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Biomedical subjects

S Dabbagh

Publications and source records attributed to S Dabbagh.

31 records · Page 2Linked to original sources
PubMed1987

Studies on renal adaptation to altered dietary amino acid intake: reduced renal cortex taurine content increases the Vmax of taurine uptake by brush border membrane vesicles.

Rats were placed on a normal taurine diet (NTD), low taurine diet (LTD) or a high taurine diet (HTD) for 14 days. beta-Alanine was fed to half of the animals in each group and resulted in a lowered renal cortex taurine content. Brush border membrane vesicle (BBMV) uptake of taurine was higher after beta-alanine feeding and was associated with an increase in Vmax of uptake. beta-Alanine feeding to HTD animals also altered the Km of uptake, possibly since the load of sulfur amino acids (6% of diet) was high. As a control, glycine (3%) feeding for 8 days along with each diet did not alter the plasma or renal cortex content; BBMV uptake as well as Km and Vmax of taurine accumulation were minimally altered. Accordingly, ingestion of a non-sulfur-containing alpha-amino acid did not change beta-amino acid transport. This study provides evidence that whole body taurine homeostasis is maintained in the presence of a taurine-depleting agent (beta-alanine feeding) by an increase in the number of Na(+)-taurine uptake sites.

Amino Acids↗
PubMed1987

Moderate hypocalcemia due to normal serum 1,25-dihydroxyvitamin D levels in an asymptomatic kindred with familial hypoparathyroidism.

Hypoparathyroidism was diagnosed in nine members of a kindred of three generations. This study investigated why these persons were asymptomatic and without developmental abnormalities, in contrast to the common presentation of idiopathic hypoparathyroidism. In the hypocalcemic subjects, serum calcium level was 7.4 +/- 0.8 mg/dl (mean +/- SD) and ionized serum calcium level was 3.48 +/- 0.21 mg/dl. Immunoreactive parathyroid hormone values were inappropriately low. Injection of EDTA in one patient lowered ionized calcium levels, but immunoreactive parathyroid hormone values did not rise. Serum levels of 1,25-dihydroxyvitamin D and other vitamin D metabolites were normal or elevated and substantially higher than in other hypoparathyroid states. The normally observed positive correlation between the fasting urinary calcium/creatinine ratio and serum 1,25-dihydroxyvitamin D that reflects the dependence of net bone resorption on 1,25-dihydroxyvitamin D was upheld in hypoparathyroid patients. It is proposed that the subjects with familial hypoparathyroidism in this kindred had moderate asymptomatic hypocalcemia without developmental abnormalities because normal or elevated serum 1,25-dihydroxyvitamin D levels enhanced intestinal calcium absorption. This may represent one point in the spectrum of idiopathic hypoparathyroidism. Alternately, both the moderate degree of hypocalcemia and the normal serum calcitriol values could have been related to mild, partial hypoparathyroidism, which could have been inherited in this kindred.

Calcium↗
PubMed1987

Severe renal osteodystrophy without elevated serum immunoreactive parathyroid hormone concentrations in hypomagnesemia due to renal magnesium wasting.

An 8 1/2-year-old girl presented with a long history of seizures, growth retardation, muscle weakness, gait disturbance, and hearing loss. Her evaluation revealed chronic moderate renal failure (serum creatinine 2.2 mg/dL), severe hypocalcemia (5 mg/dL), hyperphosphatemia (8.1 mg/dL), hypomagnesemia (1.5 mg/dL), increased urinary magnesium excretion (2 mg/kg/d), high fractional excretion of magnesium (21.7%), hypokalemia (3.2 mEq/L), and hyperkaliuria (26 mEq/L). Low circulating immunoreactive parathyroid hormone levels for the degree of the hypocalcemia (serum N-parathyroid hormone 212 pg/mL) and severe rickets without evidence of osteitis fibrosa cystica were found. The patient probably has primary renal leak hypomagnesemia (magnesuric hypomagnesemia) which caused impaired secretion of immunoreactive parathyroid hormone leading to severe hypocalcemia and calcium deficiency rickets. Treatment with magnesium and calcium supplements, calcitriol, and aluminum hydroxide resulted in marked clinical, biochemical, and radiologic improvement. Calcium deficiency rickets due to primary or secondary renal magnesium wasting in conjunction with moderate renal failure represents a largely unrecognized metabolic bone disease.

Aluminum Hydroxide↗
PubMed1985

Factors affecting the transport of beta-amino acids in rat renal brush-border membrane vesicles. The role of external chloride.

The effect of a variety of ions and other solutes on the accumulation of the beta-amino acid, taurine, was examined in rat renal brush-border membrane vesicles. Initial taurine uptake (15 and 30 s) is sodium-dependent with a typical overshoot. This Na+ effect was confirmed by exchange diffusion and gramicidin inhibition of taurine uptake. External K+ or Li+ do not increase taurine accumulation more than Na+-free mannitol, except that the combination of external K+ and Na+ in the presence of nigericin enhances uptake. Of all anions tested, including more permeant (SCN- and NO3-) or less permeant (SO4(2-)), chloride supported taurine accumulation to a significantly greater degree. Preloading vesicles with choline chloride reduced taurine uptake, suggesting that external Cl- stimulates uptake. Since this choline effect could be related to volume change, due to the slow diffusion of choline into vesicles, brush-border membrane vesicles were pre-incubated with LiCl, LiNO3 and LiSO4. Internal LiCl, regardless of the final Na+ anion mixture, reduced initial rate (15 and 60 s) and peak (360 s) taurine uptake. Internal LiNO3 or LiSO4 with external NaCl resulted in similar or higher values of uptake at 15, 60 and 360 s, indicating a role for external Cl- in taurine uptake in addition to Na+ effect. Although uptake by vesicles is greatest at pH 8.0 and inhibited at acidic pH values (pH less than 7.0), an externally directed H+ gradient does not influence uptake. Similarly, amiloride, an inhibitor of the Na+/H+ antiporter, had no influence on taurine accumulation over a wide variety of concentrations or at low Na+ concentrations. Taurine uptake is blocked only by other beta-amino acids and in a competitive fashion. D-Glucose and p-aminohippurate at high concentrations (greater than 10(-3) M) reduce taurine uptake, possibly by competing for sodium ions, although gramicidin added in the presence of D-glucose inhibits taurine uptake even further. These studies more clearly define the nature of the renal beta-amino acid transport system in brush-border vesicles and indicate a role for external Cl- in this uptake system.

