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Biomedical subjects

F L Coe

Publications and source records attributed to F L Coe.

At least 145 records · Page 8Linked to original sources
PubMed1978

Idiopathic hypercalciuria in children: prevalence and metabolic characteristics.

A group of 273 children with minor complaints was screened for idiopathic hypercalciuria by measurement of the urine Ca/Cr. Borderline or definitely high levels were noted in 17 of these children, 11 of whom were boys. More intensive metabolic studies were completed on four of these children and on three children who were noted to have symptomatic renal stones associated with idiopathic hypercalciuria. These studies suggest that IH, well recognized in adults, may have its origins in childhood and that appropriate management, if initiated in childhood, may have significant long-term benefits.

Adolescent↗
PubMed1978

Calcium-uric acid nephrolithiasis.

A small fraction of patients with nephrolithiasis form mixed stones containing calcium and uric acid or pass both calcium and uric acid stones; 23 of 539 patients we have studied fall in this category. These mixed stone formers tend to have unusually frequent stone recurrences. Although the patients are often considered to have a variant of uric acid nephrolithiasis, a high proportion harbor calcium as well as uric acid disorders. The usual treatment for uric acid lithiasis may fail to prevent calcium stone recurrence, unless concomitant calcium disorders are simultaneously corrected. Dual treatment may be very effective in preventing continued stone disease.

Adult↗
PubMed1977

Metabolic alkalosis.

Explore the source record for details and available documents.

Acid-Base Equilibrium↗
PubMed1977

The natural history of calcium urolithiasis.

The course of untreated calcium renal stones, derived from the retrospective study of 300 patients with defined metabolic disorders and from the analysis of two prospective, published studies, is complex and heterogeneous. Generally, stones provoke considerable morbidity; hyperuricosuria is associated with an unusually severe stone disease. Stone recurrence rates usually remain stable, or rise with successive stones; in a minority of patients, the reverse is true. A single stone is likely to be followed by a recurrence. The mean time to recurrence averages 6.78 years, with peaks at 1.56 and eight years. Because the disease is likely to be morbid and chronic and does not wane with age, diagnostic evaluation and treatment should be strongly considered for any patient with recurrent stones, and for those in whom recurrence is likely to pose more than the usual risk.

Adult↗
PubMed1977

Acidic peptide and polyribonucleotide crystal growth inhibitors in human urine.

Urine contains nondialyzable inhibitors of calcium oxalate crystal growth. We have pursued the hypothesis that these inhibitors may, in part, be acidic peptides and polyribonucleotide fragments. Homopolyribonucleotides and RNA inhibit calcium oxalate crystal growth at 5 x 10(-6) M of constituent ribonucleotide, whereas the monomer nucleotides are inactive at 10(-4) M. Poly-L-aspartic or glutamic acid are also inhibitory at 5 X 10(-6) M of amino acid, whereas the monomeric amino acids are inert. Gastric pepsin, a naturally occurring acidic peptide, is inhibitory. Incubation with nonspecific protease reduced the inhibitory effectiveness of normal human urine consistently and significantly, a fact compatible with an important contribution of peptides. A variable additional reduction was produced by subsequent treatment with ribonuclease, suggesting only a small role for polyribonucleotide. Sequential ion exchange and gel filtration chromatography and preparative disc gel electrophoresis yielded inhibitory material enriched with peptides that were strongly acidic and high in proline. Peptides and ribonucleotides seem to contribute to urinary nondialyzable crystal growth inhibitory activity.

Calcium↗
PubMed1977

Treated and untreated recurrent calcium nephrolithiasis in patients with idiopathic hypercalciuria, hyperuricosuria, or no metabolic disorder.

