RESUMEN
In patients with chronic kidney disease, the need for examinations using contrast media (CM) increases because of underlying diseases. Although contrast agents can affect brain cells, the blood-brain barrier (BBB) protects against brain-cell damage in vivo. However, uremia can disrupt the BBB, increasing the possibility of contrast-agent-induced brain-cell damage in patients with chronic kidney disease (CKD). ω-3 polyunsaturated fatty acids (PUFAs) have shown protective effects on various neurological disorders, including uremic brain injury. This study examined whether ω-3 PUFAs attenuate damage to the BBB caused by uremia and contrast agents in a uremic mouse model and evaluated its associated mechanisms. C57BL/6 mice (eight weeks old, male) and fat-1 mice (b6 background/eight weeks old, male) were divided into groups according to uremic induction, CM, and ω-3 PUFA administration. Uremia was induced via 24 h ischemia-reperfusion (IR) renal injury. One day after CM treatment, the brain tissue, kidney tissue, and blood were collected. The expression levels of glial fibrillary acidic protein (GFAP), claudin 5, CD31, laminin α4, and laminin α5 increased in ω-3 PUFA + CM-treated uremic mice and the brain of fat-1 + CM-treated uremic mice compared with those in the brains of CM-treated uremic mice. The pro-apoptotic protein expression decreased, whereas the anti-apoptotic proteins increased in ω-3 PUFA + CM-treated uremic mice and fat-1 + CM-treated uremic mice compared with CM-treated uremic mice. In addition, the brain-expression levels of p-JNK, p-P53, and p-P38 decreased in the ω-3 PUFA + CM-treated uremic mice and fat-1 + CM-treated uremic mice compared with those in wild-type uremic mice. Our results confirm that uremic toxin and CM damage the BBB and cause brain-cell death. ω-3 PUFAs play a role in BBB protection caused by CM in uremic mice.
Asunto(s)
Ácidos Grasos Omega-3 , Insuficiencia Renal Crónica , Daño por Reperfusión , Uremia , Ratones , Animales , Masculino , Barrera Hematoencefálica/metabolismo , Medios de Contraste , Ratones Endogámicos C57BL , Ácidos Grasos Omega-3/farmacología , Ácidos Grasos Omega-3/metabolismo , Daño por Reperfusión/metabolismo , Insuficiencia Renal Crónica/tratamiento farmacológicoRESUMEN
Recent studies have implicated mitochondrial disruption in podocyte dysfunction, which is a characteristic feature of primary and diabetic glomerular diseases. However, the mechanisms by which primary mitochondrial dysfunction in podocytes affects glomerular renal diseases are currently unknown. To investigate the role of mitochondrial oxidative phosphorylation (OxPhos) in podocyte dysfunction, glomerular function was examined in mice carrying a loss of function mutation of the gene encoding CR6-interacting factor-1 (CRIF1), which is essential for intramitochondrial production and the subsequent insertion of OxPhos polypeptides into the inner mitochondrial membrane. Homozygotic deficiency of CRIF1 in podocytes resulted in profound and progressive albuminuria from 3 weeks of age; the CRIF1-deficient mice also developed glomerular and tubulointerstitial lesions by 10 weeks of age. Furthermore, marked glomerular sclerosis and interstitial fibrosis were observed in homozygous CRIF1-deficient mice at 20 weeks of age. In cultured mouse podocytes, loss of CRIF1 resulted in OxPhos dysfunction and marked loss or abnormal aggregation of F-actin. These findings indicate that the OxPhos status determines the integrity of podocytes and their ability to maintain a tight barrier and control albuminuria. Analyses of the glomerular function of the podocyte-specific primary OxPhos dysfunction model mice demonstrate a link between podocyte mitochondrial dysfunction, progressive glomerular sclerosis, and tubulointerstitial diseases.
Asunto(s)
Albuminuria/metabolismo , Proteínas de Ciclo Celular/deficiencia , Proteínas de Ciclo Celular/metabolismo , Mitocondrias/metabolismo , Podocitos/metabolismo , Esclerosis/metabolismo , Albuminuria/genética , Albuminuria/patología , Animales , Proteínas de Ciclo Celular/genética , Nefropatías Diabéticas/metabolismo , Modelos Animales de Enfermedad , Femenino , Fibrosis , Riñón/patología , Masculino , Ratones , Ratones Noqueados , Mitocondrias/genética , Membranas Mitocondriales/metabolismo , Fosforilación Oxidativa , Péptidos/metabolismo , Esclerosis/genética , Esclerosis/patologíaRESUMEN
Although inflammation and fibrosis, which are key mechanisms of chronic kidney disease, are associated with mitochondrial damage, little is known about the effects of mitochondrial damage on the collecting duct in renal inflammation and fibrosis. To generate collecting duct-specific mitochondrial injury mouse models, CR6-interacting factor-1 (CRIF1) flox/flox mice were bred with Hoxb7-Cre mice. We evaluated the phenotype of these mice. To evaluate the effects on unilateral ureteral obstruction (UUO)-induced renal injury, we divided the mice into the following four groups: a CRIF1flox/flox (wild-type (WT)) group, a CRIF1flox/flox-Hob7 Cre (CRIF1-KO) group, a WT-UUO group, and a CRIF1-KO UUO group. We evaluated the blood and urine chemistries, inflammatory and fibrosis markers, light microscopy, and electron microscopy of the kidneys. The inhibition of Crif1 mRNA in mIMCD cells reduced oxygen consumption and membrane potential. No significant differences in blood and urine chemistries were observed between WT and CRIF1-KO mice. In UUO mice, monocyte chemoattractant protein-1 and osteopontin expression, number of F4/80 positive cells, transforming growth factor-ß and α-smooth muscle actin staining, and Masson's trichrome staining were significantly higher in the kidneys of CRIF1-KO mice compared with the kidneys of WT mice. In sham mice, urinary 8-hydroxydeoxyguanosine (8-OHDG) was higher in CRIF1-KO mice than in WT mice. Moreover, CRIF1-KO sham mice had increased 8-OHDG-positive cell recruitment compared with WT-sham mice. CRIF1-KO-UUO kidneys had increased recruitment of 8-OHDG-positive cells compared with WT-UUO kidneys. In conclusion, collecting duct-specific mitochondrial injury increased oxidative stress. Oxidative stress associated with mitochondrial damage may aggravate UUO-induced renal injury.
