Factors related to allograft survival in recipients of the same donor.
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Adult↗
Biomedical subjects
F Caravaca
Publications and source records attributed to F Caravaca.
Metabolic acidosis in advanced renal failure: differences between diabetic and nondiabetic patients.
Metabolic acidosis is almost invariably a consequence of advanced renal failure, although its severity can vary widely. To evaluate the determinants of the severity of metabolic acidosis, with special interest in determining if there is any difference in the prevalence and severity of metabolic acidosis between patients with and without diabetes, 113 predialysis patients with renal failure were studied. Criteria for inclusion onto the study were: creatinine clearance (Ccr)/1.73 m2 less than 30 mL/min, no alkali therapy within the previous 30 days, and the absence of respiratory diseases. Forty-eight patients had diabetes (33 patients with diabetic nephropathy). The following data were analyzed: demographics; cause of renal failure; hematocrit; serum urea, creatinine, uric acid, albumin, glucose, hemoglobin A1c, bicarbonate, sodium, potassium, chloride, calcium, phosphorus, and alkaline phosphatase levels; anion gap; urinary protein excretion; Ccr/1.73 m2; half of the sum of creatinine and urea clearances (Ccr-Cu); protein-equivalent nitrogen appearance (PNA); and whether the patients received diuretics (75 patients), angiotensin-converting enzyme inhibitors (54 patients), and/or calcium channel blockers (55 patients). After the exclusion of eight patients because of hypochloremia (three patients with and five patients without diabetes), mean serum bicarbonate levels were significantly greater in patients with diabetes than in the rest of the patients (20.7 +/- 2.3 v 18.2 +/- 2. 3 mmol/L; P = 0.0001). The mean anion gap (mmol/L) was also significantly less in patients with than without diabetes (19.70 +/- 3.65 v 22.35 +/- 3.64; P = 0.003). Eleven of 105 patients had serum bicarbonate levels of 23 mmol/L or greater (9 patients with and 2 patients without diabetes). Pure elevated anion gap followed by mixed (high anion gap and hyperchloremia) were the most common types of metabolic acidosis observed in both groups. There were no differences in PNA, diuretic treatment, or vomiting history between patients with and without diabetes. By multiple logistic regression analysis, the best determinants for a serum bicarbonate level greater than 19 mmol/L were: the diagnosis of diabetic nephropathy (odds ratio, 0.107; P = 0.0002), Ccr-Cu (odds ratio, 0.824; P = 0. 014), and age (odds ratio, 0.966; P = 0.046). In conclusion, patients with diabetes with advanced renal failure showed a less severe metabolic acidosis, which cannot be explained by gastrointestinal hydrogen ion losses, drugs, or reduced protein catabolic rate. Patients with diabetes may have a more efficient extrarenal generation of bicarbonate than end-stage renal failure patients without diabetes.
Acidosis, Renal Tubular↗
Parathyroid function as a determinant of the response to calcitriol treatment in the hemodialysis patient.
BACKGROUND: Bolus calcitriol (CTR) is used for the treatment of secondary hyperparathyroidism in dialysis patients. Although CTR treatment reduces parathyroid hormone (PTH) levels in many dialysis patients, a significant number fail to respond. METHODS: To learn whether or not an analysis of parathyroid function could further illuminate the response to CTR, a PTH-calcium curve was performed before and after at least two months of CTR treatment in 50 hemodialysis patients with a predialysis intact PTH of greater than 300 pg/ml. RESULTS: For the entire group (N = 50), CTR treatment resulted in a 24% reduction in predialysis (basal) PTH from 773 +/- 54 to 583 +/- 71 pg/ml (P < 0.001), whereas ionized calcium increased from 1.10 +/- 0.02 to 1.22 +/- 0.02 mM (P < 0.001); however, maximal and minimal PTH did not change from pre-CTR values. Based on whether or not the basal PTH decreased by 40% or more during CTR treatment, patients were divided into responders (Rs, N = 25) and nonresponders (NRs, N = 25). Before CTR, the NR group was characterized by a greater basal (959 +/- 80 vs. 586 +/- 51 pg/ml, P < 0.001) and maximal (1899 +/- 170 vs. 1172 +/- 108 pg/ml, P < 0. 