Hyperaldosteronism and Hypergranularity of the Juxtaglomerular Cells in Renal Hypertension

Publisher Website
Google Scholar
Abstract
Preoperative and postoperative metabolic studies were performed in a patient with hypertension, hypokalemia and metabolic alkalosis secondary to bilateral renal artery stenosis. Her most prominent symptoms were headache, profound weakness, polydipsia, polyuria and nocturia. Preoperatively, when Na intake was moderate, renal K wastage and hypokalemia occurred unless a high K intake was also provided. Either dietary Na restriction or spirono-lactone prevented excessive K excretion. These data suggest that the K loss was a function of a renal tubular cation exchange mechanism probably under the influence of high blood levels of aldosterone. The hyperaldosteronuria manifested by this patient is compatible with this concept. Surgical removal of one ischemic kidney and repair of the other stenotic renal artery was followed by "cure" of hypertension, relief of most of her preoperative symptoms and correction of her chemical and metabolic abnormalities. Histological examination of the kidneys revealed marked hypergranularity of the juxtaglomerular cells. The clinical and metabolic abnormalities of this patient may be interpreted in relation to recent knowledge of the regulation of the adrenal secretion of aldosterone. Impaired renal perfusion resulted in increased renin production by the juxtaglomerular cells. Renin enzymatically facilitated the activation of excessive quantities of angiotensin II which stimulated hypersecretion of aldosterone by the adrenals. The resultant hyperaldosteronism was responsible for many of her clinical and chemical manifestations including hypokalemia and metabolic alkalosis. Other interesting observations were persistent hyponatremia unexpalined by external balances and polydipsia not wholly explained by potassium depletion. These studies also suggested a practical clinical approach to the differential diagnosis of hypertension and hypokalemia.