The purpose of this study was to determine the effects of consumption of different cocoa-derived products on uric acid crystallization in urine of 20 healthy volunteers. Participants were requested to select the specific diet that they wished to follow during the 12 h prior to collection of urine. The only restriction was that the diet could not include any product with cocoa, coffee, or caffeine. On the first day, each volunteer followed their selected diet, and an overnight 12 h urine sample was collected as the baseline urine. After seven days on an unrestricted diet, each volunteer repeated the same diet with 20 g of milk chocolate, chocolate powder, or dark chocolate during breakfast and another 20 g during dinner. Overnight 12 h urine samples were then collected. Urine volume, pH, oxalate, creatinine, uric acid, theobromine, and a uric acid crystallization test were determined for each sample. The results for all 20 patients show that uric acid crystallization was significantly lower following the consumption of chocolate powder or dark chocolate relative to baseline or following the consumption of milk chocolate. The results indicated that increased concentrations of urinary theobromine reduced the risk of uric acid crystallization.

(1) Background: This study aimed to determine the relationship between metabolic urine conditions and the formation, severity, and composition of encrustations in ureteral stents. (2) Methods: Ninety stone-former patients requiring a double-J stent were prospectively enrolled. We collected 24 h metabolic urine samples and demographic data, including indwelling time and previous stone composition. The total deposit weight was obtained, and a macroscopic classification according to the degree of encrustation (null, low, moderate, and high) was created, allowing for intergroup comparisons. Stereoscopic and scanning electron microscopy were performed to identify the type of embedded deposits (calcium oxalate, uric acid, and infectious and non-infectious phosphates). (3) Results: In total, 70% of stents were encrusted; thereof, 42% had a moderate degree of encrustation. The most common encrustation type was calcium oxalate, but infectious phosphates were predominant in the high-encrustation group (p < 0.05). A direct correlation was observed between the purpose-built macroscopic classification and the encrustation weights (p < 0.001). Greater calciuria, uricosuria, indwelling time, and decreased diuresis were observed in stents with a higher degree of encrustation (p < 0.05). The urinary pH values were lower in patients with uric acid encrustations and higher in those with infectious phosphate encrustations (p < 0.05). When compared to non-encrusted stents, patients with calcium-oxalate-encrusted stent showed greater calciuria, phosphaturia, indwelling time, and reduced diuresis; patients with uric-acid-encrusted stent showed greater uricosuria; and patients with infectious and non-infectious phosphate encrustation showed greater urinary pH (p < 0.05). (4) Conclusions: Metabolic urine conditions play a critical role in the formation, composition, and severity of double-J stent encrustation.

This study examined the expression of the renin-angiotensin system (RAS) and inflammatory markers in cardiovascular complications associated with long-term type 1 diabetes (T1D) using a rat model. After 24 weeks of streptozotocin-induced T1D, the animals exhibited metabolic alterations indicative of both cardiac and renal dysfunction. Tissue-specific dysregulation of RAS components and pro-inflammatory markers were observed in the heart, aorta, and perivascular adipose tissue (PVAT). In the heart, there was a significant upregulation of both classical (AT1R, 1.00 (0.22) vs. 1.70 (0.45) R.U.) and counter-regulatory RAS components (ACE2, 1.00 (0.43) vs. 1.96 (0.67) R.U.; p < 0.001) and MasR (1.00 (0.56) vs. 1.33 (0.29) R.U.; p = 0.004). The aorta displayed increased expression of classical RAS components alongside a significant reduction in ACE2 expression (1.00 (0.74) vs. 0.51 (0.48) R.U.; p < 0.032). Notably, PVAT showed a significant overexpression of classical RAS components (ACE 1.00 (0.22) vs. 4.08 (1.32) R.U.; p < 0.001, AT1R 1.00 (0.59) vs. 7.22 (4.14) R.U.; p < 0.001) and MasR (1.00 (0.70) vs. 4.52 (1.91) R.U.; p < 0.001), accompanied by increased expression of TNFα and ADAM17. These findings suggest that long-term T1D induces tissue-specific activation patterns of the RAS and inflammatory pathways within the cardiovascular system, which may contribute to the progression of diabetic cardiovascular complications. Therapeutic targeting of RAS components may represent a viable strategy for mitigating cardiovascular damage in T1D.