Mycophenolic acid inhibits the phosphorylation of NF-kappaB and JNKs and causes a decrease in IL-8 release in H2O2-treated human renal proximal tubular cells.

Ischaemia-reperfusion injury is a common occurrence in renal transplantation and may affect the long-term survival of the allograft. Oxidative stress may play a crucial role in this, with reactive oxygen species formed during reperfusion causing direct cellular damage as well as activating pro-inflammatory pathways. A human proximal tubule cell line (HK-2) was subjected to hydrogen peroxide (H(2)O(2)) stress that resulted in phosphorylation of c-jun N-terminal kinases (JNKs) and the transcription factor NF-kappaB at Ser276, both of which have been associated with inflammation.

Effects of mycophenolate mofetil on acute ischaemia-reperfusion injury in rats and its consequences in the long term.

Background: Renal ischaemia-reperfusion injury (IRI) acutely decreases glomerular filtration rate (GFR) and impairs kidney function in the long term. Pre-treatment with chaetomellic acid (KM), an inhibitor of membrane-bound Ha-Ras, has demonstrated beneficial effects on acute renal ischaemia.

Methods: We tested whether mycophenolate mofetil (MMF, 20 mg/day for 4 days before IRI), an immunosuppressor with anti-inflammatory properties, improved renal outcome in uninephrectomized rats after IRI (45 min of renal ischaemia), alone or in combination with KM.

Inhibition of Ras/ERK1/2 signaling protects against postischemic renal injury.

The small GTPase p21 Ras and its downstream effectors play a central role in the control of cell survival and apoptosis. We studied the effects of Ras/ERK1/2 signaling inhibition on oxidative damage in cultured renal and endothelial cells and on renal ischemia-reperfusion injury in the rat. Primary human renal tubular and human endothelial ECV304 cells underwent significant cell death when subjected to oxidative stress.

Atorvastatin improves the course of ischemic acute renal failure in aging rats.

Statins increase the production of nitric oxide (NO) and have beneficial effects on the course of acute renal failure (ARF) in young rats. The effects of a short-term treatment with atorvastatin (ATO) on ischemic ARF in old rats, characterized by a great susceptibility to ischemia, was tested. No difference was found in renal dynamics between young (Y, 3 mo old) and old (O, 18 mo old) rats in normal conditions (CON) or after ATO treatment (12 mg/kg/d for 14 d).

Arginase inhibition slows the progression of renal failure in rats with renal ablation.

Exogenous arginine slows the progression of chronic renal failure (CRF) in remnant rats through a nitric oxide (NO)-dependent mechanism. We tested whether the inhibition of arginase could induce similar results through the increased availability of endogenous arginine. Three groups of remnant rats were studied for 8 wk: 1) untreated rats (REM); 2) remnant rats treated with 1% l-arginine (ARG); and 3) remnant rats administered a Mn(2+)-free diet to inhibit arginase (MNF).

Effect of dialysate sodium concentration on interdialytic increase of potassium.

To evaluate the role of plasma tonicity in the postdialysis increment of plasma potassium (p[K(+)]), the outcome of two hemodiafiltration treatments that differed only in the Na(+) level in dialysate (Na(D))-143 mmol/L (high dialysate sodium concentration [H-Na(D)]) and 138 mmol/L (low dialysate sodium concentration [L-Na(D)])-were compared in the same group of uremic patients from the end of treatment (T0) to the subsequent 30 to 120 min and up to 68 h. Kt/V and intradialytic K(+) removal were comparable. At T0, plasma [Na(+)] was 145+/-1 and 137+/-1 mmol/L after H-Na(D) and L-Na(D), respectively (P<0.