Asunto(s)
Proteínas de Ciclo Celular/metabolismo , Túbulos Renales Colectores/metabolismo , Mitocondrias/ultraestructura , Insuficiencia Renal Crónica/metabolismo , Animales , Modelos Animales de Enfermedad , Túbulos Renales Colectores/ultraestructura , Masculino , Ratones Endogámicos C57BL , Ratones Noqueados , Estrés Oxidativo , Insuficiencia Renal Crónica/patología , Obstrucción UreteralRESUMEN
Although the cause of neurological disease in patients with chronic kidney disease (CKD) has not been completely identified yet, recent papers have identified accumulated uremic toxin as its main cause. Additionally, omega-3 polyunsaturated fatty acid (ω-3 PUFA) plays an important role in maintaining normal nerve function, but its protective effects against uremic toxin is unclear. The objective of this study was to identify brain damage caused by uremic toxicity and determine the protective effects of ω-3 PUFA against uremic toxin. We divided mice into the following groups: wild-type (wt) sham (n = 8), ω-3 PUFA sham (n = 8), Fat-1 sham (n = 8), ischemia-reperfusion (IR) (n = 20), and ω-3 PUFA+IR (n = 20) Fat-1+IR (n = 20). Brain tissue, kidney tissue, and blood were collected three days after the operation of mice (sham and IR operation). This study showed that Ki67 and neuronal nuclei (NeuN) decreased in the brain of uremic mice as compared to wt mice brain, but increased in the ω-3 PUFA-treated uremic mice and the brain of uremic Fat-1 mice as compared to the brain of uremic mice. The pro-apoptotic protein expressions were increased, whereas anti-apoptotic protein expression decreased in the brain of uremic mice as compared to wt mice brain. However, apoptotic protein expression decreased in the ω-3 PUFA-treated uremic mice and the brain of uremic Fat-1 mice as compared to the brain of uremic mice. Furthermore, the brain of ω-3 PUFA-treated uremic mice and uremic Fat-1 mice showed increased expression of p-PI3K, p-PDK1, and p-Akt as compared to the brain of uremic mice. We confirm that uremic toxin damages the brain and causes cell death. In these injuries, ω-3 PUFA plays an important role in neuroprotection through PI(3)K-Akt signaling.
Asunto(s)
Lesiones Encefálicas , Encéfalo , Ácidos Grasos Omega-3/farmacología , Transducción de Señal/efectos de los fármacos , Uremia , Animales , Encéfalo/metabolismo , Encéfalo/patología , Lesiones Encefálicas/tratamiento farmacológico , Lesiones Encefálicas/metabolismo , Lesiones Encefálicas/patología , Línea Celular , Riñón/metabolismo , Riñón/patología , Masculino , Ratones , Fosfatidilinositol 3-Quinasas , Proteínas Proto-Oncogénicas c-akt , Uremia/tratamiento farmacológico , Uremia/metabolismo , Uremia/patologíaRESUMEN
BACKGROUND: Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. This disease, which is quickly spreading worldwide, has high potential for infection and causes rapid progression of lung lesions, resulting in a high mortality rate. This study aimed to investigate the effects of SARS-CoV-2 infection on renal function in patients with COVID-19. METHODS: From February 21 to April 24, 2020, 66 patients diagnosed with COVID-19 at Chungnam National University Hospital were analyzed; all patients underwent routine urinalysis and were tested for serum creatinine, urine protein to creatinine ratio (PCR), and urine albumin to creatinine ratio (ACR). RESULTS: Acute kidney injury (AKI) occurred in 3 (4.5%) of the 66 patients, and 1 patient with AKI stage 3 underwent hemodialysis. Upon follow-up, all 3 patients recovered normal renal function. Compared with patients with mild COVID-19, AKI (n = 3) occurred in patients with severe COVID-19, of whom both urine PCR and ACR were markedly increased. CONCLUSION: The incidence of AKI was not high in COVID-19 patients. The lower mortality rate in SARS-CoV-2 infection compared with previous Middle East respiratory syndrome and SARS-CoV infections is thought to be associated with a low incidence of dysfunction in organs other than the lungs.
