Salt and essential hypertension: pathophysiology and implications for treatment.
- Michael A Garfinkle
- Journal of the American Society of Hypertension…
Two divergent theories have been offered to explain the concentrating and diluting defects of chronic renal disease. The conventional view attributes these abnormalities to damage to specific nephron sites and assumes a significant formation of urine by partially damaged nephrons. The alternative view postulates little or no function by damaged nephrons and attributes virtually all function to the remaining "intact nephrons." It is suggested that the increased solute excretion by these fewer normal nephrons interferes with the ability to concentrate and dilute urine (1, 2). This follows from the observations in normals, under conditions of both antidiuresis and water diuresis, that an increase in solute excretion causes urine osmolality to approach that of plasma (3-6). Data supporting this latter thesis have been obtained in an animal model with unilateral kidney disease. When concentrating and diluting abilities were expressed at equivalent rates of glomerular filtration, these functions were approximately equal in the diseased and contralateral normal kidney (2, 7). However, extrapolation of such data to