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Biomedical subjects

C Y Pak

Publications and source records attributed to C Y Pak.

At least 181 records · Page 10Linked to original sources
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

Use of potassium citrate as potassium supplement during thiazide therapy of calcium nephrolithiasis.

The effectiveness of potassium citrate as a potassium supplement was compared to that of potassium chloride in 13 patients with calcium nephrolithiasis treated with thiazide. Thiazide treatment alone reduced serum potassium, urinary calcium and citrate without affecting urinary pH. Urinary saturation of calcium oxalate and brushite decreased but not as much as the decrement in urinary calcium because of reduced citrate-calcium complexation. Potassium chloride supplementation averted thiazide-induced hypokalemia and hypocitraturia without influencing hypocalciuric action of thiazide or urinary pH. The decline in urinary saturation of calcium salts paralleled the decrement in urinary calcium. Potassium citrate supplementation also kept urinary calcium low and corrected hypokalemia. Moreover, it increased urinary pH and citrate above levels in other phases. Thus, the ability of thiazide to lower the urinary saturation of calcium oxalate was accentuated by potassium citrate supplementation but not by potassium chloride supplementation, probably owing to increased citrate complexation of calcium. Moreover, the potassium citrate therapy was more effective than potassium chloride supplementation in reducing the propensity for the spontaneous precipitation of calcium oxalate in urine. In conclusion, potassium citrate supplementation may be superior to potassium chloride supplementation in patients receiving thiazide in whom stones form.

Adult↗
PubMed1984

Effect of 1,25-dihydroxyvitamin D3 on calcium absorption in the colon of healthy humans.

Calcium absorption in patients with short bowel syndrome is significantly higher when the colon is left intact. To study calcium transport in the large bowel, we investigated whether exogenous 1,25-dihydroxyvitamin D3 [1,25(OH2)D3] can induce or enhance colonic calcium absorption in healthy subjects ingesting a normal diet. Steady-state colon perfusion studies were performed before and after 1 wk of 1,25(OH)2D3 administration (2 micrograms/day, 10 subjects). Serum 1,25-dihydroxyvitamin D concentration rose from 23.0 +/- 2.2 to 39.5 +/- 4.3 pg/ml (mean +/- SE, P less than 0.01). In the basal state the mean net movement of calcium was not significantly different from zero when a 5 mM calcium gluconate solution was perfused (100 +/- 84 mumol X h-1 X entire colon secreted-1). Vitamin D administration resulted in a significant change toward calcium absorption (106 +/- 47 mumol X h-1 X entire colon absorbed-1, P less than 0.02). 1,25(OH)2D3 had no effect on colonic magnesium, phosphate, water, and electrolyte movement. This study demonstrates that in healthy humans exogenous 1,25(OH)2D3 can change colonic calcium movement toward absorption. We suspect that similar changes in colonic calcium transport are caused by endogenous 1,25(OH)2D3 when calcium deficiency has occurred in short bowel syndrome.

Adult↗
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↗
PubMed1984

Hypercalcemia associated with increased serum calcitriol levels in three patients with lymphoma.

A radioreceptor assay for serum 1,25-dihydroxyvitamin D (calcitriol) was used to screen patients with hypercalcemia of malignancy. Three patients with non-Hodgkin's lymphoma and hypercalcemia (serum Ca, 12.0, 13.4, and 13.0 mg/dL, respectively) had increased serum calcitriol levels (56, 72, and 77 pg/mL, respectively; normal, less than 50 pg/mL). Elevated levels of calcitriol, an active vitamin D metabolite, occurred in the presence of significant renal impairment (creatinine clearance, 8 to 19 mL/min) and relative parathyroid suppression (serum immunoreactive parathyroid hormone, 17 to 39 microL-eq/mL; mean value in end-stage renal disease, 182 +/- 39 microL-eq/mL). Hypercalcemia and excessive serum calcitriol levels responded to glucocorticosteroid therapy. In two patients, the hypercalcemia and increased serum calcitriol level were related to a tumor, but not to the serum immunoreactive parathyroid hormone level. Fractional intestinal 47Ca absorption, measured in one patient, was increased (0.94; normal, less than 0.61) and varied directly with the serum calcitriol level. No patient had evidence of sarcoidosis. Hypercalcemia associated with certain lymphomas may be caused by the increased synthesis of calcitriol by lymphoma cells.

Aged↗
PubMed1983

Effect of 1,25-dihydroxyvitamin D3 on calcium and magnesium absorption in the healthy human jejunum and ileum.

In calcium deficiency states such as chronic renal failure, 1,25-dihydroxyvitamin D3 increases calcium and magnesium absorption toward normal levels. In the present study, the ability of exogenous 1,25-dihydroxyvitamin D3 to increase calcium and magnesium absorption above normal rates in healthy subjects was investigated. Steady-state perfusion studies were performed in 30 cm segments of jejunum and ileum before and after one week of 1,25-dihydroxyvitamin D3 administration (2 micrograms per day, 10 subjects). Serum 1,25-dihydroxyvitamin D concentration increased from 25.8 +/- 2.5 pg/ml to 56.4 +/- 6.6 (mean +/- SEM, p less than 0.05). In the basal state, calcium absorption was significantly higher in the jejunum than in the ileum. Vitamin D administration resulted in a significant increase in calcium absorption which was quantitatively similar in both the jejunum and ileum. The changes in net movement were due to an increase in lumen-to-plasma flux of calcium; the plasma-to-lumen flux remained unchanged. Jejunal magnesium absorption also was enhanced by 1,25-dihydroxyvitamin D3. These studies demonstrate that in healthy persons, exogenous 1,25-dihydroxyvitamin D3 increases calcium absorption in both the jejunum and the ileum, and increases magnesium absorption in the jejunum.

