein binding in renal impairment appeared to be correlated with serum creatinine, creatinine clearance, blood urea nitrogen and uric acid. Significant difference in albumin and total protein concentrations were not seen between the groups of this study, so that definite conclusions on the effect of a reduced albumin or total protein concentration on the binding of VPA cannot be drawn, although the dilution experiment suggested such relationship.…”

Plasma protein binding of azapropazone in patients with kidney and liver disease.

“…warfarin site) of human serum albumin (Fehske etal., 1980 Bilirubin (mg 100ml 1) Figure 5 Free fraction values of azapropazone (0) and phenprocoumon (0) (Ghonheim & Pandya, 1975) and sulfadiazine (Boobis, 1977) while for several other drugs such correlation was apparent (Reidenberg et al, 1971;Campion, 1973;Dromgoole, 1974;O'Malley, Velasco, Pruitt & McNay, 1975;Bachmann et al, 1976;Gugler & Mueller, 1978). Several authors have suggested that the decrease in the plasma protein binding of acidic drugs in kidney disease is due to the accumulation of endogenous binding inhibitors (Craig, Evenson, Sarver & Wagnild, 1976;Sjoholm et al, 1976;OdarCederlof, 1977) which can be removed by charcoal treatment of plasma or might disappear following renal transplanation (Levy, Baliah & Procknal, 1976;Odar-Cederlof, 1977 (Fehske et al, 1980) which could explain the observed quantitative differences in the effect of disease on the binding of both drugs.…”

“…Although there is general agreement that it is primarily the protein binding of acidic drugs which decreases in kidney disease (Reidenberg, OdarCederlof, von Bahr, Borga & Sjoqvist, 1971;Andreasen, 1973;Reidenberg & Affrime, 1973) the quantitative changes in the protein binding of a particular drug of interest cannot be predicted (Yacobi & Levy, 1977). The situation seems to be even more complicated in patients with liver disease (Affrime & Reidenberg, 1975;Klotz, 1976;PerezMateo & Erill, 1977;Blaschke, 1977;Tillement et al, 1978 (Schmidt & Jahnchen, 1979).…”

Plasma protein binding of furosemide in kidney transplant patients

“…It has also been established that renal impairment may alter drug binding to plasma proteins (1)(2)(3)(4)(5), particularly with respect to acidic drugs (3) include hypoalbuminemia (2), the presence of irreversible and competitive inhibitors in the plasma (3,5), and altered albumin composition (1).…”