Abstract
PurposeTo assess the capacity of methylxanthines (caffeine, theophylline, theobromine and paraxanthine) to inhibit uric acid crystallization, and to evaluate their potential application in the treatment of uric acid nephrolithiasis.Materials and MethodsThe ability of methylxathines to inhibit uric acid nucleation was assayed turbidimetrically. Crystal morphology and its modification due to the effect of theobromine were evaluated by scanning electron microscopy (SEM). The ability of theobromine to inhibit uric acid crystal growth on calculi fragments resulting from extracorporeal shock wave lithotripsy (ESWL) was evaluated using a flow system.ResultsThe turbidimetric assay showed that among the studied methylxanthines, theobromine could markedly inhibit uric acid nucleation. SEM images showed that the presence of theobromine resulted in thinner uric acid crystals. Furthermore, in a flow system theobromine blocked the regrowth of post-ESWL uric acid calculi fragments.ConclusionsTheobromine, a natural dimethylxanthine present in high amounts in cocoa, acts as an inhibitor of nucleation and crystal growth of uric acid. Therefore, theobromine may be clinically useful in the treatment of uric acid nephrolithiasis.
Highlights
Renal lithiasis is a highly prevalent condition, currently affecting about 10% of the worldwide population [1] and estimated to affect 30% by 2050 [2]
scanning electron microscopy (SEM) images showed that the presence of theobromine resulted in thinner uric acid crystals
In a flow system theobromine blocked the regrowth of post-extracorporeal shock wave lithotripsy (ESWL) uric acid calculi fragments
Summary
Renal lithiasis is a highly prevalent condition, currently affecting about 10% of the worldwide population [1] and estimated to affect 30% by 2050 [2]. Since most renal calculi consist of calcium oxalate, some calcium oxalate crystallization inhibitors with medical application are well known, such as magnesium, citrate and phytate [3,4,5,6,7]. Other renal calculi consist of uric acid, but, except for one in vitro study of some glycosaminoglycans and saponins [8], no uric acid crystallization inhibitors have been described to date. Uric acid is the final product of purine catabolism in humans. In most other mammals, such as rats and dogs, uric acid is further degraded to allantoin by the enzyme uricase [9]. A high level of urate in blood is a pathophysiological condition, which, in patients with gout, can result in the formation of monosodium urate monohydrate crystals in the synovial fluid [10]
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