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Glenn M. Preminger - One of the best experts on this subject based on the ideXlab platform.

  • Potassium Citrate and Calcium Stones: Benefit or Risk?
    Practical Controversies in Medical Management of Stone Disease, 2014
    Co-Authors: Ramy F. Youssef, Glenn M. Preminger, Michael E. Lipkin
    Abstract:

    Nephrolithiasis is a common urological disease that will affect 5–10 % of adults during their lifetime. The natural history of nephrolithiasis is characterized by recurrence, with almost 50 % of patients recurring within 5 years of their initial stone event. Each stone episode can cause significant pain, decreases productivity, and, if not treated appropriately, may lead to renal dysfunction. Medical therapy has been used for many years in the prevention of stone growth/recurrence. Potassium Citrate is an oral alkalizing agent that has been used as the mainstay of medical nephrolithiasis management in the last three decades. With the recent increase in calcium-phosphate stone formation, concern has been raised that Potassium Citrate may be contributing to this finding.

  • impact of long term Potassium Citrate therapy on urinary profiles and recurrent stone formation
    The Journal of Urology, 2009
    Co-Authors: Marnie R. Robinson, Victor A. Leitao, George E. Haleblian, Charles D. Scales, Aravind Chandrashekar, Sean A. Pierre, Glenn M. Preminger
    Abstract:

    Purpose: Potassium Citrate therapy has become one of the cornerstones of medical stone management. We elucidated the long-term effects of Potassium Citrate on urinary metabolic profiles and its impact on stone formation rates.Materials and Methods: We performed a retrospective cohort study in patients treated at the Comprehensive Kidney Stone Center at our institution between 2000 and 2006. Patients with pre-therapy and post-therapy 24-hour urinary profiles available who remained on Potassium Citrate for at least 6 months were included in the analysis.Results: Of the 1,480 patients with 24-hour urinary profiles 503 met study inclusion criteria. Mean therapy duration was 41 months (range 6 to 168). Overall a significant and durable change in urinary metabolic profiles was noted as soon as 6 months after the onset of therapy. These changes included increased urinary pH (5.90 to 6.46, p <0.0001) and increased urinary Citrate (470 to 700 mg a day, p <0.0001). The stone formation rate also significantly decrea...

  • Impact of Long-Term Potassium Citrate Therapy on Urinary Profiles and Recurrent Stone Formation
    The Journal of urology, 2009
    Co-Authors: Marnie R. Robinson, Victor A. Leitao, George E. Haleblian, Charles D. Scales, Aravind Chandrashekar, Sean A. Pierre, Glenn M. Preminger
    Abstract:

    Purpose: Potassium Citrate therapy has become one of the cornerstones of medical stone management. We elucidated the long-term effects of Potassium Citrate on urinary metabolic profiles and its impact on stone formation rates.Materials and Methods: We performed a retrospective cohort study in patients treated at the Comprehensive Kidney Stone Center at our institution between 2000 and 2006. Patients with pre-therapy and post-therapy 24-hour urinary profiles available who remained on Potassium Citrate for at least 6 months were included in the analysis.Results: Of the 1,480 patients with 24-hour urinary profiles 503 met study inclusion criteria. Mean therapy duration was 41 months (range 6 to 168). Overall a significant and durable change in urinary metabolic profiles was noted as soon as 6 months after the onset of therapy. These changes included increased urinary pH (5.90 to 6.46, p

  • Does Potassium Citrate Medical Therapy Increase the Risk of Calcium Phosphate Stone Formation
    AIP Conference Proceedings, 2007
    Co-Authors: Victor A. Leitao, Roger L Sur, Marnie R. Robinson, George E. Haleblian, Sean A. Pierre, Glenn M. Preminger
    Abstract:

    Potassium Citrate has been extensively used in the treatment of recurrent nephrolithiasis. Recent evidence suggests that it may contribute to increasing urinary pH and, as such, increase the risk of calcium phosphate stone formation. We performed a retrospective review of our patients to further investigate this phenomenon.

