Potassium Citrate for Kidney Disease
(BICARb Trial)
Recruiting in Palo Alto (17 mi)
+1 other location
Age: Any Age
Sex: Any
Travel: May Be Covered
Time Reimbursement: Varies
Trial Phase: Phase 2 & 3
Recruiting
Sponsor: Albert Einstein College of Medicine
Must not be taking: Bisphosphonates, Denosumab, others
Disqualifiers: Hyperkalemia, Acid-base imbalance, others
Prior Safety Data
Trial Summary
What is the purpose of this trial?The goal of this clinical trial is to test whether potassium citrate improves skeletal health in adults and children with chronic kidney disease. The main questions it aims to answer are:
* To evaluate effects of potassium citrate treatment on bone quality and strength.
* To evaluate mechanism(s) underlying the effects of potassium citrate on skeletal health.
Participants will be asked to:
* provide blood, urine and answer questions about health and diet three times during an 8 months period
* undergo advanced bone imaging with high resolution-peripheral quantitative CT scan twice during 8 months
* take study pills for 4-6 weeks at the beginning of the study to ensure safety
* take either potassium citrate or placebo for 6 months during the blinded portion of the study
As part of the study, there will be a run-in period followed by the placebo-controlled randomized clinical trial. Researchers will compare the bone imaging between the potassium citrate and the placebo groups at the end of the study.
Will I have to stop taking my current medications?
The trial does not specify if you need to stop taking your current medications, but you cannot participate if you are currently taking a potassium-lowering agent or certain bone-related medications like bisphosphonates or hormone replacement therapies. It's best to discuss your specific medications with the trial team.
What data supports the effectiveness of the drug potassium citrate for kidney disease?
Research shows that potassium citrate is effective in preventing the formation of kidney stones, particularly in patients with conditions like distal renal tubular acidosis. It significantly reduces new stone formation and improves urinary conditions, making it a beneficial treatment for managing kidney stone disease.
12345Is potassium citrate safe for humans?
Potassium citrate is generally considered safe when used at therapeutic doses, with good tolerance and no significant changes in blood parameters, except for mild transient metabolic alkalosis (a temporary increase in blood pH). It is well tolerated for conditions like kidney stones and distal renal tubular acidosis, but should be avoided in certain conditions like urinary tract infections and advanced chronic renal failure.
12367How does the drug potassium citrate differ from other treatments for kidney disease?
Potassium citrate is unique because it helps prevent kidney stones by increasing urinary citrate levels, which reduces stone formation, and it is particularly effective for conditions like renal tubular acidosis and calcium oxalate nephrolithiasis. Unlike some treatments, it is well-tolerated and can be administered in a slow-release form to maintain consistent urinary citrate levels throughout the day.
238910Eligibility Criteria
This trial is for adults and children over 5 with chronic kidney disease who have normal PTH, phosphorus, and vitamin D levels. Women must use contraception and not be pregnant or breastfeeding. Participants can't join if they have certain metabolic bone diseases, high potassium levels, heart risks on ECG, severe other illnesses affecting acid-base balance, a history of kidney stones or limb amputations.Inclusion Criteria
Women of childbearing potential must be willing to use one form of effective contraception over the course of the study
My child's kidney function is moderately reduced but not severely.
I have had a menstrual period in the last month.
+6 more
Exclusion Criteria
I have had a solid or liquid organ transplant.
I have had fractures in both my wrists and shins.
My potassium levels are high or I've had high potassium in the last 6 months.
+16 more
Trial Timeline
Screening
Participants are screened for eligibility to participate in the trial
2-4 weeks
Run-in Period
Participants take study pills for 4-6 weeks to ensure safety
4-6 weeks
Treatment
Participants take either potassium citrate or placebo for 6 months during the blinded portion of the study
6 months
3 visits (in-person) for blood, urine, and health/diet assessments; 2 visits (in-person) for advanced bone imaging
Follow-up
Participants are monitored for safety and effectiveness after treatment
4 weeks
Participant Groups
The study tests if potassium citrate improves bone health in those with chronic kidney disease by comparing it to a placebo. Over 8 months, participants will take pills for safety checks then either the treatment or placebo for 6 months while undergoing blood tests, diet surveys, and advanced bone scans.
2Treatment groups
Experimental Treatment
Placebo Group
Group I: Potassium CitrateExperimental Treatment2 Interventions
Potassium Citrate extended-release tablets 30 mEq twice daily. 1 mEq/kg/day divided into two doses for children to a maximum dose of 30 mEq twice daily.
OR
(for children who cannot take pills): Potassium citrate and citric acid for oral solution 1 mEq/kg/day divided into two doses to a maximum dose of 30 mEq twice daily
Group II: PlaceboPlacebo Group1 Intervention
Placebo capsules identical to the active capsules.
