Hypernatraemia and Hyponatraemia 45 



the kidneys normally conserve sodium efficiently. For the 

 same reason, in sodium deficiency there is virtually no 

 sodium in the urine. To this there is one exception, namely, 

 when the sodium deficit is actually the result of continued 

 loss through the kidney. This happens, of course, in Addison's 

 disease, and in "salt-losing nephritis". Furthermore, in 

 certain patients with cerebral lesions persistent renal losses 

 have been observed, even when the intake of sodium is much 

 reduced (Welt et at., 1952). The renal defect has been ascribed 

 to a loss of neural impulses affecting proximal tubular func- 

 tion (Cort, 1954). But the patient of Merrill, Murray and 

 Harrison (1956) with malignant hypertension was able to 

 maintain a normal sodium balance when his own kidneys 

 were replaced by a kidney which was transplanted from his 

 twin brother and therefore deprived of its nerve supply. It 

 does not seem then that a loss of nervous impulses is alone 

 responsible for a failure of the kidneys to conserve salt, 

 though the renal nerves do play a part in the response to salt 

 deprivation (Bricker et al., 1956) and to anoxia (Foldi, 

 Kovach and Takacs, 1955a, h). The mechanism of the defect 

 in "cerebral salt-wasting" remains obscure. Water excess 

 (see below) may produce a renal loss of sodium, and some 

 instances of so-called salt wasting may therefore be examples 

 of water retention. 



Hyponatraemia from salt deficiency can, of course, be 

 corrected with salt. 



A deficiency of sodium, producing hyponatraemia, can arise 

 without a loss of sodium from the body. The sudden accumul- 

 ation of a transudate in some part of the body produces a 

 relative lack of salt and water. If only water is provided the 

 [Na] falls. This state of affairs is seen most clearly after a 

 paracentesis, w^hen water, carrying sodium with it, may rapidly 

 reaccumulate in the abdominal cavity. The fall in blood 

 volume presumably stimulates thirst and the liberation of 

 ADH; for the patient, while drinking copiously, produces 

 only a small amount of concentrated urine containing very 

 little sodium (Nelson, Rosenbaum and Strauss, 1951). 



