Ureteral stent encrustation. Pathophysiology / Incrustacion de cateteres ureterales. Fisiopatología

Ureteral stents are the most commonly used urological implants. They are used for temporary as well as for long-term ureteral stenting. Amongst others, complications of ureteral stenting are encrustation and cellular adherence which, in turn, promotes urinary tract infection and can induce impaired healing in case of ureteral damage. Biofilm formation on urological implants leads to the protection of persisting bacteria from local defense mechanisms, thereby rendering persistent urinary tract infections more common. It seems clear that antibiotics cannot penetrate into biofilms adequately. Also, bacteria persist in biofilms in a state of reduced metabolism which further reduces antibiotic efficacy. Furthermore, bacteria develop resistance more quickly in biofilms. This paper tries to give an overview of the complex pathophysiological mechanisms that underlie stent encrustation as far as we know to date

Los catéteres ureterales son los implantes urológicos más utilizados. Se utilizan de forma temporal o a largo plazo. Entre otras complicaciones la utilización de catéteres ureterales incluye la incrustación y la adherencia celular que a su vez promueven la infección del tracto urinario y pueden empeorar la cicatrización en caso de lesión ureteral. La formación de biofilms en los implantes urológicos conlleva la protección de las bacterias persistentes de los mecanismos de defensa locales, haciendo de ese modo mas común la infección urinaria. Parece claro que los antibióticos no pueden penetrar adecuadamente en los biofilms. Además, las bacterias en los biofilms persisten en un estado de metabolismo reducido que disminuye más aún la eficacia de los antibióticos. Asimismo, las bacterias en los biofilms desarrollan resistencias más rápido. Este artículo intenta ofrecer una visión de conjunto sobre los mecanismos fisiopatológicos complejos que subyacen a la incrustación de catéteres hasta donde se conoce hoy en día

Influence of body temperature on indinavir crystallization under loop of Henle conditions.

OBJECTIVES: Indinavir is a protease inhibitor used in the therapy of HIV-1+ patients. It causes indinavir stone formation. It has been shown to precipitate in the loop of Henle (LH) at plasma concentrations (conc[P]) of approximately 8 mg/L. Those experiments were performed at room temperature. Given the influence of temperature on crystallization in general, and solubility of indinavir in particular, we repeated the experiments under physiological (body) temperature conditions. METHODS: Test solutions contained indinavir concentrations of 100-750 mg/L at ionic strengths varying from 0 to 800 mM simulating conditions in the proximal tubule and the LH. Solutions were titrated with base (NaOH) to find the pH value where nucleation is initiated. Experiments were conducted at room temperature (20 degrees C) and repeated under constantly monitored (body) temperature (37 degrees C). RESULTS: Experiments at 20 degrees C confirmed our previous results. At 37 degrees C, the relationship between pH and indinavir concentration remained inversely proportional. Again, the LH was confirmed as the most likely localization of crystallization. However, at 37 degrees C precipitation occurred at a lower urinary concentration (100 versus 125 mg/L) and within a lower pH range (6.67-7.26 versus 7.23-7.44). This lower urinary concentration corresponds to a lower conc[P] [critical value (CV)] of 6.41 mg/L, as compared with 8.01 mg/L at 20 degrees C. CONCLUSIONS: The CV is even lower at 37 degrees C than previously assumed. Plasma peak concentration above the CV of 6.4 mg/L will induce crystallization in the LH and should be avoided.