Show description

Of the Progressive nephron loss (as in chronic renal failure, C R F ) means that there is less likelihood of generating fully concentrated interstitial fluid. Moreover, the surviving nephrons have high flow rates resulting from compensatory increases in their individual G F R (single nephron G F R ; S N G F R ) . Consequently, there is less likelihood of equilibration along solute gradients. Production of maximally concentrated and maximally dilute urine are, therefore, both likely to be impaired.

1988). Mutant cells without an antiporter cannot regulate ICF p H in response to acid loads, do not show a sodium influx in response to growth factors and fail to divide. Nevertheless, Ganz (1991) has suggested that some of the data regarding the role of the N a + - H + exchanger are distorted by the artificiality of the in vitro conditions, in particular the exclusion of the bicarbonate buffer system. His contention is that the antiporter serves to preserve the normality of intracellular p H during mitogenic responses rather than mediating a rise of I C F p H .

Since plasma sodium concentration is mainly regulated by control of water balance, inadequate delivery of tubular fluid to the loop and distal nephron undermines the defence of plasma sodium concentration as well as potassium and p H . T h u s , the enhancement of proximal reabsorption in defence of plasma volume undermines the defence of plasma composition by subsequent segments of the nephron. g. saline, though neutral rather than acidic, corrects metabolic alkalosis. Hypovolaemia, per se, undermines the ability of normal kidneys to resist the development of metabolic alkalosis by increasing bicarbonate excretion.