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PubMed1976

[Metabolic alkalosis and secondary hyperaldosteronism in cystic fibrosis (author's transl)].

The prolonged use of a salt restricted infant formula (1.9 mEq Na/kg/day and 1,4 mEq C1/kg/day) in a child with undiagnosed cystic fibrosis led to a life threatening metabolic disturbance. The main features were hypochloraemic alkalosis due to massive loss of electrolytes in the sweat. Urinary electrolyte excretion, however, had been lowered to a minimum due to aldosteron induced reabsorption. Plasma aldosterone levels were initially high, but returned to normal after addition of salt to the feeds. Prior to admission a sweat test had been negative. The patient clearly demonstrates the unique metabolic feature of cystic fibrosis of the ability to retain electrolytes in the tubulus and at the same time the inability of the sweat glands to reabsorb sodium and chloride. Contrary to present experience severe prolonged salt restriction is believed to be able to diminish sweat electrolytes to subpathological values.

Aldosterone↗
PubMed2003

[Investigation of hyperaldosteronism in the hypertensive patient. Why? When? How?].

Primary aldosteronism (PA) has been regarded for a long time as being a rare cause of arterial hypertension, but its prevalence has recently been reassessed as about 10%. This etiology should obviously be sought in the following settings: hypertension associated with hypokaliemia < 3.6 mmol/L (or < 3.9 mmol/L on ACE inhibitors): refractory hypertension: severe hypertension occurring before 40 years of age, especially in women. It must be reminded that more than 20% of PA are normokaliemic. Most of the authors recommend to use the aldosterone/renin ratio (ARR) as a screening test within these selected patients. When ARR turns out to be equal to or higher than 23 (if aldosterone and renin are given in pg/mL or ng/L), a suppression testing should be performed, using salt loading and/or fludrocortisone. Computed tomography scanning yields a specificity of 58% and a positive predictive value of 72%, only. Adenoma and hyperplasia have to be distinguished, using either NP-59 scintigraphy or adrenal venous samplings. Such a strategy appears to be useful, for the following reasons: removal of an adenoma results in a significant blood pressure lowering and in a blood pressure normalization in 95% and in 32% of the patients, respectively; in patients with hyperplasia, spironolactone therapy is followed by a 20% mean reduction in blood pressure.

Adenoma↗
PubMed1992

[Liddle syndrome (or pseudo-hyperaldosteronism). Long-term development and erythrocyte potassium flow study in 4 cases].

BACKGROUND: Liddle's syndrome (or pseudoprimary aldosteronism) is a rare hereditary disease; only 18 cases have been reported since 1963. Its cause remains unclear, but one of its features is increased cell membrane permeability to ions. PATIENTS AND METHODS: A diagnosis of Liddle's syndrome was made in 4 new cases, all female, two of them sisters (cases n0 3 and 4), at the ages of 2, 12, 5 and 4 years. The first manifestations were dehydratation with hypokalemia at 6 months (case n0 1), hypertension at 2 years (case n0 2), polydipsia with poor weight and height gain at 5 and 4 years of age (cases n0 3 and 4). At diagnosis, all the patients had severe hypertension, metabolic alkalosis, hypokalemia and hyperkaliuria, low plasma renin activity and serum aldosterone levels. Administration of antihypertensive agents was without effect, but the hypertension was reduced when triamterene and low-sodium diet were used. Hypercalciuria was observed in 2 cases and nephrocalcinosis in 2 (case n0 1 had both hypercalciuria and nephrocalcinosis). The 2 oldest patients (n0 3 and 4) developed progressive kidney failure, possibly due to reno-vascular disease secondary to hypertension. Patient n0 3 underwent kidney transplantation 18 years after the first symptoms of the disease. This resulted in the complete disappearance of her hypokalemia and hypertension. The red blood cell membrane permeability to K+ and Cl- was studied in all 4 cases before triamterene treatment. The passive permeability to K+ and (K+/Cl-) cotransport were both elevated. A second study, 3 years (cases n0 2 and 3) and 8 years (cases n0 1 and 4) later, of patients treated with triamterene showed low values for passive K+ permeability and (K+/Cl-)-cotransport. CONCLUSIONS: The 4 new cases of Liddle's syndrome had the classic features of the disease, except for hypercalciuria and nephrocalcinosis in 2 of them. The cell membrane permeability data are difficult to interpret. Hypokalemia and hypertension were immediately corrected after kidney transplantation in one case and remained so for 4 years, suggesting that this disease is tubular in origin.

Aldosterone↗