Urinary Calcium-creatinine Ratio Research Articles

Normal values for random urinary calcium to creatinine ratios in infancy

To determine normal values for the urinary calcium/creatinine ratio (UCa/Cr) in infants. To assess the impact of short-term supplementation of infant formula with calcium and phosphorus on UCa/Cr in a group of infants. We determined UCa/Cr in randomly collected urine samples from a group of children and adults. Short-term supplementation of infant formula with calcium glycerophosphate was carried out in 21 infants, and UCa/Cr was monitored in a before-and-after trial. A pediatric clinic at an academic center (infants and adults), and a day-care center (older children). A total of 103 infants between 5 days and 7 months of age, 40 infants between 8 and 17 months of age, 41 children between 18 months and 6 years, and 31 adults. The 95th percentiles for molar UCa/Cr for the different age groups were as follows: less than 7 months, 2.42 (0.86 mg/mg); 7 to 18 months, 1.69 (0.60 mg/mg); 19 months to 6 years, 1.18 (0.42 mg/mg); and adults, 0.61 (0.22 mg/mg). Regression analysis indicated a statistically significant decline in average UCa/Cr with age (R2 = 0.115, p < 0.0001 for log (UCa/Cr) vs log (age)). The geometric means for the two groups of infants were significantly greater than those of the older children and the adults (p < 0.05). Values for UCa/Cr in adults in our sample were comparable to those previously reported. We detected no significant changes in mean UCa/Cr during week-long periods of calcium supplementation of up to 1.8 gm of calcium and 1.39 gm of phosphorus per liter of formula. We conclude that normal values for UCa/Cr are much higher in infants than in older children and adults; UCa/Cr is age-related and declines gradually in the first several years of life, and short-term supplementation of infant formula with calcium glycerophosphate has minimal effect on UCa/Cr.

Comparison of nutrient intakes of South African elderly rural Black women in 1969 and 1989

In 1989, an investigation was made of the dietary intakes of a representative sample of 141 elderly Black women living in adjacent villages, in Western Transvaal. Results are compared with those obtained in 1969 on 43 women in a village in the same region. Energy intake averaged 6% higher, not essentially a significant increase. Fat provided 24% of energy compared with 19% in 1969, and protein, 14% versus 12% in 1969. Maize meal intake fell by a half, being replaced largely by bread, mainly brown. Intake of beans decreased slightly. Intake of vegetables and fruit rose by 40%, and of meat and dairy produce, both very low, by 75% and 20%, respectively. Sugar intake trebled. Changes were associated with significant rises in mean Body Mass Index, serum cholesterol level, and urinary calcium creatinine ratio.

The effect of hormone replacement therapy on postmenopausal bone loss

Eighty-four postmenopausal women who were randomly allocated to one of four groups, completed a 1 year follow-up. The first group ( n = 20) received 0.625 mg/day conjugated estrogens cyclically (CE; 25 days/month). The second ( n = 23) received 0.625 mg/day of CE continuously, and the third ( n = 17) received 50 μg/day of transdermal 17β-estradiol cyclically (24 days/month). All these groups also received 2.5 mg of medroxiprogesterone acetate sequentially for the last 12 days of hormone replacement therapy, while the fourth group ( n = 24) constituted a treatment-free control group. Dual photon absorptiometry was carried out before therapy and was repeated after 1 year. Serum calcium, phosphate and osteocalcine levels, and the urinary calcium creatinine and hydroxyproline creatinine ratios, were measured prior to treatment and 6 and 12 months thereafter. All treatment groups showed an increase in bone mineral content. This increase was higher in the continuous CE treatment group (4.4%, P < 0.05) and in transdermal group (7.1%, P < 0.01). Concomitant biochemical effects at 6 and 12 months, reduction in urine calcium and hydroxyproline, reduction in blood calcium, phosphate and osteocalcine, were compatible with the observed effects on bone mineral.

Intact parathyroid hormone concentration and cyclic AMP metabolism in thyroid disease.