  • Long-term combined treatment with thiazide and Potassium Citrate in nephrolithiasis does not lead to hypokalemia or hypochloremic metabolic alkalosis
    Kidney international, 2003
    Co-Authors: Clarita V. Odvina, Glenn M. Preminger, Jill S. Lindberg, Orson W. Moe, Charles Y.c. Pak
    Abstract:

    Long-term combined treatment with thiazide and Potassium Citrate in nephrolithiasis does not lead to hypokalemia or hypochloremic metabolic alkalosis. Background Potassium Citrate is commonly used in combination with a thiazide diuretic in the medical management of recurrent hypercalciuric nephrolithiasis. However, concerns have been raised that administration of this nonchloride Potassium alkali with a kaliuretic and natriuretic agent such as thiazide may not be efficacious in correcting or preventing hypokalemia, and may produce hypochloremic metabolic alkalosis. This retrospective analysis was conducted to determine if these two potential complications are encountered in patients on long-term Potassium Citrate and thiazide therapy. Methods Data were collected on 95 patients who had been on combination therapy for at least 4 months from the stone clinics of the University of Texas Southwestern Medical Center, Duke University Medical Center, and Ochsner Clinic. Results Mean serum Potassium concentration remained within normal limits without a significant decrease during combined therapy. Serum chloride was significantly lower from pretreatment but by only 1 mEq/L and remained within normal limits throughout treatment. There was a small increase in serum bicarbonate concentration compared to the baseline level of less than 1 mEq/L at 8 to 12 and 18 to 24 months, but not at other treatment periods. Conclusion Co-administration of Potassium Citrate did not induce hypokalemia or hypochloremic metabolic alkalosis in our thiazide-treated patient population.

Anthony Sebastian - One of the best experts on this subject based on the ideXlab platform.

  • Potassium Citrate PREVENTS INCREASED URINE CALCIUM EXCRETION AND BONE RESORPTION INDUCED BY A HIGH SODIUM CHLORIDE DIET
    2030 Uzbekistan Research Online, 2019
    Co-Authors: Deborah Sellmyer, Monique Schloetter, Anthony Sebastian
    Abstract:

    The amount of sodium chloride in the diet of industrialized nations far exceeds physiological requirements. The impact of abundant ietary salt on skeletal health has yet to be established, but is potentially detrimental through increased urinary calcium losses. We examined the effect of increased dietary sodium chloride on urine calcium excretion and bone turnover markers in postmenopausal women and, further, whether Potassium Citrate attenuates the effects of increased dietary salt. Postmenopausal women (n _ 60) were adapted to a low-salt (87 mmol/d sodium) diet for 3 wk, then randomized to a high-salt (225 mmol/d sodium) diet plus Potassium Citrate (90 mmol/d) or a high-salt diet plus placebo for 4 wk. Urine calcium, urine N-telopeptide, urine cAMP, serum osteocalcin, and fasting serum PTH were measured at the end of the lowand high-salt diets. On the high salt plus placebo diet, urine calcium increased 42-12 mg/d (mean _ SEM), but decreased 8-14 mg/d in the high salt plus Potassium Citrate group (P-0.008, Potassium Citrate vs. placebo, npaired t test). Ntelopeptide increased 6.4-1.4 nanomoles bone collagen equivalents per millimole creatinine in the high salt plus placebo group and 2.0-1.7 nanomoles bone collagen equivalents per millimole creatinine in the high salt plus Potassium Citrate group (P 0.05, Potassium Citrate vs. placebo, unpaired t test). Osteocalcin, PTH, and cAMP were not significantly altered. The addition of oral Potassium Citrate to a high-salt diet prevented the increased excretion of urine calcium and the bone resorption marker caused by a high salt intake. Increased intake of dietary sources of Potassium alkaline salts, namely fruit and vegetables, may be beneficial for postmenopausal women at risk for osteoporosis, particularly those consuming a diet generous in sodium chloride. (J Clin Endocrinol Metab 87: 2008–2012, 2002

