Cardiovascular and Cerebrovascular Morbidity in Patients with Urolithiasis: An Epidemiological Approach Based on Hospitalization Burden Data from 1997 to 2021.

Background: Patients with kidney stones (KSFs) are known to have a heightened risk of coronary heart disease (CHD) or stroke. The objective of the present study was to describe the natural history of these complications through the longitudinal analysis of the hospitalizations due to kidney stones in Spain from 1997 to 2021. Methods: A retrospective longitudinal observational study was developed based on nationwide hospitalization data (minimum basic data base). Three different analyses were carried out. In the first step, the prevalence of coronary or cerebrovascular events in kidney stone hospitalizations was compared with the hospitalization burden of CHD or strokes related to the general population. In the second step, a survival analysis of the kidney stones-hospitalized patients using the Kaplan-Meier method was conducted. In the third step, a Cox regression was used to assess the influence of the classical comorbidities in the development of the lithiasic patients-cardiovascular disease. Results: Kidney stone-hospitalized patients exhibit a significantly higher risk of CHD (OR = 14.8 CI95%: 14.7-14.9) and stroke (OR = 6.7 CI95%: 6.6-6.8) compared to the general population across in all age groups, although they had less cardiovascular risk factors. A total of 9352 KSFs (1.5%) developed a coronary event within an average time of 78.8 months. A total of 2120 KSFs (0.33%) suffered a stroke in an average time of 71.1 months. Diabetes, hypertension, hyperlipidemia, and being overweight were identified as risk factors for developing CHD and stroke using a univariate and multivariate analysis. Conclusions: Our study confirms previous studies in which kidney stones must be considered as a risk factor for developing CHD or cerebrovascular disease. Preventive strategies should target patients with kidney stones and classical risk cardiovascular factors to mitigate modifiable conditions associated with cardiovascular diseases.

Activation of mitoKATP channels induces penile vasodilation and inhibits mitochondrial respiration and ROS production: Role of NO.

OBJECTIVE: Mitochondrial ATP-sensitive K+ (mitoKATP) channels are involved in neuronal and cardiac protection from ischemia and oxidative stress. Penile erection is a neurovascular event mediated by relaxation of the erectile tissue via nitric oxide (NO) released from nerves and endothelium. In the present study, we investigated whether mitoKATP channels play a role in the control of penile vascular tone and mitochondrial dynamics, and the involvement of NO. METHODS: The effect of the selective mitoKATP activator BMS191095 was examined on vascular tone, on mitochondrial bioenergetics by real-time measurements with Agilent Seahorse and on ROS production by MitoSOX fluorescence in freshly isolated microarteries. RESULTS: BMS191095 and diazoxide relaxed penile arteries, BMS191095 being one order of magnitude more potent. BMS191095-induced relaxations were reduced by mechanical endothelium removal and by inhibitors of the nitric oxide synthase (NOS) and PI3K enzymes. The NO-dependent component of the relaxation to BMS191095 was impaired in penile arteries from insulin resistant obese rats. The blockers of mitoKATP channel 5-HD, sarcolemma KATP (sarcKATP) channel glibenclamide, and large conductance Ca2+-activated K+ (BKCa) channel iberiotoxin, inhibited relaxations to BMS191095 and to the NO donor SNAP. BMS191095 reduced the mitochondrial bioenergetic profile of penile arteries and attenuated mitochondrial ROS production. Blockade of endogenous NO impaired and exogenous NO mimicked, respectively, the inhibitory effects of BMS191095 on basal respiration and oxygen consumed for ATP synthesis. Exogenous NO exhibited dual inhibitory/stimulatory effects on mitochondrial respiration. CONCLUSIONS: These results demonstrate that selective activation of mitoKATP channels causes penile vasodilation, attenuates ROS production and inhibits mitochondrial respiration in part by releasing endothelial NO. These mechanisms couple blood flow and metabolism in penile arterial wall and suggest that activation of vascular mitoKATP channels may protect erectile tissue against ischemic injury.

Hospitalization Burden of Patients with Kidney Stones and Metabolic Comorbidities in Spain during the Period 2017-2020.