Find a Clinic Near You
Research Locations NearbySelect from list below to view details:
University of Pittsburgh Medical CenterPittsburgh, PA
Albert Einstein College of MedicineBronx, NY
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Who Is Running the Clinical Trial?
Albert Einstein College of MedicineLead Sponsor
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)Collaborator
University of UtahCollaborator
University of Pittsburgh Medical CenterCollaborator
Columbia UniversityCollaborator
References
Safety, efficacy, and acceptability of ADV7103 during 24 months of treatment: an open-label study in pediatric and adult patients with distal renal tubular acidosis. [2021]A new prolonged-release formulation of potassium citrate and potassium bicarbonate, ADV7103, has been shown to improve metabolic control, palatability, and gastrointestinal safety in patients with distal renal tubular acidosis (dRTA) when compared to standard of care (SoC) treatments. The present work evaluates safety and efficacy of ADV7103 during 24 months.
[Granulated potassium citrate in the prevention of calcium oxalate lithiasis]. [2013]Since the approval of potassium citrate for the treatment of urolithiasis, there are many patients in other countries who have benefited from this drug. This paper describes the biochemical changes and tolerance seen in fifteen patients treated for one month with granulated potassium citrate. Some significant changes are observed in serum potassium and creatinine, and in urinary pH, citrate and potassium. Tolerance was good. Our results confirm that potassium citrate is an effective, easy to use, and well tolerated drug for the prophylaxis of oxalocalcium lithiasis.
[Therapeutic use of potassium citrate]. [2022]Therapeutic indications of potassium citrate include: 1. Oxaluric renal stone disease and some cases of uric acid stone disease. Prevention of stone formation in patients with renal polycystic disease. Prevention of stone relapse after ESWL or lithotomy; 2. Distal renal tubular acidosis complicated by hypercalciuria, mainly in children. 3. Renal hypercalciuria and hyperoxaluria. 4. Prevention of renal complications at the time of glaucoma treatment with acetazolamide. 5. Potassium supplementation during treatment of hypertension. Potassium citrate is usually contraindicated in the case of: 1. Urinary tract infection. 2. Struvite renal stone disease. 3. Hyperpotassemia and advanced chronic renal failure. 4. Peptic ulcer or gastritis. 5. Gastrointestinal bleeding. 6. Disorders of coagulation, crural varices. 7. Metabolic alkalosis. Potassium citrate, when used at therapeutic doses, is to be considered as quite safe. The average daily dose even if admitted as a single dose day engages 60-75% of free renal capacity for potassium excretion. Physiologic and therapeutic citrate concentration in urine exceeds much those available for other inhibitors. The therapeutic dose does not induce any significant changes in any biochemical or endocrine parameter of blood except mild transient metabolic alkalosis. The decrease of urine calcium and increase in oxalate calcium phosphate excretion is observed. In hypo-cytriaturic patients the response to therapeutic dose of citrate is smaller. One-year remission of stone disease is observed in 70-75% cases.
Comparative efficacy of "specific" potassium citrate therapy versus conservative management in nephrolithiasis of mild to moderate severity. [2019]It generally is believed that conservative measures of high fluid intake and dietary modification in the setting of a stone clinic could favorably influence the course of renal stone disease. To establish the effect of specific medical treatment from the stone clinic effect, we compared the results of potassium citrate therapy to those of 11 reported conservative or placebo trials. The 54 patients receiving potassium citrate chosen for this comparison had mild to moderately severe stone disease (less than 1 stone per patient per year), similar to that encountered in conservative placebo trials (mean 0.54 stones per patient per year). New stone formation was virtually eliminated by potassium citrate therapy (a decrease from 0.52 to 0.02 stones per patient per year, a remission rate of 96 per cent, p less than 0.001), whereas it continued in 39 per cent of the patients during conservative or placebo trials. However, in patients participating in conservative or placebo trials new stone formation decreased by only 54 per cent (from 0.54 to 0.25 stones per patient per year). The superior response to potassium citrate suggested that this specific medical treatment exerted an additional favorable effect on the course of stone disease above the stone clinic effect.