001) PTH and serum phosphorus (6.14 +/- 0.25 vs. 5.14 +/- 0.34 mg/dl, P < 0.01). Logistical regression analysis showed that the pre-CTR basal PTH was the most important predictor of the post-CTR basal PTH, and a pre-CTR basal PTH of 750 pg/ml represented a 50% probability of a response. Basal PTH correlated with the ionized calcium in the NR group (r = 0.59, P = 0.002) but not in the R group (r = 0.06, P = NS). In the R group, an inverse correlation was present between ionized calcium and the basal/maximal PTH ratio, an indicator of whether calcium is suppressing basal PTH secretion relative to the maximal secretory capacity (maximal PTH) r = -0.55, P = 0.004; in the NR group, this correlation approached significance but was positive (r = 0.34, P = 0.09). After CTR treatment, serum calcium increased in both groups, and despite marked differences in basal PTH (Rs, 197 +/- 25 vs. NRs, 969 +/- 85 pg/ml), an inverse correlation between ionized calcium and basal/maximal PTH was present in both groups (Rs, r = -0.61, P = 0.001, and NRs, r = -0.60, P = 0.001). CONCLUSIONS: (a) Dynamic testing of parathyroid function provided insights into the pathophysiology of PTH secretion in hemodialysis patients. (b) The magnitude of hyperparathyroidism was the most important predictor of the response to CTR. (c) Before CTR treatment, PTH was sensitive to calcium in Rs, and serum calcium was PTH driven in NRs, and (d) after the CTR-induced increase in serum calcium, calcium suppressed basal PTH relative to maximal PTH in both groups.
Calcitriol↗
Effects of oral phosphorus supplementation on mineral metabolism of renal transplant recipients.
BACKGROUND: Persistent hyperparathyroidism (HPT) is frequently observed in kidney transplant recipients. Hypophosphataemia is a common biochemical consequence of HPT. Theoretically, oral phosphorus administration may induce negative effects on the control of HPT, though this point has never been demonstrated in kidney-transplant recipients. This study was designed to evaluate the effects of oral phosphorus supplementation on the mineral metabolism of successful kidney transplant recipients. METHODS: Thirty-two kidney transplant recipients with serum creatinine < 2 mg/dl and serum phosphate levels <3.5 mg/dl were included in the study. After a washout period in which oral phosphorus supplementation was discontinued, the following parameters were determined (F0 period): serum calcium, phosphate, alkaline phosphatase, uric acid, bicarbonate, PTH, 1,25-dihydroxyvitamin D3 (1,25 (OH)(2)D) and 25-hydroxyvitamin D3 (25OHD). Creatinine clearance, calcium, and phosphate excretion were determined from a 24-h urine sample. The same determinations were repeated (F1 period) after all patients received 1.5 g of oral phosphorus for 15 days. For data analysis, patients were divided into two subgroups (optimal and suboptimal) according to allograft function (Ccr>or < 70 ml/min/1.73 m2). RESULTS: In the F0 period, only nine of 32 patients had PTH levels within the normal range (<65 pg/ml). The mean concentrations of PTH, 1,25(OH)(2)D and 25OHD were 132+/-97pg/ml, 40.5+16pg/ml and 12.5+/-8.2 ng/ml respectively. Phosphorus supplementation led to significant reductions in serum calcium and 1,25(OH)(2)D concentrations, as well as in urinary calcium excretion in the whole group. On the contrary, serum phosphate, PTH, and urinary phosphate excretion increased significantly. The percentage increase in PTH concentrations after phosphorus supplementation were similar in patients with optimal and suboptimal allograft function (33 vs 36%). The reduction of 1,25 (OH)(2)D concentrations after phosphorus supplementation was observed mainly in the subgroup with optimal allograft function (21% reduction with respect to baseline values), while the mean 1,25(OH)(2)D concentrations in patients with suboptimal allograft function scarcely changed (1.4% increase). Changes in 1,25(OH)(2)D concentrations after phosphorus supplementation, expressed as a percentage of the initial concentrations, correlated positively with the percentage changes in PTH concentrations for the whole group, as well as for each subgroup. The best determinants for the percentage and the absolute increase in PTH concentration after phosphorus supplementation was the final serum phosphate concentration (F=4.84, r=0.37, P=0.035) and the increase in serum phosphate (F=7.69, r=0.45, P= 0.009) respectively. CONCLUSIONS: Oral phosphorus supplementation led to a significant increase in the PTH concentration of kidney transplant recipients. The mean 1,25(OH)(2)D concentration decreased mainly in recipients with optimal allograft function. The counterbalance effect of PTH on 1,25(OH)(2)D production may account for the relative preservation of 1,25(OH)2D levels in recipients with suboptimal allograft function.