Asunto(s)
Lesión Renal Aguda/virología , Albuminuria/orina , Infecciones por Coronavirus/patología , Creatinina/sangre , Neumonía Viral/patología , Proteinuria/orina , Lesión Renal Aguda/epidemiología , Lesión Renal Aguda/patología , Anciano , Albúminas/análisis , Betacoronavirus , COVID-19 , Femenino , Tasa de Filtración Glomerular/fisiología , Humanos , Pruebas de Función Renal , Masculino , Persona de Mediana Edad , Pandemias , República de Corea/epidemiología , SARS-CoV-2RESUMEN
BACKGROUND AND PURPOSE: As intraarterial thrombectomy (IAT) has been actively practiced, blood biomarkers that can predict outcomes after IAT have drawn attention. Growth differentiation factor-15 (GDF-15) is a stress-responsive cytokine and the levels are increased during inflammation or other pathological conditions of various tissues, including the brain. However, GDF-15 levels have not been reported as a biomarker for IAT outcomes. This study was performed to evaluate whether GDF-15 was related to the extent of brain damage and whether it could predict patient prognosis after IAT. METHODS: Patients who showed large arterial occlusion and significant diffusion-perfusion mismatch on imaging underwent IAT. A total of 62 patients who underwent IAT and had blood samples for GDF-15 measurements were enrolled from July 2013 to May 2015. We assessed the infarct severity by consecutive changes on the National Institutes of Health Stroke Scale (NIHSS) during admission and the size of the infarction on brain imaging. Modified Rankin Scale scores (mRS) from 0 to 2 were considered good outcomes, representing functional independence at discharge and three months later. RESULTS: The levels of GDF-15 at the time of admission were significantly correlated with the NIHSS scored at 24 hours (râ¯=â¯0.306, pâ¯=â¯0.016), three days after IAT (râ¯=â¯0.261, pâ¯=â¯0.041), and at discharge (râ¯=â¯0.266, pâ¯=â¯0.037), as well as the infarct size on diffusion-weighted image taken 24 h after IAT (râ¯=â¯0.452, pâ¯=â¯0.001), but the levels were not correlated with the initial NIHSS or the infarct size before IAT. Multiple logistic regression showed that GDF-15 levels were an independent predictor of functional independence (mRS 0 - 2) at discharge (pâ¯=â¯0.028) and three months after IAT (pâ¯=â¯0.019). Other factors that could predict prognosis were good collateral status on the initial brain angiography and rapid recanalization within six hours from symptom onset. CONCLUSION: The GDF-15 level at the time of admission showed a significant positive correlation with the severity of cerebral damage and clinical outcome after IAT. This suggests that GDF-15 can provide useful prognostic information for patients who successfully underwent IAT in an emergency setting.
Asunto(s)
Isquemia Encefálica/terapia , Factor 15 de Diferenciación de Crecimiento/sangre , Accidente Cerebrovascular/terapia , Trombectomía , Anciano , Biomarcadores/sangre , Isquemia Encefálica/sangre , Isquemia Encefálica/diagnóstico , Angiografía Cerebral , Imagen de Difusión por Resonancia Magnética , Evaluación de la Discapacidad , Femenino , Humanos , Masculino , Persona de Mediana Edad , Valor Predictivo de las Pruebas , Accidente Cerebrovascular/sangre , Accidente Cerebrovascular/diagnóstico , Trombectomía/efectos adversos , Factores de Tiempo , Resultado del TratamientoRESUMEN
AIMS: The long-term safety and efficacy of gemigliptin was evaluated in the present extension study after a 12-week study during a 40-week follow-up period. METHODS: The main study was a randomized, placebo-controlled, double-blinded, phase IIIb study in which 50 mg of gemigliptin (N = 66) or placebo (N = 66) was administered to patients with type 2 diabetes mellitus (T2DM) and moderate or severe renal impairment over a 12-week period. Patients with a glycated haemoglobin (HbA1c) level of 7% to 11% and an estimated glomerular filtration rate (eGFR) of 15 to 59 mL/min/1.73 m2 were enrolled in the main study. After 12 weeks, patients in the gemigliptin group continued to receive gemigliptin (N = 50), whereas patients in the placebo group were transitioned from placebo to linagliptin (N = 52). Each group received the indicated treatment over the subsequent 40-week period. A total of 102 patients consented to participate in the extension study, and 79 patients ultimately completed the study. RESULTS: The HbA1c levels of both groups were significantly reduced at week 52 compared with baseline. Specifically, the adjusted mean change ± standard error in HbA1c level in the gemigliptin and placebo/linagliptin groups was 1.00% ± 0.21% and 0.65% ± 0.22% lower at week 52 than at baseline (P < .001 and P = .003), respectively. No significant difference in the change in HbA1c level was found between the 2 groups (P = .148). Trends in fasting plasma glucose, fructosamine and glycated albumin levels in the 2 groups were similar to trends in HbA1c levels. The eGFR of both groups was also significantly lower at week 52 than at baseline, and no significant difference in change in eGFR was found between the 2 groups. In contrast, both drugs had little effect on urinary albumin excretion, although both drugs significantly reduced the urinary type IV collagen level. The overall rates of adverse events were similar between the 2 groups. CONCLUSIONS: Gemigliptin and linagliptin did not differ with respect to safety and efficacy in patients with T2DM and renal impairment. The 2 drugs had similar glucose-lowering effects, and the changes in eGFR and albuminuria were also similar. Additionally, the risk of side effects, including hypoglycaemia, was similar between the 2 groups.
