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Biomedical subjects

K Sakhaee

Publications and source records attributed to K Sakhaee.

At least 73 records · Page 4Linked to original sources
PubMed1985

Prevention of recurrent calcium stone formation with potassium citrate therapy in patients with distal renal tubular acidosis.

Distal renal tubular acidosis is a common cause of intractable calcium nephrolithiasis. We examined the effect of oral potassium citrate therapy in 9 patients with incomplete distal renal tubular acidosis diagnosed on the basis of an abnormal response to an oral ammonium chloride load. Patients were studied during a control phase and after 3 months of potassium citrate treatment (60 to 80 mEq. daily). Potassium citrate caused a significant increase in urinary pH and urinary citrate, and a decrease in urinary calcium. The urinary relative saturation ratio of calcium oxalate significantly decreased during treatment, while that of brushite did not change. Potassium citrate also was shown to inhibit new stone formation. During a mean treatment period of 34 months none of the 9 patients had new stones, although 39.3 plus or minus 79.7 (standard deviation) stones per patient formed during the 3 years preceding treatment. The results support the potential clinical advantage of potassium citrate therapy in patients with distal renal tubular acidosis and recurrent calcium nephrolithiasis.

Acidosis, Renal Tubular↗
PubMed1985

Lack of effect of prostaglandin inhibition on calcium excretion in normal volunteers.

Recent data have shown that administration of indomethacin to patients with hypercalciuric nephrolithiasis decreased urinary calcium excretion, implying a possible pathogenic role for renal prostaglandins in hypercalciuria. To explore this hypothesis we administered indomethacin, ketoprofen and aspirin to normal volunteers for 6 days and assessed daily creatinine clearance and urinary excretion of sodium and calcium. In contrast to previous studies, subjects were maintained on a constant metabolic diet. These nonsteroidal anti-inflammatory drugs decreased urinary sodium excretion but had no effect on creatinine clearance or urinary calcium excretion. In summary, our data do not support an important physiologic role of renal prostaglandins in renal calcium excretion in normal subjects.

Adult↗
PubMed1985

Short-term 1,25-dihydroxyvitamin D3 administration raises serum osteocalcin in patients with postmenopausal osteoporosis.

In order to evaluate whether 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] could increase the serum concentration of osteocalcin (BGP) in patients with post-menopausal osteoporosis, we administered 2 micrograms/d of 1,25(OH)2D3 to 14 patients with biopsy proven osteoporosis for two weeks. An additional 13 age and sex-matched patients with osteoporosis received no drug and served as the control. Administration of 1,25(OH)2D3 significantly increased the serum concentration of 1,25(OH)2D from 31 +/- 2 SE to 56 +/- 5 pg/ml (p less than 0.01). Commensurate with the rise in 1,25(OH)2D was a significant increase in BGP from 3.9 +/- 0.6 to 6.4 +/- 0.9 ng/ml (p less than 0.001). There were no significant changes for these parameters in the control group. It is concluded that short term 1,25(OH)2D3 administration is effective in raising BGP concentrations in patients with post-menopausal osteoporosis.

Calcitriol↗
PubMed1985

Postmenopausal osteoporosis as a manifestation of renal hypercalciuria with secondary hyperparathyroidism.

An apparently unique presentation of osteoporosis was encountered in eight postmenopausal women (mean age, 56.8 yr). They had renal hypercalciuria, since they had fasting hypercalciuria [0.17 +/- 0.04 (+/- SD) mg/100 ml glomerular filtrate (GF)] in the setting of normocalcemia and parathyroid stimulation (high serum immunoreactive PTH and/or urinary cAMP). Serum 1,25-dihydroxyvitamin D was not significantly different (28 +/- 7 vs. 34 +/- 2 pg/ml) from that in a nonelderly control group, but fractional intestinal calcium (Ca) absorption was significantly lower (0.382 +/- 0.123 vs. 0.49 +/- 0.06; P less than 0.025). Thus, the patients did not have compensatory intestinal hyperabsorption of Ca despite PTH excess. Treatment with hydrochlorothiazide (50 mg/day) produced a decline in fasting urinary Ca (to 0.07 +/- 0.02 mg/100 ml GF; P less than 0.01), serum PTH (from 39 +/- 19 to 21 +/- 1 microliters eq/ml; P less than 0.05), and urinary cAMP excretion (from 5.30 +/- 0.57 to 3.57 +/- 0.59 nmol/100 ml GF; P less than 0.0025). The results suggested that hyperparathyroidism was secondary. Histomorphometric analysis of bone showed reduced trabecular bone volume without mineralization defect, compatible with osteoporosis. Four of eight patients had high or high normal fractional resorption surfaces, fractional formation surfaces, and fractional osteoid volumes. That these abnormalities may reflect PTH-dependent osteoclastic resorption and bone turnover was supported by the reduction of these indices after correction of secondary hyperparathyroidism with hydrochlorothiazide therapy. The remaining four patients, however, had normal histomorphometric results. In summary, postmenopausal osteoporosis may occur sometimes with renal hypercalciuria and secondary hyperparathyroidism. The lack of compensatory intestinal hyperabsorption of Ca predisposes to negative Ca balance, and the hyperparathyroid state may be manifested by stimulated osteoclastic and osteoblastic activities.

Aged↗
PubMed1985

Exaggerated natriuretic and calciuric responses to hydrochlorothiazide in renal hypercalciuria but not in absorptive hypercalciuria.

Patients with hypercalciuria have been reported to have an exaggerated response to hydrochlorothiazide (HCTZ), implying a renal tubular defect in solute reabsorption. To determine whether this disturbance is generalized or unique to a particular pathogenetic type of hypercalciuria, we measured the increments in urinary sodium (delta Na), calcium (delta Ca), and magnesium after a 100-mg dose of oral HCTZ in 10 normal subjects and 31 patients with different types of hypercalciuric nephrolithiasis. Eleven patients with renal hypercalciuria had significantly greater delta Na (P less than 0.005) and delta Ca (P less than 0.005) than the normal subjects. Ten patients with absorptive hypercalciuria and 10 patients with fasting hypercalciuria without parathyroid stimulation had delta Na and delta Ca indistinguishable from those of normal subjects. In all groups, urinary HCTZ and basal 24-h urinary Na did not differ. The results suggest that the unique natriuretic and calciuric responses to HCTZ occur only in renal hypercalciuric patients with secondary hyperparathyroidism. The data support a renal tubular defect in renal hypercalciuric in contrast to other diagnostic categories of hypercalciuric nephrolithiasis.

Absorption↗
PubMed1985

Disturbances in mineral metabolism after successful renal transplantation.

Abnormalities of mineral metabolism remain a clinical problem after successful renal transplantation. These disturbances may be the result of derangements in divalent ion, parathyroid hormone (PTH) and/or vitamin D metabolism. We therefore measured serum Ca, phosphorus, PTH and 1,25-dihydroxyvitamin D [1,25(OH)2D] levels and fractional intestinal Ca absorption (alpha) in 6 patients before and after successful transplantation (early, less than or equal to 6 months). 3 were reexamined later (late, greater than or equal to 24 months after transplantation). The patients exhibited decreased serum levels of 1,25(OH)2D and alpha before the renal transplantation. In the early stages, renal transplantation reduced serum phosphorus from 5.55 +/- (SD)1.96 to 2.96 +/- 0.95 mg/dl (p less than 0.02); this was accompanied by a rise in serum 1,25(OH)2D from 8.7 +/- 1.5 to 26.3 +/- 8.4 pg/ml (p less than 0.005). The calcemic response to PTH infusion became normal, since the increment in serum Ca rose from 0.45 +/- 0.21 mg/dl before transplantation to 1.03 +/- 0.18 mg/dl early after transplantation. Although the mean value for alpha increase significantly from 0.263 +/- 0.048 to 0.402 +/- 0.175 (p less than 0.05), alpha was subnormal in 3 patients (alpha less than 0.37). Urinary Ca was high in 3 patients, and it exceeded absorbed Ca (from intestines) in 4 patients (indicative of negative Ca balance). Serum PTH fell significantly but remained above normal. It was hoped that late after transplantation, when patients were maintained on smaller doses of oral glucocorticoids, these abnormalities would be ameliorated. However, hypercalciuria was found in 2 of 3 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Augmentation of renal citrate excretion by oral potassium citrate administration: time course, dose frequency schedule, and dose-response relationship.

