Deflazacort and Nephrolithiasis Risk
Deflazacort, like other corticosteroids, does not have established evidence linking it to increased nephrolithiasis risk, and the available pharmacokinetic data suggests it can be safely used in patients with renal conditions without dose adjustment. 1
Evidence Assessment
Direct Evidence on Deflazacort and Kidney Stones
No clinical trials or observational studies have specifically evaluated deflazacort's association with nephrolithiasis. The available literature on deflazacort focuses on its efficacy in inflammatory conditions and its metabolic effects compared to other corticosteroids, but kidney stone formation has not been systematically studied. 2
Deflazacort has been safely used in pediatric patients with chronic renal failure and after renal transplantation without requiring dose adjustments for renal function, suggesting acceptable renal safety. 1
One study evaluated deflazacort as medical expulsive therapy for existing distal ureteral stones (facilitating stone passage), which is a different clinical context than causing stone formation. 3
Corticosteroid Class Effects on Stone Formation
Corticosteroids as a class are not listed among the established risk factors for nephrolithiasis in major guidelines from the American College of Physicians, American Urological Association, or National Kidney Foundation. 4
The primary established risk factors for calcium stone formation include hypercalciuria, hyperoxaluria, hypocitraturia, hyperuricosuria, low fluid intake, high sodium intake, and high animal protein consumption—none of which are prominently induced by deflazacort. 5, 4
Metabolic Considerations
Deflazacort causes dose-dependent increases in plasma calcium levels, similar to prednisolone, though the clinical significance for stone formation remains unclear. 6
Deflazacort appears to have less negative metabolic impact than prednisone on parameters associated with bone metabolism and may be associated with fewer serious metabolic sequelae, though this does not specifically address stone risk. 2
The overall adverse event incidence with deflazacort (16.5%) is lower than prednisone (20.5%), with gastrointestinal symptoms being most common rather than renal complications. 2
Clinical Context: Known Stone-Promoting Medications
Calcium supplements (not corticosteroids) are associated with increased nephrolithiasis risk (relative risk 1.17 in the Women's Health Initiative trial), particularly when taken between meals rather than with food. 5
Vitamin D supplementation combined with calcium has shown increased stone risk in large trials, which is relevant since some patients on corticosteroids may also receive vitamin D. 5
Practical Recommendations
Do not withhold deflazacort based on nephrolithiasis concerns when it is otherwise indicated for inflammatory or immunosuppressive therapy, as there is no evidence supporting this association. 2
If a patient on deflazacort develops kidney stones, investigate the established risk factors: obtain 24-hour urine collection to assess for hypercalciuria, hyperoxaluria, hypocitraturia, hyperuricosuria, and low urine volume. 4
Ensure adequate hydration (urine output >2 liters/day) in all patients on corticosteroid therapy as a general preventive measure, since low fluid intake is a major modifiable risk factor for stone formation. 7, 4
Monitor for hypercalciuria if deflazacort is used long-term, given the documented calcium-elevating effects, though this has not been directly linked to stone formation. 6