Evidence of increased proximal sodium and water reabsorption in experimental glomerulonephritis. Role of a natriuretic factor of renal origin.

Abstract

In previous work, we have demonstrated that rats with experimental glomerulonephritis (GN) were unable to increase fractional and absolute sodium excretion after saline loading. This inability appears to be related to the disappearance of a natriuretic material that we have shown to be of renal origin. Similar results were obtained in human GN. In order to identify the nephronic site of the enhanced tubular sodium reabsorption, two techniques were used: (1) study of TmG in normal and glomerulonephritic rats during a progressive saline loading, and (2) micropuncture studies of sodium and water reabsorption. The results clearly demonstrate that: (1) in GN rats, TmG is increased in proportion with Na reabsorption; (2) TmG decreases, of the same magnitude, in GN and normal rats during progressive saline loading; (3) one site of the increased sodium and water reabsorption is proximal as evidenced by glucose titration curve and micropuncture studies, and (4) there is a disruption of glomerulotubular balance in GN rats. Moreover, the parallel behavior of TmG and proximal sodium reabsorption strongly suggests that the part of sodium transport presumbably linked to glucose transport is selectively involved. These results also suggest that the observed disorders are due to the disappearance of a renal natriuretic factor, the site of action of which being presumably proximal.