Administration, Oral↗
Are plasma 1,25-dihydroxyvitamin D3 concentrations appropriate after successful kidney transplantation?
We studied 28 patients with parathyroid hormone (PTH) concentrations >65 pg/ml immediately prior to kidney transplant and who had stable allograft function with serum creatinine <2 mg/dl. After 12-18 months of transplantation, biochemical parameters (including 25-hydroxy- and 1,25-dihydroxy-vitamin D3) were studied. Patients were divided into three groups according to their PTH concentrations. Patients with renal transplant were compared with 50 healthy subjects and 20 patients with primary hyperparathyroidism. The mean 1,25-dihydroxy-vitamin D3 concentration of the transplant patients did not differ from the controls, but was lower than in patients with primary hyperparathyroidism. Using univariate linear regression analysis, 1,25-dihydroxy vitamin D3 correlated positively with PTH (P=0.008) and serum calcium (P=0.0015), and inversely with creatinine clearance (P=0.01). However, it did not correlate significantly with serum phosphorus. Our data suggest that renal transplant recipients may have an inappropriate production of 1,25-dihydroxy vitamin D3; suboptimal allograft function may be a major limiting factor.
Adult↗
Hypertensive crises following platelet transfusions in a patient on erythropoietin therapy.
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Adolescent↗
Evidence for both abnormal set point of PTH stimulation by calcium and adaptation to serum calcium in hemodialysis patients with hyperparathyroidism.
In vitro studies of parathyroid glands removed from dialysis patients with secondary hyperparathyroidism and hypercalcemia have demonstrated the presence of an increased set point of parathyroid hormone (PTH) stimulation by calcium (set point [PTHstim]), suggesting an intrinsic abnormality of the hyperplastic parathyroid cell. However, clinical studies on dialysis patients have not observed a correlation between the set point (PTHstim) and the magnitude of hyperparathyroidism. In the present study, 58 hemodialysis patients with moderate to severe hyperparathyroidism (mean PTH 780 +/- 377 pg/ml) were evaluated both before and after calcitriol treatment to establish the relationship among PTH, serum calcium, and the set point (PTHstim) and to determine whether changes in the serum calcium, as induced by calcitriol treatment, modified these relationships. Calcitriol treatment decreased serum PTH levels and increased the serum calcium and the setpoint (PTHstim); however, the increase in serum calcium was greater than the increase in the setpoint (PTHstim). Before treatment with calcitriol, the correlation between the set point (PTHstim) and the serum calcium was r = 0.82, p < 0.001, and between the set point (PTHstim) and PTH was r = 0.39, p = 0.002. After treatment with calcitriol, the correlation between the set point (PTHstim) and the serum calcium remained significant (r = 0.70, p < 0.001), but the correlation between the set point (PTHstim) and PTH was no longer significant (r = 0.09); moreover, a significant correlation was present between the change in the set point (PTHstim) and the change in serum calcium that resulted from calcitriol treatment (r = 0.73, p < 0.001). The correlation between the residual values (deviation from the regression line) of the set point (PTHstim), derived from the correlation between PTH and the set point (PTHstim), and serum calcium was r = 0.77, p < 0.001 before calcitriol and r = 0.72, p < 0.001 after calcitriol. In conclusion, the set point (PTHstim) increased after a sustained increase in the serum calcium, suggesting an adaptation of the set point to the existing serum calcium; the increase in serum calcium resulting from calcitriol treatment was greater than the increase in the set point (PTHstim); the set point (PTHstim) was greater in hemodialysis patients with higher serum PTH levels; and the correlation between PTH and the set point (PTHstim) may be obscured because the serum calcium directly modifies the set point (PTHstim).
Adaptation, Physiological↗
Drug action of ritodrine on the sarcoplasmic reticulum Ca(2+)-ATPase from skeletal muscle.
