Benign persistent asymptomatic proteinuria with incomplete foot process disease in adolescents: a new clinical entity?

A distinct glomerular damage characterized by the following clinical and pathological findings was verified in 20 children with a proteinuria. The clinical features were: 1) glomerular damage was frequent in adolescent males, the male to female ratio being 3:1; 2) the onset was initiated by asymptomatic proteinuria which remitted spontaneously after 3-5 years, with no resulting nephrotic syndrome; 3) there was no apparent cause for the proteinuria such as postural proteinuria, wandering kidney, hypertension or heart disease; 4) in no patient was there a past history of infection or occurrence of other diseases; 5) there were no morphological alterations except for fusion of the epithelial foot processes in about 40% of the glomerular capillary wall; and 6) immunofluorescence microscopy revealed the lack of deposition of immunoglobulins in 20 patients and deposits of complement (C3) or fibrinogen in 4 out of 20. The degree of fusion of epithelial foot processes in incomplete foot process disease was significantly different from that seen in orthostatic proteinuria, thin basement membrane syndrome and minimal change nephrotic syndrome. Compared to the latter, incomplete foot process disease is likely to occur at a higher age with a peak at adolescence, then remit spontaneously without therapy. These events may constitute a distinct entity.