The time course, dose frequency schedule, and dose-response relationship of the citraturic response to orally administered potassium citrate was examined in 22 normal volunteers and 21 patients with uric acid or calcium nephrolithiasis. The slow-release (wax matrix) preparation of potassium citrate produced a rapid and sustained rise in urinary citrate lasting for up to 12 hours following a single oral administration. Probably owing to this prolonged action, the slow-release preparation when given in a twice-daily or thrice-daily schedule at a dosage of 60 meq or 3.78 Gm citrate/day virtually eliminated the normally wide circadian fluctuation in urinary citrate and maintained urinary citrate at a higher, more constant level throughout the day. The liquid preparation of potassium citrate was less effective in this regard. However, the two preparations of potassium citrate caused an equivalent rise in total 24-hour urinary citrate. When 24-hour excretions of citrate were examined, urinary citrate was shown to reach its peak level by the second day of potassium citrate treatment and to return to the pretreatment level by the second day after the treatment was stopped. The rise in urinary citrate produced by treatment was directly proportional to the dose of potassium citrate. In most hypocitraturic patients with renal stones, potassium citrate 60 meq/day restored normal urinary citrate (greater than 320 mg/day).

Administration, Oral↗
PubMed1984

Reduction in intestinal calcium absorption by hydrochlorothiazide in postmenopausal osteoporosis.

In six women with postmenopausal osteoporosis, most of whom responded to 50 micrograms/day 25-hydroxyvitamin D (25-OHD) therapy with a rise in intestinal calcium (Ca) absorption, 50 mg/day hydrochlorothiazide (TZ) were added to determine whether the resulting decline in urinary Ca would cause Ca retention in the skeleton. Urinary Ca decreased from 183 +/- 48 (SD) mg/day to 142 +/- 67 mg/day (P less than 0.05) when TZ was added. However, fractional Ca absorption also declined from 0.532 +/- 0.077 during 25-OHD treatment to 0.401 +/- 0.064 during combined 25-OHD and TZ therapy (P less than 0.0025). The above changes were accompanied by a significant decline in urinary cAMP from 4.29 +/- 1.64 to 3.19 +/- 1.44 mumol/g creatinine (P less than 0.05) and in serum 1,25-dihydroxyvitamin D from 41 +/- 14 to 22 +/- 11 pg/ml (P less than 0.01). The results suggest that TZ lowers urinary Ca, suppresses parathyroid function, inhibits 1,25-dihydroxyvitamin D synthesis, and thereby reduces intestinal Ca absorption. Thus, combined 25-OHD and TZ therapy probably does not improve Ca balance.

Aged↗
PubMed1983

Low urinary citrate excretion in nephrolithiasis.

The urinary citrate excretion was examined in patients with nephrolithiasis who were categorized on the basis of different physiologic or metabolic abnormalities. A wide prevalence of low citrate excretion (hypocitraturia) was observed, with over one half of our patients with stones exhibiting it. Hypocitraturia was found in all patient categories except primary hyperparathyroidism and hyperuricosuric calcium oxalate nephrolithiasis. As expected, hypocitraturia was present in renal tubular acidosis and in enteric hyperoxaluria. However, urinary citrate was also low in absorptive and renal hypercalciurias, and in patients in whom an acid-base disturbance was clearly excluded.

Acidosis, Renal Tubular↗
PubMed1983

Contrasting effects of potassium citrate and sodium citrate therapies on urinary chemistries and crystallization of stone-forming salts.

Effects of potassium citrate therapy (60 mEq/day) on urinary chemistries and crystallization were compared to those of sodium citrate treatment in five patients with uric acid lithiasis. Both alkali treatments significantly increased urinary pH (P less than 0.001), from 5.35 +/- 0.18 SD to 6.68 +/- 0.14 for potassium citrate and 6.73 +/- 0.20 for sodium citrate. During potassium citrate therapy, urinary calcium significantly declined from 154 +/- 47 mg/day to 99 +/- 23 mg/day (P less than 0.01) and urinary citrate rose from 398 +/- 119 mg/day to 856 +/- 103 mg/day (P less than 0.001). The urinary saturation (activity product ratio) of calcium oxalate decreased from 3.21-fold to 1.69-fold saturation (P less than 0.01), and the inhibitor activity against calcium oxalate precipitation (formation product ratio) significantly increased. However, sodium citrate therapy did not significantly decrease urinary calcium (to 139 +/- 24 mg/day), although it increased urinary citrate substantially (to 799 +/- 89 mg/day, P less than 0.01). Urinary environment became supersaturated with respect to brushite (calcium phosphate) and monosodium urate. The inhibitor activity against calcium oxalate precipitation was not significantly altered for the whole group; in two patients, it decreased by more than 30%. The results indicate that (1) both alkali therapies are equally effective in preventing uric acid stone formation because of their ability to increase urinary pH, and (2) potassium citrate may prevent the complication of calcium nephrolithiasis in patients with uric acid stones, whereas sodium citrate may not.