Ritodrine inhibits the steady-state Ca(2+)-ATPase activity of isolated sarcoplasmic reticulum vesicles in a dose-dependent manner. The observed K0.5 value for inhibition (approximately 3 mM) gives proof of a low-affinity interaction. Ritodrine also interferes with the steady-state Ca2+ transport ability decreasing the maximal rate without modification of the Ca2+ or ATP affinity for the enzyme. This is consistent with an absence of competition for the transport and the catalytic sites. Analysis of the catalytic and transport cycle shows that: (i) ritodrine inhibits the phosphorylation partial reaction. This is supported by pre-steady-state kinetic experiments of Ca2+ transport and also by the temperature dependence of the phosphoenzyme level. (ii) At high ritodrine concentrations the dephosphorylation step becomes rate-limiting. This is suggested by the biphasic profile (V-shape) of phosphoenzyme accumulation at different ritodrine concentrations. This was also confirmed by chase experiments of radioactive phosphoenzyme decomposition at steady state. These data reveal a complex pattern of inhibition involving two sites for interaction with low and high ritodrine concentrations. It is envisaged that ritodrine does not exert any direct effect on the smooth muscle sarcoplasmic reticulum Ca(2+)-ATPase when used in the treatment of preterm birth.
Adenosine Triphosphate↗
Effect of the mode of calcitriol administration on PTH-ionized calcium relationship in uraemic patients with secondary hyperparathyroidism.
To assess the effect of the different modes of calcitriol administration on PTH-ionized calcium relationship we conducted a prospective clinical trial in 33 patients on chronic haemodialysis with secondary hyperparathyroidism (four times upper normal limit intact PTH) who were randomly assigned, with stratification to PTH levels, to receive daily oral, intermittent oral, or intermittent intravenous calcitriol at the same dose of 0.045 micrograms/kg/weekly. PTH-iCa curves were generated by inducing hypo- or hypercalcaemia in sequential haemodialysis 1 week apart, before and after 10 weeks on treatment. All patients were dialysed against a dialysate calcium concentration of 2.5 mEq/l throughout the study period. After drop-outs, 26 patients completed the study: 11 on intravenous calcitriol (mean basal PTH +/- SD: 666 +/- 280 pg/ml), eight on intermittent oral calcitriol (mean basal PTH: 831 +/- 361), and seven on daily oral calcitriol (mean basal PTH: 719 +/- 280). Serum ionized calcium and phosphorus significantly increased in intravenous and daily oral groups after calcitriol treatment, but not in the intermittent oral group. Basal PTH did not significantly change in the three groups after 10 weeks on treatment. Maximal PTH significantly decreased in intravenous group (1449 +/- 660 versus 1122 +/- 691 pg/ml, P = 0.0085) and at the limit of statistical significance in the intermittent oral group (1701 +/- 774 versus 1445 +/- 634, P = 0.12), but it did not change in the daily oral group. Minimal PTH did not modify in the three groups. In all three groups, a shift to the right in the PTH-iCa relationships were observed, with significant changes in the set point of calcium.(ABSTRACT TRUNCATED AT 250 WORDS)
Administration, Oral↗
Haemodynamic changes induced by the correction of anaemia by erythropoietin: role of antiplatelet therapy.
BACKGROUND: In a retrospective study, antiplatelet therapy has been shown to be associated with a decreased incidence of erythropoietin-induced hypertension. In order to ascertain the role of antiplatelet drugs in the haemodynamic response to the correction of anaemia by rHuEpo, 18 patients on chronic haemodialysis who started rHuEpo therapy were prospectively studied. METHODS: The subjects were randomly assigned to receive or not, one of the following antiplatelet drugs: ditazole (3 patients), ticlopidine (3 patients) or aspirin plus dipyridamole (3 patients). Cardiac index (CI) by echo-Doppler, total peripheral resistance (TPR) and mean arterial pressure (MAP) were determined at baseline 10 and 20 weeks following the initiation of rHuEpo therapy. rHuEpo therapy was administered subcutaneously at the same dose (40 U/kg thrice weekly) during the first 10 weeks. Ten uraemic patients on haemodialysis who had never received rHuEpo therapy served as the control group. RESULTS: One patient in the group without antiplatelet drugs discontinued the study due to the development of severe hypertension after 12 weeks on rHuEpo therapy. There were no significant differences in the haemodynamic parameters at baseline. At 10 weeks, MAP was higher in patients without than with antiplatelet drugs or controls untreated with rHuEpo (128.5 +/- 28 versus 100.6 +/- 13.5 versus 98.7 +/- 14 mmHg respectively, P = 0.0047), TPR was also higher in patients without antiplatelet drugs than in the 2 other groups (1919 +/- 433 versus 1576 +/- 359 versus 1418 +/- 324 din.seg.cm-5m2 respectively, P = 0.0231), but CI did not differ among the three groups. At 20 weeks, MAP was still higher in patients without antiplatelet drugs than in patients with antiplatelet drugs or controls not on rHuEpo therapy respectively (112.9 +/- 24.6 versus 91.0 +/- 9.0 versus 101.7 +/- 14.1 mmHg respectively, P = 0.075), but at this stage TPR and Cl did not differ among the three groups. CONCLUSIONS: These data reinforce the previous observation that antiplatelet therapy may prevent the development of rHuEpo-induced hypertension.