Nephrolithiasis has become an increasing worldwide problem during the last decades. Metabolic syndrome, its components, and related dietary factors have been pointed out as responsible for the increasing incidence. The objective of this study was to evaluate the trends in the hospitalization rates of patients with nephrolithiasis, hospitalization features, costs, and how metabolic syndrome traits influence both the prevalence and complications of lithiasic patients. An observational retrospective study was conducted by analyzing hospitalization records from the minimum basic data set, including all patient hospitalizations in Spain in which nephrolithiasis has been coded as a main diagnosis or as a comorbidity during the period 2017-2020. A total of 106,407 patients were hospitalized and coded for kidney or ureteral lithiasis in this period. The mean age of the patients was 58.28 years (CI95%: 58.18-58.38); 56.8% were male, and the median length of stay was 5.23 days (CI95%: 5.06-5.39). In 56,884 (53.5%) patients, kidney or ureteral lithiasis were coded as the main diagnosis; the rest of the patients were coded mostly as direct complications of kidney or ureteral stones, such as "non-pecified renal colic", "acute pyelonephritis", or "tract urinary infection". The hospitalization rate was 56.7 (CI95%: 56.3-57.01) patients per 100,000 inhabitants, showing neither a significant increasing nor decreasing trend, although it was influenced by the COVID-19 pandemic. The mortality rate was 1.6% (CI95%: 1.5-1.7), which was higher, if lithiasis was coded as a comorbidity (3.4% CI95%: 3.2-3.6). Metabolic syndrome diagnosis component codes increased the association with kidney lithiasis when age was higher, reaching the highest in the eighth decade of life. Age, diabetes, and hypertension or lithiasis coded as a comorbidity were the most common causes associated with the mortality of lithiasic patients. In Spain, the hospitalization rate of kidney lithiasis has remained stable during the period of study. The mortality rate in lithiasic patients is higher in elderly patients, being associated with urinary tract infections. Comorbidity conditions such as diabetes mellitus and hypertension are mortality predictors.

Hyperoxaluria Induces Endothelial Dysfunction in Preglomerular Arteries: Involvement of Oxidative Stress.

Urolithiasis is a worldwide problem and a risk factor for kidney injury. Oxidative stress-associated renal endothelial dysfunction secondary to urolithiasis could be a key pathogenic factor, similar to obesity and diabetes-related nephropathy. The aim of the present study was to characterize urolithiasis-related endothelial dysfunction in a hyperoxaluria rat model of renal lithiasis. EXPERIMENTAL APPROACH: Endothelial dysfunction was assessed in preglomerular arteries isolated from control rats and in which 0.75% ethylene glycol was administered in drinking water. Renal interlobar arteries were mounted in microvascular myographs for functional studies; superoxide generation was measured by chemiluminescence and mRNA and protein expression by RT-PCR and immunofluorescence, respectively. Selective inhibitors were used to study the influence of the different ROS sources, xanthine oxidase, COX-2, Nox1, Nox2 and Nox4. Inflammatory vascular response was also studied by measuring the RNAm expression of NF-κB, MCP-1 and TNFα by RT-PCR. RESULTS: Endothelium-dependent vasodilator responses were impaired in the preglomerular arteries of the hyperoxaluric group along with higher superoxide generation in the renal cortex and vascular inflammation developed by MCP-1 and promoted by NF-κB. The xanthine oxidase inhibitor allopurinol restored the endothelial relaxations and returned superoxide generation to basal values. Nox1 and Nox2 mRNA were up-regulated in arteries from the hyperoxaluric group, and Nox1 and Nox2 selective inhibitors also restored the impaired vasodilator responses and normalized NADPH oxidase-dependent higher superoxide values of renal cortex from the hyperoxaluric group. CONCLUSIONS: The current data support that hyperoxaluria induces oxidative stress-mediated endothelial dysfunction and inflammatory response in renal preglomerular arteries which is promoted by the xanthine oxidase, Nox1 and Nox2 pathways.

Endothelial Dysfunction: An Intermediate Clinical Feature between Urolithiasis and Cardiovascular Diseases.