Asunto(s)
Diabetes Mellitus Tipo 2/tratamiento farmacológico , Nefropatías Diabéticas/fisiopatología , Inhibidores de la Dipeptidil-Peptidasa IV/uso terapéutico , Riñón/efectos de los fármacos , Linagliptina/uso terapéutico , Piperidonas/uso terapéutico , Pirimidinas/uso terapéutico , Insuficiencia Renal Crónica/fisiopatología , Anciano , Diabetes Mellitus Tipo 2/sangre , Diabetes Mellitus Tipo 2/complicaciones , Nefropatías Diabéticas/complicaciones , Inhibidores de la Dipeptidil-Peptidasa IV/efectos adversos , Método Doble Ciego , Monitoreo de Drogas , Quimioterapia Combinada/efectos adversos , Femenino , Estudios de Seguimiento , Humanos , Hiperglucemia/prevención & control , Hipoglucemiantes/uso terapéutico , Insulina/uso terapéutico , Riñón/fisiopatología , Linagliptina/efectos adversos , Masculino , Persona de Mediana Edad , Pacientes Desistentes del Tratamiento , Piperidonas/efectos adversos , Pirimidinas/efectos adversos , Insuficiencia Renal Crónica/complicaciones , Índice de Severidad de la Enfermedad , Compuestos de Sulfonilurea/uso terapéuticoRESUMEN
BACKGROUND: It is well known that renal dysfunction and cerebral small-vessel disease (SVD), including microbleed, lacunar infarction, and white matter lesion (WML), are associated with poor prognosis after ischemic stroke. However, the prognostic relationship between renal dysfunction and SVD has not been well evaluated in acute ischemic stroke survivors. Therefore, in this study, we evaluated the prognostic relationships between estimated glomerular filtration rate (eGFR) and cerebral SVD after acute ischemic stroke. METHODS: We retrospectively reviewed the clinical and radiological data of acute ischemic stroke survivors with decreased eGFR (<60 mL/min/1.73 m2, n = 128) and controls (eGFR ≥60 mL/min/1.73 m2, n = 128). The presence of SVD was evaluated according to magnetic resonance imaging performed on admission. Mortality data were obtained from medical chart reviews and telephone interviews. RESULTS: Patients with silent lacunar infarction, WML, or microbleed had lower eGFR than patients without such lesions (60.4 ± 34.8 versus 87.5 ± 28.4 mL/min/1.73 m2, 60.5 ± 37.1 versus 73.9 ± 33.3 mL/min/1.73 m2, and 57.6 ± 33.3 versus 73.9 ± 32.9 mL/min/1.73 m2, respectively). In addition, the multivariate adjusted odds ratio for the presence of SVD increased inversely with eGFR. Three-year survival was lower in patients with renal dysfunction and each type of SVD. The presence of WML was an independent risk factor for cardiovascular death. CONCLUSIONS: Renal impairment was associated with the presence of SVD in acute ischemic stroke survivors. Both renal impairment and the presence of SVD were predictors of poor poststroke survival.
Asunto(s)
Isquemia Encefálica/diagnóstico , Encéfalo/diagnóstico por imagen , Insuficiencia Renal Crónica/complicaciones , Accidente Cerebrovascular/diagnóstico , Sustancia Blanca/diagnóstico por imagen , Anciano , Isquemia Encefálica/mortalidad , Isquemia Encefálica/fisiopatología , Femenino , Tasa de Filtración Glomerular , Humanos , Modelos Logísticos , Imagen por Resonancia Magnética , Masculino , Pronóstico , Insuficiencia Renal Crónica/mortalidad , Insuficiencia Renal Crónica/fisiopatología , Estudios Retrospectivos , Factores de Riesgo , Índice de Severidad de la Enfermedad , Accidente Cerebrovascular/mortalidad , Accidente Cerebrovascular/fisiopatología , Análisis de SupervivenciaRESUMEN
BACKGROUND/AIMS: Both endothelin-1 (ET-1) and the renin-angiotensin system (RAS) may play important roles in renal fibrosis in the obstructed kidney. However, there have been few clear demonstrations of a relationship between their activation and additive or synergistic roles in renal fibrosis. We investigated the protective roles and relationship between renal RAS and ET-1 in unilateral ureteral obstruction (UUO) mice. METHODS: 8-week-old male C57BL/6 mice were divided into seven groups: sham, bosentan+sham, valsartan+sham, vehicle+UUO, bosentan+UUO, valsartan+UUO, and valsartan+bosentan+UUO. Valsartan and bosentan were administered orally using an NG tube (valsartan 10 mg/kg/day, bosentan 100 mg/kg/day for 8 days, after which the molecular and structural kidney parameters were evaluated. Bosentan treatment elevated plasma renin activity, renal renin, and AT1R expression in UUO mice. RESULTS: Although valsartan decreased plasma ET-1 in these mice, it did not affect ET(A) or ET(B) in their kidneys. Co-treatment with valsartan and bosentan decreased ET-1 in these mice compared to the single treatments. Bosentan, but not valsartan, elevated eNOS expression in their kidneys. Co-treatment with valsartan and bosentan reduced TGF-ß, α-SMA, and collagen IV expression, and the Masson's trichrome stained area in their kidneys. CONCLUSIONS: Bosentan and valsartan acted complementarily, and co-treatment with both drugs had an additive protective effect against renal fibrosis.
