In response to a high sodium (Na + ) intake, salt-sensitive in salt-resistant (؉55 ؎ 16.0 ml/min/1.73 m 2 ) and saltsensitive patients (؉22 ؎ 21.5 ml/min/1.73 m 2 ). patients with hypertension retain more Na + and manifest a greater rise in arterial pressure than salt-resistant This study has shown that salt-sensitive AfricanAmericans manifest different systemic and renal patients. Because there is limited information regarding the role of nitric oxide (NO) in salt-sensitivity we examhaemodynamic responses to L-arginine than salt-resistant patients and controls. The fall in mean blood pressined the effects of L-arginine (500 mg/kg, i.v. for 30 min) on mean arterial pressure and renal haemodynamics in ure following L-arginine was greater in salt-sensitive than in salt-resistant patients and controls, whereas the 21 hypertensive and five normotensive African-Americans. At the end of L-arginine infusion mean arterial increase in ERPF was reduced in salt-sensitive compared to salt-resistant and normal subjects. The data are pressure fell more in salt-sensitive (−11.5 ؎ 2.5) than in salt-resistant (؊3.7 ؎ 1.5 mm Hg) and control subjects in keeping with the notion that a defect in NO production may participate to the genesis of blood pressure sensi-(؊3.2 ؎ 3.8 mm Hg). At the end of L-arginine infusion effective renal plasma flow (ERPF) increased more tivity to salt. (P Ͻ 0.05) in controls (+108 ؎ 13.9 ml/min/1.73 m 2 ) than

A remission-inducing regimen of LD-CYC (cumulative dose 3 g) followed by AZA for SLE patients with proliferative LN achieves clinical results comparable to those obtained with HD-CYC without serious infection in both regimens.

Background and objectivesCisplatin is a nephrotoxic chemotherapeutic agent. So, preventive measures worth to be evaluated. Human amniotic fluid stem cells (hAFSCs) in prevention or amelioration of cisplatin-induced acute kidney injury (AKI) in Sprague-Dawley rates have been tested.Methods80 Sprague-Dawley rats (250~300 g) were used and divided into 4 major groups, 20 rats each. Group I: Saline-injected group. Group II: Cisplatin-injected group (5 mg/kg I.P). Group III: Cisplatin-injected and hAFSCs-treated group (5×106 hAFSCs I.V. one day after cisplatin administration). Group IV: Cisplatin-injected and culture media-treated group. Each major group was further divided into 4 equal subgroups according to the timing of sacrifice; 4, 7, 11 and 30 days post-cisplatin injection. Renal function tests were done. Kidney tissue homogenate oxidative stress parameters malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione (GSH) were determined. Histopathological scoring systems for active injury, regenerative and chronic changes were analyzed separately.ResultshAFSCs characterization and differentiation was proved. Cisplatin injection resulted in a significant increase in serum creatinine and MDA and decrease in SOD, GSH and creatinine clearance. These changes were attenuated early by day 4 with the use of hAFSCs. Cisplatin injection induced tubular necrosis, atrophy, inflammatory cells infiltration and fibrosis. The use of hAFSCs was associated with significantly lowered injury score at day 4, 7, 11 and 30 with marked regenerative changes starting from day 4.ConclusionhAFSCs have both a protective and regenerative activities largely through an antioxidant activity. This activity cut short the acuteness of cisplatin nephrotoxicity.

Aim: L-carnitine is a short organic hydrosoluble molecule and is present in biological materials

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