In 35 thyrotoxic patients and 35 patients receiving thyroxine replacement therapy mean serum intact parathyroid hormone concentrations were lower than in euthyroid normal volunteer controls. In 20 hypothyroid patients intact PTH was increased relative to euthyroid controls. Mean serum adjusted calcium was increased in thyrotoxic patients relative to euthyroid controls and in 8 toxic patients with elevated serum adjusted calcium (greater than 2.60 mmol/l) intact PTH was below the assay detection limit (less than 0.5 pmol/l). Indices of PTH activity were consistent with intact PTH measurements in thyrotoxic patients with nephrogenous cyclic adenosine monophosphate lower, tubular maximum reabsorption of phosphate higher, and urinary calcium creatinine ratio higher than controls. In hypothyroid patients these indices of PTH activity suggest relative end organ resistance to PTH with nephrogenous cyclic adenosine monophosphate similar, tubular maximum reabsorption of phosphate similar, and calcium creatinine ratio lower than in controls. In treated hypothyroid patients nephrogenous cyclic adenosine monophosphate was higher, tubular maximum reabsorption of phosphate similar, and calcium creatinine ratio higher than in controls. These results are compatible with the hypothesis that thyroid status modifies the renal responses to PTH (1-84).

Effects of amino-butylidene diphosphonate in hypercalcemia due to malignancy

We studied the effect of a single 5 mg intravenous infusion of amino-butylidene diphosphonate (ABDP) in nine patients with hypercalcemia of malignancy, in whom serum calcium values were stable or rising after intravascular volume expansion. Serum calcium fell progressively in all patients and in seven reached the normal reference range by day 6 ( p < 0.001). The decrease in serum calcium was associated with a decrease in the fasting urinary calcium creatinine ratio ( p < 0.05). Hypercalcemia recurred in seven of the patients by day 12, but two patients remained normocalcemic for 21 days. We conclude that ABDP is a highly potent diphosphonate and that a single intravenous infusion is capable of inhibiting tumour-mediated bone resorption for several days.

Hyperphosphaturia and Hypermagnesuria in Children With IDDM

Urinary excretion of calcium, inorganic phosphorus, magnesium, glucose, and creatinine was measured in first-void spot urine samples collected 4 days apart in 220 insulin-dependent diabetic (IDDM) children (mean age 11.9 yr) attending a summer camp. A single control urine sample was obtained from 33 healthy nondiabetic siblings (mean age 11.2 yr). Mean +/- SD urinary calcium-creatinine ratios (UCa/Cr) did not significantly differ between IDDM and control subjects (0.14 +/- 0.09 vs. 0.12 +/- 0.09, respectively, P = 0.156). Mean urinary magnesium-creatinine ratios (UMg/Cr) were elevated in IDDM compared with control subjects (0.15 +/- 0.06 vs. 0.08 +/- 0.03, respectively, P = 0.0001). Similarly, mean urinary phosphorus-creatinine ratios (UP/Cr) were significantly increased over those in control subjects (1.12 +/- 0.33 vs. 0.40 +/- 0.22, respectively, P = 0.0001). UCa/Cr, UMg/Cr, and UP/Cr were correlated with increasing mean urine glucose content (P = 0.0001). No correlations were found when UCa/Cr, UMg/Cr, or UP/Cr were compared with patient age, duration of diabetes, glycosylated hemoglobin, or insulin dosage. Urine losses of phosphorus and magnesium were present even when glycemic control was considered good by several methods (glycosylated hemoglobin, short-term glycemic index, or urinary glucose content). Glomerular hyperfiltration was unable to account for increased urinary mineral content. In conclusion, the data indicate that urinary excretion of phosphorus and magnesium is elevated in children with IDDM, regardless of glycemic control. In the presence of glucosuria, this loss is further enhanced. Urinary calcium excretion is significantly higher only during periods of glucosuria. The data suggest that children with IDDM could be at risk for mineral deficiencies in the absence of intensive insulin management.

Effects of infusion of human parathyroid hormone-related protein-(1-40) in nude mice: histomorphometric and biochemical investigations.

