Potassium Citrate for Uric Acid Kidney Stones: Long-Term Study Summary

The study “ Successful Management of Uric Acid Nephrolithiasis with Potassium Citrate “ by C. Y. Pak et al. (1986) examined urine chemistry changes and reported stone outcomes during long-term potassium citrate use in uric acid nephrolithiasis. This summary is a plain-language paraphrase of that scientific paper only; it does not add new data or independent medical advice. Pak, Sakhaee, Fuller, and colleagues followed 18 people with uric acid nephrolithiasis, including some who also had calcium stones, and measured how potassium citrate affected urine chemistry and stone events over several years. The authors also described five detailed case reports comparing sodium-based alkali therapy with potassium-based alkali therapy in the same patients.

In this scientific paper, the authors focused on uric acid nephrolithiasis, a form of kidney stone disease in which stones are mainly composed of uric acid. These stones tend to form in acidic urine, where more uric acid stays in an undissociated (non-ionized) form that is less soluble and more likely to crystallize. The patients in this study were described as having “uric acid nephrolithiasis,” with six having only uric acid stones and twelve having both uric acid and calcium-containing stones.

Alkali therapy is commonly used to raise urine pH. When urine becomes less acidic, more uric acid shifts toward a more soluble urate form, which is generally considered less favorable for uric acid crystal formation. In this study, the authors used potassium citrate as the primary alkali and, in a subset of patients, compared potassium-based alkali with sodium-based alkali such as sodium bicarbonate or sodium citrate.

This scientific paper reports a clinical study in which 18 patients with uric acid nephrolithiasis were treated with potassium citrate for 1 to 5.33 years. Six patients had uric acid stones only, while twelve had a combination of uric acid and calcium stones. Mean follow-up was 2.78 years.

Potassium citrate was given at daily doses between 30 and 80 milliequivalents (mEq), most commonly 60 mEq per day. During therapy, the researchers monitored several urine parameters, including:

• Urine pH (a measure of acidity)
• Amount of undissociated uric acid in the urine (in milligrams per day)
• Urinary citrate (in milligrams per day)
• Urinary saturation of calcium oxalate (a measure of how close urine is to forming calcium oxalate crystals)

They also tracked the rate of new stone formation, calculated as the number of stones per patient per year, before and during potassium citrate treatment.

In addition to this main group, the authors presented detailed case reports for five patients. These patients had been treated first with sodium-based alkali (sodium bicarbonate or sodium citrate) and then with potassium-based alkali (potassium citrate or potassium bicarbonate). The case reports allowed the authors to compare how sodium versus potassium alkali affected stone outcomes in individuals with persistent low urine pH and uric acid stones.

At baseline, the patients had acidic urine, with a mean urine pH of about 5.30 ± 0.31. During potassium citrate treatment, urine pH increased into a more normal range, reported as 6.19 to 6.46 during therapy. This shift means that the urine became less acidic, which is generally associated with higher uric acid solubility in urine.

The amount of undissociated uric acid in the urine was high before treatment, averaging 204 ± 82 mg per day. With potassium citrate therapy, this value decreased into the normal range, reported as 64 to 108 mg per day. At the same time, urinary citrate rose from an average of 503 ± 225 mg/day to a higher range of about 852 to 998 mg/day. The study also reports that urinary saturation of calcium oxalate fell significantly during potassium citrate treatment, indicating a lower tendency for calcium oxalate crystals to form.

Together, these measurements show that potassium citrate use coincided with higher urine pH and citrate and lower undissociated uric acid and calcium oxalate saturation in this cohort, as reported by the authors.

One key outcome is the change in stone formation rate reported by the authors. Before potassium citrate therapy, the group had a mean stone formation rate of 1.20 ± 1.68 stones per year per patient. During treatment, the reported rate was 0.01 ± 0.04 stones per year per patient. The authors used the term “remission” to mean no new stone events during follow-up and reported this outcome in 94.4% of patients. They further reported a 99.2% reduction in the group stone formation rate when comparing the pre-treatment period with the treatment period. These findings describe outcomes observed in this small cohort during the follow-up window reported in the paper.

In five patients, the authors had the opportunity to compare sodium-based alkali treatment with potassium-based alkali treatment over time. All five had persistent low urine pH (often below 5.5) and normal uric acid excretion, and four had elevated serum uric acid levels (hyperuricemia). Before any alkali therapy, these patients had either surgically removed or spontaneously passed pure uric acid stones.

When they were treated with sodium alkali (either sodium bicarbonate or sodium citrate at 60 to 118 mEq/day), new stone formation continued in four of the five patients. In the remaining patient, a radiolucent uric acid stone became “calcified,” and stone analysis later showed calcium oxalate and calcium phosphate components. Stone analyses during the sodium alkali phase reported calcium oxalate components in stones from all five patients and calcium phosphate components in stones from three patients.

Later, the same patients were treated with potassium-based alkali (potassium citrate in four cases, potassium bicarbonate in one case) at doses of 60 to 80 mEq/day for periods between 1 and 3.5 years. During this potassium alkali therapy, the authors report that no new stones formed in these five patients.

The authors interpret these case reports as suggesting a difference between sodium and potassium alkali in these individuals, with potassium-based alkali associated with fewer reported stone events during follow-up in this small subgroup.

Within the limits of a small clinical trial, this scientific paper reports that potassium citrate use was associated with higher urine pH and citrate, lower undissociated uric acid, reduced calcium oxalate saturation, and fewer observed new stone events during follow-up in patients with uric acid nephrolithiasis, with or without associated calcium stones.

They also note that in five patients who had previously received sodium-based alkali, stone formation persisted or stones changed composition, whereas changing to potassium-based alkali was associated with no new stones over 1 to 3.5 years. The authors conclude that these findings provide “physiological and physicochemical rationale” and describe therapeutic benefit in the context of this study for potassium citrate in uric acid lithiasis, whether or not calcium stones are also present.

All of these implications come directly from the study’s own data and conclusions. This summary does not extend those conclusions beyond what Pak and colleagues reported in their original 1986 scientific paper.

In this 1986 clinical investigation, Pak and co-authors report that long-term potassium citrate therapy was associated with improved urine chemistry and a 99.2% reduction in the reported group stone formation rate among 18 patients with uric acid nephrolithiasis, many of whom also had calcium stones. The paper also describes a small case-report series in which sodium-based alkali coincided with continued stone events in several patients, while later potassium-based alkali coincided with no reported new stones over follow-up periods of 1 to 3.5 years. As presented by the authors, these findings describe potassium citrate as an alkali approach discussed for uric acid nephrolithiasis, based on physiologic and physicochemical changes observed in this cohort. This conclusion reflects the wording and data reported by Pak et al. and does not add new clinical guidance.