An epidemiological relationship between urolithiasis and cardiovascular diseases has extensively been reported. Endothelial dysfunction is an early pathogenic event in cardiovascular diseases and has been associated with oxidative stress and low chronic inflammation in hypertension, coronary heart disease, stroke or the vascular complications of diabetes and obesity. The aim of this study is to summarize the current knowledge about the pathogenic mechanisms of urolithiasis in relation to the development of endothelial dysfunction and cardiovascular morbidities. METHODS: A non-systematic review has been performed mixing the terms "urolithiasis", "kidney stone" or "nephrolithiasis" with "cardiovascular disease", "myocardial infarction", "stroke", or "endothelial dysfunction". RESULTS: Patients with nephrolithiasis develop a higher incidence of cardiovascular disease with a relative risk estimated between 1.20 and 1.24 and also develop a higher vascular disease risk scores. Analyses of subgroups have rendered inconclusive results regarding gender or age. Endothelial dysfunction has also been strongly associated with urolithiasis in clinical studies, although no systemic serum markers of endothelial dysfunction, inflammation or oxidative stress could be clearly related. Analysis of urine composition of lithiasic patients also detected a higher expression of proteins related to cardiovascular disease. Experimental models of hyperoxaluria have also found elevation of serum endothelial dysfunction markers. CONCLUSIONS: Endothelial dysfunction has been strongly associated with urolithiasis and based on the experimental evidence, should be considered as an intermediate and changeable feature between urolithiasis and cardiovascular diseases. Oxidative stress, a key pathogenic factor in the development of endothelial dysfunction has been also pointed out as an important factor of lithogenesis. Special attention must be paid to cardiovascular morbidities associated with urolithiasis in order to take advantage of pleiotropic effects of statins, angiotensin receptor blockers and allopurinol.

Differential contribution of renal cytochrome P450 enzymes to kidney endothelial dysfunction and vascular oxidative stress in obesity.

Arachidonic acid (AA)-derived cytochrome P450 (CYP) derivatives, epoxyeicosatrienoic acids (EETs) and 20-hidroxyeicosatetranoic acid (20-HETE), play a key role in kidney tubular and vascular functions and blood pressure. Altered metabolism of CYP epoxygenases and CYP hydroxylases has differentially been involved in the pathogenesis of metabolic disease-associated vascular complications, although the mechanisms responsible for the vascular injury are unclear. The present study aimed to assess whether obesity-induced changes in CYP enzymes may contribute to oxidative stress and endothelial dysfunction in kidney preglomerular arteries. Endothelial function and reactive oxygen species (ROS) production were assessed in interlobar arteries of obese Zucker rats (OZR) and their lean counterparts lean Zucker rats (LZR) and the effects of CYP2C and CYP4A inhibitors sulfaphenazole and HET0016, respectively, were examined on the endothelium-dependent relaxations and O2- and H2O2 levels of preglomerular arteries. Non-nitric oxide (NO) non-prostanoid endothelium-derived hyperpolarization (EDH)-type responses were preserved but resistant to the CYP epoxygenase blocker sulfaphenazole in OZR in contrast to those in LZR. Sulfaphenazole did not further inhibit reduced arterial H2O2 levels, and CYP2C11/CYP2C23 enzymes were downregulated in intrarenal arteries from OZR. Renal EDH-mediated relaxations were preserved in obese rats by the enhanced activity and expression of endothelial calcium-activated potassium channels (KCa). CYP4A blockade restored impaired NO-mediated dilatation and inhibited augmented O2- production in kidney arteries from OZR. The current data demonstrate that both decreased endothelial CYP2C11/ CYP2C23-derived vasodilator H2O2 and augmented CYP4A-derived 20-HETE contribute to endothelial dysfunction and vascular oxidative stress in obesity. CYP4A inhibitors ameliorate arterial oxidative stress and restore endothelial function which suggests its therapeutic potential for the vascular complications of obesity-associated kidney injury.

Urolithiasis Develops Endothelial Dysfunction as a Clinical Feature.

An increased risk of cardiovascular morbidity has been reported in lithiasic patients. In this context, endothelial dysfunction (ED), an earlier status of atherogenesis, has been identified in hyperoxaluria rat models of urolithiasis. OBJECTIVE: The purpose of this study was to determine the endothelial vascular function in patients with urolithiasis in relation to systemic inflammatory, oxidative stress, and vascular function serum markers. METHODS: A cross-sectional study was performed between 27 urolithiasic patients, matched for age and sex, with 27 healthy patients. Endothelial function was assessed by measuring flow-mediated dilation (Celermajer method). Fasting blood was collected to determine metabolic parameters (glucose and lipid profile), along with serum CRP, IL-6, MDA, ADMA, and VCAM-1. RESULTS: Both the control and urolithiasis groups were homogenous in anthropometric, exploration, and general laboratory measures. Flow-mediated dilation (%FMD) was 11.85% (SE: 2.78) lower in the lithiasis group (p < 0.001). No significant differences were achieved between groups when CRP, IL-6, MDA, ADMA, and VCAM-1 were compared, although slightly higher values of CRP, ADMA, and VCAM-1 were detected in the lithiasic group. A correlation was not reached in any of the serum markers when they were related to flow-mediated values, although a slight negative correlation trend was observed in MDA, VCAM-1, and IL-6 values. CONCLUSIONS: Endothelial dysfunction constitutes an important disorder related to urolithiasis patients. It must be considered as an early feature responsible for future cardiovascular events. Our study did not find a significant association between inflammatory, oxidative stress, endothelial serum markers, and flow-mediated dilation.