Female nude mice were infused with 5.0, 3.0, or 1.0 micrograms/day of synthetic human parathyroid hormone-related protein (PTHrP) or control diluent with subcutaneous Alzet miniosmotic pumps for 7 days. Serum calcium was increased (p less than 0.01) on days 3 (13.9 mg/dl), 5 (13.6 mg/dl), and 7 (12.9 mg/dl) in mice infused with PTHrP at 5.0 micrograms/day compared with control nude mice (8.8 mg/dl). Serum calcium was significantly increased to a lesser degree in mice infused with 1.0 micrograms/day PTHrP (day 3) or 3.0 micrograms/day (days 3 and 7). Serum phosphorus was decreased (p less than 0.01) in all three groups of mice infused with PTHrP (4.6 mg/dl, 5.0 micrograms/day; 6.7 mg/dl, 3.0 micrograms/day; and 6.4 mg/dl, 1.0 micrograms/day) compared with controls (8.5 mg/dl). Serum 1,25-dihydroxycholecalciferol was increased (2.4-fold) in mice infused with PTHrP (5.0 and 3.0 micrograms/day). The urinary calcium-creatinine ratio (0.74 compared with 0.034 in controls) was increased (p less than 0.03) in mice infused with PTHrP (5.0 micrograms/day), but the urinary phosphorus-creatinine ratio was not different from that in controls. The urinary cAMP-creatinine ratio was increased (1.6-fold) in mice infused with PTHrP (5.0 micrograms/day). Static bone histomorphometry revealed increased (p less than 0.01) trabecular bone area, osteoblast perimeter, osteoid perimeter, osteoid width, wall width, osteoclast area, number of osteoclasts, and osteoclast perimeter in trabecular bone of lumbar vertebrae from mice infused with PTHrP. Dynamic bone histomorphometry demonstrated increased (p less than 0.01) double-labeled perimeter, mineralizing perimeter, and bone formation rate. The results of this study indicated that PTHrP increased serum calcium and 1,25-dihydroxycholecalciferol, decreased serum phosphorus, increased urinary excretion of calcium, phosphorus, and cAMP, and increased both bone resorption and formation in nude mice. PTHrP mimics the action of native PTH in vivo and is likely to be an important protein in the pathogenesis of humoral hypercalcemia of malignancy.

Atypical idiopathic hypercalciuria in an adolescent

Idiopathic hypercalciuria (IH) in adults is recognized as a cause of urolithiasis. If IH is symptomatic, the symptoms are hematuria, renal colic, or obstructive uropathy with or without infection. In children, IH has been linked to the spectrum of urinary symptoms including hematuria, pyuria, dysuria, recurrent urinary infections, abdominal or suprapubic pain, proteinuria, and the frequency-urgency syndrome. Hematuria may appear prior to the appearance of stones, and thiazide therapy appears to prevent stone formation by decreasing urinary calcium excretion. This report describes an older adolescent with hematuria and flank pain. His urinary chemistry values were not consistently typical of IH, but a thiazide trial with withdrawal challenge was diagnostic. His case is remarkable because, though essentially an adult, his disease was typical of prepubertal disease. Adolescents with unexplained urinary symptoms should be evaluated for IH. The urinary calcium-creatinine ratio may not be elevated, and timed urinary calcium may be equivocal. In some cases a thiazide trial may be valuable and cost effective.

Possibility of elevated parathyroid function in patients with calcium-containing nephrolithiasis as compared with normal controls.

109 patients with calcium-containing nephrolithiasis and 10 normal controls underwent oral calcium load test. After thorough examination, 6 of the 109 patients were diagnosed as having primary hyperparathyroidism (PHPT) and the remainder as having normocalcemic nephrolithiasis without PHPT. Following the oral calcium load test, the latter were operationally divided into 3 groups - normocalciuric nephrolithiasis (NN), n = 78; absorptive hypercalciuria (AH), n = 10, and renal hypercalciuria (RH), n = 15 - according to the criteria reported by Pak et al. Before the oral calcium load test, nephrogenous adenosine 3',5'-monophosphate (NcAMP), urinary adenosine 3'-5'-monophosphate (urinary cAMP), and plasma immunoreactive parathyroid hormone (iPTH) were determined to evaluate parathyroid function. This function, as assessed by mean basal NcAMP in the NN, AH and RH groups as well as the PHPT group, was significantly increased as compared with that in the normal controls. Within the NcAMP-elevated 4 groups, the mean basal NcAMP was highest in the PHPT group followed by the RH, AH and NN groups. In view of the mean basal NcAMP, disregarding the PHPT group, the NN and AH groups seemed to be intermediate types between the normal controls and the RH groups. Similar, but less distinctive results were obtained in the determination of urinary cAMP and plasma iPTH. On the other hand, when leaving the PHPT group out, the mean basal urinary calcium creatinine ratio (Ca/Cr) was highest in the RH group followed by the AH and NN groups, and lowest in normal controls, suggesting that the NN and AH groups were intermediate between normal controls and the RH group. The mean basal urinary Ca/Cr ratio in the PHPT group was moderately elevated but not remarkable. Almost similar tendencies were observed in 24-hour urinary calcium excretions on a calcium-restricted diet. A weakly positive correlation (r = 0.232, p less than 0.05) between basal NcAMP and basal urinary Ca/Cr ratio was observed in accumulated cases of the NN, AH and RH groups, whereas a negative correlation (r = -0.664, p less than 0.05) was obtained in normal controls. It is concluded that a possible abnormal calcium metabolism is suggested in stone formers without PHPT. Additionally, it is speculated that 'relative hypercalciuria' in NN and hypercalciuria in AH and RH might be accounted for in a single line of a primary renal leak of calcium.