Asunto(s)
Endotelina-1/antagonistas & inhibidores , Cirrosis Hepática/tratamiento farmacológico , Receptores de Angiotensina/efectos de los fármacos , Sulfonamidas/farmacología , Obstrucción Ureteral/tratamiento farmacológico , Valsartán/farmacología , Lesión Renal Aguda/tratamiento farmacológico , Lesión Renal Aguda/prevención & control , Animales , Antihipertensivos/farmacología , Antihipertensivos/uso terapéutico , Bosentán , Sinergismo Farmacológico , Cirrosis Hepática/prevención & control , Masculino , Ratones , Ratones Endogámicos C57BL , Sulfonamidas/uso terapéutico , Valsartán/uso terapéuticoRESUMEN
UNLABELLED: Backgound: This study evaluated whether the hydration status affected health-related quality of life (HRQOL) during 12 months in peritoneal dialysis (PD) patients. METHODS: The hydration status and the HRQOL were examined at baseline and after 12 months using a bioimpedance spectroscopy and Kidney Disease Quality of Life-Short Form, respectively in PD patients. Four hundred eighty-one patients were included and divided according to the baseline overhydration (OH) value; normohydration group (NH group, -2L≤ OH ≤+2L, n=266) and overhydration group (OH group, OH >+2L, n=215). Baseline HRQOL scores were compared between the two groups. The subjects were re-stratified into quartiles according to the OH difference (OH value at baseline - OH value at 12 months; <-1, -1 - -0.1, -0.1 - +1, and ≥+1L). The relations of OH difference with HRQOL scores at 12 months and the association of OH difference with the HRQOL score difference (HRQOL score at baseline - HRQOL score at 12 months) were assessed. RESULTS: The OH group showed significantly lower baseline physical and mental health scores (PCS and MCS), and kidney disease component scores (KDCS) compared with the NH group (all, P<0.01). At 12 months, the adjusted PCS, MCS, and KDCS significantly increased as the OH difference quartiles increased (P<0.001, P=0.002, P<0.001, respectively). In multivariate analysis, the OH difference was independently associated with higher PCS (ß = 2.04, P< .001), MCS (ß=1.02, P=0.002), and KDCS (ß=1.06, P<0.001) at 12 months. The OH difference was independently associated with the PCS difference (ß = -1.81, P<0.001), MCS difference (ß=-0.92, P=0.01), and KDCS difference (ß=-0.90, P=0.001). CONCLUSION: The hydration status was associated with HRQOL and increased hydration status negatively affected HRQOL after 12 months in PD patients.
Asunto(s)
Deshidratación/fisiopatología , Insuficiencia Cardíaca/fisiopatología , Enfermedades Renales/terapia , Diálisis Peritoneal/efectos adversos , Adulto , Anciano , Deshidratación/complicaciones , Espectroscopía Dieléctrica , Femenino , Insuficiencia Cardíaca/etiología , Humanos , Enfermedades Renales/complicaciones , Enfermedades Renales/fisiopatología , Masculino , Persona de Mediana Edad , Calidad de Vida , Rigidez Vascular/fisiologíaRESUMEN
In this study, we characterized cerebral blood flow changes by assessment of blood flow parameters in neck arteries using carotid duplex ultrasonography and predictive factors for these hemodynamic changes. Hemodynamic variables were measured before and during hemodialysis in 81 patients with an arteriovenous access in their arm. Hemodialysis produced significant lowering in peak systolic velocity and flow volume of neck arteries and calculated total cerebral blood flow (1,221.9 ± 344.9 [before hemodialysis] vs. 1,085.8 ± 319.2 [during hemodialysis], P < 0.001). Effects were greater in vessels on the same side as the arteriovenous access and these changes were influenced by arteriovenous access flow during hemodialysis, both in the CCA (r = -0.277, P = 0.015) and the VA (r = -0.239, P = 0.034). The change of total cerebral blood flow during hemodialysis was independently related with age, presence of diabetes, and systemic blood pressure.
