title: High sodium sensitivity and glomerular hypertension/hyperfiltration in primary aldosteronism.
abstract: OBJECTIVE
  To assess sodium sensitivity and glomerular haemodynamics in patients with primary aldosteronism.
  
  
  METHODS
  Two-week studies were performed in six patients with primary aldosteronism whose diagnosis had been confirmed by histology of the removed adrenal adenoma. Patients were fed normal or sodium-restricted diets for 1 week each and renal clearance measured during the normal sodium diet. Pressure-natriuresis relationships were drawn by plotting the urinary sodium excretion on the y-axis as a function of the systemic mean arterial pressure on the x-axis.
  
  
  RESULTS
  The extrapolated x-intercept of the pressure-natriuresis curve was 118 +/- 9 mmHg. The sodium sensitivity, which corresponds to the reciprocal of the slope, was augmented to 0.111 +/- 0.013 mmHg/mmol per day, and the reduction in mean arterial pressure by sodium restriction was 11 +/- 2%. As we had reported previously, the difference between the mean arterial pressure (137 +/- 5 mmHg) with the normal-sodium diet and the x-intercept was assumed to be the effective filtration pressure across the glomerular capillary walls (18.2 +/- 2.0 mmHg). By dividing the glomerular filtration rate (128 +/- 10 ml/min per 1.73 m2) by the effective filtration pressure, the whole kidney ultrafiltration coefficient in these patients was estimated to be 0.127 +/- 0.021 ml/s per mmHg, which was approximately normal. The glomerular capillary pressure was calculated to be 54 +/- 2 mmHg.
  
  
  CONCLUSIONS
  Compared with non-sodium-sensitive essential hypertension patients (n = 18) whose glomerular filtration rate and capillary hydraulic pressure were 84 +/- 3 ml/min per 1.73 m2 and 47 +/- 1 mmHg, the sodium sensitivity of blood pressure in patients with primary aldosteronism was augmented, and both glomerular hyper-filtration and glomerular capillary hypertension were observed. We confirmed that the glomerular haemodynamic characteristics in primary aldosteronism are typical of those expected for sodium-sensitive hypertension caused by enhanced tubular sodium reabsorption.
authors.affiliation: Department of Medicine, National Cardiovascular Centre, Osaka, Japan.
authors.forename: G
authors.initials: G
authors.lastname: Kimura
authors.forename: T
authors.initials: T
authors.lastname: Uzu
authors.forename: S
authors.initials: S
authors.lastname: Nakamura
authors.forename: T
authors.initials: T
authors.lastname: Inenaga
authors.forename: T
authors.initials: T
authors.lastname: Fujii
mesh_terms: D000328:Adult; D005260:Female; D005919:Glomerular Filtration Rate; D006439:Hemodynamics; D006801:Humans; D006929:Hyperaldosteronism / Q000503:physiopathology*; D006973:Hypertension / Q000209:etiology*; D007678:Kidney Glomerulus / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D012982:Sodium, Dietary / Q000008:administration & dosage*
chemical_list: D012982:Sodium, Dietary