  • Potassium Citrate supplementation results in sustained improvement in calcium balance in older men and women
    Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2013
    Co-Authors: Kendall F. Moseley, Connie M. Weaver, Lawrence J. Appel, Anthony Sebastian, Deborah E. Sellmeyer
    Abstract:

    The dietary acid load created by the typical Western diet may adversely impact the skeleton by disrupting calcium metabolism. Whether neutralizing dietary acid with alkaline Potassium salts results in sustained improvements in calcium balance remains controversial. In this randomized, double-blind, placebo-controlled study, 52 men and women (mean age 65.2 ± 6.2 years) were randomly assigned to Potassium Citrate 60 mmol/d, 90 mmol/d, or placebo daily with measurements of bone turnover markers, net acid excretion, and calcium metabolism, including intestinal fractional calcium absorption and calcium balance, obtained at baseline and at 6 months. At 6 months, net acid excretion was significantly lower in both treatment groups compared to placebo and it was negative, meaning subjects' dietary acid was completely neutralized (-11.3 mmol/d on 60 mmol/d; -29.5 mmol/d on 90 mmol/d, p < 0.001 compared to placebo). At 6 months, 24-hour urine calcium was significantly reduced in persons taking Potassium Citrate 60 mmol/d (-46 ± 15.9 mg/d) and 90 mmol/d (-59 ± 31.6 mg/d) compared with placebo (p < 0.01). Fractional calcium absorption was not changed by Potassium Citrate supplementation. Net calcium balance was significantly improved in participants taking Potassium Citrate 90 mmol/d compared to placebo (142 ± 80 mg/d on 90 mmol/d versus -80 ± 54 mg/d on placebo; p = 0.02). Calcium balance was also improved on Potassium Citrate 60 mmol/d, but this did not reach statistical significance (p = 0.18). Serum C-telopeptide decreased significantly in both Potassium Citrate groups compared to placebo (-34.6 ± 39.1 ng/L on 90 mmol/d, p = 0.05; -71.6 ± 40.7 ng/L on 60 mmol/d, p = 0.02) whereas bone-specific alkaline phosphatase did not change. Intact parathyroid hormone was significantly decreased in the 90 mmol/d group (p = 0.01). Readily available, safe, and easily administered in an oral form, Potassium Citrate has the potential to improve skeletal health. Longer-term trials with definitive outcomes such as bone density and fracture are needed.

  • Potassium Citrate prevents increased urine calcium excretion and bone resorption induced by a high sodium chloride diet
    The Journal of Clinical Endocrinology and Metabolism, 2002
    Co-Authors: Deborah E. Sellmeyer, Monique Schloetter, Anthony Sebastian
    Abstract:

    The amount of sodium chloride in the diet of industrialized nations far exceeds physiological requirements. The impact of abundant dietary salt on skeletal health has yet to be established, but is potentially detrimental through increased urinary calcium losses. We examined the effect of increased dietary sodium chloride on urine calcium excretion and bone turnover markers in postmenopausal women and, further, whether Potassium Citrate attenuates the effects of increased dietary salt. Postmenopausal women (n = 60) were adapted to a low-salt (87 mmol/d sodium) diet for 3 wk, then randomized to a high-salt (225 mmol/d sodium) diet plus Potassium Citrate (90 mmol/d) or a high-salt diet plus placebo for 4 wk. Urine calcium, urine N-telopeptide, urine cAMP, serum osteocalcin, and fasting serum PTH were measured at the end of the low- and high-salt diets. On the high salt plus placebo diet, urine calcium increased 42 +/- 12 mg/d (mean +/- SEM), but decreased 8 +/- 14 mg/d in the high salt plus Potassium Citrate group (P = 0.008, Potassium Citrate vs. placebo, unpaired t test). N-telopeptide increased 6.4 +/- 1.4 nanomoles bone collagen equivalents per millimole creatinine in the high salt plus placebo group and 2.0 +/- 1.7 nanomoles bone collagen equivalents per millimole creatinine in the high salt plus Potassium Citrate group (P < 0.05, Potassium Citrate vs. placebo, unpaired t test). Osteocalcin, PTH, and cAMP were not significantly altered. The addition of oral Potassium Citrate to a high-salt diet prevented the increased excretion of urine calcium and the bone resorption marker caused by a high salt intake. Increased intake of dietary sources of Potassium alkaline salts, namely fruit and vegetables, may be beneficial for postmenopausal women at risk for osteoporosis, particularly those consuming a diet generous in sodium chloride.

