Boron for Kidney Stones

Boron has not been shown to prevent, shrink or help pass kidney stones. In the only placebo-controlled trial, 60 adults with nephrolithiasis (kidney stone disease) took 10 mg of boric acid, 10 mg of boron citrate or placebo daily for 8 weeks. Stone numbers did not fall significantly (incidence rate ratio 1.09, 95% CI 0.65-1.85 for boric acid; 1.30, 0.79-2.13 for boron citrate), stone size did not differ, and the authors reported no beneficial evidence for boron (Vousoughi 2025).

The idea has a thin base: small metabolic studies in postmenopausal women in which 3 mg a day of boron lowered urinary calcium or oxalate in some but not all analyses (Nielsen 1987; Hunt 1997; Beattie 1993), a handful of reports from one research group, and rat studies that point both ways (Bahadoran 2016; Ergul 2018). We rate the evidence insufficient. Nothing yet justifies using boron in place of the fluids, diet changes and medicines that guidelines recommend (Skolarikos 2024; Asher 2026).

The mechanism idea is that boron changes how the body handles the minerals that turn up in stones. In a metabolic-unit study of 12 postmenopausal women, 3 mg a day of boron markedly reduced urinary calcium and magnesium, more so when dietary magnesium was low; it also raised serum oestradiol and testosterone (Nielsen 1987). In an 11-woman ward study, 3 mg a day lowered the share of dietary calcium lost in the urine in women on the basal magnesium diet but raised it in those given 200 mg of magnesium, and total urinary oxalate fell on boron in the women on the basal diet; the authors saw a possible role for boron in controlling urolithiasis when magnesium is low (Hunt 1997).

Other human data do not line up. Healthy postmenopausal women who went from 0.33 mg to 3.33 mg a day of boron showed no effect on minerals, sex steroids or bone turnover markers, so the hormone finding was not repeated, though the authors thought the low-boron diet had itself caused calcium hyperabsorption that may have hidden an effect (Beattie 1993). In athletic and sedentary women, calcium excretion rose over time in all groups combined, and the abstract gives no boron-versus-placebo difference in it (Meacham 1995). None of these studies enrolled people with kidney stones.

In rats given ethylene glycol to produce kidney crystals, 3 mg of boron a day lowered the crystal calcium deposition score, probably by reducing oxidative stress, according to the authors (6 rats per group) (Bahadoran 2016). A larger study of 50 rats gave boric acid at 25, 50 and 100 mg/kg/day, equal to 4, 8 and 16 mg of boron, and found no difference in stone formation, tissue calcium or oxalate, or oxidative markers compared with stone-induced animals given no boron (Ergul 2018). Its authors note that boron's effects are dose-dependent and U-shaped.

Neither rat study tells you what happens in a person. Stones were induced chemically, the doses and routes differ, and the two studies reached opposite conclusions. The mechanism also cannot tell you whether a change in urinary calcium or oxalate in healthy women means fewer stones. The one placebo-controlled trial that counted stones found no benefit (Vousoughi 2025).

There is no established dose of boron for kidney stones. The placebo-controlled trial gave 10 mg a day of boric acid or boron citrate for 8 weeks (Vousoughi 2025). The lithotripsy trial gave 10 mg twice a day for 2 weeks after shock wave lithotripsy (ESWL), a procedure that breaks stones with sound waves; its abstract does not say whether that is elemental boron, which if so would total 20 mg a day, the adult upper limit (Jalali 2023; NIH ODS). The metabolic studies used 3 mg a day (Nielsen 1987; Hunt 1997; Beattie 1993). For comparison, median dietary boron intake in US adults is 0.87-1.35 mg a day (NIH ODS).

Supplement Facts labels declare elemental boron, not the weight of the whole compound (NIH ODS), so compare like with like before copying a trial number onto a label.

Sixty adults aged 20-65 with nephrolithiasis were randomised, double-blind, to boric acid 10 mg, boron citrate 10 mg or placebo daily for 8 weeks. The primary outcomes were stone size and number. In fully adjusted models neither form reduced stone number (incidence rate ratio 1.09, 95% CI 0.65-1.85, P = 0.740 for boric acid; 1.30, 0.79-2.13, P = 0.296 for boron citrate), and a Quade analysis found no significant difference in stone size. Of the laboratory measures, only urine phosphorus was significantly higher with boric acid than placebo, and no other clinically relevant effects were seen (Vousoughi 2025).