Activation of AMP kinase ameliorates kidney vascular dysfunction, oxidative stress and inflammation in rodent models of obesity.

BACKGROUND AND PURPOSE: Obesity is a risk factor for the development of chronic kidney disease independent of diabetes, hypertension and other co-morbidities. Obesity-associated nephropathy is linked to dysregulation of the cell energy sensor AMP-activated protein kinase (AMPK). We aimed here to assess whether impairment of AMPK activity may cause renal arterial dysfunction in obesity and to evaluate the therapeutic potential of activating renal AMPK. EXPERIMENTAL APPROACH: Effects of the AMPK activator A769662 were assessed on intrarenal arteries isolated from ob/ob mice and obese Zucker rats and then mounted in microvascular myographs. Superoxide and hydrogen peroxide production were measured by chemiluminescence and fluorescence, respectively, and protein expression was analysed by western blotting. KEY RESULTS: Endothelium-dependent vasodilation and PI3K/Akt/eNOS pathway were impaired in preglomerular arteries from genetically obese rats and mice, along with impaired arterial AMPK activity and blunted relaxations induced by the AMPK activator A769662. Acute ex vivo exposure to A769662 restored endothelial function and enhanced activity of PI3K/Akt/eNOS pathway in obese rats, whereas in vivo treatment with A769662 improved metabolic state and ameliorated endothelial dysfunction, reduced inflammatory markers and vascular oxidative stress in renal arteries and restored redox balance in renal cortex of obese mice. CONCLUSION AND IMPLICATIONS: These results demonstrate that AMPK dysregulation underlies obesity-associated kidney vascular dysfunction and activation of AMPK improves metabolic state, protects renal endothelial function and exerts potent vascular antioxidant and anti-inflammatory effects. The beneficial effects of vascular AMPK activation might represent a promising therapeutic approach to the treatment of obesity-related kidney injury.

Activation of the AMP-related kinase (AMPK) induces renal vasodilatation and downregulates Nox-derived reactive oxygen species (ROS) generation.

AMP-activated protein kinase (AMPK) is a cellular energy sensor activated during energy stress to stimulate ATP production pathways and restore homeostasis. AMPK is widely expressed in the kidney and involved in mitochondrial protection and biogenesis upon acute renal ischemia, AMPK activity being blunted in metabolic disease-associated kidney disease. Since little is known about AMPK in the regulation of renal blood flow, the present study aimed to assess the role of AMPK in renal vascular function. Functional responses to the selective AMPK activator A769662 were assessed in intrarenal small arteries isolated from the kidney of renal tumour patients and Wistar rats and mounted in microvascular myographs to perform simultaneous measurements of intracellular calcium [Ca2+]i and tension. Superoxide (O2.-) and hydrogen peroxide (H2O2) production were measured by chemiluminescence and fluorescence and protein expression by Western blot. Activation of AMPK with A769662 increased AMPKα phosphorylation at Thr-172 and induced potent relaxations compared to AICAR in isolated human and rat intrarenal arteries, through both endothelium-dependent mechanisms involving nitric oxide (NO) and intermediate-conductance calcium-activated potassium (IKCa) channels, as well as activation of ATP-sensitive (KATP) channels and sarcoplasmic reticulum Ca2+-ATPase (SERCA) in vascular smooth muscle (VSM). Furthermore, AMPK activator reduced NADPH oxidase 4 (Nox4) and Nox2-derived reactive oxygen species (ROS) production. These results demonstrate that A769662 has potent vasodilator and antioxidant effects in intrarenal arteries. The benefits of AMPK activation in rat kidney are reproduced in human arteries and therefore vascular AMPK activation might be a therapeutic target in the treatment of metabolic disease-associated kidney injury.

Differential contribution of Nox1, Nox2 and Nox4 to kidney vascular oxidative stress and endothelial dysfunction in obesity.