  • Potassium Citrate Prevents Increased Urine Calcium Excretion and Bone Resorption Induced by a High Sodium Chloride Diet
    The Journal of clinical endocrinology and metabolism, 2002
    Co-Authors: Deborah E. Sellmeyer, Monique Schloetter, Anthony Sebastian
    Abstract:

    The amount of sodium chloride in the diet of industrialized nations far exceeds physiological requirements. The impact of abundant dietary salt on skeletal health has yet to be established, but is potentially detrimental through increased urinary calcium losses. We examined the effect of increased dietary sodium chloride on urine calcium excretion and bone turnover markers in postmenopausal women and, further, whether Potassium Citrate attenuates the effects of increased dietary salt. Postmenopausal women (n = 60) were adapted to a low-salt (87 mmol/d sodium) diet for 3 wk, then randomized to a high-salt (225 mmol/d sodium) diet plus Potassium Citrate (90 mmol/d) or a high-salt diet plus placebo for 4 wk. Urine calcium, urine N-telopeptide, urine cAMP, serum osteocalcin, and fasting serum PTH were measured at the end of the low- and high-salt diets. On the high salt plus placebo diet, urine calcium increased 42 ± 12 mg/d (mean ± sem), but decreased 8 ± 14 mg/d in the high salt plus Potassium Citrate group...

Charles Y.c. Pak - One of the best experts on this subject based on the ideXlab platform.

  • Long-term combined treatment with thiazide and Potassium Citrate in nephrolithiasis does not lead to hypokalemia or hypochloremic metabolic alkalosis
    Kidney international, 2003
    Co-Authors: Clarita V. Odvina, Glenn M. Preminger, Jill S. Lindberg, Orson W. Moe, Charles Y.c. Pak
    Abstract:

    Long-term combined treatment with thiazide and Potassium Citrate in nephrolithiasis does not lead to hypokalemia or hypochloremic metabolic alkalosis. Background Potassium Citrate is commonly used in combination with a thiazide diuretic in the medical management of recurrent hypercalciuric nephrolithiasis. However, concerns have been raised that administration of this nonchloride Potassium alkali with a kaliuretic and natriuretic agent such as thiazide may not be efficacious in correcting or preventing hypokalemia, and may produce hypochloremic metabolic alkalosis. This retrospective analysis was conducted to determine if these two potential complications are encountered in patients on long-term Potassium Citrate and thiazide therapy. Methods Data were collected on 95 patients who had been on combination therapy for at least 4 months from the stone clinics of the University of Texas Southwestern Medical Center, Duke University Medical Center, and Ochsner Clinic. Results Mean serum Potassium concentration remained within normal limits without a significant decrease during combined therapy. Serum chloride was significantly lower from pretreatment but by only 1 mEq/L and remained within normal limits throughout treatment. There was a small increase in serum bicarbonate concentration compared to the baseline level of less than 1 mEq/L at 8 to 12 and 18 to 24 months, but not at other treatment periods. Conclusion Co-administration of Potassium Citrate did not induce hypokalemia or hypochloremic metabolic alkalosis in our thiazide-treated patient population.

  • Prevention of spinal bone loss by Potassium Citrate in cases of calcium urolithiasis.
    The Journal of urology, 2002
    Co-Authors: Charles Y.c. Pak, Roy D. Peterson, John R. Poindexter
    Abstract:

    Purpose: We determine if Potassium Citrate treatment stabilizes spinal bone density among patients with recurrent calcium oxalate nephrolithiasis.Materials and Methods: We studied a group of 16 men and 5 women with stones taking Potassium Citrate from 11 to 120 months. They represented all patients from the Stone Clinic who took Potassium Citrate alone for at least 11 months. L2–L4 bone mineral density data before and after Potassium Citrate treatment were retrieved retrospectively and analyzed.Results: In the combined group L2–L4 bone mineral density increased significantly by 3.1% over mean duration of 44 months. Z score, corrected for age matched normal values, increased significantly by 3.8%. Urinary pH, Citrate and Potassium increased significantly during treatment but urinary calcium did not change.Conclusions: Potassium Citrate, a commonly used drug for the prevention of recurrent nephrolithiasis, may avert age dependent bone loss. Spinal bone density increased in most patients when it normally dec...

