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The present review summarizes current concepts on glomerular non-inflammatory and inflammatory immune injury. Non-inflammatory glomerular injury can be ascribed to mechanisms involving antibody alone, terminal component of complement (C5b-9) or cytokines having as primary target the glomerular epithelial cells. These mechanisms induce changes in cell cytoskeleton and in surface distribution of adhesion molecules leading to functional alterations which may account for loss of glomerular permselectivity. Inflammatory glomerular injury is mediated by neutrophils, macrophages, platelets and lymphocytes as well as by resident glomerular cells. Cell derived mediators include proteases, reactive oxygen species, cationic proteins, cytokines and growth factors that may variably affect recruitment of inflammatory cells, proliferation of resident glomerular cells and production of extracellular matrix. These alterations may determine proteinuria, impairment of renal function and eventually progression of glomerular injury to sclerosis. The inflammatory type of glomerular injury is mainly initiated by subendothelial-mesangial immune deposits and/or activation of cell mediated immunity. The role of factors such as the nature, intensity and persistence of initiating mechanisms, the types of inflammatory cells involved and the response of intrinsic glomerular cells, in expression and progression of glomerular injury are discussed.

Renal biopsies from 32 patients, whose light microscopy showed a pattern of minimal changes nephropathy, have been submitted to immunohistological examination. On the basis of immunofluorescence pattern we separated the cases into three groups: the first group (12 cases) was characterized by absence of any glomerular deposit. The second group (9 cases) showed focal and segmental deposits of IgM and sometimes C3 on capillary walls. In the third group (11 cases) we observed slight deposits of IgM and sometimes C3 "comma like" over glomerular structures in all glomeruli. The site of these last deposits was sometimes mesangium and sometimes the capillary walls. The results of immunohistological examinations gave no information about the pathogenetic mechanisms of minimal changes nephropathy. We observed that the patients enclosed in the second group had a worse clinical prognosis, compared with the other two groups.

During phenytoin therapy, a male patient showed hypertermia, myalgias and mediastinal and abdominal lymphadenopathy. Despite the impossibility of histological diagnosis, he was treated with antiblastic polychemotherapy with little benefit. Another female patient on the same therapy showed splenomegaly with pancytopenia. The spleen and some abdominal lymph nodes were removed; they revealed a pattern of tubercular-like gigantocellular-epithelioid chronic flogosis. As in the first patient, the suspension of therapy gave a disease-free period. A third female patient on diphenylhydantoin therapy undervent some hemolytic crysis and, finally, SLE with cardiac involvement. We point out the complexity of the pathogenesis of hydantoinic immunologic syndromes, the polymorphism of the clinical patterns and the difficulty to make a correct diagnosis, mostly on presence exclusively deep involvement.

Following a review of the most recent aetiopathogenetic theories and therapeutic records of Goodpasture's syndrome, a personal case is reported. Stress is laid on the extreme clinical variability of the disease and on the role which disseminated intravascular clotting can have on its course.