Rise In Urinary Calcium Research Articles

MP43-06 BAKING SODA EXERTS A SIGNIFICANT ALKALINIZING EFFECT IN PATIENTS WITH UROLITHIASIS WITHOUT INCREASING URINARY CALCIUM EXCRETION

You have accessJournal of UrologyStone Disease: Medical & Dietary Therapy (MP43)1 Apr 2020MP43-06 BAKING SODA EXERTS A SIGNIFICANT ALKALINIZING EFFECT IN PATIENTS WITH UROLITHIASIS WITHOUT INCREASING URINARY CALCIUM EXCRETION Kristina Penniston*, Scott Quarrier, Shuang Li, and R. Allan Jhagroo Kristina Penniston*Kristina Penniston* More articles by this author , Scott QuarrierScott Quarrier More articles by this author , Shuang LiShuang Li More articles by this author , and R. Allan JhagrooR. Allan Jhagroo More articles by this author View All Author Informationhttps://doi.org/10.1097/JU.0000000000000898.06AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail Abstract INTRODUCTION AND OBJECTIVE: Baking soda (sodium bicarbonate, NaHCO3) has been used for decades as an alkalinizing agent. When taken orally, NaHCO3 increases urine pH and citrate. Despite rising prices of prescriptive urinary alkalinizing agents, urologists may be reluctant to recommend NaHCO3 due to fear of Na-induced hypercalciuria. To assess this potential adverse event, we reviewed our recent clinical experience with baking soda as alkali treatment. METHODS: A convenience sample of patients from our metabolic stone prevention clinic who used baking soda within the past year was assembled from an IRB-approved prospectively maintained database. In addition to taking 1/4 tsp baking soda BID (dissolved in water or other liquid), providing approximately 25 mEq alkali, most patients were counseled to increase intake of bicarbonate precursors from fruits and vegetables. Results from patients’ 24-h urine collections before and during treatment were retrospectively reviewed. The primary outcome was change in urinary calcium (UCa) excretion. Patients were excluded for urine creatinine variation >40% and/or no follow-up urine collection. In order to assess only patients compliant with treatment, those with no increases in either urine citrate or pH and/or 24-h urine Na:Cl ratio <0.9 while on treatment were excluded. RESULTS: Patients (n=21) were mostly male (71%) and were 60±10 y. Urine collections were 9.1±2.1 months apart. Overall, significant increases were observed in urinary citrate excretion (523 to 822 mg/d), pH (5.83 to 6.26), and 24-h urine Na:Cl ratio (1.03 to 1.17); p≤0.003 for all comparisons (paired t-tests). The increase in urinary Na excretion (40±102 mEq) was >3-fold higher than change in Cl excretion, confirming higher Na intake from NaHCO3 vs. dietary salt (NaCl). UCa excretion was not different before and during treatment (191 mg and 217 mg respectively; p=0.18, paired t-test). Before treatment, 4 patients had UCa>250 mg; 2 of these resolved on treatment. Of 5 patients with new-onset hypercalciuria, higher dietary NaCl intake, suggested by higher post-treatment Cl excretion (delta >200 mEq), was deemed to have explained the rise in UCa in a subset of these. CONCLUSIONS: Treatment with baking soda providing 25 mEq alkali daily in patients who achieved increases in urinary citrate excretion and/or urine pH was not associated with higher UCa. Moreover, treatment with baking soda did not exacerbate hypercalciuria in patients with high pre-treatment urine calcium. A prospective trial to confirm these results is currently underway. Source of Funding: none © 2020 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 203Issue Supplement 4April 2020Page: e649-e649 Advertisement Copyright & Permissions© 2020 by American Urological Association Education and Research, Inc.MetricsAuthor Information Kristina Penniston* More articles by this author Scott Quarrier More articles by this author Shuang Li More articles by this author R. Allan Jhagroo More articles by this author Expand All Advertisement PDF downloadLoading ...