Prevention of recurrent calcium stone formation with potassium citrate therapy in patients with distal renal tubular acidosis. [2022]Distal renal tubular acidosis is a common cause of intractable calcium nephrolithiasis. We examined the effect of oral potassium citrate therapy in 9 patients with incomplete distal renal tubular acidosis diagnosed on the basis of an abnormal response to an oral ammonium chloride load. Patients were studied during a control phase and after 3 months of potassium citrate treatment (60 to 80 mEq. daily). Potassium citrate caused a significant increase in urinary pH and urinary citrate, and a decrease in urinary calcium. The urinary relative saturation ratio of calcium oxalate significantly decreased during treatment, while that of brushite did not change. Potassium citrate also was shown to inhibit new stone formation. During a mean treatment period of 34 months none of the 9 patients had new stones, although 39.3 plus or minus 79.7 (standard deviation) stones per patient formed during the 3 years preceding treatment. The results support the potential clinical advantage of potassium citrate therapy in patients with distal renal tubular acidosis and recurrent calcium nephrolithiasis.
Rationale and Design of a Randomized Placebo-Controlled Clinical Trial Assessing the Renoprotective Effects of Potassium Supplementation in Chronic Kidney Disease. [2023]Dietary potassium (K+) has beneficial effects on blood pressure and cardiovascular (CV) outcomes. Recently, several epidemiological studies have revealed an association between urinary K+ excretion (as proxy for dietary intake) and better renal outcomes in subjects with chronic kidney disease (CKD). To address causality, we designed the "K+ in CKD" study.
Single-dose sodium polystyrene sulfonate for hyperkalemia in chronic kidney disease or end-stage renal disease. [2023]Label="BACKGROUND" NlmCategory="BACKGROUND">The use of sodium polystyrene sulfonate (SPS) for the treatment of hyperkalemia lacks sufficient efficacy data in patients with chronic kidney disease (CKD) and end-stage renal disease (ESRD); however, use remains widespread. Recent evidence suggests that this population may be at risk for serious gastrointestinal adverse effects with SPS. Methods. We conducted a single-center retrospective cohort study. Adult patients with CKD Stages 4, 5, or ESRD maintained on renal replacement therapy with serum potassium >5 mEq/L and receipt of SPS were screened for inclusion. Our primary outcome was decrease in potassium within 24 h post-30 g oral SPS suspended in 33% sorbitol. Secondary outcomes included decrease in potassium within 24 h from 15 or 30 g SPS doses and gastrointestinal adverse events.
Citrate and renal calculi. [2013]Potassium citrate is a new and exciting therapeutic approach which has considerably broadened our capability for the medical control of stone disease. The discussion summarizes the data supporting utility of potassium citrate in the management of renal tubular acidosis with calcium stones, hypocitraturic calcium oxalate nephrolithiasis ('idiopathic', or secondary to chronic diarrheal syndrome or thiazide therapy) and uric acid lithiasis with or without calcium stones.
Augmentation of renal citrate excretion by oral potassium citrate administration: time course, dose frequency schedule, and dose-response relationship. [2019]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).
Dosage of potassium citrate in the correction of urinary abnormalities in pediatric distal renal tubular acidosis patients. [2013]Potassium citrate is an alkaline agent that has been recommended for the prevention of nephrolithiasis in distal renal tubular acidosis (RTA). Information on the effectiveness and the optimal dose of potassium citrate in the correction of urinary abnormalities in pediatric distal RTA is limited, however. We conducted this study to determine the effectiveness and the optimal dose of potassium citrate for the correction of urinary abnormalities and the prevention of nephrolithiasis in children with distal RTA. Eight pediatric distal RTA patients participated in this study. The mean +/- SEM age was 9.7 +/- 1.2 years, and mean body weight was 29.1 +/- 4.7 kg. After initial evaluation, all patients were treated with increasing dosages of potassium citrate starting from 2 mEq/kg/d in three divided doses. The dosage was increased progressively in a stepwise fashion every 2 months from 2 mEq/kg/d to 3 mEq/kg/d, then to 4 mEq/kg/d. Blood and 8-hour overnight urine samples were obtained at baseline and every 2 months before increasing the dosage of potassium citrate. Urinary saturations for calcium oxalate and calcium phosphate were estimated by using Tiselius's indices. The basal urinary calcium-to-creatinine, phosphate-to-creatinine, and calcium-to-citrate ratios and urinary saturation for calcium oxalate and calcium phosphate were elevated significantly, whereas citrate-to-creatinine ratio was reduced significantly in distal RTA patients. These ratios were normalized gradually with the increasing dosage of potassium citrate. All the aforementioned abnormalities were normalized only after the dosage of potassium citrate was raised to 4 mEq/kg/d. The elevation in urinary saturation of calcium phosphate could not be normalized throughout the study, however. These results suggest that 4 mEq/kg/d of potassium citrate supplement can correct successfully most of the urinary abnormalities and the elevated urinary saturation for calcium oxalate but not for calcium phosphate in children with distal RTA. Monitoring of urinary calcium-to-creatinine ratio or citrate-to-creatinine ratio is valuable to ensure adequate potassium citrate supplementation in this group of patients.