Renal clearance of endogenous hippurate correlates with expression levels of renal organic anion transporters in uremic rats.

Hippurate (HA) is a harmful uremic toxin that accumulates during chronic renal failure, and failure of the excretion system for uremic toxins is thought to be responsible. Recently, we reported that rat organic anion transporter 1 (rOat1) is the primary mediator of HA uptake in the kidney, and so now we have studied the pharmacokinetics and tissue distribution of HA after a single i.v.

Lopinavir protein binding in vivo through the 12-hour dosing interval.

Most protease inhibitors available for the treatment of human immunodeficiency virus (HIV) infection are highly bound to plasma proteins, mainly alpha-1 acid glycoprotein. Therapeutic drug monitoring (TDM) of total protease inhibitor (PI) concentrations has been increasing in the past few years; however, the pharmacological activity of the PIs is dependent on unbound drug entering cells harboring HIV. There is little information available on unbound drug concentrations of these drugs in vivo.

Renal disposition of a furan dicarboxylic acid and other uremic toxins in the rat.

The aim of this study was to understand the mechanisms that underlie the renal elimination of albumin-bound uremic toxins, particularly the highly bound furan acid 3-carboxy-4-methyl-5-propyl-2-furanpropanoic acid (CMPF), that accumulate in chronic renal failure. These toxins inhibit the binding of acidic drugs and have various other untoward effects. The pharmacokinetics and tissue distribution of CMPF plus three other such toxins, indoxyl sulfate, indole acetic acid, and hippuric acid, have been examined in the anesthetized rat.

Albumin, bilirubin, and activated carbon: new edges of an old triangle.

The problem of interaction of human serum albumin (HSA), unconjugated bilirubin (UB) and high porosity activated HSGD carbons is investigated in this study. The decrease of UB to HSA molecular ratio by more than 300 times was demonstrated while the batch experiments in HSA-UB admixtures after contact with HSGD. HSGD carbons express extremely high activity for the removal of UB from HSA containing solutions (more than 100 mg of UB per 1 g of activated carbon).