Increased blood viscosity as the pathogenic agent in minimal change nephrosis: a new hypothesis.
It is proposed that minimal change nephrosis (MCN) is the result of impaired glomerular blood flow to slightly increased blood viscosity or to an abnormality of an autoregulatory mechanism controlling glomerular perfusion pressure or to unusually small efferent arterioles, or to combinations of these factors. The functional response to any of such changes would be an increase in intraglomerular pressure. If the pressure exceeded a critical level albumin would be able to pass into Bowman's space after deforming the pressure-dependent thixotropic basement membrane. In response to the presence of albumin in Bowman's space, epithelial cell foot process retraction would be initiated. The concentration of albumin capable of stimulating this reversible change in unknown. If it can be shown that MCN is a consequence of increased blood viscosity, then drugs having direct effects on blood viscosity might offer alternatives to steroid treatment.
D000419:Albuminuria / Q000209:etiology; D001160:Arterioles / Q000503:physiopathology; D001794:Blood Pressure; D001809:Blood Viscosity; D006801:Humans; D007678:Kidney Glomerulus / Q000098:blood supply*; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology; D009402:Nephrosis, Lipoid / Q000097:blood* / Q000188:drug therapy; D012212:Rheology; D013256:Steroids / Q000627:therapeutic use
D013256:Steroids