Imbalance between production and scavenging of hydroxyl radicals in patients maintained on hemodialysis.

Background: Reactive oxygen species are as being related to the pathophysiology of endstage renal disease (ESRD). We measured the plasma hydroxyl radical (.OH)-producing ability and .

More stable and reliable pharmacokinetics with preprandial administration of cyclosporine compared with postprandial administration in patients with refractory nephrotic syndrome.

Study Objective: To compare the absorption profile of cyclosporine after preprandial administration with that after postprandial administration, and to determine which administration time resulted in a more stable absorption profile and the timing of the drug concentration that was the most reliable marker for monitoring drug absorption.

Design: Prospective analysis.

Setting: University teaching hospital in Japan.

Urinary excretion of fatty acid-binding protein reflects stress overload on the proximal tubules.

Urinary excretion of human liver-type fatty acid-binding protein (hL-FABP), which is expressed in human proximal tubules and engaged in free fatty acid (FFA) metabolism, was reported to reflect the clinical prognosis of chronic kidney disease. Here we have investigated the pathophysiological significance of hL-FABP in a model of protein overload nephropathy. Because L-FABP is not expressed in the wild-type mice, we generated hL-FABP chromosomal gene transgenic (Tg) mice.

Aquaporin-1 is recruited to the plasma membrane by hyperosmotic stimuli via a protein kinase A-dependent pathway in rat peritoneal mesothelial cells.

Aquaporin-1 (AQP1) has been reported to play an important role in water permeability in peritoneal dialysis. To determine the mechanism involved in this process, we used cultured rat peritoneal mesothelial cells (RPMCs) to examine the glucose-induced translocation of AQP1 to the plasma membrane. Cultured RPMCs obtained from male Sprague-Dawley rats were incubated in a combination of Dulbecco modified Eagle medium (DMEM) and F12 medium at 37 degrees C for 15 minutes.

Hypertension accelerates diabetic nephropathy in Wistar fatty rats, a model of type 2 diabetes mellitus, via mitogen-activated protein kinase cascades and transforming growth factor-beta1.

Although it is known that diabetic nephropathy is accelerated by hypertension, the mechanisms involved in this process are not clear. In this study we aimed to clarify these mechanisms using male Wistar fatty rats (WFR) as a type 2 diabetic model and male Wistar lean rats (WLR) as a control. Each group was fed a normal or high sodium diet from the age of 6 to 14 weeks.