Search PubMed⌕ Search

Biomedical subjects

J C Chan

Publications and source records attributed to J C Chan.

At least 415 records · Page 23Linked to original sources
PubMed1980

Renal hypophosphatemic rickets: growth acceleration after long-term treatment with 1,25-dihydroxyvitamin-D3.

Treatment with 1,25-dihydroxyvitamin-D3 and phosphorus supplementation for as long as 48 months was evaluated in six patients with renal hypophosphatemic rickets. Previous phosphorus supplementation of 1,800 to 4,000 mg/sq m of body surface area per day was continued while 1,25-dihydroxyvitamin-D3 at 17 to 80 ng/kg of body weight per day was given orally in place of vitamin-D2. The serum calcium concentration stayed within the normal range in the majority of patients, while the serum phosphorus concentration rose from 2.5 +/- 0.4 to 3.4 +/- 1.2 mg/100 ml after one month (P < .01). With rare exceptions, serum alkaline phosphatase and parthyroid hormone concentrations stayed normal throughout the study. Healing of rickets was demonstrated by radiography. In five patients, growth velocity was evaluated for 12 months before and after therapy. Growth accelerations were 123% to 235% of that expected for changes in chronologic age and 114% to 200% expected for changes in bone age after therapy. Orally administered, 1,25-dihydroxyvitamin-D3 increased renal calcium excretion and calcium retention was achieved by virtue of the decreased fecal calcium loss. In contrast, 1,25-dihydroxyvitamin-D3, even at doses up to 4 micrograms/day (80 ng/kg/day) did not significantly alter renal phosphaturia. The phosphorus retention was therefore achieved as the result of the decreased fecal phosphate excretion. The absence of hypercalcemia even at high doses of 1,25-dihydroxyvitamin-D3 and the enhanced linear growth support the long-term therapeutic value of 1,25-dihydroxyvitamin-D3 in renal hypophosphatemic rickets.

Adolescent↗
PubMed1980

Acute renal failure in children: diagnosis and treatment.

The rate of survival in children with acute renal failure is 70%, with death due to sepsis, gastrointestinal bleeding, or fluid-electrolyte imbalances. The author outlines evaluation and treatment procedures conducive to survival.

Acute Kidney Injury↗
PubMed1979

Calcium and parathyroid disorders in children. Chronic renal failure and treatment with calcitriol.

Progression of renal failure, represented by rising serum creatinine concentrations, was correlated with progressive elevation of serum parathyroid hormone (PTH) concentrations in 23 children. A significant linear relationship was established. Despite normal serum calcium concentrations in 11 children receiving maintenance hemodialysis, circulating PTH concentrations were elevated after six months. Progressive deterioration with time occurred in all variables tested, at six-month intervals. These complications were reversible with kidney transplantation or treatment with 0.25 to 2 microgram/day of calcitriol for four to 20 weeks.

Adolescent↗
PubMed1979

Clinical disorders of calcium, phosphate, magnesium, and hydrogen ion metabolism: diagnostic approach.

Information concerning normal concentrations of serum calcium, phosphate, magnesium, and hydrogen ion, as well as clinically useful data concerning absorption and excretion of these physiologically important ions, are reviewed. Clinical approaches to diagnosis of these electrolyte disturbances are summarized with special emphasis on interpretations of these disorders in children.

Acidosis↗
PubMed1979

Quantitative measurement of intracellular RNA genomes of Rauscher murine leukemia virus by competition hybridization in DNA excess.

The technique of competition hybridization in DNA excess was used to determine the intracellular distribution of RNA genomes of Rauscher murine leukemia virus. An examination of subcellular RNA fractions revealed that 59% of intracellular viral RNA genomes were associated with the nuclear-enriched fraction, 41% with the cytoplasmic fraction, and 18% with the polysomal-enriched fraction. Also, an analysis of total cellular RNA disclosed that 20% of intracellular viral RNA genomes were polyadenylated and 80% were not polyadenylated.

Cell Line↗
PubMed1979

Control of aldosterone secretion.

This paper reviews the control of aldosterone secretion, including the role played by hepatic metabolic clearance, ACTH, and the renin-angiotensin system, and the interrelationships of aldosterone secretion with sodium and potassium metabolism. The physiological modulations of aldosterone secretion by the upright posture, progesterone, estriol and estradiol are also discussed.

Adrenocorticotropic Hormone↗
PubMed1979

Acid-base, calcium, potassium and aldosterone metabolism in renal tubular acidosis.

Classic renal tubular acidosis is characterized by a primary defect in establishment of a large hydrogen ion gradient across the distal renal tubule. Thus the development of hyperchlorenic metabolic acidosis follows. In addition, hypokalemia results from renal potassium wasting secondary hyperaldosteronism from sodium wasting and contraction of the extracellular fluid. The presenting signs and symptoms are growth retardation, fatigue, periodic paralysis, polyuria, polydipsia, vomiting and constipation as well as nephrocalcinosis and nephrolithiasis. It is suggested that effective treatment with alkali therapy requires markedly higher doses than formerly recommended, and may related to a higher rate of endogenous acid production from (1) intermediary metabolism of sulfur amino acids and organic acids, (2) impaired tubular reabsorption of bicarbonate and (3) hydrogen ion release from hydroxyapatite formation. It is also suggested that acidosis may interfere with vitamin D metabolism and thus play an important role in the pathoetiology of the growth failure in children with this disorder.

Acid-Base Equilibrium↗
PubMed1979

Long-term hemodialysis and nerve conduction in children.

Initial observations in adults revealed that peripheral neuropathy, as documented by reduced conduction velocity is common in chronic renal failure. Critical analysis of this problem in children on long-term dialysis is scarce, consisting of a simgle report which demonstrated that the motor nerve conduction velocities were decreased early and frequently with more severe depression in peroneal nerve velocities. This is in distinct contrast to data from adults, in whom uniform rates of deterioration are encountered. In addition, a direct correlation of the degree of nerve conduction defect with the severity of the renal failure is found in adult patients. The present study showed a relative lack of nerve conduction defects in 11 children on long-term hemodialysis. With rare exceptions, the conduction velocities were normal. To date, no clinical symptoms of neuropathy were evident in our patients. It would seem that, with the short-dialysis schedule of 12--14 h/wk over a period of up to 5 yr, there is no progressive neuropathy as quantitated by nerve conduction measurements.

Adolescent↗
PubMed1979

Renal osteodystrophy in children with end-stage kidney failure.

The discovery that the kidney is the site of production of calcitriol clarifies our understanding of calcium metabolic disorders in chronic renal failure and carries with it clinical implications in the treatment of renal rickets. The author presents data on the action of calcium and reviews the therapeutic effects on uremic osteodystrophy in children of calcitriol and its analogue.

Adolescent↗