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Circulación Cerebrovascular/fisiología , Hemodinámica/fisiología , Fallo Renal Crónico/fisiopatología , Anciano , Arterias Carótidas/diagnóstico por imagen , Mareo/etiología , Femenino , Humanos , Masculino , Persona de Mediana Edad , Diálisis Renal , Factores de Riesgo , Ultrasonografía Doppler DúplexRESUMEN
In hemodialysis patients, vascular access infection remains a significant cause of morbidity and mortality. It has various complications, including bacterial endocarditis, spinal epidural abscess, osteomyelitis, septic arthritis, and septic pulmonary emboli. However, aortitis with infected pseudoaneurysm formation is very rare. Here, we report a case of necrotizing aortitis in a hemodialysis patient with an arteriovenous graft infection.
Asunto(s)
Aneurisma Falso/patología , Aortitis/patología , Derivación Arteriovenosa Quirúrgica/efectos adversos , Fallo Renal Crónico/terapia , Diálisis Renal/efectos adversos , Aneurisma Falso/microbiología , Aorta Torácica/lesiones , Aorta Torácica/patología , Aortitis/microbiología , Resultado Fatal , Humanos , Fallo Renal Crónico/microbiología , Fallo Renal Crónico/patología , Masculino , Persona de Mediana Edad , Diálisis Renal/métodos , Rotura EspontáneaRESUMEN
Cognitive dysfunction is more frequent in end-stage renal disease (ESRD) patients undergoing hemodialysis compared with the healthy population, emphasizing the need for early detection. Interest in serum markers that reflect cognitive function has recently increased. Elevated serum growth differentiation factor 15 (GDF-15) levels are known to be associated with an increased risk of decreased renal function and cognitive dysfunction. This study investigated the relationship between GDF-15 and cognitive dysfunction in hemodialysis patients using a retrospective analysis of 92 individuals aged ≥ 18 years. Cognitive function was assessed using the Korean version of the Mini-Mental Status Examination (K-MMSE), categorizing patients into normal (≥24 points) and cognitive dysfunction (<24 points). As a result, serum GDF-15 concentrations were at significantly higher levels in the cognitive dysfunction group (7500.42 pg/mL, p = 0.001). Logistic regression indicated an increased risk of K-MMSE scores < 24 points when serum GDF-15 exceeded 5408.33 pg/mL. After indoxyl sulfate exposure in HT22 cells, HT22 cells survival was decreased and GDF-15 expression in HT22 cells was increased. Similarly, exposure to indoxyl sulfate in mouse brain tissue resulted in an increased expression of GDF-15. This study highlights the potential of serum GDF-15 as a marker for cognitive dysfunction in hemodialysis patients, offering a valuable screening tool. Serum GDF-15 is related to cognitive dysfunction in hemodialysis patients and may be helpful in screening for cognitive dysfunction in hemodialysis patients.
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Background: The global prevalence of chronic kidney disease (CKD) is increasing, with diabetes accounting for the highest proportion. We analyzed the influence of clinical factors on the incidence of CKD according to the renal function, primary focusing on patients with diabetes. Methods: We used the Sample Cohorts Database provided by the National Health Insurance Sharing Service (NHISS) in Korea. Participants aged ≥ 40 years who underwent a health checkup in 2009 were categorized into six groups based on their eGFR values (<60 mL/min, 60-89 mL/min, ≥90 mL/min) and the presence of diabetes. And all patients with CKD at 2009 screening were excluded. The participants were tracked from 2010 to 31 December 2019. The CKD incidence rate according to the eGFR values and the effect of the accompanying factors on CKD incidence were confirmed. Results: 148,089 people without CKD were analyzed. The CKD incidence rate was highest in those with eGFR < 60 mL/min with diabetes and lowest in those with eGFR ≥ 90 mL/min without diabetes. The CKD incidence rates were similar between the eGFR < 60 mL/min group without diabetes and the eGFR 60-89 mL/min group with diabetes. Compared to under 44 years of age, the hazard ratio of CKD incidence was 8 times higher in over 75 years of age. Men had a 1.7-fold higher risk of developing CKD than women. Current smoker, hypertension, dyslipidemia, myocardial infarction history, and atrial fibrillation and flutter increased the risk of CKD incidence. Age, diabetes, and baseline eGFR are important factors in the occurrence of CKD. As age increases, the risk of developing CKD in men increases compared to women. Conclusions: These results will be helpful in predicting risk groups for CKD and establishing strategies to lowering CKD incidence.
RESUMEN
Background: Malnutrition is common in patients undergoing hemodialysis and is a powerful predictor of morbidity and mortality. This study aimed to investigate the effect of nutritional status on permanent catheter patency in elderly patients aged >75 years of age undergoing dialysis using tunneled dialysis catheters; Methods: Records of 383 patients whose nutritional factors and body cell mass (BCM) were measured simultaneously at the start of dialysis between 14 January 2020 and 30 September 2023, at Chungnam National University Hospital, were retrospectively reviewed. The relationships between permanent catheter patency at 180 days and BCM parameters and clinical parameters were studied using Kaplan-Meier survival curves and multivariate Cox proportional hazards analysis. Results: Age and sexual differences were significant (p ≤ 0.05), and most of the BCM parameters and BCM were not significant (p ≤ 0.05), except for intracellular water. Permanent catheter patency was superior at low controlling nutritional status (CONUT) scores (p < 0.05). After adjustment for covariates, the CONUT score remained an independent factor associated with permanent catheter-patency survival; Conclusions: CONUT scores measured before the start of dialysis are expected to play an important role in predicting the prognosis of permanent catheter-patency survival in patients aged >75 years.