The authors wrote that, despite previous preliminary evidence, they found no beneficial evidence for boron. The limits are the size and length: 60 people across three arms for 8 weeks could miss a modest effect, or one that takes longer to show, and the abstract does not describe side effects separately.

After ESWL, 200 eligible patients were randomised to boron 10 mg twice daily or tamsulosin 0.4 mg nightly for 2 weeks; 89 and 81 completed. Stone expulsion was 46.6% with boron and 38.7% with tamsulosin. The abstract reports no statistically significant difference between groups, but the P value it prints for that comparison (0.003) contradicts its own conclusion, so the result is unclear. Time to clearance (7.47 ± 22.4 versus 6.52 ± 18.45 days, P = 0.648) and pain were similar, and no significant side effects were reported (Jalali 2023).

The authors concluded that boron could be effective as adjuvant therapy, but the design cannot support that. Tamsulosin, an alpha-blocker used to help stone passage, was the comparator, not a placebo, so similar results mean boron was not clearly better or worse than tamsulosin, not that it beat doing nothing. And 30 of 200 patients did not finish.

Two single-patient case reports describe stones passing with boron: a woman with a 10.0 mm lower-pole stone who had lithotripsy and took 10 mg of boron a day for two weeks (Naghii 2013), and a man given boron plus antioxidants, dairy products and fluids, who passed a 9 x 20 mm stone (his abstract does not mention lithotripsy) (Naghii 2014). Each ends by saying boron deserves further study. One patient with no comparison cannot separate boron from natural passage or, in the first case, from the lithotripsy, and the second combined several measures.

Most of the positive signals trace to one author. M. R. Naghii wrote both case reports and a 2012 letter on preliminary evidence (not summarised here because it has no abstract), and is an author of the low-dose rat study (Naghii 2012; Bahadoran 2016). The one placebo-controlled trial and the high-dose rat study, both null, were published by other authors (Vousoughi 2025; Ergul 2018).

No trial has followed stone formers for a year or more on boron, counted new stones, or reported 24-hour urine calcium and oxalate on boron in people with stones. By contrast, a 2026 systematic review of 31 prevention studies concluded that increased fluid intake, a diet with normal to high calcium and low protein and sodium, thiazides, alkali therapy and allopurinol may prevent recurrence in adults with calcium oxalate or phosphate stones, with low strength of evidence, and its summary does not mention boron (Asher 2026). The 2026 AUA guideline and the 2024 EAU update likewise build prevention on dietary measures and targeted drug therapy (Pearle 2026 Parts I and II; Skolarikos 2024).

At the doses in the trials, no clinically relevant effects other than higher urine phosphorus with boric acid were reported at 10 mg a day for 8 weeks (Vousoughi 2025), and no significant side effects over 2 weeks at 10 mg twice a day (Jalali 2023). The adult tolerable upper intake level is 20 mg a day, with lower limits of 3 mg for ages 1-3, 6 mg for 4-8, 11 mg for 9-13 and 17 mg for 14-18, and the European Food Safety Authority's level is cited as 10 mg a day (NIH ODS; Stübing 2026). The US limits were set for healthy people from animal reproductive and developmental data (NIH ODS), so they are a ceiling, not a target, for stone formers with reduced kidney function. Large doses can cause nausea, vomiting, diarrhoea, headache and kidney injury (NIH ODS).

Boron is absorbed quickly and leaves mostly in the urine, with a half-life in humans of about a day (Moseman 1994); in a ward study, faecal and urinary excretion accounted for nearly 100% of dietary boron with no accumulation (Hunt 1997). A 2005 review of boron and the kidney noted that boron exposure has been implicated as a potential cause of chronic kidney disease in Southeast Asia (Pahl 2005). Recurrent stones can themselves lead to kidney damage (Asher 2026), so anyone with reduced kidney function should settle the question with a clinician before adding a supplement cleared through the kidney.

In animal studies, boron caused developmental and reproductive effects (Dourson 1998). With no proven benefit for stones, discuss any supplement with your obstetric clinician first.

Boron is not known to have clinically relevant interactions with medicines (NIH ODS). The practical cautions are hormones, adding to your total boron intake, and not displacing the stone medicines that have the best evidence.