Research directions for kidney stone disease

Kidney stone disease poses a major burden to patients and healthcare systems around the world. The formation of kidney stones may occur over months or years, but many patients are diagnosed at a late stage, suffer excruciating pain, and require surgical intervention to physically remove the stones. The prevalence of kidney stones has increased during recent decades to over 10% in many developed countries, suggesting a link with environmental and behavioral factors. Recurrence rates are also high. In terms of their impact and scale, kidney stones are an ongoing pandemic. The causes and mechanisms of kidney stone formation are diverse and often unknown, resulting in varied compositions and different anatomical locations being affected. A better understanding of these processes could enable earlier diagnoses through more sensitive and scalable biomarkers, as well as more effective preventives and therapeutics

Química i vida

Abstract not availabl

Characterization of deposits on double J stents

We have characterized the types of encrustations that form on ureteral stents. The deposit that generates blocks is composed of hydroxyapatite/magnesium ammonium phosphate (44%). Calcium oxalate dihydrate was also detected at a high degree of encrustation (13%). Hydroxyapatite deposits, also of high degree of encrustation (13%) are generated due to their formation as a consequence of persistently high urinary pH values. The formation of large uric acid deposits (31%) must be attributed to the persistence of urinary $\mathrm{pH} < 5.5$. To avoid development of encrustations of ureteral stents, urinary calcium levels and urinary pH control should be carried out, avoiding urinary infections

Characterization of deposits on double J stents

We have characterized the types of encrustations that form on ureteral stents. The deposit that generates blocks is composed of hydroxyapatite/magnesium ammonium phosphate (44%). Calcium oxalate dihydrate was also detected at a high degree of encrustation (13%). Hydroxyapatite deposits, also of high degree of encrustation (13%) are generated due to their formation as a consequence of persistently high urinary pH values. The formation of large uric acid deposits (31%) must be attributed to the persistence of urinary $\mathrm{pH} < 5.5$. To avoid development of encrustations of ureteral stents, urinary calcium levels and urinary pH control should be carried out, avoiding urinary infections

Key Aspects of Myo-Inositol Hexaphosphate (Phytate) and Pathological Calcifications

Phytate (myo-inositol hexaphosphate, InsP6) is an important component of seeds, legumes, nuts, and whole cereals. Although this molecule was discovered in 1855, its biological effects as an antinutrient was first described in 1940. The antinutrient effect of phytate results because it can decrease the bioavailability of important minerals under certain circumstances. However, during the past 30 years, researchers have identified many important health benefits of phytate. Thus, 150 years have elapsed since the discovery of phytate to the first descriptions of its beneficial effects. This long delay may be due to the difficulty in determining phytate in biological media, and because phytate dephosphorylation generates many derivatives (InsPs) that also have important biological functions. This paper describes the role of InsP6 in blocking the development of pathological calcifications. Thus, in vitro studies have shown that InsP6 and its hydrolysates (InsPs), as well as pyrophosphate, bisphosphonates, and other polyphosphates, have high capacity to inhibit calcium salt crystallization. Oral or topical administration of phytate in vivo significantly decreases the development of pathological calcifications, although the details of the underlying mechanism are uncertain. Moreover, oral or topical administration of InsP6 also leads to increased urinary excretion of mixtures of different InsPs; in the absence of InsP6 administration, only InsP2 occurs at detectable levels in urine

Theobromine inhibits uric acid crystallization. A potential application in the treatment of uric acid nephrolithiasis.

To 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.The 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.The 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.Theobromine, 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