Impact of potassium citrate on urinary risk profile, glucose and lipid metabolism of kidney stone formers in Switzerland

Anna Wiegand; Gioia Fischer; Harald Seeger; Daniel Fuster; Nasser Dhayat; Olivier Bonny; Thomas Ernandez; Min-Jeong Kim; Carsten A Wagner; Nilufar Mohebbi

doi:10.1093/ckj/sfz098

Impact of potassium citrate on urinary risk profile, glucose and lipid metabolism of kidney stone formers in Switzerland

Clin Kidney J. 2019 Aug 19;13(6):1037-1048. doi: 10.1093/ckj/sfz098. eCollection 2020 Dec.

Authors

Anna Wiegand¹, Gioia Fischer¹, Harald Seeger^{1

2}, Daniel Fuster^{2

3}, Nasser Dhayat^{2

3}, Olivier Bonny^{2

4}, Thomas Ernandez^{2

5}, Min-Jeong Kim^{2

6}, Carsten A Wagner^{2

7}, Nilufar Mohebbi^{1

2}

Affiliations

¹ Division of Nephrology, University Hospital of Zurich, Zurich, Switzerland.
² Swiss Kidney Stone Cohort, National Center of Competence in Research, NCCR-Kidney, Switzerland.
³ Department of Nephrology and Hypertension, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.
⁴ Service of Nephrology, University Hospital of Lausanne, Lausanne, Switzerland.
⁵ Service of Nephrology, University Hospital of Geneva, Geneva, Switzerland.
⁶ Clinic for Transplantation Immunology and Nephrology, University Hospital Basel, Basel, Switzerland.
⁷ Institute of Physiology, University of Zurich, Zurich, Switzerland.

Abstract

Background: Hypocitraturia and hypercalciuria are the most prevalent risk factors in kidney stone formers (KSFs). Citrate supplementation has been introduced for metaphylaxis in KSFs. However, beyond its effects on urinary parameters and stone recurrence, only a few studies have investigated the impact of citrate on other metabolic pathways such as glucose or lipid metabolism.

Methods: We performed an observational study using data from the Swiss Kidney Stone Cohort. Patients were subdivided into two groups based on treatment with potassium citrate or not. The outcomes were changes of urinary risk parameters, haemoglobin A1c (HbA_1c), fasting glucose, cholesterol and body mass index (BMI).

Results: Hypocitraturia was present in 19.3% of 428 KSFs and potassium citrate was administered to 43 patients (10.0%) at a mean dosage of 3819 ± 1796 mg/day (corresponding to 12.5 ± 5.9 mmol/ day). Treatment with potassium citrate was associated with a significantly higher mean change in urinary citrate (P = 0.010) and urinary magnesium (P = 0.020) compared with no potassium citrate treatment. Exogenous citrate administration had no effect on cholesterol, fasting glucose, HbA_1c and BMI. Multiple linear regression analysis demonstrated no significant association of 1,25-dihydroxyvitamin D₃ [1,25(OH)₂ D₃] levels with urinary citrate excretion.

Conclusion: Potassium citrate supplementation in KSFs in Switzerland resulted in a beneficial change of the urinary risk profile by particularly increasing anti-lithogenic factors. Fasting glucose, HbA_1c, cholesterol levels and BMI were unaffected by potassium citrate therapy after 3 months, suggesting that potassium citrate is safe and not associated with unfavourable metabolic side effects. Lastly, 1,25(OH)₂ D₃ levels were not associated with urinary citrate excretion.

Keywords: 1,25(OH)2 D3; hypocitraturia; metaphylaxis; nephrolithiasis; urolithiasis.