The nephrotic syndrome is a consequence of urinary loss of intermediate sized plasma proteins and the resulting homeostatic responses to those losses. Plasma protein composition is changed greatly. Intermediate sized proteins, including albumin, transferrin, IgG, hormone binding proteins, and low molecular weight inhibitors of the clotting cascade, are lost in the urine and their concentration in plasma reduced. Synthesis of many proteins secreted by the liver is increased either at the level of transcription or posttranscriptionally. Synthesis of several liver-derived proteins is increased in the absence of their urinary loss, suggesting that hypoalbuminemia or reduced plasma oncotic pressure (Π) stimulates the production or reduces the rate of catabolism of these proteins. Their plasma levels, including those of lipoproteins and elements of the coagulation cascade, are increased. Plasma Πfalls and plasma viscosity increases because of the replacement of intermediate sized plasma proteins by larger ones. The plasma concentration of several proteins lost in the urine but not secreted by the liver, such as erythropoietin and IgG, are not defended by increased synthesis, suggesting that increased synthesis of plasma proteins is primarily confined to the liver. Loss of both liver-derived and non-liver-derived proteins may cause reduced immunity, anemia, and deficiency syndromes. Urinary loss of albumin alone is not responsible for decreased plasma Π. The relationship between plasma protein concentration and Πis greatly disturbed in nephrotic rats. In contrast, the relationship between Πand plasma protein concentration is nearly the same in rats with hereditary analbuminemia (NAR) and normal rats, despite the absence of albumin from the plasma of NAR. When proteinuria is induced in NAR the relationship between plasma protein concentration and Πbecomes identical to that in nephrotic animals, although no albumin was lost in the urine of NAR.

Keywords:
Oncotic pressure, Albumin, Transferrin, Lipoproteins, Analbuminemia, Fibrinogen, Protein synthesis
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© 1993 S. Karger AG, Basel
1993
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