B. Di Paolo

Protective Effect of Calcium-Channel Blockers on the Cyclosporins (CyA)-Related Nephrotoxicity

Cyclosporine (CyA) represents an entirely different class of immunosuppressive agents (1). Acute and chronic nephrotoxicity directly attributable to CyA has tempered the initial enthusiasm surrounding this drug (1). At present the pathogenesis of CyA nephrotoxicity has not been fully elucidated but so far it has been suggested that can be divided chronologically into three broad components: 1) a functional toxicity, due mainly to afferent renal arteriolar vasocontriction (2); 2) a reversible tubulo-toxicity manifested by giant mitochondria and tubular vacuolization and dilatation (3); 3) an obliterative and irreversible arteriolopathy, eventually leading to interstitial fibrosis and nephron loss. Recently a number of reports have suggested that renal allograft recipients receiving CyA and Calcium-channel antagonists have better graft function, a lower incidence of delayed graft function and fewer rejection episodes than those receiving CyA alone (4). The use of calcium-channel antagonists as nifedipine (NIF) in combination with CyA therapy in renal transplant recipients is attractive, as hypertension is common, and because they may potentiate the inhibition of lymphocyte proliferation induced by CyA, the effects of NIF on overall glomerular and tubular functions has not been investigated in patients with stable graft function. Aim of our paper is to assess the effects of NIF on glomerular and tubular function and CyA levels in patients with stable allograft function at least six months after transplantation.

Serum Branch-Chain Amino and Keto Acids in the Nutritional and Immunological Assessment of Uremics on Conservative and Dialysis Treatment

Defective cell-mediated immunity (CMI) is well documented in patients with chronic renal failure (CRF) due to many factors (1). The aim of our study was to examine the effects of CRF on serum branch-chain amino and keto acids (BCAA-BCKA), visceral proteins and CMI.