Adult↗
PubMed1983

Long term 25-hydroxyvitamin D3 therapy in postmenopausal osteoporosis: demonstration of responsive and nonresponsive subgroups.

Previous studies from our laboratory have demonstrated that 25-hydroxyvitamin D3 (25OHD3) therapy is effective in raising the impaired intestinal calcium absorption (alpha) associated with postmenopausal osteoporosis. In the present study we have assessed the effects of long term 25-OHD3 therapy (50 micrograms/day; mean treatment period, 1.3 yr) in 12 women with postmenopausal osteoporosis (mean age, 62.5 yr). Our results indicate that there was a significant increase in alpha for the group during therapy. However, we found that the patients could be divided into 2 groups based upon their ability to raise alpha in response to 25OHD3 therapy. In those who responded (n = 7), alpha increased from 0.36 +/- 0.05 to 0.49 +/- 0.08 (+/- SD; P less than 0.005) while no significant change was observed for the nonresponders (0.44 +/- 0.03 to 0.48 +/- 0.07). During therapy, there were significant increases in serum 25OHD and 24,25-dihydroxyvitamin D [25,25-(OH)2D] for both groups. Serum 1,25-(OH)2D significantly increased in the responders (21 +/- 8 to 39 +/- 13 pg/ml; P less than 0.01), but not in nonresponders (25 +/- 11 to 28 +/- 8 pg/ml). Between-group comparisons for responders vs. nonresponders before therapy disclosed significant reductions in 24,25-(OH)2D (0.4 +/- 0.3 vs. 2.2 +/- 0.8 ng/ml; P less than 0.005) and alpha (0.36 +/- 0.05 vs. 0.44 +/- 0.03; P less than 0.01). During therapy, there were no significant differences in any parameter between the two groups, except for serum I,25-(OH)2D which was significantly higher in the responders (39 +/- 13 vs. 28 +/- 8 pg/ml; P less than 0.05). These data would suggest that in postmenopausal osteoporosis, the ability to raise alpha in response to 25OHD3 therapy is due in part to increases in serum 1,25-(OH)2D during therapy. This suggests that in some patients with menopausal osteoporosis, renal 25OHD3-1 alpha-hydroxylase may be impaired.

24,25-Dihydroxyvitamin D 3↗
PubMed1983

Physiological and physiochemical correction and prevention of calcium stone formation by potassium citrate therapy.

Long-term effects of potassium citrate therapy (usually 60 mEq/day) were examined in 53 patients with renal stones (11 with uric acid lithiasis with complication of calcium stones, 10 with hypocitraturia as the sole abnormality, and 28 with hypocitraturia occurring with other abnormalities such as absorptive hypercalciuria, renal tubular acidosis, hyperuricosuric calcium oxalate nephrolithiasis, and enteric hyperoxaluria). Potassium citrate was given alone in 29 patients, added to thiazide and/or allopurinol treatments in 12 patients who continued to form stones on these treatments, and begun concurrently with thiazide and/or allopurinol in 12 patients with hypocitraturia and other defects (hypercalcuria and/or hyperuricosuria). In all three groups of patients, urinary citrate and pH significantly increased during potassium citrate treatment. Urinary saturation of calcium oxalate significantly declined while that of brushite remained unchanged. The propensity for the spontaneous nucleation of calcium oxalate, determined from the minimum amount of added oxalate required to elicit precipitation, declined. The treatment was effective in preventing new stone formation in all three groups. Stone passage rate declined from 5.14-7.41 stones/patient year before potassium citrate treatment to 0.66-1.33 stones/patient year during treatment, and 75.0-91.7% of patients were in remission. In patients who relapsed on other treatments (with passage of 5.14 stones/patient year), the addition of potassium citrate to the ongoing treatment program reduced stone formation to 1.33 stones/patient year and caused remission in 91.7% of patients. In 14 of 33 patients with preexisting radiopaque stones, there was radiological evidence of a reduced number of stones after 8 months-2 years of potassium citrate treatment. In conclusion, potassium citrate restores normal urinary citrate, decreases saturation and propensity for spontaneous nucleation of calcium oxalate, and inhibits new stone formation.