ENHANCED RENAL TUBULAR CALCIUM REABSORPTION INDEPENDENT OF PARATHORMONE ACTIVITY, IN CHILDREN ON LONG TERM ANTICONVULSANT THERAPY

A significant reduction in the urinary calcium-creatinine ratio, was found in thirty-four ambulatory epileptic children on long term anticonvulsant therapy, studied during wintertime. No significant difference in the urinary excretion of cyclic AMP, phosphate or amino-acids was observed when the study-group was compared to an age-matched control group. Serum calcium and phosphate values were normal, but a significant increment in alkaline phosphatase was noted. Since there was no evidence of hyperactivity of the parathormone, it is suggested that the enhanced renal tubular calcium reabsorption in children on long term anticonvulsant therapy is a nonparathormone mediated phenomenon, possibly compensating for reduced calcium absorption in the gastrointestinal tract.

THE EFFECT OF ENDOGENOUS OESTROGEN ON PLASMA AND URINARY CALCIUM AND PHOSPHATE IN OOPHORECTOMIZED WOMEN

SUMMARY Using a specific radioimmunoassay, significant levels of plasma oestradiol can be detected in the blood of oophorectomized women. In these women the plasma concentration of oestradiol correlates positively with the body fat content. Low circulating concentrations of oestradiol are associated with increased values for serum phosphate and alkaline phosphatase, but no significant change in serum calcium. The fasting urinary calcium creatinine ratio is inversely related to circulating plasma oestradiol concentration which also correlates, in a more complex way, with the renal threshold for phosphate (TmPO4/GFR). It is suggested that oestrogen production may be an important factor in determining bone loss in post-menopausal women.

The effect of endogenous oestrogen on plasma and urinary calcium and phosphate in oophorectomized women.

Using a specific radioimmunoassay, significant levels of plasma oestradiol can be detected in the blood of oophorectomized women. In these women the plasma concentration of oestradiol correlates positively with body fat content. Low circulating concentrations of oestradiol are associated with increased values for serum phosphate and alkaline phosphatase, but no significant change in serum calcium. The fasting urinary calcium creatinine ratio is inversely related to circulating plasma oestradiol concentration which also correlates, in a more complex way, with the renal threshold for phosphate (TmPO4/GFR). It is suggested that oestrogen production may be an important factor in determining bone loss in postmenopausal women.

The urinary calcium-creatinine ratio as a measure of urinary calcium excretion.

Urine specimens were collected from 26 normal subjects, 10 patients with proven primary hyperparathyroidism, and eight patients with hypercalcaemia due to other causes. After overnight urine concentration, an oral water load was given to induce a diuresis and provide urine specimens with a relatively wide range of creatinine concentration for each subject. In normal subjects the urinary calcium/creatinine ratio was found to be independent of urine concentration. In eight out of 10 patients with primary hyperparathyroidism and in two out of eight patients with hyper-calcaemia due to other causes, the urinary calcium/creatinine ratio was found to be high when the creatinine concentration was low, but usually normal when the creatinine concentration was high. The results suggest that if the urinary calcium/creatinine ratio of random urine specimens is used as a ;screening' procedure to detect hypercalciuria the latter cannot be excluded if the urinary creatinine concentration is more than 40 mg per 100 ml.