Amiloride↗
PubMed1985

Renal cortex taurine content regulates renal adaptive response to altered dietary intake of sulfur amino acids.

Rats fed a reduced sulfur amino acid diet (LTD) or a high-taurine diet (HTD) demonstrate a renal adaptive response. The LTD results in hypotaurinuria and enhanced brush border membrane vesicle (BBMV) accumulation of taurine. The HTD causes hypertaurinuria and reduced BBMV uptake. This adaptation may relate to changes in plasma or renal cortex taurine concentration. Rats were fed a normal-taurine diet (NTD), LTD, or HTD for 14 d or they underwent: (a) 3% beta-alanine for the last 8 d of each diet; (b) 3 d of fasting; or (c) a combination of 3% beta-alanine added for 8 d and 3 d of fasting. Each maneuver lowered the cortex taurine concentration, but did not significantly lower plasma taurine values compared with controls. Increased BBMV taurine uptake occurred after each manipulation. Feeding 3% glycine did not alter the plasma, renal cortex, or urinary taurine concentrations, or BBMV uptake of taurine. Feeding 3% methionine raised plasma and urinary taurine excretion but renal tissue taurine was unchanged, as was initial BBMV uptake. Hence, nonsulfur-containing alpha-amino acids did not change beta-amino acid transport. The increase in BBMV uptake correlates with the decline in renal cortex and plasma taurine content. However, since 3% methionine changed plasma taurine without altering BBMV uptake, it is more likely that the change in BBMV uptake and the adaptive response expressed at the brush border surface relate to changes in renal cortex taurine concentrations. Finally, despite changes in urine and renal cortex taurine content, brain taurine values were unchanged, which suggests that this renal adaptive response maintains stable taurine concentrations where taurine serves as a neuromodulator.

Amino Acids, Sulfur↗
PubMed1984

Renal-nonresponsive, bone-responsive pseudohypoparathyroidism. A case with normal vitamin D metabolite levels and clinical features of rickets.

Clinical signs of rickets developed in a previously healthy 13-year-old girl with normal features. She had hypocalcemia, hyperphosphatemia, elevated alkaline phosphatase and parathyroid hormone levels, and normal vitamin D metabolite levels, with osteitis fibrosa cystica on bone biopsy specimen. Her renal function was normal. Treatment with 1 microgram of calcitriol each day resulted in symptomatic and clinical relief and improvement of the serum chemical values. This patient probably has pseudohypoparathyroidism type 1, with renal nonresponsiveness and bone responsiveness. This disorder has the clinical features of rickets, but represents hyperparathyroid bone disease.

Adolescent↗
PubMed1982

Prolonged anuria and aortic insufficiency in a child with Wegener's granulomatosis.

A 16 year-old boy developed generalized Wegener's granulomatosis with rapidly progressive renal insufficiency resulting in prolonged anuria. He was treated with cyclophosphamide, prednisone and anticoagulants, and was maintained on peritoneal dialysis for seven weeks, after which he regained a GFR of 35 ml/min. Recovery of renal function following prolonged anuria has not been previously reported in a child with Wegener's granulomatosis. The patient also developed aortic regurgitation, a cardiac lesion not previously described in this disorder.

Adolescent↗
PubMedDate not supplied

Divergent membrane maturation in rat kidney: exposure by dietary taurine manipulation.

Taurinuria is characteristic of the immature rat. The excessive taurine loss could be the result of brush border or basal lateral membrane immaturity. The beta-amino acid, taurine, and D-glucose were examined using isolated brush border membrane vesicles (BBMV), slices and tubules prepared from 28-day-old rats. In BBMV, taurine accumulation was inversely proportional to osmolarity, indicating uptake rather than binding, and taurine accumulation was Na+-dependent. BBMV from 28-day rats did not accumulate D-glucose to the same degree as in adult BBMV, and the initial rate of uptake was slower. Taurine uptake had a similar Km and Vmax in BBMV from immature rats. Despite similarities in the kinetics of taurine uptake, higher urinary taurine concentrations are found in younger rats. The efflux of taurine from slices and tubules was much slower than in adults and probably accounts for the taurinuria of young animals. A diet low in methionine and taurine (LTD) given for seven days resulted in a lower excretion and fractional excretion of taurine than in animals fed a normal sulfur amino acid diet (NTD). A high-taurine diet (HTD) causes excessive taurinuria. These patterns of excretion are reflected at the brush border membrane surface with greater uptake after the LTD and reduced uptake after the HTD. A kinetic analysis of adult and 28-day-old animal BBMV reveals that the Vmax of accumulation is altered by diet, whereas the Km remains unchanged. The Vmax is higher in BBMV from LTD animals and lower in BBMV from HTD animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