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Biomedical subjects

A S Brem

Publications and source records attributed to A S Brem.

11 recordsLinked to original sources
PubMed1992

Central nervous system and renal investigations in patients with Lowe syndrome.

We describe three patients with Lowe (oculocerebrorenal) syndrome, emphasizing primarily the central nervous system and renal pathology. Using magnetic resonance imaging, we noted diffuse high T2 signals periventricularly, indicating significant white matter destruction, which may be responsible in part for the mental retardation, seizure disorder, hypotonia, and areflexia observed in the patients. In contrast to previously published reports, there was minimal renal tubular dysfunction; however, proteinuria was significantly increased in all patients. We believe that the observed proteinuria is primarily the result of glomerular pathology rather than renal tubular dysfunction and may represent a net loss of negative charges within the glomerular filter. This loss of charge may be linked to the increased excretion of glycosaminoglycans in the urine.

Adolescent↗
PubMed1992

Effect of carbenoxolone sodium on steroid-induced sodium transport in the toad bladder: further studies.

The licorice derivative, carbenoxolone sodium, is a potent inhibitor of the enzyme 11 beta-hydroxysteroid dehydrogenase. When this enzyme is suppressed or is absent, endogenous glucocorticoids induce mineralocorticoid-like sodium retention by the kidney. Carbenoxolone sodium administered in vivo to an adrenalectomized rat has also recently been shown to enhance the mineralocorticoid response to submaximal concentrations of aldosterone, deoxycorticosterone (DOC) and 11-dehydrocorticosterone (compound A). In the present studies conducted on the urinary bladder isolated from the Dominican toad, Bufo marinus, a concentration of carbenoxolone sodium shown previously to increase glucocorticoid-induced sodium transport (2.5 x 10(-5) M) did not appear to alter the response to submaximal concentrations of aldosterone 10(-8) M, DOC 10(-7) M, or compound A 10(-5) M. These findings are consistent with the view that in the whole animal carbenoxolone sodium may modify additional steroid metabolic pathways and/or physiological processes in several organs to produce the enhanced renal response to mineralocorticoids and compound A.

Aldosterone↗
PubMed1992

Electrolyte disorders associated with respiratory distress syndrome and bronchopulmonary dysplasia.

In understanding the various electrolyte disorders associated with respiratory failure, one has to appreciate how the otherwise healthy premature infant maintains extracellular fluid homeostasis. The same physiologic processes that regulate body fluids are affected to varying degrees in the infant with respiratory failure. Maintenance of sodium conservation by the kidney is of critical importance for survival and growth. The immature kidney tends to exhibit excessive sodium wasting especially early on, but appropriate positive sodium balance is achieved generally within the first week. Appropriate reduction in extracellular fluid occurring during the first week or so of life is expected and if it is not allowed to occur may result in dilutional hyponatremia and an increase in pulmonary interstitial water. Diuretics, when used to promote an increase in lung compliance, can themselves generate significant morbidity. Sodium depletion, hypokalemia, alkalosis, and calcium wasting all can either be caused by or exaggerated by the loop diuretics. Thus, one must consider the maturational state of the infant, the infant's response to pulmonary failure, and iatrogenic factors influencing the outcome.

Acid-Base Equilibrium↗
PubMed1991

Primary renal lymphoma.

Lymphomatous involvement of the kidneys is a common manifestation of systemic non-Hodgkin's lymphoma but associated renal dysfunction is uncommon. In contrast, lymphoma originating within the kidneys is a rare event. We report a case of primary renal lymphoma presenting with renal insufficiency and hypertension in a 10-year-old boy.

Child↗
PubMed1991

Changes in intracellular sodium during the hydroosmotic response to vasopressin.

During vasopressin (VP)-induced water movement, toad urinary bladder epithelial cells undergo unique morphological changes. The osmolality within these responding cells remains relatively stable despite the large transcellular transport of water. We hypothesized that the hydroosmotic response to VP may be associated with a net increase in sodium either as an aid in maintaining the intracellular osmolality or as part of a Na-Ca exchange process. Changes in intracellular sodium (Nai) were monitored over time in individual hemibladders using 23Na NMR. Hemibladders were mounted as bags on glass pipets and filled with deionized water. During NMR studies, the serosal bath consisted of aerated 2.4 mM HCO3 amphibian Ringer's (pH 8.1) made up with 15% D2O containing the shift reagent, dysprosium tripolyphosphate (1 mM). This reagent allowed for visualization of Nai by shifting the extracellular Na signal; it did not affect basal or VP stimulated water flow, short-circuit current, or high energy phosphate metabolism as seen by 31P NMR. Changes in Nai were determined by integrating the area under the unshifted Na peak at each measurement and expressing differences as a ratio relative to baseline. The initial Nai signal from unstimulated hemibladders remained stable in these tissues over at least 180 minutes. Within 30 minutes of VP (20 mU/ml) exposure, however, the Nai peak increased 2.47 times above pretreatment baseline (N = 16, P less than 0.001). The Nai signal returned toward baseline values with removal of VP from the serosal bath but only after approximately 90 minutes. When change in cell shape and water movement were prevented by having isotonic sorbitol in the mucosal bath, VP produced no change in the Nai signal (N = 10).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

11-Dehydrocorticosterone, a glucocorticoid metabolite, inhibits aldosterone action in toad bladder.

