Biomedical subjects

C L Wabner

Publications and source records attributed to C L Wabner.

8 recordsLinked to original sources

PubMed1993

Effect of orange juice consumption on urinary stone risk factors.

The value of orange juice consumption in kidney stone prevention was examined in 8 healthy men and 3 men with documented hypocitraturic nephrolithiasis. They underwent 3 phases of a metabolic study, a placebo phase and 2 treatment phases in which they ingested either 1.2 l. orange juice (containing 60 mEq. potassium and 190 mEq. citrate per day) with meals or potassium citrate tablets (60 mEq. per day) with water and meals. Compared to potassium citrate, orange juice delivered an equivalent alkali load and caused a similar increase in urinary pH (6.48 versus 6.75 from 5.71) and urinary citrate (952 versus 944 from 571 mg. per day). Therefore, orange juice, like potassium citrate, decreased urinary undissociated uric acid levels and increased the inhibitor activity (formation product) of brushite (calcium phosphate). However, orange juice increased urinary oxalate and did not alter calcium excretion, whereas potassium citrate decreased urinary calcium without altering urinary oxalate. Thus, orange juice lacked the ability of potassium citrate to decrease urinary saturation of calcium oxalate. Overall, orange juice should be beneficial in the control of calcareous and uric acid nephrolithiasis.

Adult↗

PubMed1993

Calcium citrate without aluminum antacids does not cause aluminum retention in patients with functioning kidneys.

It has been suggested that calcium citrate might enhance aluminum absorption from food, posing a threat of aluminum toxicity even in patients with normal renal function. We therefore measured serum and urinary aluminum before and following calcium citrate therapy in patients with moderate renal failure and in normal subjects maintained on constant metabolic diets with known aluminum content (967-1034 mumol/day, or 26.1-27.9 mg/day, in patients and either 834 or 1579 mumol/day, or 22.5 and 42.6 mg/day, in normal subjects). Seven patients with moderate renal failure (endogenous creatinine clearance of 43 ml/min) took 50 mmol (2 g) calcium/day as effervescent calcium citrate with meals for 17 days. Eight normal women received 25 mmol (1 g) calcium/day as tricalcium dicitrate tablets with meals for 7 days. In patients with moderate renal failure, serum and urinary aluminum were normal before treatment at 489 +/- 293 SD nmol/l (13.2 +/- 7.9 micrograms/l) and 767 +/- 497 nmol/day (20.7 +/- 13.4 micrograms/day), respectively. They remained within normal limits and did not change significantly during calcium citrate treatment (400 +/- 148 nmol/l and 600 +/- 441 nmol/day, respectively). Similarly, no significant change in serum and urinary aluminum was detected in normal women during calcium citrate administration (271 +/- 59 vs 293 +/- 85 nmol/l and 515 +/- 138 vs 615 +/- 170 nmol/day, respectively). In addition, skeletal bone aluminum content did not change significantly in 14 osteoporotic patients (endogenous creatinine clearance of 68.5 ml/min) treated for 24 months with calcium citrate, 10 mmol calcium twice/day separately from meals (29.3 +/- 13.9 ng/mg ash bone to 27.9 +/0- 10.4, P = 0.727). In them, histomorphometric examination did not show any evidence of mineralization defect. Thus, calcium citrate given alone without aluminum-containing drugs does not pose a risk of aluminum toxicity in subjects with normal or functioning kidneys, when it is administered on an empty stomach at a recommended dose of 20 mmol calcium/day.

Absorption↗

PubMed1992

Modification by food of the calcium absorbability and physicochemical effects of calcium citrate.

The food-calcium (Ca) interaction was examined in 12 healthy women (mean age 38 years) maintained on a constant metabolic diet. They underwent three phases of study, comprised of control (no Ca), Ca citrate (1 g Ca/day) during meals, and Ca citrate separately from meals. Each phase was 7 days in length and two 24-hour urine samples were collected on days 6 and 7. The rise from the control phase in urinary Ca was slightly more prominent when Ca citrate was given with meals than without (68 and 62%, respectively). The fall in urinary phosphorus was equivalent at about 25% between Ca citrate phases. The rise in urinary citrate and pH and the decline in urinary ammonium were more prominent when Ca citrate was given with meals; however, the changes were small or nonsignificant. The urinary saturation of Ca oxalate, brushite or monosodium urate did not differ between the two Ca citrate phases. There was a nonsignificant rise in serum iron during Ca citrate phases. The results suggest that: 1) dissolution and absorption of Ca citrate might be slightly greater when given with food than without; 2) that the ability of Ca citrate to attenuate crystallization of stone-forming Ca salts in urine is not modified by food; and 3) that Ca citrate may not impair iron absorption from food.

Adult↗

PubMed1991

A simple method for quantitating the propensity for calcium oxalate crystallization in urine.