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Handgrip strength (HGS) is suggested as an indirect assessment of nutritional status in chronic kidney disease (CKD) patients, but evidence is limited for non-dialysis-dependent CKD (NDD-CKD) patients. This cross-sectional study included 404 patients from the Phase II KoreaN Cohort Study for Outcome in Patients With CKD. HGS, measured twice in each hand, was the exposure, and malnutrition status was defined by a malnutrition-inflammation score (MIS) of 6 or higher. A logistic regression analysis adjusted for age, sex, diabetes mellitus (DM), hypertension, CKD stages, smoking, overhydration, education, and income status was used to assess malnutrition risk. The predictability of HGS for malnutrition was evaluated using the area under the curve (AUC). Patients with lower HGS were older, had a higher prevalence of DM, and lower estimated glomerular filtration rate. Higher HGS was significantly associated with lower malnutrition risk after adjustment (per 1 standard deviation increase, adjusted odds ratio, 0.47 [0.30-0.75]). Subgroup analyses showed no significant interaction between HGS and malnutrition risk across age, sex, DM, and CKD stage. HGS showed fair predictability for malnutrition in men (AUC 0.64 [0.46-0.83]) and women (AUC 0.71 [0.55-0.86]). In conclusion, HGS is a useful diagnostic indicator of malnutrition in NDD-CKD patients.
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Fuerza de la Mano , Desnutrición , Estado Nutricional , Insuficiencia Renal Crónica , Humanos , Masculino , Femenino , Insuficiencia Renal Crónica/fisiopatología , Insuficiencia Renal Crónica/epidemiología , Persona de Mediana Edad , Estudios Transversales , Anciano , Desnutrición/epidemiología , Desnutrición/diagnóstico , Evaluación Nutricional , Factores de Riesgo , República de Corea/epidemiología , Tasa de Filtración GlomerularRESUMEN
BACKGROUND: The target blood pressure (BP) value is unclear for diabetic kidney disease (DKD). Therefore, we aimed to evaluate the effect of strict BP control or 'on treatment' BP on clinical outcomes in patients with DKD. METHODS: A post-hoc analysis of the prespecified secondary outcomes of the FimAsartaN proTeinuriA SusTaIned reduCtion in comparison with losartan in diabetic chronic kidney disease (FANTASTIC) trial, a randomized multicenter double-blind phase III trial. Eligible patients were aged ≥ 19 years with DKD. We assigned 341 participants with DKD to BP control strategy (standard-systolic BP [SBP] < 140 mmHg versus strict-SBP < 130 mmHg). The outcome was the occurrence of cardiovascular events and renal events. Separate analyses were performed to compared the risk of outcome according to achieved average BP levels. RESULTS: A total of 341 participants were included in the analysis. Over a median follow-up of 2.8 years, cardiovascular/renal events were observed in 25 (7.3%) participants. Mean (SD) SBPs in the standard and strict BP control group were 140.2 (11.6) and 140.2 (11.9) mmHg, respectively. The strict BP control group did not show significantly reduced risk of cardiovascular/renal events (HR 1.32; 95% CI 0.60-2.92]). In the post-hoc analyses using achieved BP, achieved average SBP of 130-139 mmHg resulted in reduced risk of cardiovascular/renal events (HR 0.15; 95% CI 0.03-0.67) compared to achieved average SBP ≥ 140 mmHg, whereas further reduction in achieved average SBP < 130 mmHg did not impart additional benefits. CONCLUSION: In patients with DKD, targeting a SBP of less than 130 mmHg, as compared with less than 140 mmHg, did not reduce the rate of a composite of cardiovascular and renal events. Achieved SBP of 130-139 mmHg was associated with a decreased risk for the primary outcome in patients with DKD. TRIAL REGISTRATION: ClinicalTirals.gov Identifier: NCT02620306, registered December 3, 2015. ( https://clinicaltrials.gov/study/NCT02620306 ).
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BACKGROUND: The presence of tubuloreticular inclusions (TRIs) in endothelial cells (ECs) always evokes suspicion of an association with underlying viral infections or autoimmune diseases. However, other underlying diseases can be associated with TRI expression. Since identification of the underlying disease is of primary consideration for management of glomerulonephritis (GN), it is important to clarify the clinical significance of TRI expression. METHODS: The authors studied 104 renal biopsy cases having TRI. They investigated their clinicopathological profiles and focused on potential connections with underlying diseases. RESULTS: Among 104 renal biopsy cases, 62 cases (59.6%) were associated with lupus nephritis (LN) and 20 cases (19.2%) were associated with a viral infection (hepatitis B virus (13), hepatitis C virus (4), and human immunodeficiency virus (3)). Other underlying disease groups included membranous GN (MGN) (7), IgA nephropathy (7), Henoch-Schoenlein purpura (HSP) nephritis (2), and others (6). The incidence of TRIs in both LN and viral infections was significantly higher than for other diseases (p < 0.0001). Among 7 MGN cases, 2 cases were diabetes, 1 case was associated with lung cancer, another case with antineutrophilic cytoplasmic antibody (ANCA), and the others showed no evidence of systemic disease. On immunofluorescence (IF) study, 2 MGN cases, 2 IgA nephropathy cases, and 1 HSP nephritis case showed C1q deposition, with no evidence of SLE. CONCLUSIONS: TRIs were identified in MGN and other glomerular diseases, including IgA nephropathy and HSP nephritis. However, a diagnosis of LN should be considered because TRIs associated with a full-house IF pattern are usually found in LN.