Oxidative stress-associated endothelial dysfunction is a key pathogenic factor underlying the microvascular complications of metabolic disease. NADPH oxidase (Nox) is a major source of oxidative stress in diabetic nephropathy and chronic kidney disease, despite Nox4 and Nox2 have been identified as relevant sources of vasodilator endothelial H2O2.The present study was sought to investigate the role of Nox enzymes in renal vascular oxidative stress and endothelial dysfunction in a rat model of genetic obesity. Endothelial function was assessed in intrarenal arteries of obese Zucker rats (OZR) and their counterparts lean Zucker rats (LZR) mounted in microvascular myographs, and superoxide (O2.-) and H2O2 production were measured. Impaired endothelium-dependent relaxations to acetylcholine (ACh) were associated to augmented O2.- generation, but neither ROS scavengers nor the Nox inhibitor apocynin significantly improved these relaxant responses in renal arteries of OZR. Whereas NO contribution to endothelial relaxations was blunted, catalase-sensitive non-NO non-prostanoid relaxations were enhanced in obese rats. Interestingly, NADPH-dependent O2.- production was augmented while NADPH-dependent H2O2 generation was reduced, and cytosolic and mitochondrial SOD were up-regulated in kidney of obese rats. Nox4 was down-regulated in renal arteries and Nox4-dependent H2O2 generation and endothelial relaxation were reduced in OZR. Up-regulation of both Nox2 and Nox1 was associated with augmented O2.- production but reduced H2O2 generation and blunted endothelial Nox2-derived H2O2-mediated in obese rats. Moreover, increased Nox1-derived O2.- contributed to renal endothelial dysfunction in OZR. In summary, the current data support a main role for Nox1-derived O2.- in kidney vascular oxidative stress and renal endothelial dysfunction in obesity, while reduced endothelial Nox4 expression associated to decreased H2O2 generation and H2O2-mediated vasodilatation might hinder Nox4 protective renal effects thus contributing to kidney injury. This suggests that effective therapies to counteract oxidative stress and prevent microvascular complications must identify the specific Nox subunits involved in metabolic disease.

Hydrogen peroxide derived from NADPH oxidase 4- and 2 contributes to the endothelium-dependent vasodilatation of intrarenal arteries.

The role of NADPH oxidase (Nox)-derived reactive oxygen species in kidney vascular function has extensively been investigated in the harmful context of oxidative stress in diabetes and obesity-associated kidney disease. Since hydrogen peroxide (H2O2) has recently been involved in the non-nitric oxide (NO) non-prostanoid relaxations of intrarenal arteries, the present study was sought to investigate whether NADPH oxidases may be functional sources of vasodilator H2O2 in the kidney and to assess their role in the endothelium-dependent relaxations of human and rat intrarenal arteries. Renal interlobar arteries isolated from the kidney of renal tumor patients who underwent nephrectomy, and from the kidney of Wistar rats, were mounted in microvascular myographs to assess function. Superoxide (O2.-) and H2O2 production was measured by chemiluminescence and Amplex Red fluorescence, and Nox2 and Nox4 enzymes were detected by Western blotting and by double inmunolabeling along with eNOS. Nox2 and Nox4 proteins were expressed in the endothelium of renal arterioles and glomeruli co-localized with eNOS, levels of expression of both enzymes being higher in the cortex than in isolated arteries. Pharmacological inhibition of Nox with apocynin and of CYP 2C epoxygenases with sulfaphenazol, but not of the NO synthase (NOS), reduced renal NADPH-stimulated O2.- and H2O2 production. Under conditions of cyclooxygenase and NOS blockade, acetylcholine induced endothelium-dependent relaxations that were blunted by the non-selective Nox inhibitor apocynin and by the Nox2 or the Nox1/4 inhibitors gp91ds-tat and GKT136901, respectively. Acetylcholine stimulated H2O2 production that was reduced by gp91ds-tat and by GKT136901. These results suggest the specific involvement of Nox4 and Nox2 subunits as physiologically relevant endothelial sources of H2O2 generation that contribute to the endothelium-dependent vasodilatation of renal arteries and therefore have a protective role in kidney vasculature.

Metabolic syndrome contributes to renal injury mediated by hyperoxaluria in a murine model of nephrolithiasis.

