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P Candi

Publications and source records attributed to P Candi.

3 recordsLinked to original sources

Hemodialysis leukopenia and complement function with different dialyzers.

The relationship between leukopenia and the complement system during hemodialysis was re-examined by studying not only the in vivo effects of four different dialyzer membranes (cellulose hydrate, cuprophan, cellulose acetate, and polyacrilonitrile) on leukocyte counts and complement levels, but especially by investigating the effects of these membranes on complement function in vitro. Whereas from in vivo studies no definite conclusions could be drawn, in vitro investigations provided clear-cut information. When more sophisticated technical approaches were undertaken, it became evident that hemodialysis leukopenia has to be thought of in terms of chemotactic factor generation. In fact, a strict correlation was demonstrated between the degree of leukopenia induced by the dialyzers tested and the ability of the relative membrane to generate chemotactic activity in vitro. Moreover, the previously observed ability of polyacrilonitrile membrane to induce a decrement in complement function was due to the ability of polyacrilonitrile to adsorb complement activity and did not correspond to effective complement consumption. This finding explained why polyacrilonitrile dialysis is not accompanied by a decrease in circulating granulocytes. Taken together, our data strongly point to a pivotal role of complement system in the pathogenesis of hemodialysis leukopenia.

Acrylic Resins

Cell mediated immunity in idiopathic glomerulonephritis.

Various recent reports have suggested the presence of a functional defect of lymphocyte subpopulations in minimal-change nephropathy during the active phase. A probable role of inhibitory humoral factor(s) has been hypothesized. However, other authors have been unable to detect a significant difference between plasma from patients with nephrotic syndrome due to minimal-change nephropathy and plasma from other glomerulonephritis in the degree of inhibition of mitogen-induced lymphocyte transformation. In our study, T cell function, as measured by the response to PHA in autologous plasma, was depressed only in patients with minimal-change nephrotic syndrome and in patients with membranoproliferative glomerulonephritis. The lymphocyte function returned to normal when lymphocytes were cultured in homologous plasma. The lymphocyte responsiveness of patients with other glomerulonephritis with or without nephrotic syndrome was normal in both autologous and homologous plasma. Moreover, only plasma from patients with minimal-change nephropathy in the active phase and with membranoproliferative glomerulonephritis were able to induce inhibition of mitogenesis of lymphocytes from healthy donors. These data seem to confirm the presence of specific humoral inhibitory factor(s) in the plasma of these patients. Finally, preliminary findings seem to demonstrate an increase of the number of TG cells in patients with minimal-change nephropathy in remission who relapse early in the subsequent follow-up.

Adult