Editorial Comment

This manuscript by Canales et al describes the effects of calcium and vitamin B6 supplementation on oxalate excretion in a rat Roux-en-Y gastric bypass model. Medical advances in the treatment of calcium oxalate stones have only made modest gains over the past several decades and the common misconception that excessive calcium in one's diet exacerbates stone formation has been hard to overcome. While this study deals specifically with enteric hyperoxaluria and Roux-en-Y gastric bypass, it does hold similarities between other calcium oxalate stone forming patients. The primary principles proven in this rat model indicate the importance of oral dietary calcium supplementation in patients with excessive oxalate in the gut. In the case of enteric hyperoxaluria, calcium becomes saponified by excessive fat in the intestine and is therefore unavailable to bind to dietary oxalate. In this study, dietary calcium supplementation decreased urinary oxalate excretion by 28% without a rise in urinary calcium. This same principle is often true in many calcium oxalate stone formers. Dietary supplementation with either milk or calcium-fortified orange juice taken with meals is an important treatment to reduce urinary oxalate. Prescribing calcium citrate to your stone forming patient with hyperoxaluria is also beneficial and should be in the armamentarium of all practicing urologists.

The Effect of Calcium and Vitamin B6 Supplementation on Oxalate Excretion in a Rodent Gastric Bypass Model of Enteric Hyperoxaluria

To test the effect of calcium and vitamin B6 therapies on urinary oxalate excretion in a rodent model of enteric hyperoxaluria after Roux-en Y gastric bypass (RYGB) surgery. Obese male Sprague-Dawley rats underwent sham (n = 7) or RYGB (n = 10). Animals were maintained on low oxalate (1.5%) and fat (10%; LOF), normal calcium (0.6 %) diet for 8 weeks and then completed a 2-phase crossover metabolic study. In the first 2-week phase, animals were fed a Low oxalate and fat (LOF), high calcium (2.4%; HC) diet. After a 2-week washout, rats were fed a LOF/normal calcium diet highly enriched with vitamin B6. Urine was collected before and after each intervention. Plasma pyridoxal 5'-phosphate (PLP) and metabolites were measured baseline and 11 weeks after sham or RYGB. Compared to baseline, sham animals on LOF/HC diet doubled their urinary calcium excretion but not oxalate. RYGB animals on LOF/HC diet decreased urinary oxalate excretion 28% (P = .001) without a significant rise in urinary calcium. Vitamin B6 supplementation decreased RYGB urinary oxalate by approximately 15% (P = .06), and serum PLP explained 63% of urinary oxalate variability. Based on the findings in this model, calcium supplementation appears to be a reasonable therapy to decrease urinary oxalate in RYGB patients who maintain a low fat and oxalate diet. Serum PLP had a fair correlation to urinary oxalate excretion and may be a useful screening tool in hyperoxaluric RYGB patients. Further experimental human studies after RYGB are necessary to determine whether these commonly employed supplements truly provide a benefit in enteric hyperoxaluria.

Evidence for metabolic origin of absorptive hypercalciuria Type II

The objective of this retrospective data analysis was to test the hypothesis that absorptive hypercalciuria Type II (AH-II) is a less severe variant of absorptive hypercalciuria Type I (AH-I), a common cause of calcareous stones. 24-h urinary calcium obtained on constant metabolic diets was retrieved from several data sources, including those of the authors and another group. On a low calcium diet (10 mmol calcium), 35 patients with AH-II were compared with 70 non-stone formers (NSF) and 76 patients with AH-I. On a high calcium diet (25 mmol calcium/day), 10 patients with AH-II were compared with 35 NSF and 32 with AH-I. On a low calcium diet for all participants, 24-h urinary calcium in AH-II (4.13 ± 0.63 mmol/day) was significantly higher than in NSF (3.06 ± 1.17 mmol/day), but significantly lower than in AH-I (6.11 ± 1.14 mmol/day) (p < 0.001). In a smaller subset, fractional intestinal calcium absorption in AH-II (65.0 ± 11.1%) was intermediate between NSF (50.0 ± 6.4%) and AH-I (71.0 ± 6.7%) (p < 0.001 between AH-II and other groups). On a high calcium diet, the rise in urinary calcium in AH-II was significantly higher than in NSF, but not as marked as in AH-I. Estimated calcium balance in AH-II was similar to NSF, but significantly more positive than AH-I. In conclusion, AH-II shares with AH-I the same metabolic disturbance(s) stimulating intestinal absorption and renal excretion of calcium but to a lesser degree. Bone might be spared in AH-II.

