C3 glomerulonephritis is a clinicopathologic entity defined by the presence of isolated or dominant deposits of C3 on immunofluorescence. To explore the effect of immunosuppression on C3 glomerulonephritis, we studied a series of 60 patients in whom a complete registry of treatments was available over a median follow-up of 47 months. Twenty patients had not received immunosuppressive treatments. In the remaining 40 patients, 22 had been treated with corticosteroids plus mycophenolate mofetil while 18 were treated with other immunosuppressive regimens (corticosteroids alone or corticosteroids plus cyclophosphamide). The number of patients developing end-stage renal disease was significantly lower among treated compared with untreated patients (3 vs. 7 patients, respectively). No patient in the corticosteroids plus mycophenolate mofetil group doubled serum creatinine nor developed end-stage renal disease, as compared with 7 (significant) and 3 (not significant), respectively, in patients treated with other immunosuppressive regimens. Renal survival (100, 80, and 72% at 5 years) and the number of patients achieving clinical remission (86, 50, and 25%) were significantly higher in patients treated with corticosteroids plus mycophenolate mofetil as compared with patients treated with other immunosuppressive regimens and untreated patients, respectively. Thus, immunosuppressive treatments, particularly corticosteroids plus mycophenolate mofetil, can be beneficial in C3 glomerulonephritis.

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(PRL) secretion was investigated in 12 undialyzed patients with chronic renal failure (CRF), 30 hemodialyzed patients (HD), 19 renal transplant (RT) recipients and 17 controls. Basal PRL levels in CRF and HD patients were higher than in controls and RT subjects. Plasma PRL values were higher in CRF than in HD patients. In the HD group, plasma PRL concentrations were significantly higher in men with reduced sexual potency than in those in which it was normal. After TRH stimulation in CRF and HD the PRL response was considerably less and the time of peak delayed with respect to the controls. In RT subjects PRL did not return towards baseline after 120 min. After bromocriptine, plasma PRL suppression in CFR and HD patients was lower than in controls and RT subjects. These findings suggest that some factor which accumulates in uremia, is only partially removed by hemodialysis, and might be responsible for the hyperprolactinemia and might also interfere with the binding of TRH and bromocriptine to their respective pituitary receptors. Although a pituitary defect seems to be prevalent, a concomitant hypothalamic disorder cannot be excluded. Hyperprolactinemia seems to play a role in the sexual disturbances showed by some HD men. Whatever the alterations responsible for the impaired PRL regulation in uremia are, they are reversed by successful renal transplant.