Adult↗
Antiplatelet therapy and development of hypertension induced by recombinant human erythropoietin in uremic patients.
The pathogenesis of hypertension induced by recombinant human erythropoietin (rHuEPO) remains a subject of intense interest. The observation that patients treated with antiplatelet drugs never developed hypertension following rHuEPO therapy prompted us to study retrospectively the incidence and risk factors associated with the development of hypertension in 91 patients on renal replacement therapy who had commenced rHuEPO therapy in the last three years. Logistic regression analysis was used to determine the risk factors associated with the development or aggravation of hypertension during the first six months on rHuEPO therapy. The predictors were: age, gender, number of months on dialysis, antecedent of hypertension, use of antiplatelet drugs, and those parameters related with dose, route and magnitude of the hematological response to rHuEPO. Of the 91 patients studied, 34 developed hypertension (37%). Of the 34 patients who were on antiplatelet treatment, 2 (5.8%) developed hypertension, whereas among 57 who did not receive antiplatelet drugs, 32 (56%) developed it. By multiple logistic regression analysis, the best predictive variables over the development of hypertension were: age (odds ratio: 0.959, P = 0.02), antecedent of hypertension (odds ratio: 6.52, P = 0.002), and use of antiplatelet therapy (odds ratio: 0.030, P < 0.0001). The rest of the studied variables failed to explain the development of hypertension. Antiplatelet therapy may prevent the development of hypertension in patients treated with rHuEPO. Since the antiplatelet drugs used in this study did not have a significant hemodynamic effect, we infer that changes in platelet aggregability induced by rHuEPO may be involved in the pathogenesis of hypertension induced by this hormone.
Adolescent↗
Lean body mass as an index of nutrition in CAPD patients.
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Body Mass Index↗
Epidemic asthma in Cartagena, Spain, and its association with soybean sensitivity.
We conducted a matched case-control study to assess the association between epidemic asthma and soybean sensitivity in Cartagena, Spain. In skin tests, 81% of the cases and no control subjects were positive to the commercial soybean allergen; 87% of the cases and 12% of the controls were positive to the prepared soybean allergen; and 69% of the cases and 6% of the controls showed high levels of specific immunoglobulin E antibodies (odds ratio = 10; 95% confidence interval = 1.4-433). The association remained strong after adjustment for total immunoglobulin E and for 28 other allergens. The results indicate that soybean sensitivity may be causing asthma epidemics in Cartagena.
Adolescent↗
Vasovagal syncope related to peritoneal dialysate infusion.
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Aged↗
Assessment of iron status by erythrocyte ferritin in uremic patients with or without recombinant human erythropoietin therapy.
