[Tubular functions in the regulation of osmotic and acid-base homeostasis in chronic hypertensive compensated glomerulonephritis].

In 45 patients with chronic compensated hypertensive glomerulonephritis and in 184 others suffering from different clinical variants of the same disease the state of tubular functions controlling the osmotic and acid-base homeostasis was investigated. The objective was to assess in this connection the scope of renal processes in this connection the scope of renal processes peculiar to the hypertensive from that keep up these function, to reveal (by studying the materials of renal biopsies) the morphological substrate of the dysfunctional under consideration and also to determine its ossible importance in maintaining hypertension. As a criterion for the mass of active nephrons the magnitude of glomerular filtration (from clearance of endogenous creatinine with a minute-long diuresis of 1.5-2.5 ml/min) was used. It was established that, as distinct from the latent forms, in cases of benign hypertensive form of chronic glomerulonephritis, as well as in those of nephritic one, the ammonium excretion is halved and so is also the maximum osmotic concentration. Common to the hypertonic syndrome proved to be a particularly steep, by 70%, fall of CH2O. The disclosed disturbances, except for reduced excretion of "osmotically free" water, may be attributed to the nature of morphological changes inherent in this form of the disease, i.e. in the atrophy of the tubular epithelium and of the tubulo-interstitial component. The major fall of CH2O is largely determined by an increased proximal transport of sodium and inhibition of this process in the distal part of the nephron. A derangement of the studied tubular functions may, though in part, be considered as a factor keeping up the arterial pressure.