  • Dissolution of Calcium Calculi with Potassium Citrate
    Urolithiasis 2, 1994
    Co-Authors: S. Womack, Charles Y.c. Pak, J. Fine, G. Miller, N. Mandel, Glenn M. Preminger
    Abstract:

    We have noted radiological evidence of diminution and even complete disappearance of pre-existing calcium stones in a number of patients being treated with Potassium Citrate (K-Cit) for the prevention of new stone formation. Two prospective studies were initiated to more closely investigate this clinical phenomenon.

  • Randomized double-blind study of Potassium Citrate in idiopathic hypocitraturic calcium nephrolithiasis.
    The Journal of urology, 1993
    Co-Authors: P. Barcelo, O. Wuhl, E. Servitge, A. Rousaud, Charles Y.c. Pak
    Abstract:

    AbstractIn an attempt to document the efficacy of Potassium Citrate in stone formation, 57 patients with active lithiasis (2 or more stones during the preceding 2 years) and hypocitraturia were randomly allocated into 2 groups, with 1 group taking 30 to 60 mEq. Potassium Citrate daily in wax matrix tablet formation and the other group receiving placebo. In 18 patients receiving Potassium Citrate for 3 years stone formation significantly declined after treatment from 1.2 ± 0.6 to 0.1 ± 0.2 per patient year (p < 0.0001), in 13 patients (72%) the disease was in remission and all patients showed a reduced stone formation rate individually. In contrast, 20 patients taking placebo medication for 3 years showed no significant change in stone formation rate (1.1 ± 0.4 to 1.1 ± 0.3 per patient year) and in only 4 patients (20%) was the disease in remission. The stone formation rate during Potassium Citrate treatment was significantly lower than during the placebo treatment (0.1 ± 0.2 versus 1.1 ± 0.3 per patient y...

  • Effect of meal on the physiological and physicochemical actions of Potassium Citrate.
    The Journal of urology, 1991
    Co-Authors: Charles Y.c. Pak, Sioni Baker, James S. Morris
    Abstract:

    AbstractThe effect of meals on the physiological and physicochemical actions of Potassium Citrate was examined in 8 patients with nephrolithiasis maintained on a constant metabolic dietary regimen. Potassium Citrate (20mEq. 3 times per day), whether given with food or on an empty stomach, significantly increased urinary pH, Citrate and Potassium, and decreased urinary calcium and ammonium. Moreover, Potassium Citrate decreased urinary saturation of calcium oxalate and uric acid, although it slightly increased that of brushite. However, there was no significant difference in these measures when the drug was given with meals from the time when it was given on an empty stomach. Thus, the effect of Potassium Citrate on urinary risk factors is unaffected by food.

Marnie R. Robinson - One of the best experts on this subject based on the ideXlab platform.

  • impact of long term Potassium Citrate therapy on urinary profiles and recurrent stone formation
    The Journal of Urology, 2009
    Co-Authors: Marnie R. Robinson, Victor A. Leitao, George E. Haleblian, Charles D. Scales, Aravind Chandrashekar, Sean A. Pierre, Glenn M. Preminger
    Abstract:

    Purpose: Potassium Citrate therapy has become one of the cornerstones of medical stone management. We elucidated the long-term effects of Potassium Citrate on urinary metabolic profiles and its impact on stone formation rates.Materials and Methods: We performed a retrospective cohort study in patients treated at the Comprehensive Kidney Stone Center at our institution between 2000 and 2006. Patients with pre-therapy and post-therapy 24-hour urinary profiles available who remained on Potassium Citrate for at least 6 months were included in the analysis.Results: Of the 1,480 patients with 24-hour urinary profiles 503 met study inclusion criteria. Mean therapy duration was 41 months (range 6 to 168). Overall a significant and durable change in urinary metabolic profiles was noted as soon as 6 months after the onset of therapy. These changes included increased urinary pH (5.90 to 6.46, p <0.0001) and increased urinary Citrate (470 to 700 mg a day, p <0.0001). The stone formation rate also significantly decrea...