Adult↗
PubMed1981

Is selective therapy of recurrent nephrolithiasis possible?

We evaluated, in 128 patients with recurrent nephrolithiasis, the efficacy of special treatment programs for some of the common causes of nephrolithiasis, chosen on the basis of their ability to correct underlying physicochemical and physiologic derangements. Therapy included sodium cellulose phosphate for 18 patients with absorptive hypercalciuria, thiazide diuretics for 27 patients with absorptive hypercalciuria and for 10 with renal hypercalciuria, orthophosphate for eight patients with hypophosphatemic absorptive hypercalciuria, allopurinol for 21 patients with hyperuricosuric calcium oxalate nephrolithiasis, thiazide and allopurinol for 26 patients with absorptive hypercalciuria with hyperuricosuria, and high fluid intake and/or low calcium diet for 22 patients with normocalciuric nephrolithiasis. Patients in all seven groups had a significant reduction in stone formation during 1.70 to 3.37 years of treatment, as compared with the pretreatment period of three years. Remission was found in 70 to 91 percent of patients and reduced stone formation rate was encountered in 88 to 100 percent. Each treatment program produced a significant decline in stone formation rate from 1.90 to 2.28 stones per year to 0.09 to 0.55 stones per year. The actual number of stones formed during treatment was significantly lower than the number predicted from the pretreatment frequency of stone formation (less than 26 percent). The results provide evidence supporting a selective approach to therapy of nephrolithiasis.

Allopurinol↗
PubMed1981

Utility and limitation of calciuric response to oral calcium load as a measure of intestinal calcium absorption: comparison with isotopic fractional calcium absorption.

The intestinal absorption of calcium (Ca), indirectly measured from the calciuric response to oral Ca load (1g), was compared to the more directly obtained isotopic fractional absorption, alpha (from the fecal recovery of orally administered 47Ca). In 17 normal subjects and 30 patients with absorptive hypercalciuria (AH), there was a significant (P less than 0.001) correlation of alpha with the Ca load responses, (r = 0.81). However, this correlation was not observed in patients with renal hypercalciuria (RH), and those with AH receiving thiazide or orthophosphate. In RH, 38 per cent of patients had elevated Ca load responses, despite normal values for alpha. The point correlating the calciuric response and alpha in these patients was below the 95 per cent confidence limit of the line correlating alpha and the load response. Thus, Ca load response often overestimated intestinal Ca absorption, because of the high basal (fasting) urinary Ca. Thiazide therapy in RH improved the correlation between the two tests of Ca absorption. However, thiazide therapy in AH produced normal Ca load responses despite persistently high alpha in 60 per cent of patients. Similarly, 50 per cent of patients with AH receiving orthophosphate had normal Ca load response, although alpha remained elevated. Thus, Ca load response underestimated Ca absorption when patients with AH took thiazide or orthophosphate, probably because these drugs augment renal tubular reabsorption of Ca. These data support the Ca load test as a valid indirect measure of intestinal Ca absorption in normal subjects and patients with AH, in whom fasting urinary Ca is not elevated. In conditions of renal Ca, leak or with various drugs known to alter renal Ca handling, there seen to be large deviations of Ca load response from alpha. Care should be exercised before reaching conclusions regarding the intestinal Ca absorption in these situations.

Administration, Oral↗
PubMed1980

Ambulatory evaluation of nephrolithiasis. Classification, clinical presentation and diagnostic criteria.

