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Long-term treatment of calcium nephrolithiasis with potassium citrate.
J Urol. 1985 Jul; 134(1):11-9.JU

Abstract

The long-term effects of potassium citrate therapy (usually 20 mEq. 3 times daily during 1 to 4.33 years) were examined in 89 patients with hypocitraturic calcium nephrolithiasis or uric acid lithiasis, with or without calcium nephrolithiasis. Hypocitraturia caused by renal tubular acidosis or chronic diarrheal syndrome was associated with other metabolic abnormalities, such as hypercalciuria or hyperuricosuria, or occurred alone. Potassium citrate therapy caused a sustained increase in urinary pH and potassium, and restored urinary citrate to normal levels. No substantial or significant changes occurred in urinary uric acid, oxalate, sodium or phosphorus levels, or total volume. Owing to these physiological changes, uric acid solubility increased, urinary saturation of calcium oxalate decreased and the propensity for spontaneous nucleation of calcium oxalate was reduced to normal. Therefore, the physicochemical environment of urine following treatment became less conducive to the crystallization of calcium oxalate or uric acid, since it stimulated that of normal subjects without stones. Commensurate with the aforementioned physiological and physicochemical changes the treatment produced clinical improvement, since individual stone formation decreased in 97.8 per cent of the patients, remission was obtained in 79.8 per cent and the need for surgical treatment of newly formed stones was eliminated. In patients with relapse after other treatment, such as thiazide, the addition of potassium citrate induced clinical improvement. Thus, our study provides physiological, physicochemical and clinical validation for the use of potassium citrate in the treatment of hypocitraturic calcium nephrolithiasis and uric acid lithiasis with or without calcium nephrolithiasis.

Authors

No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Clinical Trial
Comparative Study
Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

3892044

Citation

Pak, C Y., et al. "Long-term Treatment of Calcium Nephrolithiasis With Potassium Citrate." The Journal of Urology, vol. 134, no. 1, 1985, pp. 11-9.
Pak CY, Fuller C, Sakhaee K, et al. Long-term treatment of calcium nephrolithiasis with potassium citrate. J Urol. 1985;134(1):11-9.
Pak, C. Y., Fuller, C., Sakhaee, K., Preminger, G. M., & Britton, F. (1985). Long-term treatment of calcium nephrolithiasis with potassium citrate. The Journal of Urology, 134(1), 11-9.
Pak CY, et al. Long-term Treatment of Calcium Nephrolithiasis With Potassium Citrate. J Urol. 1985;134(1):11-9. PubMed PMID: 3892044.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Long-term treatment of calcium nephrolithiasis with potassium citrate. AU - Pak,C Y, AU - Fuller,C, AU - Sakhaee,K, AU - Preminger,G M, AU - Britton,F, PY - 1985/7/1/pubmed PY - 1985/7/1/medline PY - 1985/7/1/entrez SP - 11 EP - 9 JF - The Journal of urology JO - J. Urol. VL - 134 IS - 1 N2 - The long-term effects of potassium citrate therapy (usually 20 mEq. 3 times daily during 1 to 4.33 years) were examined in 89 patients with hypocitraturic calcium nephrolithiasis or uric acid lithiasis, with or without calcium nephrolithiasis. Hypocitraturia caused by renal tubular acidosis or chronic diarrheal syndrome was associated with other metabolic abnormalities, such as hypercalciuria or hyperuricosuria, or occurred alone. Potassium citrate therapy caused a sustained increase in urinary pH and potassium, and restored urinary citrate to normal levels. No substantial or significant changes occurred in urinary uric acid, oxalate, sodium or phosphorus levels, or total volume. Owing to these physiological changes, uric acid solubility increased, urinary saturation of calcium oxalate decreased and the propensity for spontaneous nucleation of calcium oxalate was reduced to normal. Therefore, the physicochemical environment of urine following treatment became less conducive to the crystallization of calcium oxalate or uric acid, since it stimulated that of normal subjects without stones. Commensurate with the aforementioned physiological and physicochemical changes the treatment produced clinical improvement, since individual stone formation decreased in 97.8 per cent of the patients, remission was obtained in 79.8 per cent and the need for surgical treatment of newly formed stones was eliminated. In patients with relapse after other treatment, such as thiazide, the addition of potassium citrate induced clinical improvement. Thus, our study provides physiological, physicochemical and clinical validation for the use of potassium citrate in the treatment of hypocitraturic calcium nephrolithiasis and uric acid lithiasis with or without calcium nephrolithiasis. SN - 0022-5347 UR - https://www.unboundmedicine.com/medline/citation/3892044/Long_term_treatment_of_calcium_nephrolithiasis_with_potassium_citrate_ L2 - https://www.jurology.com/doi/full/10.1016/s0022-5347(17)46962-x?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -