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Studies have highlighted the significant involvement of kidney pericytes in renal fibrosis. Kidney pericytes, classified as interstitial mesenchymal cells, are extensively branched, collagen-producing cells that closely interact with endothelial cells. This article aims to provide an overview of the recent advancements in understanding the physiological functions of pericytes and their roles in kidney diseases. In a healthy kidney, pericytes have essential physiological function in angiogenesis, erythropoietin (EPO) production, and the regulation of renal blood flow. Nevertheless, pericyte-myofibroblast transition has been identified as the primary cause of disease progression in acute kidney injury (AKI)-to-chronic kidney disease (CKD) continuum. Our recent research has demonstrated that hypoxia-inducible factor-2α (HIF-2α) regulates erythropoietin production in pericytes. However, this production is repressed by EPO gene hypermethylation and HIF-2α downregulation which were induced by transforming growth factor-ß1-activated DNA methyltransferase and activin receptor-like kinase-5 signaling pathway during renal fibrosis, respectively. Additionally, AKI induces epigenetic modifications in pericytes, rendering them more prone to extracellular matrix production, cell migration and proliferation, thereby contributing to subsequent capillary rarefaction and renal fibrosis. Further investigation into the specific functions and roles of different subpopulations of pericytes may contribute for the development of targeted therapies aimed at attenuating kidney disease and mitigating their adverse effects.
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Lesión Renal Aguda , Eritropoyetina , Enfermedades Renales , Insuficiencia Renal Crónica , Humanos , Pericitos/metabolismo , Células Endoteliales/metabolismo , Riñón/patología , Eritropoyetina/genética , Lesión Renal Aguda/patología , Fibrosis , Factores de Transcripción con Motivo Hélice-Asa-Hélice Básico/metabolismoRESUMEN
INTRODUCTION: Cardiovascular (CV) events are the major cause of morbidity and mortality associated with blood pressure (BP) in hemodialysis (HD) patients. BP varies significantly during HD treatment, and the dramatic variation in BP is a well-recognized risk factor for increased mortality. The development of an intelligent system capable of predicting BP profiles for real-time monitoring is important. Our aim was to build a web-based system to predict changes in systolic BP (SBP) during HD. METHODS: In this study, dialysis equipment connected to the Vital Info Portal gateway collected HD parameters that were linked to demographic data stored in the hospital information system. There were 3 types of patients: training, test, and new. A multiple linear regression model was built using the training group with SBP change as the dependent variable and dialysis parameters as the independent variables. We tested the model's performance on test and new patient groups using coverage rates with different thresholds. The model's performance was visualized using a web-based interactive system. RESULTS: A total of 542,424 BP records were used for model building. The accuracy was greater than 80% in the prediction error range of 15%, and 20 mm Hg of true SBP in the test and new patient groups for the model of SBP changes suggested the good performance of our prediction model. In the analysis of absolute SBP values (5, 10, 15, 20, and 25 mm Hg), the accuracy of the SBP prediction increased as the threshold value increased. DISCUSSION: This databae supported our prediction model in reducing the frequency of intradialytic SBP variability, which may help in clinical decision-making when a new patient receives HD treatment. Further investigations are needed to determine whether the introduction of the intelligent SBP prediction system decreases the incidence of CV events in HD patients.
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Macrodatos , Diálisis Renal , Humanos , Presión Sanguínea , Diálisis Renal/efectos adversos , Factores de Riesgo , Análisis MultivarianteRESUMEN
BACKGROUND: Renal erythropoietin (EPO)-producing (REP) cells produce EPO through hypoxia-inducible factor (HIF) 2α-activated gene transcription. Insufficient EPO production leads to anemia in patients with chronic kidney disease. Although recombinant EPO is effective to improve anemia, no reliable REP cell lines limit further progress of research and development of novel treatment. METHODS: We screened Epo mRNA expression in mouse fibroblast cell lines. Small interfering RNA specific for HIF1α or HIF2α was transfected to study Epo expression in C3H10T1/2 cells. The effect of transforming growth factor-ß1 (TGF-ß1) on HIF-EPO axis was studied in C3H10T1/2 cells and mice. RESULTS: Similar to mouse REP pericytes, C3H10T1/2 cells differentiated to α-smooth muscle actin+ myofibroblasts after exposure to TGF-ß1. Specific HIF knockdown demonstrated the role of HIF2α in hypoxia-induced Epo expression. Sustained TGF-ß1 exposure increased neither DNA methyltransferase nor methylation of Epas1 and Epo genes. However, TGF-ß1 repressed HIF2α-encoding Epas1 promptly through activating activin receptor-like kinase-5 (ALK5), thereby decreasing Epo induction by hypoxia and prolyl hydroxylase domain inhibitor roxadustat. In mice with pro-fibrotic injury induced by ureteral obstruction, upregulation of Tgfb1 was accompanied with downregulation of Epas1 and Epo in injured kidneys and myofibroblasts, which were reversed by ALK5 inhibitor SB431542. CONCLUSION: C3H10T1/2 cells possessed the property of HIF2α-dependent Epo expression in REP pericytes. TGF-ß1 induced not only the transition to myofibroblasts but also a repressive effect on Epas1-Epo axis in C3H10T1/2 cells. The repressive effect of TGF-ß1 on Epas1-Epo axis was confirmed in REP pericytes in vivo. Inhibition of TGF-ß1-ALK5 signaling might provide a novel treatment to rescue EPO expression in REP pericytes of injured kidney.
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Factores de Transcripción con Motivo Hélice-Asa-Hélice Básico/genética , Eritropoyetina/genética , Factor de Crecimiento Transformador beta1/genética , Células 3T3 , Animales , Factores de Transcripción con Motivo Hélice-Asa-Hélice Básico/metabolismo , Eritropoyetina/metabolismo , Fibroblastos/metabolismo , Ratones , Ratones Endogámicos C57BL , Factor de Crecimiento Transformador beta1/metabolismoRESUMEN
BACKGROUND/PURPOSE: Substantial progress was made in acute kidney injury (AKI) over the past 10 years, but no therapeutic interventions have been shown to prevent AKI or accelerate functional recovery after injury. A large number of preclinical studies supports the use of recombinant human erythropoietin (rHuEPO) to prevent AKI, but the clinical trial data are inconclusive. To address concerns about preclinical study design and reporting in AKI, we here presented our rigorous experiments on the use of rHuEPO in a mouse model simulating the most common post-ischemic AKI in patients. METHODS: Use of saline vehicle or rHuEPO (100 or 1000 U/KgBW) in mice subjected to AKI induced by ischemia-reperfusion injury of left kidney 2 weeks after right nephrectomy (NX + IRI). RESULTS: NX + IRI resulted in a reproducible AKI model. Use of rHuEPO as a pretreatment or posttreatment did not affect AKI severity, functional recovery, and mouse survival regardless of gender, injury severity, or doses of rHuEPO. Administering rHuEPO with 1000 U/KgBW did increase hematocrit and modulate AKI kidney macrophages by Nos2 downregulation and Ccl17 upregulation. Active expression of erythropoietin receptor (EPOR) was not identified in renal cells by lineage tracing study, whereas expression of colony-stimulating factor 2 receptor ß (CSF2Rß) was identified in kidney macrophages and upregulated after AKI. Both EPOR and CSF2Rß were identified in cultured bone marrow derived macrophages, possibly mediated the robust inhibition of cytokine-induced phenotype switching by rHuEPO. CONCLUSION: Use of rHuEPO can modulate macrophage function but not the post-ischemic AKI severity, functional recovery and survival in mice.