The enzyme 11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD) metabolizes glucocorticoid hormones and diminishes their ability to induce sodium transport. In these studies, we determined the location of this enzyme in toad bladder and assessed the biological role for its 11-dehydro end product. Employing a polyclonal antibody directed toward 11 beta-OHSD and immunofluorescence techniques, we located the enzyme in the epithelial cell layer of the toad bladder. Although corticosterone (10(-7) M) can partially suppress aldosterone (10(-7) M)-stimulated short-circuit current (SCC), a clear excess of corticosterone (10(-6) M) did not inhibit the aldosterone-induced induced (10(-8) M) rise in SCC (n = 6). The 11-dehydro product of corticosterone, 11-dehydrocorticosterone (compound A) added to the serosal bath suppressed aldosterone (10(-8) M) peak SCC (360 min) in a dose-dependent fashion reaching 46 +/- 5% of control values at 10(-5) M (n = 6; P less than 0.001). Compound A (10(-5) M) in the mucosal bath also was capable of partially inhibiting the peak aldosterone rise in SCC to 63 +/- 7% of control values with aldosterone at 10(-8) M (n = 6; P less than 0.01) and to 64 +/- 10% of control values with aldosterone at 10(-7) M (n = 9; P less than 0.01). Compound A alone at 10(-5) M did not have any effect on SCC. Isolated toad bladders were not able to transform compound A (at 10(-8) and 10(-5) M) back to corticosterone. Thus the 11-dehydro end product of 11 beta-OHSD (compound A) may play a biologic role by regulating a component of mineralocorticoid-induced sodium transport.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1990

Disorders of potassium homeostasis.

Derangements in potassium homeostasis affect the body's bioelectric processes, including muscle contraction, nerve conduction, and myocardial electric pacing. Changes in extracellular potassium concentration occur with altered routes of elimination (renal or gastrointestinal) or with pathologic shifts in potassium from one body fluid compartment to another. The therapeutic interventions may either restore a normal resting potential for excitable cells or affect the threshold potential. Thus, an understanding of the basic pathophysiology is the foundation for treatment.

Humans↗
PubMed1989

Effect of carbenoxolone on glucocorticoid metabolism and Na transport in toad bladder.

In humans, diminished 11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD) enzyme activity has been associated with sodium retention and hypertension. These studies show that the toad bladder, another target tissue epithelium displaying steroid-induced sodium transport, possesses the enzyme 11 beta-OHSD. The toad urinary bladder rapidly transformed corticosterone (3 x 10(-8) M) (50% by 10 min and 90% by 180 min) with 11-dehydrocorticosterone being the major metabolite. The 11-dehydrocorticosterone produced reached an apparent plateau when the tissue incubations were repeated with higher concentrations of corticosterone (10(-7) and 10(-6) M). Carbenoxolone sodium (2.5 x 10(-5) M), a water soluble derivative of glycyrrhetinic acid, markedly inhibited the metabolism of corticosterone (3 x 10(-8) M) to 11-dehydrocorticosterone similar to previous observations in the mammalian kidney. Carbenoxolone sodium (2.5 x 10(-5) M) did not significantly affect short-circuit current (SCC) in toad bladders when added to either the serosal or mucosal bath. However, when carbenoxolone sodium was added to the mucosal bath and 60 min later corticosterone 10(-6) M was placed in the serosal bath, bladders generated a SCC 2.07 +/- 0.17 (mean +/- SE) times above base line at 360 min compared with 1.48 +/- 0.11 in bladders exposed to corticosterone alone (P less than 0.02). In parallel experiments, carbenoxolone sodium in the mucosal bath enhanced the rise in SCC induced by cortisol 10(-6) M; 1.66 +/- 0.16 times above base line at 360 min compared with 1.07 +/- 0.14 with cortisol alone (P less than 0.02). We conclude that the toad bladder contains 11 beta-OHSD and inhibition of this enzyme with carbenoxolone sodium is associated with amplification of glucocorticoid-induced transepithelial sodium transport in this tissue. However, since the quantity of 11-dehydro-product produced appears to be limited, other factors in addition to inhibition of 11 beta-OHSD may play a role in this amplification of sodium transport.

Animals↗
PubMed1977

Toxicity from tea ingestion in an infant: a computer simulation analysis.

A seven-week-old infant presented with tonic posturing and nervous irritability after concentrated tea ingestion. The tea was analyzed and found to contain caffeine, a methylxanthine central nervous system stimulant. With the aid of a computer, projected blood levels were calculated over a thirty-hour time period and comared to the infant's clinical status. It is recommended that beverages containing xanthines be given to infants and small children with caution.

Caffeine↗