Metabolic syndrome (MS) individuals have a higher risk of developing chronic kidney disease through unclear pathogenic mechanisms. MS has been also related with higher nephrolithiasis prevalence. To establish the influence of MS on renal function, we designed a murine model of combined metabolic syndrome and hyperoxaluria. Four groups of male Sprague-Dawley rats were established: (1) control group (n = 10) fed with standard chow; (2) stone former group (SF) (n = 10) fed with standard chow plus 0.75% ethylene glycol administered in the drinking water; (3) metabolic syndrome group (MS) (n = 10), fed with 60% fructose diet; (4) metabolic syndrome + stone former group (MS + SF) (n = 10), 60% fructose diet and 0.75% EG in the drinking water. MS group showed a significant injury to renal function when hyperoxaluria was induced. It was demonstrated by a significant decrease of creatinine clearance (p < 0.001), with higher tubular damage (34.3%, CI 95% 23.9-44.7, p < 0.001), produced by deposition of crystals, and increased tubular synthesis of osteopontin as a response to tubular damage. Induction of hyperoxaluria in rats with MS causes severe morphological alterations with a significant impairment of renal function. This impairment is not produced in rats without MS. Therefore, this model can be useful for the study of the influence of MS in stone formation.

[Laparoscopic Boari Flap ureteral reimplantation.] / Reimplante ureteral laparoscópico con Flap de Boari.

OBJECTIVES: To report our initial experience with laparoscopic Boari flap ureteral reimplantation and to review the main technical elements in ureteral reconstructive surgery. METHODS: In a 10-year period we performed 23 laparoscopic ureteral reimplantations. Three cases required a Boari flap. Two patients presented ureteral stenosis above the iliac vessels and the third one a urothelial tumor of the pelvic ureter. RESULTS: Two cases were completed laparoscopically; the third one was electively converted to open surgery to avoid prolonged OR time. Mean operative time was 276 minutes (270-290 min). There were no intraoperative complications. Mean hospital stay was 6.6 days. One patient presented postoperative UTI (Clavien 2). One patient developed with history of sever arteriopathy and aortorenal by pass developed ureteral stenosis proximal to the ureteral reimplantation eight months after the operation. CONCLUSIONS: Laparoscopic Boari flap ureteral reimplantation is an affective technique for ureteral reconstruction, safe and reproducible, reserved for cases of ureteral pathology in which the distance to bridge between the bladder and the ureteral stump is long.

Reimplante ureteral laparoscópico con Flap de Boari / Laparoscopic Boari Flap ureteral reimplantation

OBJETIVO: Presentamos nuestra experiencia inicial con el flap de Boari laparoscópico y revisamos los principales recursos quirúrgicos de la cirugía reconstructiva del uréter. MÉTODOS: En un periodo de 10 años hemos realizado 23 reimplantes ureterales laparoscópicos de los que 3 requirieron la utilización de un flap de Boari. En dos casos se trataba de estenosis ureterales por encima de los vasos iliacos, en el tercero un tumor ureteral. RESULTADOS: Dos de los tres casos se completaron por vía laparoscópica. El caso del tumor ureteral se convirtió de forma electiva para evitar la prolongación del tiempo quirúrgico. El tiempo medio de operación fue de 276 minutos (270-290 min). No hubo complicaciones intraoperatorias. La estancia media fue de 6,6 días. Uno de los pacientes presentó una infección urinaria después del alta, tratada con antibióticos orales (Clavien 2). Uno de los pacientes, con una arteriopatía aortoiliaca severa y by pass aortorenal previo presentó estenosis ureteral proximal al reimplante a los ocho meses de la cirugía, requiriendo colocación de un stent ureteral. CONCLUSIONES: El flap de Boari laparoscópico es una técnica eficaz para la reconstrucción del uréter, reproducible y segura, reservada para los casos de patología ureteral en los que la distancia a salvar entre la vejiga y el extremo ureteral es larga

OBJECTIVES: To report our initial experience with laparoscopic Boari flap ureteral reimplantation and to review the main technical elements in ureteral reconstructive surgery. METHODS: In a 10-year period we performed 23 laparoscopic ureteral reimplantations. Three cases required a Boari flap. Two patients presented ureteral stenosis above the iliac vessels and the third one a urothelial tumor of the pelvic ureter.RESULTS: Two cases were completed laparoscopically; the third one was electively converted to open surgery to avoid prolonged OR time. Mean operative time was 276 minutes (270-290 min). There were no intraoperative complications. Mean hospital stay was 6.6 days One patient presented postoperative UTI (Clavien 2). One patient developed with history of sever arteriopathy and aortorenal by pass developed ureteral stenosis proximal to the ureteral reimplantation eight months after the operation. CONCLUSIONS: : Laparoscopic Boari flap ureteral reimplantation is an affective technique for ureteral reconstruction, safe and reproducible, reserved for cases of ureteral pathology in which the distance to bridge between the bladder and the ureteral stump is long

Ureteroscopy for the treatment of urinary stones. Past, present and future.