Adult↗
PubMed1983

A simple technique for assessing the propensity for crystallization of calcium oxalate and brushite in urine from the increment in oxalate or calcium necessary to elicit precipitation.

In an effort to develop a simple and reliable method with which to assess the propensity for spontaneous nucleation of calcium oxalate and brushite in urine, the permissible increment of oxalate and calcium was calculated. This represented the additional amount of oxalate or calcium that could be added to urine in three hours before spontaneous precipitation of calcium oxalate or brushite was initiated. The permissible increment of oxalate inversely correlated (P less than 0.001) with the formation-product ratio-activity-product ratio discriminant score of calcium oxalate, which was previously shown to reflect a quantitative measure of the likelihood for spontaneous nucleation. Similarly, the permissible increment of calcium inversely correlated (P less than 0.001) with the formation-product ratio-activity-product ratio discriminant score of brushite. The permissible increments in oxalate and calcium were significantly lower (P less than 0.001) in patients with renal stones than in control subjects. Moreover, treatment with thiazides, allopurinol, sodium cellulose phosphate, orthophosphate, and diphosphonate significantly raised the permissible increment of oxalate in patients with stones. Thus, the permissible increment was reliable in discriminating "stone-forming" from control urine and in assessing response to treatment.

Calcium↗
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

Lack of effect of salt intake on urinary uric acid excretion.

Although it has been established that acute expansion of the extracellular fluid volume results in enhanced uric acid clearance, the effect of chronic volume expansion by a high salt diet on urinary uric acid excretion has not been examined. Eleven normal subjects were placed on a constant diet containing 10 mEq. sodium per day for 10 days, followed by 240 mEq. sodium daily for another 10 days. Measurements were performed on the final 3 days of each phase. Urinary sodium increased from 9 plus or minus 3 standard error to 221 plus or minus 9 mEq. per day (p less than 0.001), and uric acid clearance increased from 5.9 plus or minus 0.4 to 7.1 plus or minus 0.6 ml. per minute (p less than 0.01). However, serum uric acid decreased from 6.4 plus or minus 0.4 to 5.5 plus or minus 0.3 mg./dl. (p less than 0.001). Total urinary excretion of uric acid did not change (533 plus or minus 24 to 535 plus or minus 26 mg. per day). A high salt diet does not result in sustained hyperuricosuria, although it may predispose to kidney stone formation in other ways.

Adult↗
PubMed1983

Assessment of cystine solubility in urine and of heterogeneous nucleation.

Factors affecting cystine solubility were sought in an effort to derive a reliable method for estimating urinary saturation with respect to cystine. In synthetic solutions, cystine solubility was measured from the maximum ambient cystine concentration reached after incubation with an excess of solid cystine. It rose progressively as the ionic strength increased from addition of mineral electrolytes. The increment in cystine solubility between ionic strength of 0.005 and 0.3 ranged from 13 mg./1. for potassium chloride to 70 mg./1. for calcium chloride. Urinary macromolecules (less than 5,000 daltons, obtained by ultrafiltration), at concentrations normally expected to be found in urine, increased cystine solubility by as much as 45 mg./1. Because of these actions of electrolytes and macromolecules, cystine solubility in urine (from control subjects and patients with cystinuria) exceeded solubility in synthetic solution containing 5 mM sodium cacodylate by 68 to 89 mg./1. Thus, the saturation of cystine in individual urine samples cannot be estimated by comparing the original cystine concentration with a defined cystine solubility curve. It may be more accurately measured as the ratio of original cystine concentration and the directly determined cystine solubility in urine. The estimated assessment of urinary saturation with respect to cystine was shown to deviate from the empirically derived measure from -33 to +44 per cent. In conclusion, cystine is more soluble in urine because of the effects of electrolytes and macromolecules. Thus, urinary saturation of cystine cannot be estimated from solubility curves but must be empirically derived from the direct assessment of cystine solubility in individual urine samples.

Calcium Oxalate↗
PubMed1983

Natural urinary macromolecular inhibitors: attenuation of inhibitory activity by urate salts.

The interaction between naturally occurring urinary macromolecular inhibitors of calcium oxalate nucleation and crystal growth and the various urate salts was explored in vitro. The fraction of macromolecules chosen for the study was the one which was previously shown to have a potent inhibitor activity against calcium oxalate nucleation and one which gave a satisfactory yield. As little as 0.025 mg/ml of this fraction (Y-b) was found to inhibit calcium oxalate nucleation by nearly 50% and crystal growth by 31%. Prior incubation of the solution containing Y-b with increasing crystal surface areas (1.1 to 26.2 mm2/ml) of monosodium urate (NaU), monopotassium urate (KU), or uric acid (UA) attenuated the inhibitory action of the Y-b fraction for both nucleation and crystal growth of calcium oxalate. The most prominent effect was elicited by NaU at surface areas as small as 1.1 mm2/ml. Potassium urate and UA were without significant effects until surface areas of 13.1 and 2.6 mm2/ml, respectively, were achieved. These results support an important pathogenetic role for urates (particularly NaU) in the development of hyperuricosuric calcium urolithiasis.

Calcium Oxalate↗