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E J Lennon

Publications and source records attributed to E J Lennon.

18 recordsLinked to original sources
PubMed1974

The effect of glucose on urinary cation excretion during chronic extracellular volume expansion in normal man.

Both glucose administration and extracellular volume expansion augment urinary calcium and magnesium excretion. While volume expansion also augments sodium excretion, glucose induces an antinatriuresis. To examine the interrelationships of volume expansion and of glucose administration on sodium, calcium, and magnesium excretion, the effects of glucose were evaluated during clearance studies in the same subjects before and after chronic extracellular volume expansion produced by desoxycorticosterone acetate (DOCA) and a normal dietary sodium intake. The augmentation of U(Ca)V and U(Mg)V by glucose was simply additive to the increments in divalent cation excretion caused by "escape" from the sodium-retaining effects of DOCA. Glucose administration reduced U(Na)V, an effect exaggerated after DOCA escape and associated with reductions in volume/glomerular filtration rate (V/GFR) and C(Na) + C(H2O)/GFR, suggesting augmented proximal tubular reabsorption. Before glucose, U(Na) was inversely correlated with U(G), and after glucose administration C(Na)/GFR was inversely correlated with T(G)/GFR. We propose that the availability of glucose in the proximal tubule stimulates Na reabsorption while delaying development of a chloride diffusion potential, thereby inhibiting tubular reabsorption of Ca and Mg.

Bicarbonates↗
PubMed1970

A comparison of the effects of glucose ingestion and NH4Cl acidosis on urinary calcium and magnesium excretion in man.

Both glucose ingestion and NH(4)Cl acidosis have been reported to augment urinary calcium (U(Ca) V) and magnesium (U(Mg) V) excretion. Both also cause acidification of the urine and an increase in renal acid excretion. To examine whether a common mechanism of action was involved, the effects of glucose ingestion and NH(4)Cl acidosis on U(Ca) V and U(Mg) V were tested in the same subjects. Glucose ingestion caused significant increases in both U(Ca) V and U(Mg) V. During stable NH(4)Cl acidosis, U(Ca) V increased significantly, while U(Mg) V was unaffected. When a glucose load was given during acidosis, the separate effects of acidosis and glucose on U(Ca) V were additive, whereas U(Mg) V increased less than observed during normal acid-base balance. Although renal acid excretion increased and the urine was acidified after glucose in the normal steady state, when glucose was administered during NH(4)Cl acidosis urine pH rose and there was no change in renal acid excretion. We concluded that NH(4)Cl acidosis and glucose ingestion reduce the renal tubular reabsorption of magnesium and (or) calcium, but they act through separate mechanisms.

Acidosis↗
PubMed1967

The effect of treatment of acidosis on calcium balance in patients with chronic azotemic renal disease.

Small but statistically significant negative calcium balances were found in each of eight studies in seven patients with chronic azotemic renal disease when stable metabolic acidosis was present. Only small quantities of calcium were excreted in the urine, but fecal calcium excretion equaled or exceeded dietary intake. Complete and continuous correction of acidosis by NaHCO(3) therapy reduced both urinary and fecal calcium excretion and produced a daily calcium balance indistinguishable from zero. Apparent acid retention was found throughout the studies during acidosis, despite no further reduction of the serum bicarbonate concentration. The negative calcium balances that accompanied acid retention support the suggestion that slow titration of alkaline bone salts provides an additional buffer reservoir in chronic metabolic acidosis. The treatment of metabolic acidosis prevented further calcium losses but did not induce net calcium retention. It is suggested that the normal homeostatic responses of the body to the alterations in ionized calcium and calcium distribution produced by raising the serum bicarbonate might paradoxically retard the repair of skeletal calcium deficits.

Acidosis, Renal Tubular↗
PubMed1967

Studies of the mechanism by which chronic metabolic acidosis augments urinary calcium excretion in man.

We carried out clearance studies in nine healthy adults and four patients with hypoparathyroidism before and after inducing stable metabolic acidosis with either NH(4)Cl or acetazolamide. Clearances were repeated in seven normal subjects and three of the patients 3 days after stopping these agents.During acidosis in the normal subjects, serum ultrafilterable calcium concentration rose significantly, but inulin clearance fell to a greater extent, so that the calculated filtered load of calcium fell significantly. Despite this, urinary calcium excretion rose. Urinary calcium excretion remained elevated in the recovery studies when the serum ultrafilterable calcium concentration and filtered load of calcium had returned to control levels. Evidence is presented indicating that the increased calcium excretion which occurred during acidosis and recovery clearances was not due to natriuresis or to increased excretion of complexing anions. The comparable results in the four patients with hypoparathyroidism, two of whom also had hypothyroidism, suggest that the capacity to alter secretion rates of parathyroid hormone, thyrocalcitonin or both is not a critical determinant of the augmented rates of calcium excretion during acidosis.We conclude that metabolic acidosis produces increased urinary calcium excretion by causing decreased renal tubular calcium reabsorption. Evidence is presented which suggests that this is a direct effect of metabolic acidosis on metabolic processes within renal tubular cells.

Journal Article↗