Erythrocyte ferritin may be a better estimator of iron bioavailability than the conventional markers of iron stores (serum ferritin and transferrin saturation). To investigate the accuracy of these conventional markers in uremic patients compared with erythrocyte ferritin, we studied 29 chronic hemodialysis patients on erythropoietin (EPO) therapy, 18 without EPO therapy, and 22 healthy control subjects. Apart from the red blood cell indices, serum ferritin, transferrin saturation, and erythrocyte ferritin, the analytical study included red blood cell protoporphyrin and plasma aluminum levels. The control group showed erythrocyte ferritin concentrations between 8.3 and 12.5 attograms/cell (95% confidence interval). In the EPO group, red blood cell protoporphyrin correlated negatively with erythrocyte ferritin, but not with serum ferritin or transferrin saturation. In the non-EPO group, serum ferritin, erythrocyte ferritin, and transferrin saturation did not correlate with red blood cell protoporphyrin. Even though erythrocyte ferritin correlated well with serum ferritin in the EPO group (r = 0.61, P = 0.0003), the sensitivity of normal serum ferritin levels (30 to 300 ng/mL) to discard a low erythrocyte ferritin concentration (erythrocyte ferritin less than 7 ag/cell) was 0.53, while the sensitivity of serum ferritin at levels less than 30 ng/mL to indicate an absolute iron deficiency expressed as a low erythrocyte ferritin concentration was 0.28. Only values of serum ferritin and transferrin saturation greater than 300 ng/mL and 35%, respectively, could rule out a relative iron deficiency expressed as a low erythrocyte ferritin and high red blood cell protoporphyrin concentration. Plasma aluminum levels did not correlate with red blood cell protoporphyrin or erythrocyte ferritin levels in either uremic group.(ABSTRACT TRUNCATED AT 250 WORDS)
Anemia, Hypochromic↗
Purification and characterization of major inhalant allergens from soybean hulls.
Proteins responsible for respiratory allergy to soybean have been purified from an extract of soybean hulls. The purification procedure combined size exclusion and reverse-phase HPLC. Two pure glycoproteins (S1 and S2) exhibiting IgE-binding ability, as demonstrated by immunoblotting and ELISA techniques, were obtained. Both proteins displayed low molecular weight values on SDS-PAGE (S1, 7.0 kD; S2 7.5 kD). Protein S1 showed charge microheterogeneity, rendering two bands at pH 6.1-6.2 on IEF, whereas S2 showed a single band at pH 6.8. Amino acid composition analyses revealed a strong homology between S1 and S2 and, as a characteristic feature, a high percentage of hydrophobic residues, mainly leucine and isoleucine. Concerning the allergenic activity, both proteins were recognized by the specific IgE from 95% of patients who suffered asthma attacks during the asthma outbreaks of 1987 and 1988 in Cartagena (Spain), caused by soybean dust. Besides, proteins S1 and S2 were able to, separately, inhibit up to 75% the binding of specific IgE to the whole extract. Moreover, purified proteins totally crossreacted, even though protein S2 seemed to be slightly more active in all the immunochemical techniques employed. Results presented allow us to conclude that both proteins are isoallergens and to name them as Gly m IA (protein S2) and Gly m IB (protein S1), according to the IUIS-allergen nomenclature system.
Allergens↗
More about anaphylactoid reactions in patients dialyzed with AN69 filter and on angiotensin converting enzyme inhibitors treatment.
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Acrylic Resins↗
Calcium acetate versus calcium carbonate as phosphate binders in hemodialysis patients.
We conducted a randomized unblinded parallel clinical trial to compare the effectiveness, side effects and tolerance between calcium acetate (CA) and calcium carbonate (CC) in 80 stable chronic hemodialysis patients selected on the basis of their acceptable control of serum phosphorus (P) levels with aluminum hydroxide (AH). All patients were dialyzed against the same calcium dialyzate (1.62 mmol/l). The serum analytical tests included: calcium corrected to total protein, P, PTH (intact molecule) and bicarbonate. The study was divided into the following periods: P0: baseline measurements; P1: washout (withdrawal of AH for 15 days); P2: random allocation to CA and CC treatment at doses equivalent to 75 mEq of elemental calcium, stratified according to previous doses of AH (2 months); P3: adjustment of doses until control P (2 months). CA was poorly tolerated in 7 patients and CC in 2 (NS). The changes in serum P levels between P0 and P2 periods were lower in the CA group (1.73 +/- 0.25 vs. 1.80 +/- 0.50 mmol/l; p = 0.26) than in the CC group (1.77 +/- 0.35 vs. 1.93 +/- 0.48 mmol/l; p = 0.03, paired t test). Serum calcium was hardly modified by CA (2.42 +/- 0.20 vs. 2.47 +/- 0.17 mmol/l; NS) while in the CC group, it rose significantly (2.40 +/- 0.12 vs. 2.55 +/- 0.22 mmol/l; p = 0.0004). There were no differences in the control of PTH or bicarbonate.(ABSTRACT TRUNCATED AT 250 WORDS)
Acetates↗