Using the ambulatory protocol previously described, 241 patients with nephrolithiasis were evaluated. They could be categorized into 10 groups from the results obtained. Absorptive hypercalciuria type I (87 per cent male) comprised 24.5 per cent and was characterized by normocalcemia, normal fasting urinary calcium (less than 0.11 mg/100 ml glomerular filtration), an exaggerated urinary calcium following an oral calcium load (greater than 0.20 mg/mg creatinine), normal urinary cyclic adenosine monophosphate (AMP) (less than 5.4 nmol/100 ml glomerular filtration) and serum parathyroid hormone (PTH), and hypercalciuria (greater than 200 mg/day during a calcium- and sodium-restricted diet). Absorptive hypercalciuria type II (50 per cent male) accounted for 29.8 per cent; its biochemical features were the same as those for absorptive hypercalciuria type I, except for normocalciuria during a restricted diet and low urine volume (1.42 +/- 0.55 SD liter/day). Renal hypercalciuria (56 per cent male), disclosed in 8.3 per cent, was represented by normocalcemia and high values for fasting urinary calcium (0.160 +/- 0.054 mg/100 ml glomerular filtration), urinary cyclic AMP (6.80 +/- 2.10 nmol/100 ml glomerular filtration) and serum PTH. Primary hyperparathyroidism (57 per cent female), accounted for 5.8 per cent, typically included hypercalcemia, hypophosphatemia, hypercalciuria and high urinary cyclic AMP. Hyperuricosuric calcium urolithiasis (100 per cent male) comprised 8.7 per cent, and was characterized by hyperuricosuria (776 +/- 164 mg/day) and urinary pH exceeding pK for uric acid (5.91 +/- 0.33). In enteric hyperoxaluria (60 per cent female), encountered in 2.1 per cent of cases, urinary oxalate was increased (6.29 +/- 13.2 mg/day). Noncalcium-containing stones were found in 2.1 per cent of the patients with uric acid lithiasis (100 per cent male) and in another 2.1 per cent of the patients with infection lithiasis (60 per cent female). These conditions were typified by low urinary pH (5.29 +/- 0.12) and high urinary pH (6.69 +/- 1.16), respectively. Renal tubular acidosis was found in one patient (male, 0.4 per cent). In 10.8 per cent of the patients (81 per cent male), no metabolic abnormality could be found, although urine volume was low (1.41 +/- 0.51 liter/day). Hypercalciuria could not be differentiated between absorptive hypercalciuria and renal hypercalciuria in 5.4 per cent of the patients. Thus, this ambulatory protocol disclosed a physiologic disturbance in nearly 90 per cent of the cases and provided a definitive diagnosis in 95 per cent of the patients.

Adult↗
PubMed1980

Evidence justifying a high fluid intake in treatment of nephrolithiasis.

We quantitatively assessed the effect of urinary dilution on the crystallization of calcium salts. Urinary dilution was achieved in vitro (1 to 2 L/d) by addition of water to urine from six patients with renal stones and two normal subjects, and in vivo (1.023 to 2.383 L/d) by an increased ingestion of distilled water in four patients with nephrolithiasis and three normal subjects. Both forms of urinary dilution significantly reduced the urinary activity product ratio (state of saturation) of calcium phosphate (brushite), calcium oxalate, and monosodium urate. Moreover, the formation product ratio (limit of metastability or minimum supersaturation needed to elicit spontaneous nucleation) of calcium oxalate significantly increased, although that for brushite did not change significantly. Thus, there was a reduced propensity for crystallization of calcium salts. The results provide objective evidence for the beneficial role of an increased fluid intake in the management of nephrolithiasis.

Calcium Oxalate↗
PubMed1979

Critical appraisal of oral calcium load test for indirect assessment of intestinal calcium absorption.

Two methods of oral calcium load or tolerance test for the indirect assessment of calcium absorption were compared. In 16 patients in whom the diagnosis of absorptive hypercalciuria was made independently, an exaggerated urinary total calcium excretion during four hours following calcium load, indicative of increased calcium absorption according to the method of Pak et al., was found in 15 patients. An abnormally high increment in urinary calcium during third and fourth hours post-calcium load, suggestive of enhanced calcium absorption by the criteria of Broadus et al., was encountered in 14 patients. However, an exaggerated urinary total calcium following calcium load was found in all 7 patients with renal hypercalciuria, whereas only 4 were shown to have an enhanced increment in calcium excretion. It is concluded that both methods are equally reliable in the detection of increased calcium absorption in absorptive hypercalciuria. However, the technique of Broadus et al. is probably superior to that of Pak et al. in the disclosure of increased calcium absorption in renal hypercalciuria.

Administration, Oral↗