To assess the propensity for spontaneous crystallization of calcium oxalate in urine, the permissible increment in oxalate is calculated. The previous method required visual observation of crystallization with the addition of oxalate, this warranted the need for a large volume of urine and a sacrifice in accuracy in defining differences between small incremental changes of added oxalate. Therefore, this method has been miniaturized and spontaneous crystallization is detected from the depletion of radioactive oxalate. The new "micro" method demonstrated a marked decrease (p < 0.001) in the permissible increment in oxalate in urine of stone formers versus normal subjects. Moreover, crystallization inhibitors added to urine, in vitro (heparin or diphosphonate) or in vivo (potassium citrate administration), substantially increased the permissible increment in oxalate. Thus, the "micro" method has proven reliable and accurate in discriminating stone forming from control urine and in distinguishing changes of inhibitory activity.

Adult↗

PubMed1990

Life span differences in digoxin uptake and excretion.

Little is known about the underlying mechanisms for the altered susceptibility to digitalis with age. To this end, we investigated the digoxin uptake and excretion in mice and rats of different ages through the life span, including the periods of growth, maturity, and aging. Digoxin uptake by cardiac slices was linear from 0 to 15 min, with steady state occurring at 45 min. The rate in the mature 12-month mouse was significantly less than that of the senescent 30-month mouse. The kinetic parameters revealed a significant decrease in Km with a concomitant increase in Vmax during senescence. On the other hand, digoxin uptake by renal cortical slices was highest during growth, decreased to a maturation plateau and then declined further during senescence. Renal clearance and the secretory capacity for digoxin increased 30 and 62%, respectively, during growth and progressively decreased from maturity through senescence and were 59 and 77%, respectively, during aging. In summary, there was an increase in digoxin clearance and tubular activity during growth, and an increase in myocardial uptake of digoxin and a decrease in renal excretion during aging. Thus, these results may explain the clinical observations of altered susceptibility to digitalis with age.

Aging↗

PubMed1990

Intestinal transport during the life span of the mouse.

Intestinal malabsorption of nutrients may be a critical factor in aging. For this reason, we investigated the nutrient absorption in mice of different ages of the life span, representing growth (3 mo), young adult (12 mo), mature (24 mo), old (30 mo), and very old (33-36 mo) periods. The everted sac technique was used to study the transepithelial transport of D-glucose, 3-O-methyl-D-glucose (3MG), and L-tyrosine. There was a 32% increase in the rate of D-glucose transepithelial transport during growth followed by a 55% decrease in the old mouse, and the same pattern occurred with 3MG, a nonmetabolized glucose derivative. However, L-tyrosine transepithelial transport was not impaired until the mouse reached the very old, 33-36 mo period. Also, the rate of D-glucose metabolism measured by lactate production in the very old mouse was only 45% of the mature mouse value. In addition, these transepithelial transport changes were accompanied by decreases in the number and the height of villi. The results indicate that intestinal transepithelial transport and the surface area for absorption decrease in aging.

3-O-Methylglucose↗

PubMed1988

Crystal adsorption and growth slowing by nephrocalcin, albumin, and Tamm-Horsfall protein.

Urine inhibition of calcium oxalate monohydrate (COM) crystal growth (CG) seems due to a glycoprotein that contains gamma-carboxyglutamic acid and has been named nephrocalcin (NC); however, Tamm-Horsfall protein (THP) and albumin resemble NC and make its measurement and role uncertain. NC in urine is aggregated to molecular mass 64 kDa and higher, similar to albumin (64 kDa) and THP (87 kDa). Albumin and THP are calcium binding, albumin adsorbs to COM crystals, and THP has been described as an inhibitor of COM growth. Antisera to NC have cross-reacted with THP even though the NC was isolated from cultured renal cells. Here we have compared highly purified NC, THP, and albumin adsorption with COM crystals and CG inhibition; also we compared their patterns of cross-reactivities with a new antiserum against NC and a monoclonal antibody to THP. NC adsorbs to COM crystals, THP does not. Albumin and THP do not inhibit CG. Cross-reactivity of albumin and THP to the antiserum is slight by direct enzyme-linked immunosorbent assay and nonexistent by competitive ELISA; reaction of NC to the anti-THP monoclonal antibody is absent.

Adsorption↗

PubMed1987

Aging changes in renal handling of p-aminohippurate.

Aging alterations in the renal transport of p-aminohippurate (PAH) were investigated using cortical slices from C57BL/6 mice and standard clearance techniques in 5-ethyl-5-(1-methylpropyl)-2-thiobarbituric acid (Inactin)-anesthetized Fischer 344 rats. Life-span stages were classified as growth, maturity, and aging. PAH uptake was linear from 0 to 20 min with steady state occurring at 30 min in the growing and mature mouse and 20 min in the aging mouse. Km values for PAH uptake in the growing, mature, and aging mouse were 250, 123, and 643 microM, respectively, and maximal rate of uptake values were 0.756, 0.926, and 0.586 mumol X g-1 X 30 min-1, respectively. The efflux half-life (t 1/2) for PAH was similar in all age groups. The PAH acetylation rate was similar in the growing and mature mouse but decreased by 40% in the aging mouse. There were statistically significant correlations between aging (12-27 mo) and renal plasma flow [(RPF) r2 = 0.33, P less than 0.05] and between aging and tubular maximal (Tm) activity for PAH transport (r2 = 0.84, P less than 0.001). Maximal decreases of 25 and 40% were found for RPF and Tm, respectively, in the aging rat. It is concluded that aging affects PAH transport at the receptor level.

Aging↗