Evidence for a Renal Calcium Leak in Postmenopausal Women

We have measured calcium, albumin, globulin, bicarbonate, and anion gap in the plasma; and calcium, sodium, and creatinine in the urine, in 115 premenopausal and 140 postmenopausal normal women after an overnight fast, and calculated the calcium fractions in the plasma and the calcium/and sodium/creatinine ratios in the urine. The total ultrafiltrable calcium was significantly higher in the postmenopausal group, mainly due to their higher complexed calcium fraction, due in turn to their higher bicarbonate and anion gap concentrations. Urinary calcium was also significantly higher in the postmenopausal group even after correcting for sodium. After matching for total calcium and each of the calcium fractions in turn, the urinary calcium remained significantly higher in the post- than in the premenopausal sets even after correction for sodium. The implication is that the rise in urinary calcium at the menopause is due to reduced tubular reabsorption of calcium rather than to an increase in filtered load. We suggest that estrogens promote tubular reabsorption of calcium and that the rise in bone resorption at the menopause could be accounted for, at least in part, by the effect of estrogen deficiency on the kidney.

Dose dependency of calcium absorption: a comparison of calcium carbonate and calcium citrate.

Calcium supplementation is recommended as a prophylaxis against bone loss. This study was performed to determine the dose dependency of calcium absorption in an attempt to derive an optimum dose schedule. Using the well-described oral calcium load technique, we measured the calcium absorption from three different calcium doses (0.5, 1.0, and 2.0 g) of both calcium carbonate and calcium citrate administered to 21 normal subjects (4 men and 17 women, 22-60 years). Nine subjects underwent two additional loads with 0.2 g of elemental calcium as calcium carbonate and as calcium citrate. The intestinal calcium absorption from calcium carbonate and calcium citrate was estimated from the rise in urinary calcium following oral ingestion of the respective calcium salt. The increment in urinary calcium post-load, reflective of intestinal calcium absorption, rose rapidly from 0 to 0.5 g calcium loads with only slight subsequent increases from the 0.5 g to 2.0 g calcium doses. Thus, results indicate that 0.5 g of calcium is the optimum dose of either calcium salt. Moreover, the increment in urinary calcium post-load was higher from calcium citrate than from calcium carbonate at all four dosage levels. The increment in urinary calcium (during the second 2 hr) following calcium citrate load (0.5 g calcium) was 0.104 +/- 0.096 mg/dl glomerular filtrate (GF), which was higher than that of 0.091 +/- 0.068 mg/dl GF obtained from 2.0 g calcium as calcium carbonate. These results confirm the superior calcium bioavailability from calcium citrate as compared with calcium carbonate.(ABSTRACT TRUNCATED AT 250 WORDS)

Assessment of adenosine 3',5'-monophosphate excretion and an oral calcium tolerance test in the diagnosis of mild primary hyperparathyroidism.

An oral calcium tolerance test was administered to 22 hyperparathyroid patients and 162 normal subjects to determine its value in the diagnosis of mild primary hyperparathyroidism. Basal urinary excretion of calcium was higher in patients [0.217 mg/100 ml glomerular filtrate (GF)] than in normal subjects (0.090 mg/100 ml GF), but there was 50% overlap between the two groups. Phosphorus excretion, expressed as the ratio of the maximal tubular reabsorption of phosphorus to the glomerular filtration rate, was lower in patients (2.77) than in normal subjects (3.7), but 38% of the patients fell within the normal range. Urinary excretion of total cAMP also failed to separate hyperparathyroid patients from normal subjects [5.8 +/- 0.32 (+/- SEM) nmol/100 ml GF in patients vs. 3.41 +/- 0.11 in normal subjects]. Determination of nephrogenous cAMP failed to increase the utility of cAMP as a predictor of hyperparathyroidism. In response to oral calcium, the elevation in serum calcium concentration was the same in both groups. The rise in urinary calcium was greater in patients, but showed 77% overlap with that in normal subjects. Conversely, serum immunoreactive PTH, measured with a midregion-specific RIA, was elevated in 90% of the patients. Some normal subjects also had high levels of PTH, but none of these had hypercalcemia. We conclude that the oral calcium tolerance test and measurement of urinary cAMP do not adequately distinguish hyperparathyroid patients from normal subjects. In the absence of renal insufficiency, the combination of hypercalcemia and elevated serum PTH concentration most accurately predicts the diagnosis of primary hyperparathyroidism.

Renal tubular acidosis: effects of etacrynic acid on renal acid and calcium excretion.

The fundamental disorder in renal tubular acidosis--the impaired excretions of hydrogen ions--can favourably be influenced by etacrynic acid (Hydromedin). Net acid and calcium excretion was measured in eight patients with incomplete RTA I and five controls before and during treatment with the diuretic: urinary pH was lowered and net acid excretion increased (p less than 0.05) with only slight rise in urinary calcium. Etacrynic acid appears to be particularly suitable for the long term treatment of patients with incomplete RTA I and calculous disease.

Preliminary trial of low doses of human parathyroid hormone 1–34 peptide in treatment of osteoporosis

It has recently been suggested that parathyroid hormone (PTH), administered chronically in low doses so as to induce a positive calcium balance, may be effective in the treatment of osteoporosis (11). This hypothesis was based in part on the relative sensitivity of the multiple effects of the parathyroids on calcium metabolism (12) and in part on the known anabolic effects of PTH in low doses on young rat bone (17, 5, 21). In the adult dog, which provides a better model than the rat of adult human calcium metabolism, Parsons and Reit demonstrated that chronic low-dose infusions of bovine PTH (0.025 to 0.1 µg/kg/h) resulted in increased calcium absorption without a concomitant rise in urinary calcium, in spite of moderate hypercalcaemia at the higher dose levels. These results provided the justification for a preliminary trial of low doses of a synthetic amino-terminal fragment of human PTH (hPTH 1–34 (8, 20)) in the treatment of primary osteoporosis.

Isolated human growth hormone deficiency. IV. The response of sexual ateliotic dwarfs to exogenous growth hormone

Sexual ateliotic dwarfs react acutely to human growth hormone treatment with a decrease in nitrogen and phosphorus excretion, a fall in serum urea nitrogen, and a rise in urinary calcium. The plasma insulin response to glucose is considerably augmented. A single subject, treated for one year, has exhibited an impressive increase in linear growth.

A Guide to the Adequacy of Therapy in Resistant Rickets due to Familial or Essential Hypophosphatemia

The regulation of vitamin-D dosage in resistant rickets (familial or essential hypophosphatemia) is best accomplished by measuring the twenty-four-hour urinary calcium output against the curve of normal excretion. For such comparison the subject's weight and a fairly close estimate of calcium intake are also necessary. Qualitative tests for urine calcium are of no real value in determining the child's status with respect to vitamin-D therapy. Urinary calcium values before treatment are usually three standard deviations or more below the normal mean excretion value. With high doses of vitamin D, urinary calcium rises toward the mean, the rate of rise paralleling the size of the dose. Maintenance of urine calcium at values approximating the normal mean will promote healing of clinical rickets and avoid hypervitaminosis D. A rise of urinary calcium to approximately three standard deviations above the mean, or higher, means hypervitaminosis, and the dosage should be decreased sharply. The abnormal rise in urinary calcium from overtreatment precedes a rise in serum calcium by days or weeks, except after operative treatment when the child will be thrown into acute hypervitaminosis D unless the vitamin is discontinued for a time starting before operation.

Progressive changes in renal phosphate and calcium excretion in rats following parathyroidectomy or parathyroid administration.

SummaryThis study has dealt with progressive changes which occur in renal phosphate and calcium excretion rates in rats during the first 27 hours after parathyroidectomy or the first injection of parathyroid extract. Following parathyroidectomy there is an immediate drop in urinary phosphate and a rise in urinary calcium. Within 24 hours the excretory rates for both these ions return to normal despite the continued high phosphate and low calcium levels of the serum. Following the initiation of parathyroid extract administration to normal rats the reverse is true. There is an immediate drop in urinary calcium and a rise in urinary phosphate. Twenty-four hours later the excretory rate for calcium returns to or rises above normal. The urinary phosphate, however, continues high throughout the entire period. These data are explained on the basis that immediate changes in renal excretory rates resulting from changes in parathyroid hormone titer are due to shifts in the renal threshold for these two ions. Excret...