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Abstract: SA-PO280

Effect of Hydroxycitrate (HCA) on Urinary Risk Factors for Calcium-Based Kidney Stones

Session Information

Category: Bone and Mineral Metabolism

  • 402 Bone and Mineral Metabolism: Clinical


  • Adiga, Avinash Govinda, NYU School of Medicine, New York, New York, United States
  • Norris, Briony L., The Royal Melbourne Hospital, Parkville, New South Wales, Australia
  • Granja, Ignacio, Litholink Corporation, Chicago, Illinois, United States
  • Rohit, Kumar, New York University, Jersey City, New Jersey, United States
  • Modersitzki, Frank, New York University School of Medicine, New York, New York, United States
  • Borin, James, NYU Langone Health, New York, New York, United States
  • Bushinsky, David A., University of Rochester Medical Center, Rochester, New York, United States
  • Rimer, Jeffrey D., University of Houston, Houston, Texas, United States
  • Asplin, John R., Litholink Corp, Chicago, Illinois, United States
  • Goldfarb, David S., New York Harbor VAMC, New York, New York, United States

Potassium citrate is a mainstay of treatment to prevent calcium stones. However, it can increase urine pH and calcium phosphate (CaP) supersaturation (SS). HCA, extracted from garcinia cambogia, is a potent inhibitor of calcium oxalate (CaOx) crystal growth in vitro and may not yield HCO3. It is “generally regarded as safe” and available over the counter. We studied how HCA supplementation affects urine chemistry.


We enrolled 2 groups: calcium stone formers (SF) and non-stone forming (NSF) controls. Thiazides and potassium citrate were held for 2 weeks prior to study. Participants recorded a self-selected diet for 2 days and performed 24-hour urine collection on day 2. HCA 300 mg 3 times daily was taken orally for 7 days, and 24-hour urine collected on day 7 while the patient replicated the initial, self-selected diet.


13 people, aged 26 - 76 years, participated. There were 6 SF and 7 NSF, combined into 1 group of 13. Patients replicated their diets well, as urine Na, volume, and creatinine were similar (data not shown). Results presented in Table. HCA increased urine K and citrate (P < 0.001 and 0.013 respectively). Mean urine pH was unchanged (6.25 to 6.47, P=0.14), while urinary NH4 fell (P = 0.017). 24h excretion of Ca and Ox did not change. SS of CaOx and CaP did not change. Serum values did not change: baseline HCO3 and K were 23.5 + 2.5 and 4.0 + 0.2 meq/L and 23.7 + 1.8 and 4.4 + 0.6 meq/L after HCA.


Urine K excretion rose by 29 meq/day compared with an expected increase based on the label of 14 meq, suggesting the label was not accurate. Increased citrate and lower NH4 suggest some K is in the form of alkali salts or that some HCA is metabolized to bicarbonate. There was no change in CaP or CaOx SS. The lack of effect on SS may not reflect the potential ability of HCA to inhibit calcium crystallization, as it inhibits Ca crystal growth in vitro in supersaturated media.

Effect of HCA Supplementation on 24h Urine Chemistry; n=13, mean (SD)
Baseline171.5 (68.5)31.7 (8.1)59.8 (16.6)520.0 (191.1)6.25 (0.58)38.7 (12.8)4.8 (1.7)1.2 (0.8)
Hydroxycitrate188.5 (77.9)29.8 (8.1)89.0 (22.1)*660.8 (237.9)*6.47 (0.58)29.8 (8.6)*5.2 (3.0)1.6 (1.2)

SS CaOx and CaP: supersaturation of calcium oxalate and calcium phosphate. * = P<0.05


  • Commercial Support – Litholink Corp