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Células Endoteliales/ultraestructura , Glomerulonefritis/patología , Cuerpos de Inclusión/ultraestructura , Glomérulos Renales/ultraestructura , Nefritis Lúpica/patología , Virosis/patología , Adolescente , Adulto , Anciano , Biopsia , Células Endoteliales/inmunología , Células Endoteliales/virología , Femenino , Glomerulonefritis/epidemiología , Glomerulonefritis/inmunología , Glomerulonefritis/virología , Humanos , Incidencia , Cuerpos de Inclusión/inmunología , Cuerpos de Inclusión/virología , Glomérulos Renales/inmunología , Glomérulos Renales/virología , Nefritis Lúpica/epidemiología , Nefritis Lúpica/inmunología , Masculino , Persona de Mediana Edad , República de Corea/epidemiología , Estudios Retrospectivos , Virosis/epidemiología , Virosis/inmunología , Virosis/virología , Adulto JovenRESUMEN
Renal disease associated with type 2 diabetes mellitus (T2DM) has become the leading cause of chronic kidney disease (CKD). Renal ultrasonography is an imaging examination required in the work-up of renal disease. This study aimed to identify the differences in renal ultrasonographic findings between patients with and without DM, and to evaluate the relationship between renal ultrasound findings and renal prognosis in patients with DM. A total of 252 patients who underwent renal ultrasonography at Chungnam National University Hospital were included. Kidney disease progression was defined as a ≥10% decline in the annual estimated glomerular filtration rate (eGFR), which, in this paper, is referred to as ΔeGFR/year, or the initiation of renal replacement therapy after follow-up. The renal scoring system was evaluated by summing up the following items: the value of renal parenchymal echogenicity (0: normal; 1: mildly increased; and 2: increased) and the shape of the cortical margin (0: normal and 1: irregular; right kidney length/height (RH-0 or 1), mean cortical thickness/renal length/height (CKH-0 or 1), and cortical thickness/parenchymal thickness (CK/PK-0 or 1) based on the median: 0-above median, and 1-below median). Patients with DM had thicker renal PKH than those without, despite having lower eGFRs (0.91 ± 0.15, 0.86 ± 0.14, p = 0.006). In the progression group, the renal scores were significantly higher than those from the non-progression group. In the multivariate logistic regression analysis, the higher renal scores, presence of DM, and younger age were independently predicted for renal disease progression after adjusting for confounding variables, such as the presence of hypertension, serum hemoglobin and albumin levels, and UPCR. In conclusion, patients with high renal scores were significantly associated with renal disease progression. Our results suggest that renal ultrasonography at the time of diagnosis provides useful prognostic information in patients with kidney disease.
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For reducing the high mortality rate of severe acute kidney injury (AKI) patients initiating continuous renal replacement therapy (CRRT), diagnosing sepsis and predicting prognosis are essential. However, with reduced renal function, biomarkers for diagnosing sepsis and predicting prognosis are unclear. This study aimed to assess whether C-reactive protein (CRP), procalcitonin, and presepsin could be used to diagnose sepsis and predict mortality in patients with impaired renal function initiating CRRT. This was a single-center, retrospective study involving 127 patients who initiated CRRT. Patients were divided into sepsis and non-sepsis groups according to the SEPSIS-3 criteria. Of the 127 patients, 90 were in the sepsis group and 37 were in the non-sepsis group. Cox regression analysis was performed to determine the association between the biomarkers (CRP, procalcitonin, and presepsin) and survival. CRP and procalcitonin were superior to presepsin for diagnosing sepsis. Presepsin was closely related to the estimated glomerular filtration rate (eGFR) (r = -0.251, p = 0.004). These biomarkers were also evaluated as prognostic markers. Procalcitonin levels ≥3 ng/mL and CRP levels ≥31 mg/L were associated with higher all-cause mortality using Kaplan-Meier curve analysis. (log-rank test p = 0.017 and p = 0.014, respectively). In addition, procalcitonin levels ≥3 ng/mL and CRP levels ≥31 mg/L were associated with higher mortality in univariate Cox proportional hazards model analysis. In conclusion, a higher lactic acid, sequential organ failure assessment score, eGFR, and a lower albumin level have prognostic value to predict mortality in patients with sepsis initiating CRRT. Moreover, among these biomarkers, procalcitonin and CRP are significant factors for predicting the survival of AKI patients with sepsis-initiating CRRT.