Renal retention of sodium in nephrotic syndrome
Experimental evidence from rats in whom nephrosis is induced by puromycin aminonucleoside (PAN), shows that sodium retention occurs beyond the last nephron segment accessible to micropuncture i.e. between the late distal convoluted tubule and the tip of the collecting duct. This includes the connecting tubule and the cortical and outer medullary collecting ducts, which reabsorb sodium and are the major sites of the adjustment of sodium balance under the homeostatic control of aldosterone, and the inner medullary collecting duct, which is able to secrete an overload of sodium in response to atrial natriuretic peptide.
In vitro analysis of isolated subsegments of the distal nephron has shown a marked stimulation of sodium reabsorption in the cortical collecting duct of PAN nephrotic rats. In addition, the inner medullary collecting duct becomes insensitive to the natriuretic action of atrial natriuretic peptide, thereby preventing any compensation of sodium retention in upstream nephron segments.
Further studies have shown that the main reason for this increased sodium reabsorption in the cortical collecting duct is stimulation of the basolateral Na-K-ATPase.