OBJECTIVES: Ureteroscopy has been considered one of the most revolutionary techniques in modern urology for the treatment of urinary stones. The developments of new ureteroscopes, ancillary techniques or fragmentation devices have contributed to that evolution. To describe the evolution of imaging systems, auxiliary techniques and fragmentation methods for treatment of urinary stones from its beginnings to present time, with special emphasis on the different trends in the technique for the nearest future. METHODS: A bibliographic review is performed highlighting the development of technical details, and the impact on the results in terms of stone-free rate, and complications. CONCLUSIONS: Ureteroscopy has evolved into a first-line technique for the treatment of upper urinary tract stones. Technological advances in both imaging equipment and on different ancillary techniques and fragmentation methods have enabled improved stone free rates and decreased morbidity of the technique. Improvements in imaging systems, auxiliary instruments and fragmentation methods allow the treatment of stones progressively more complex.

Ureteroscopia para el tratamiento de la litiasis. Pasado, presente y futuro / Ureteroscopy for the treatment of urinary stones. Past, present and future

OBJETIVO: La ureteroscopia ha constituido una de las técnicas más revolucionarias de la urología moderna para el tratamiento de la litiasis urinaria. El desarrollo de nuevos ureteroscopios, de las diferentes técnicas auxiliares, así como de los métodos de fragmentación han sido las causas de esta evolución. Describir la evolución de los sistemas de imagen, las técnicas auxiliares para el manejo de los cálculos, así como los métodos de fragmentación desde sus inicios a nuestros días, poniendo especial énfasis en las diferentes tendencias relativas a la técnica que nos deparará el futuro próximo. MÉTODOS: Se realiza una revisión bibliográfica destacando el desarrollo de los detalles técnicos, así como el impacto sobre los resultados en términos de tasa libre de litiasis, y desarrollo de complicaciones. CONCLUSIONES: La ureteroscopia ha evolucionado hasta convertirse actualmente en una técnica de primera línea para el tratamiento de la litiasis del tracto urinario superior. Los avances tecnológicos producidos tanto en los equipos de imagen como en las diferentes técnicas auxiliares y en los métodos de fragmentación han permitido la mejora de las tasas libres de litiasis y han disminuido la morbilidad de la técnica. Las mejoras en los sistemas de imagen, los instrumentos auxiliares y los métodos de fragmentación permitirán progresivamente el tratamiento de litiasis más complejas del tracto urinario superior

OBJECTIVES: Ureteroscopy has been considered one of the most revolutionary techniques in modern urology for the treatment of urinary stones. The developments of new ureteroscopes, ancillary techniques or fragmentation devices have contributed to that evolution. To describe the evolution of imaging systems, auxiliary techniques and fragmentation methods for treatment of urinary stones from its beginnings to present time, with special emphasis on the different trends in the technique for the nearest future. METHODS: A bibliographic review is performed highlighting the development of technical details, and the impact on the results in terms of stone-free rate, and complications. CONCLUSIONS: Ureteroscopy has evolved into a first-line technique for the treatment of upper urinary tract stones. Technological advances in both imaging equipment and on different ancillary techniques and fragmentation methods have enabled improved stone free rates and decreased morbidity of the technique. Improvements in imaging systems, auxiliary instruments and fragmentation methods allow the treatment of stones progressively more complex

Análisis de decisión en la evaluación económica del tratamiento de la uropatía obstructiva crónica / Decision analysis for economic evaluation of the management of chronic obstructive uropathy

OBJETIVO: Demostrar cuál es la mejor decisión para tratar una uropatía obstructiva de larga evolución: la derivación urinaria convencional mediante un catéter ureteral doble J o la prótesis metálica termoexpandible Memokath 051, en base a la supervivencia estimada del enfermo, la cantidad de recambios de catéter que va a necesitar y el coste que cada acto terapeútico va a conllevar.MÉTODO: Se recogieron los datos de costes de la inserción de un catéter ureteral doble J teniendo en cuenta visitas preoperatorias y postoperatorias, acto quirúrgico con costes estructurales, médicos, de material fungible y de la prótesis. A continuación se hizo una simulación de los costes de inserción de una prótesis Memokath 051, en base a los datos del cateterismo ureteral. Se realizó un árbol de decisión y un análisis económico de Coste Efectividad (ACE) para medir la efectividad de las dos intervenciones sanitarias. A través de él se identificaron, cuantificaron y valoraron los costes de las dos alternativas de intervención sanitaria disponibles para alcanzar la resolución de la obstrucción ureteral.RESULTADOS: Los datos de costes de cada procedimiento son: catéter doble J en régimen de cirugía Mayor Ambulatoria (CMA) 1.275,44 €, prótesis metálica termoexpandible en CMA 4865,16 €, doble J con ingreso de 1 día 1424,52 € y prótesis con ingreso de un día 5014,24 €.La diferencia de costes entre el catéter ureteral y la prótesis metálica termoexpandible es de 3589,72 € por cada tratamiento en CMA a favor del catéter ureteral.CONCLUSIÓN: A pesar de su alto coste inicial la prótesis metálica termoexpandible ofrece ventajas económicas añadidas al catéter ureteral convencional doble J en el tratamiento de la obstrucción ureteral maligna. A partir del tercer cambio de catéter ureteral doble J, y si la supervivencia del paciente es lo suficientemente prolongada, la opción más coste efectiva es la prótesis metálica en régimen de CMA(AU)