  • Impact of Long-Term Potassium Citrate Therapy on Urinary Profiles and Recurrent Stone Formation
    The Journal of urology, 2009
    Co-Authors: Marnie R. Robinson, Victor A. Leitao, George E. Haleblian, Charles D. Scales, Aravind Chandrashekar, Sean A. Pierre, Glenn M. Preminger
    Abstract:

    Purpose: Potassium Citrate therapy has become one of the cornerstones of medical stone management. We elucidated the long-term effects of Potassium Citrate on urinary metabolic profiles and its impact on stone formation rates.Materials and Methods: We performed a retrospective cohort study in patients treated at the Comprehensive Kidney Stone Center at our institution between 2000 and 2006. Patients with pre-therapy and post-therapy 24-hour urinary profiles available who remained on Potassium Citrate for at least 6 months were included in the analysis.Results: Of the 1,480 patients with 24-hour urinary profiles 503 met study inclusion criteria. Mean therapy duration was 41 months (range 6 to 168). Overall a significant and durable change in urinary metabolic profiles was noted as soon as 6 months after the onset of therapy. These changes included increased urinary pH (5.90 to 6.46, p

  • Does Potassium Citrate Medical Therapy Increase the Risk of Calcium Phosphate Stone Formation
    AIP Conference Proceedings, 2007
    Co-Authors: Victor A. Leitao, Roger L Sur, Marnie R. Robinson, George E. Haleblian, Sean A. Pierre, Glenn M. Preminger
    Abstract:

    Potassium Citrate has been extensively used in the treatment of recurrent nephrolithiasis. Recent evidence suggests that it may contribute to increasing urinary pH and, as such, increase the risk of calcium phosphate stone formation. We performed a retrospective review of our patients to further investigate this phenomenon.

Deborah E. Sellmeyer - One of the best experts on this subject based on the ideXlab platform.

  • Potassium Citrate supplementation results in sustained improvement in calcium balance in older men and women
    Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2013
    Co-Authors: Kendall F. Moseley, Connie M. Weaver, Lawrence J. Appel, Anthony Sebastian, Deborah E. Sellmeyer
    Abstract:

    The dietary acid load created by the typical Western diet may adversely impact the skeleton by disrupting calcium metabolism. Whether neutralizing dietary acid with alkaline Potassium salts results in sustained improvements in calcium balance remains controversial. In this randomized, double-blind, placebo-controlled study, 52 men and women (mean age 65.2 ± 6.2 years) were randomly assigned to Potassium Citrate 60 mmol/d, 90 mmol/d, or placebo daily with measurements of bone turnover markers, net acid excretion, and calcium metabolism, including intestinal fractional calcium absorption and calcium balance, obtained at baseline and at 6 months. At 6 months, net acid excretion was significantly lower in both treatment groups compared to placebo and it was negative, meaning subjects' dietary acid was completely neutralized (-11.3 mmol/d on 60 mmol/d; -29.5 mmol/d on 90 mmol/d, p < 0.001 compared to placebo). At 6 months, 24-hour urine calcium was significantly reduced in persons taking Potassium Citrate 60 mmol/d (-46 ± 15.9 mg/d) and 90 mmol/d (-59 ± 31.6 mg/d) compared with placebo (p < 0.01). Fractional calcium absorption was not changed by Potassium Citrate supplementation. Net calcium balance was significantly improved in participants taking Potassium Citrate 90 mmol/d compared to placebo (142 ± 80 mg/d on 90 mmol/d versus -80 ± 54 mg/d on placebo; p = 0.02). Calcium balance was also improved on Potassium Citrate 60 mmol/d, but this did not reach statistical significance (p = 0.18). Serum C-telopeptide decreased significantly in both Potassium Citrate groups compared to placebo (-34.6 ± 39.1 ng/L on 90 mmol/d, p = 0.05; -71.6 ± 40.7 ng/L on 60 mmol/d, p = 0.02) whereas bone-specific alkaline phosphatase did not change. Intact parathyroid hormone was significantly decreased in the 90 mmol/d group (p = 0.01). Readily available, safe, and easily administered in an oral form, Potassium Citrate has the potential to improve skeletal health. Longer-term trials with definitive outcomes such as bone density and fracture are needed.

