Portal de Periódicos da CAPES

Étude clinique et expérimentale

1965; Taylor & Francis; Volume: 20; Issue: sup1 Linguagem: Inglês

10.1080/17843286.1965.11717825

2295-3337

M Verbanck,

Parathyroid Disorders and Treatments

SummaryThe purpose of this work was to study, in clinical and experimental conditions, the influence of hypercalcemia on renal function and on plasma electrolytes.I. — Clinical and biological data of 24 adult hypercalcémie patients admitted to the medical department of the Brugmann University Hospital were described.Hypercalcemia was related to secondary neoplasm of lxinc in 14 patients. (Sites of origin were as follows : Lung : 4 eases, breast : 3 cases, prostate gland : 1 case, (esophagus : 1 case, kidney : 1 case, multiple myeloma : 2 cases, unknown : 2 cases.) In 9 patients, hyperparathyroidism was considered as the most likely diagnosis. One of these showed the features of an acute hypercalcémie crisis with a blood calcium level above 200 mg/1. Burnett's syndrome was responsible of hypercalcemia in the last patient.1. It was noted that hypercalcemia of most cancers though not that of parathyroid origin was accompanied by a systemic alkalosis, hypokaliema and an acid urine. A slight degree of potassium depletion occurred in 3 cases. In hyper-parathyroid patients, alkalosis was observed only in two patients and could be explained by vomiting or ingestion of alcalini/.ing salts.2. We have measured the pbosphatc/creatinine clearance ratios in most of our hypercalcémie patients; they were invariably increased, and thus the diagnostic approach of hypercalcémie states does not seem to lie made any easier by assessing these ratios.3. High urinary calcium output was observed in most cases. The patient with the milk alkali syndrome had a rather low calciuria, as is usually described in this condition.4. In most cases of hypercalcemia, renal insufficiency remained moderate. This was especially true in hyperparathyroidism. A severe degree of renal failure was never directly related to hypercalcemia, but associated with kidney stones or urinary infection.II. — Our experimental work was performed with dogs.The effects of acute hypercalcemia were studied in two different conditions :— or by injection of calcium chloride alone during 5 hours; between the end of the 1 st and the end of the 5th hour a single urinary collection was performed;— or bv simultaneous injection of calcium chloride and sodium bicarlxmate.Acute hypercalcemia induced by these procedures showed the following major changes in the urinary water and electrolyte excretion pattern :1) a definite diuretic effect accompanied by an increase of the free water clearance was observed.2) H+ and NH4+ output by the kidney was markedly enhanced.3) urinary bicarbonate decreased and chloride increased.4) a sharp raising of plasma inorganic phosphorus was invariably observed during calcium chloride infusions and in most cases the urinary excretion rose as a result of this procedure. Thus, it is obvious that hyperphosphoremia may not be considered as a consequence of reduced parathyroid activity.5) renal excretion of sodium and magnesium was well above control values during acute hypercalcemia. Potassium urinary excretion is not influenced by calcium infusion after tubular exchange mechanism of K is already stimulated by injection of sodium bicarbonate.III. — Chronic hypercalcemia was induced in 14 dogs: in 10 by daily ingestion of 900.000 Units vitamin D3 without any calcium supplements. In 4, lower doses of vitamin D were used, but together with calcium chloride or calcium lactate administration.1) During the first weeks of this treatment, plasma phosphorus rised and urinary 24-hours phosphate excretion was reduced; in most cases, blood pll and plasma potassium increased.A moderate raising of urinary output of water, calcium, magnesium, chloride and sodium was observed.2) After 6 to 10 weeks of vitamin D3 treatment, a definite hypercalcémie state developed. Glomerular filtration rate was reduced to about 50 % of its control state value. At this stage of toxicity, alkalosis occurred, without potassium depletion. Vomiting seemed to plav no part in this acid-base balance disturbance. A chloride depletion of renal origin appeared most likedv, but was not formally demonstrated.3) The administration of an acid load indicated that chronic hypercalcemia was associated with an impaired ammonium production by the kidneys. However, titrable acidity production and lowering of the urine pH were not significantly different from their control values.4) During sodium phosphate or bicarbonate infusions, blood calcium fell in dogs treated with toxic doses of vitamin D. Ammonium chloride ingestion had the same effect but at the same time improved the renal function, as demonstrated by an increase in the glomerular filtration rate.