Nephrotic syndrome: new concepts in the pathophysiology of sodium retention

The nephrotic syndrome is a frequent clinical condition
characterized by fluid and salt retention. Although several
theories have been put forward to explain the salt-retaining
status, recent data have confirmed previous renal
micropuncture observations indicating that the distal
nephron is the site for increased salt reabsorption, eventually
leading to sodium retention. Target proteomic approaches
and immunocytochemistry experiments have identified
the epithelial sodium channel (ENaC) and basolateral
Na+,K+-ATPase as the main transport proteins responsible
for increased transepithelial sodium reabsorption
in various forms of experimental nephrotic syndrome.
Although the fine-tuning for the up-regulation of
these transporters has not been so far elucidated, it is
clear from clinical studies that the use of amiloride, a selective,
dose-dependent ENaC inhibitor, is an appropriate
tool to reduce distal sodium reabsorption and thus to
offset edema formation.