Two hundred two recurrent calcium oxalate stone-forming patients with idiopathic hypercalciuria or hyperuricosuria, or both, were treated for an average of 2.91 years (1 to 7 years) with thiazide or allopurinol, or both. The frequency of new stone formation was drastically reduced. During the treatment period of 625 patient years, 220.0 new stones should have occurred, whereas 22 were actually formed (chi-square=178, P less than 0.001). Thirty-four patients without discernible metabolic disturbances and treated only with increased fluid intake and dietary advice formed 29 new stones compared to a predicted 33.2 stones (87.3%). Thirty similar patients treated with thiazide and allopurinol formed six stones compared to a predicted 31.8, P less than 0.001. Chronic reversal of idiopathic hypercalciuria and hyperuricosuria with thiazide and allopurinol is an effective way to prevent recurrent calcium oxalate stones. Conservative measures are only of marginal effectiveness in treating metabolically normal stone forming patients; however, thiazide and allopurinol appear to decrease new stone formation.

Allopurinol↗
PubMed1976

Compensatory phosphaturia after unilateral nephrectomy in the rat.

Within 24 hr after unilateral nephrectomy, fractional excretion of phosphate (FEp) by the remaining kidney is markedly increased. This increase in FEp occurs in throparathyroidectomized rats receiving fixed replacement doses of parathyroid hormone and, therefore, cannot be due to secondary hyperparathyroidism occurring in response to unilateral nephrectomy. In the avsence of any hormone replacement, the increase in FEp is much reduced, but still present. The increase in FEp cannot be ascribed to depression of overall tubular sodium reabsorption because it could be demonstrated in the absence of an increase in FENa. Phosphaturia following unilateral nephrectomy in the rat appears to be part of the complex of events that occur after acute reduction of renal mass; the exact mechanisms of its genesis are uncertain.

Animals↗
PubMed1975

Effect of acute and chronic metabolic acidosis on serum immunoreactive parathyroid hormone in man.

The effects of acute and chronic metabolic acidosis on serum immunoreactive parathyroid hormone (iPTH) were studied. Acute metabolic acidosis induced by administration of ammonium chloride (NH4Cl) produced a barely detectable increase in serum iPTH. Chronic NH4Cl administration produced a marked elevation of serum iPTH that was well correlated with the magnitude of acid-induced hypercalciuria but not with the degree of acidosis. Acetazolamide administration produced an equivalent degree of acidosis, but hypercalciuria was minimal and iPTH increased only marginally. Methionine administration caused moderate hypercalciuria and a significant but moderate increase in iPTH. Chronic NH4Cl-induced acidosis produced no hypercalciuria when dietary sodium intake was rigidly restricted, and under these conditions serum iPTH remained normal. When sodium intake was suddenly increased while maintaining the acid load, hypercalciuria appeared and was followed by progressive rise in serum iPTH equivalent to that observed during chronic NH4Cl-induced acidosis in subjects consuming salt ad lib. These results indicate that chronic acidosis elevates iPTH mainly by producing hypercalciuria and that acidosis itself is not a primary stimulus to PTH secretion.

Acetazolamide↗
PubMed1975

Sodium urate accelerates precipitation of calcium oxalate in vitro.

Precipitation of calcium oxalate crystals from a metastable solution can be detected within 10 min if crystalline sodium urate is added at a solid to liquid ratio of 0.1 mM or more. Without urate, precipitation begins after 50 min. Uric acid is not effective. Pyrophosphate inhibits the effects of sodium urate.

Calcium↗
PubMed1975

Evidence for mild reversible hyperparathyroidism in distal renal tubular acidosis.

Circulating levels of immunoreactive parathyroid hormone were measured in six patients with distal renal tubular acidosis before and during two years of long-term alkali therapy. Parathyroid hormone level was elevated modestly in five patients before treatment and fell, gradually during treatment to normal or near normal levels. Urine calcium level fell, serum calcium level rose, and renal phosphorus reabsorption rose during treatment. Stopping treatment briefly caused reversion of serum parathyroid hormone and calcium levels and renal phosphorus reabsorption to pretreatment values within eight weeks. Mild hyperparathyroidism is present in renal tubular acidosis and reverses with alkali treatment.

Acidosis, Renal Tubular↗