  • Potassium Citrate prevents increased urine calcium excretion and bone resorption induced by a high sodium chloride diet
    The Journal of Clinical Endocrinology and Metabolism, 2002
    Co-Authors: Deborah E. Sellmeyer, Monique Schloetter, Anthony Sebastian
    Abstract:

    The amount of sodium chloride in the diet of industrialized nations far exceeds physiological requirements. The impact of abundant dietary salt on skeletal health has yet to be established, but is potentially detrimental through increased urinary calcium losses. We examined the effect of increased dietary sodium chloride on urine calcium excretion and bone turnover markers in postmenopausal women and, further, whether Potassium Citrate attenuates the effects of increased dietary salt. Postmenopausal women (n = 60) were adapted to a low-salt (87 mmol/d sodium) diet for 3 wk, then randomized to a high-salt (225 mmol/d sodium) diet plus Potassium Citrate (90 mmol/d) or a high-salt diet plus placebo for 4 wk. Urine calcium, urine N-telopeptide, urine cAMP, serum osteocalcin, and fasting serum PTH were measured at the end of the low- and high-salt diets. On the high salt plus placebo diet, urine calcium increased 42 +/- 12 mg/d (mean +/- SEM), but decreased 8 +/- 14 mg/d in the high salt plus Potassium Citrate group (P = 0.008, Potassium Citrate vs. placebo, unpaired t test). N-telopeptide increased 6.4 +/- 1.4 nanomoles bone collagen equivalents per millimole creatinine in the high salt plus placebo group and 2.0 +/- 1.7 nanomoles bone collagen equivalents per millimole creatinine in the high salt plus Potassium Citrate group (P < 0.05, Potassium Citrate vs. placebo, unpaired t test). Osteocalcin, PTH, and cAMP were not significantly altered. The addition of oral Potassium Citrate to a high-salt diet prevented the increased excretion of urine calcium and the bone resorption marker caused by a high salt intake. Increased intake of dietary sources of Potassium alkaline salts, namely fruit and vegetables, may be beneficial for postmenopausal women at risk for osteoporosis, particularly those consuming a diet generous in sodium chloride.

  • Potassium Citrate Prevents Increased Urine Calcium Excretion and Bone Resorption Induced by a High Sodium Chloride Diet
    The Journal of clinical endocrinology and metabolism, 2002
    Co-Authors: Deborah E. Sellmeyer, Monique Schloetter, Anthony Sebastian
    Abstract:

    The amount of sodium chloride in the diet of industrialized nations far exceeds physiological requirements. The impact of abundant dietary salt on skeletal health has yet to be established, but is potentially detrimental through increased urinary calcium losses. We examined the effect of increased dietary sodium chloride on urine calcium excretion and bone turnover markers in postmenopausal women and, further, whether Potassium Citrate attenuates the effects of increased dietary salt. Postmenopausal women (n = 60) were adapted to a low-salt (87 mmol/d sodium) diet for 3 wk, then randomized to a high-salt (225 mmol/d sodium) diet plus Potassium Citrate (90 mmol/d) or a high-salt diet plus placebo for 4 wk. Urine calcium, urine N-telopeptide, urine cAMP, serum osteocalcin, and fasting serum PTH were measured at the end of the low- and high-salt diets. On the high salt plus placebo diet, urine calcium increased 42 ± 12 mg/d (mean ± sem), but decreased 8 ± 14 mg/d in the high salt plus Potassium Citrate group...