Cellular immune mechanisms have been shown to play a prominent role in glomerulonephritis. Cellular mediators of inflammation cause both acute and progressive glomerular and tubular injury. Understanding the mediation pathways offers the opportunity for therapeutic manipulation. In addition to polymorphonuclear leucocytes, monocytes/macrophages, B-cells and T-cells subsets are being enumerated in normal and diseased renal tissues. The correlation between immunological findings in peripheral blood and infiltrate composition in renal tissue, by using weekly Fine Needle Aspiration Biopsy (FNAB), for assessing the clinical status and monitoring the immunosuppressive therapy was the aim of this study. When determining the intensity of inflammation the numerical values of the Total Corrected Increment (T.C.I.) were defined as follows: less than 1.5 no inflammation; from 1.5 to 2.0 inflammation possible; greater than 2.0 inflammation. The ratio between OKT4 and OKT8 was used as the index: greater than 2.0 immunologic activation; greater than 2.0 no immunologic activation. When the T.C.I. was greater than 1.5 and the OKT4/OKT8 less than 2.0, or the T.C.I. less than 1.5 and the OKT4/OKT8 greater than 2.0 we used only a standard treatment. When both activation indexes were in the normal range we have not treated the patients. When the T.C.I. was greater than 1.5 and the OKT4/OKT8 was greater than 2.0 we treated the patients with standard treatment plus methylprednisolone pulses every time the activation indexes monitored by FNAB, showed an increase. A spontaneous improvement was obtained in untreated patients. The patients treated by standard therapy alone showed a different outcome. All patients treated with standard therapy plus methyl-prednisolone pulses showed a progressive clinical improvement.(ABSTRACT TRUNCATED AT 250 WORDS)