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1.
Rev Med Inst Mex Seguro Soc ; 61(Suppl 3): S372-S379, 2023 Oct 02.
Artículo en Español | MEDLINE | ID: mdl-37934678

RESUMEN

Background: COVID-19 challenged our health system, within the broad clinical spectrum acute kidney injury was presented as a catastrophic event, acute kidney injury and the risk of dependency after dialysis constitute a clinical problem with high repercussions in the funcionality. Objective: To identify risk factors for dialysis dependence after acute kidney injury from COVID-19. Material and methods: A retrospective observational cohort study was carried out at the Hospital de Especialidades del Centro Médico Nacional Siglo XXI, of the Mexican Institute of Social Security, from March 2020 to March 2021. 317 patients were included, we performed descriptive statistics, we compared differences between the stages of acute kidney injury, finding a difference in obesity with a frequency of 2.2% in stage 1, 20.82% stage 2 and 14.51% stage 3, with p value = 0.018. Results: We found dialysis dependence one year after hospital-acquired acute kidney injury induced by COVID-19 in 58 patients (18.9%), we analyzed by KDIGO stage, in those patients who had AKI KDIGO 1 (2.83%) it depended on dialysis at one year, in the KDIGO stage 2 (3.78%), in the KDIGO stage 3 (11.67%). Conclusions: Our study allowed us to identify that the risk factors associated with dialysis dependence are: male gender, type 2 diabetes mellitus, obesity, cardiovascular disease.


Introducción: la COVID-19, retó a nuestro sistema de salud, dentro del amplio espectro clínico la lesión renal aguda se presentó como un evento catastrófico, la lesión renal aguda y el riesgo de dependencia posterior a diálisis constituye un problema clínico con alta repercusión en la funcionalidad. Objetivo: identificar los factores de riesgo para la dependencia a diálisis posterior a lesión renal aguda por COVID-19. Material y métodos: se realizó un estudio de cohorte observacional retrospectivo en el Hospital de Especialidades del Centro Médico Nacional Siglo XXI, del Instituto Mexicano del Seguro Social, del periodo de marzo del 2020 a marzo del 2021. Se incluyeron 317 pacientes, realizamos estadística descriptiva, comparamos diferencias entre los estadios de lesión renal aguda encontrando diferencia en obesidad con frecuencia de 2.2% en estadio 1, de 20.82% estadio 2 y de 14.51% estadio 3, con valor p = 0.018. Resultados: encontramos la dependencia a diálisis a un año posterior a lesión renal aguda intrahospitalaria inducida por COVID-19 en 58 pacientes (18.9%), analizamos por estadio de KDIGO, en aquellos pacientes que cursaron con LRA KDIGO 1 (2.83%) dependió de diálisis a un año, en el estadio KDIGO 2 (3.78%), en el estadio KDIGO 3 (11.67%). Conclusiones: nuestro estudio permitió identificar que los factores de riesgo que se asocian con dependencia a diálisis son: sexo masculino, diabetes mellitus tipo 2, obesidad, enfermedad cardiovascular.


Asunto(s)
Lesión Renal Aguda , COVID-19 , Diabetes Mellitus Tipo 2 , Humanos , Masculino , Estudios Retrospectivos , Pacientes Internos , Diabetes Mellitus Tipo 2/complicaciones , Diálisis Renal , COVID-19/epidemiología , Factores de Riesgo , Lesión Renal Aguda/epidemiología , Lesión Renal Aguda/etiología , Lesión Renal Aguda/terapia , Obesidad/complicaciones , Mortalidad Hospitalaria
2.
Toxins (Basel) ; 13(8)2021 08 09.
Artículo en Inglés | MEDLINE | ID: mdl-34437422

RESUMEN

Acute kidney injury (AKI), defined as an abrupt increase in serum creatinine, a reduced urinary output, or both, is experiencing considerable evolution in terms of our understanding of the pathophysiological mechanisms and its impact on other organs. Oxidative stress and reactive oxygen species (ROS) are main contributors to organ dysfunction in AKI, but they are not alone. The precise mechanisms behind multi-organ dysfunction are not yet fully accounted for. The building up of uremic toxins specific to AKI might be a plausible explanation for these disturbances. However, controversies have arisen around their effects in organs other than the kidney, because animal models usually depict AKI as a kidney-specific injury. Meanwhile, humans present AKI frequently in association with multi-organ failure (MOF). Until now, medium-molecular-weight molecules, such as inflammatory cytokines, have been proven to play a role in endothelial and epithelial injury, leading to increased permeability and capillary leakage, mainly in pulmonary and intestinal tissues.


Asunto(s)
Lesión Renal Aguda/metabolismo , Insuficiencia Multiorgánica/metabolismo , Tóxinas Urémicas/metabolismo , Animales , Humanos , Unión Proteica
4.
Contrib Nephrol ; 192: 116-124, 2018.
Artículo en Inglés | MEDLINE | ID: mdl-29393127

RESUMEN

BACKGROUND: Uric acid (UA) stones are responsible for 5-10% of the formation of all kidney stones. Recently, an association between UA stones and insulin resistance, diabetes mellitus, and obesity has been demonstrated and so the incidence has increased. The development of UA stones is dependent on several risk factors, including genetic predisposition, geographical location, dietary indiscretion, and various metabolic characteristics. SUMMARY: UA nephrolithiasis can arise from diverse etiologies, all with distinct underlying defects converging to one or more of 3 defects of hyperuricosuria, acidic urine pH, and low urinary volume. Low urinary pH is the commonest and by far the most important factor in UA nephrolithiasis, but the reason for this defect is unknown. Patients with UA nephrolithiasis have normal acid-base parameters assessed according to conventional clinical tests. Studies have revealed that there could be an insufficient production of urinary ammonium buffer. Many transport proteins are candidate participants in urate handling, with URAT1 and GLUT9 being the best characterized to date. Because low urine pH is the most important pathogenic factor of UA stone formation, urine alkalinization is an effective intervention to reduce UA crystallization and dissolve UA stones. Key Messages: Epidemiological and metabolic studies have indicated an association between UA nephrolithiasis and insulin resistance. Some potential mechanisms include impaired ammoniagenesis caused by resistance to insulin action in the renal proximal tubule or due to substrate competition by free fatty acids. The identification of novel complementary DNA has provided an interesting insight into the renal handling of UA, including one genetic cause of renal UA wasting.


Asunto(s)
Hiperuricemia/complicaciones , Nefrolitiasis/etiología , Ácido Úrico/metabolismo , Amoníaco/metabolismo , Humanos , Concentración de Iones de Hidrógeno , Hiperuricemia/sangre , Hiperuricemia/genética , Resistencia a la Insulina , Nefrolitiasis/tratamiento farmacológico , Nefrolitiasis/epidemiología , Factores de Riesgo , Orina/química
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