OBJECTIVES: To test which is the best treatment for chronic obstructive uropathy: urinary diversion using a conventional double-J ureteral stent or the metal thermo-expandable Memokath 051 prosthesis.METHODS: We collected cost data of the insertion of a double-J stent taking into account preoperative and postoperative visits and surgery. Structural, medical, consumables and the prosthesis costs were considered. The estimated survival of the patient, number of spare stents and cost of each therapeutic measure were computed. Then, a simulation of the cost of inserting a Memokath 051 prosthesis was conducted, based on data of ureteral catheterization.We performed a decision tree and Cost Effectiveness economic analysis to measure the effectiveness of both health interventions.RESULTS: Cost data of each procedure were: 1275.44 € for the double J catheter in a program of day case surgery (DCS), 4865.16 € for the metal thermo-expandable prosthesis as DCS, and 1424.52 € for the double J stent with 1 day admission and 5014.24 € for the prosthesis with 1 day admission.The cost difference between ureteral stent and metal thermo-expandable prosthesis is 3589.72 € per treatment for the ureteral stent as DCS.CONCLUSIONS: Despite its high initial cost, the metal thermo-expandable prosthesis potentially offers economic advantages over the conventional double-J ureteral stent in the treatment of long evolution ureteral obstruction. After the third change of double-J stent, and if the patient survival is long enough, the metal prosthesis as DCS should be the most cost effective option(AU)

Renocolic fistula as a complication of radiofrequency in the treatment of renal cell carcinoma.

METHOD: Beyond postoperative suspicion, retrograde pyelogram was performed, the images of which are displayed, and demonstrated the fistula. RESULTS: Treatment has been definitive nephrectomy after failed attempt to seal the fistula with suture and TachoSil. CONCLUSIONS: Although radiofrequency ablation can be a valid technique for treating small renal tumors in patients with high morbidity, it is not without significant complications as described in this case, despite the precautions taken.

Fístula renocólica como complicación de radiofrecuencia para tratamiento de carcinoma renal de células claras / Renocólic fistula as a complication of ratiofrequency in the treatment of renal cell carcinoma

OBJETIVO: Describir un caso clínico de fístula reno cólica como complicación de ablación por radiofrecuencia de carcinoma de células renales. Se revisa la literatura y se exponen las diferentes actitudes diagnósticas y terapéuticas. MÉTODO: Tras la sospecha postoperatoria se realizó pielografía retrograda, cuyas imágenes se muestran, que demuestra la fístula. RESULTADO: El tratamiento definitivo ha sido la nefrectomía tras intento fallido de sellar la fístula con sutura y tachosil. CONCLUSIÓNES: Si bien la ablación por radiofrecuencia puede ser una técnica válida para el tratamiento del tumores renales de pequeño tamaño en pacientes con elevada morbilidad, no está exenta de complicaciones importantes como la descrita en este caso, a pesar de las precauciones tomadas(AU)

OBJECTIVES: To describe a clinical case of renocolic fistula as a complication of radiofrequency ablation of renal cell carcinoma. We reviewed the literature and presented different diagnostic and therapeutic approaches. METHOD: Beyond postoperative suspicion, retrograde pyelogram was performed, the images of which are displayed, and demonstrated the fistula. RESULTS: Treatment has been definitive nephrectomy after failed attempt to seal the fistula with suture and TachoSil. CONCLUSIONS: Although radiofrequency ablation can be a valid technique for treating small renal tumors in patients with high morbidity, it is not without significant complications as described in this case, despite the precautions taken(AU)