Impaired sodium excretion in experimental glomerulonephritis: an explanation for the controversies in the literature.

Considerable discrepancies exist in the literature concerning Na excretion by the rat kidney in experimental antiglomerular basement membrane (GBM) glomerulonephritis (GN). Previous studies in our laboratories demonstrated a disturbance in Na excretion with an impaired absolute (UNa X V) and fractional (FENa) excretion of Na after saline loading. However, most of the other authors in the literature failed to observe similar findings. The present study was undertaken to elucidate some of these controversies: We showed that a difference in Na excretion between anesthetized GN and normal rats might not be detected after a volume expansion if the latter is small or slow (FENa in GN 2 +/- 0.1%, in normals 2 +/- 0.2%; not significant). Only a rapid and important volume expansion is sufficient to unmask such a difference between the two groups (FENa 3 +/- 0.3 and 6 +/- 1%, respectively, p less than 0.001), and detect an impaired Na excretion in GN animals. The same amount of NaCl was nevertheless administered during slow and rapid volume expansion. Similarly, in GN conscious rats only after a saline load or repeated water loads did we observe a significantly smaller UNa X V compared to normals while no difference was present between the two groups after a single water load. In the literature, all the authors, that failed to demonstrate a disturbance in Na excretion in anti-GBM GN, administered slow and small isotonic saline loads to their rats. The hypothesis we formulate to explain these controversies is that the nonobserved disturbance in sodium excretion in most of these studies is probably secondary to insufficient natriuretic stimuli.