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Neurological abnormalities specifically related to uremia constantly occur in patients with end-stage renal disease (ESRD), although they only become clinically well defined in severe acute renal failure (ARF) or late in the course of chronic renal failure (CRF) and sometimes in connection with metabolic acidosis and/or electrolyte disturbances secondary to renal disease (1–5).

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.

As long as the use of r-HuEPO and of high-efficiency techniques as HDF raised-up, a growing interest in the complications induced by uremia on various systems and organs and mainly on the Nervous Systems seems to appear. An intense look in the Central and Peripheral Nervous System is fluorished when the effects of SD and HDF with the r-HuEPO became available and the finest modifications of these treatments could be recorded electrophysiologically and re-checked in the same patient at suitable intervals, giving the nephrologist the possibility of tracing back from the neurological impairment to the degree of uremic intoxication ([1]). It is still too early to assess the impact of long-term HDF-r-HuEPO therapy as subjective indicators of well-being, as well as patients manifested increased energy, improved appetite, taste, cold tolerance, sleeping habits and so on. The paper’s aim is to describe the main effects of SD and of HDF that allow a separate control of removal for small and larger toxins from blood. Because of the efficiency of the dialyzer/hemodiafilter and the r-HuEPO treatment the dialysis can be handled in SD and in HDF in order to explore whether part of the uremic syndrome can be attributed to the effects of uremia and anemia on the various organs and on the Central and Peripheral Nervous System (CNS). Because the treatment with r-HuEPO reduces anemia, in turn improving brain and multiorgans functions, in our study we assessed the effects of SD, HDF and of r-HuEPO on CNS and organs activity.

Clinical and electrophysiological findings show that, in spite of conventional conservative and regular dialysis treatment, uremic neuropathy persists and progresses [1] until after kidney transplant normality has been reached. However, papers referring to this topic do not generally give details of the diet, which is vaguely referred as a low-protein diet. No conclusions can thus be drawn on the real role of such a treatment on the progression of uremic neuropathy.

Neurological abnormalities specifically related to uremia occur constantly in chronic renal failure (CRF), although they do not become clinically well defined until late in the course of the uremic syndrome. These abnormalities can affect the central (encephalopathy) or peripheral (polyneuropathy) nervous system or both.

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.