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Lesión Renal Aguda/tratamiento farmacológico , Eritropoyetina/farmacología , Macrófagos/efectos de los fármacos , Daño por Reperfusión/fisiopatología , Transducción de Señal/efectos de los fármacos , Lesión Renal Aguda/etiología , Animales , Apoptosis/efectos de los fármacos , Modelos Animales de Enfermedad , Femenino , Riñón/efectos de los fármacos , Riñón/cirugía , Macrófagos/patología , Masculino , Ratones , Ratones Endogámicos C57BL , Ratones Transgénicos , Nefrectomía , Proteínas Recombinantes/farmacologíaRESUMEN
BACKGROUND/AIMS: Fabry disease (FD), a rare x-lined genetic disorder is a cause of renal deterioration. The phenotype of FD is highly variable and nonspecific, and correct diagnosis has always been delayed. We aimed to explore the prevalence and clinical presentation of FD in this high-risk male population in a Northern Taiwan medical center. METHODS: This is the first study to survey the incidence of FD in this high-risk population through the platform of a chronic kidney disease (CKD) education program in Asia. A total of 1,012 male patients with unknown CKD causes were screened using an assay of alpha-galactosidase A activity (α-Gal A) by dried blood spots (DBS). A final GLA gene analysis was also done for those with low enzyme activity. RESULTS: We identified two new patients with classic FD and four patients with late-onset FD. One novel GLA mutation with c.413 G>A was found in one classic FD patient (index 5). The prevalence of FD is about 0.59 % (6 in 1,012) in the high-risk population group with CKD. The clinical symptoms of FD patients are nonspecific except in those with various degrees of renal failure. Those patients' correct diagnosis was delayed, taking years and even decades. Three patients received enzyme replacement therapy and one started regular hemodialysis due to persistent renal function deterioration. Another two patients were found from family screening through a new index. In addition, a false negative result occurred in one patient who was proved to have FD by his kidney pathology as determined by this screening. CONCLUSION: FD is not such as rare a disease and its prevalence is greater in this high-risk male population. Clinicians need to be aware that FD should be included in the differential diagnosis in CKD with unknown etiology.
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Enfermedad de Fabry/diagnóstico , Fallo Renal Crónico/etiología , Adulto , Anciano , Anciano de 80 o más Años , Diagnóstico Diferencial , Enfermedad de Fabry/epidemiología , Humanos , Isoenzimas/sangre , Isoenzimas/genética , Masculino , Tamizaje Masivo , Persona de Mediana Edad , Prevalencia , Proteínas Recombinantes/sangre , Proteínas Recombinantes/genética , Insuficiencia Renal Crónica , Taiwán , Adulto Joven , alfa-Galactosidasa/sangre , alfa-Galactosidasa/genéticaRESUMEN
Anemia is a common complication and contributes to increased morbidity and mortality in chronic kidney disease (CKD) patients. Whereas there has been a significant improvement of understanding the underlying mechanism of erythropoiesis, the treatment of renal anemia is still restricted to erythropoietin (EPO)-stimulating agents. The purpose of this article is to review the physiology of erythropoiesis, functional role of EPO and underlying molecular and cellular basis that regulate EPO production. Regulation of EPO production is at mRNA level. When anemia or hypoxia occurs, transcriptional factor, hypoxia-inducible factor (HIF), binds to EPO 5' hypoxic response element and EPO gene transcription increases. The renal EPO is mainly produced by pericytes. In CKD, pericytes transdifferentiate to myofibroblasts, and subsequently the ability of EPO production decreases, leading to renal anemia. Recent experimental and clinical studies show the promising efficacy of prolyl hydroxylase inhibitors in renal anemia through increasing EPO production by stabilizing HIF. Recent advances on epigenetics create a new field to study EPO gene expression at chromatin level. We will discuss the role of demethylating agent on restoring EPO expression, providing a novel approach to the treatment of renal anemia.
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Anemia/genética , Eritropoyesis , Eritropoyetina/fisiología , Miofibroblastos/metabolismo , Insuficiencia Renal Crónica/complicaciones , Anemia/tratamiento farmacológico , Anemia/etiología , Animales , Eritropoyetina/genética , Regulación de la Expresión Génica , Humanos , Factor 1 Inducible por Hipoxia/metabolismo , Pericitos/metabolismoRESUMEN
BACKGROUND: Intradialytic hypotension (IDH) is a serious complication and a major risk factor of increased mortality during hemodialysis (HD). However, predicting the occurrence of intradialytic blood pressure (BP) fluctuations clinically is difficult. This study aimed to develop an intelligent system with capability of predicting IDH. METHODS: In developing and training the prediction models in the intelligent system, we used a database of 653 HD outpatients who underwent 55,516 HD treatment sessions, resulting in 285,705 valid BP records. We built models to predict IDH at the next BP check by applying time-dependent logistic regression analyses. RESULTS: Our results showed the sensitivity of 86% and specificity of 81% for both nadir systolic BP (SBP) of <90 mmHg and <100 mmHg, suggesting good performance of our prediction models. We obtained similar results in validating via test data and data of newly enrolled patients (new-patient data), which is important for simulating prospective situations wherein dialysis staff are unfamiliar with new patients. This compensates for the retrospective nature of the BP records used in our study. CONCLUSION: The use of this validated intelligent system can identify patients who are at risk of IDH in advance, which may facilitate well-timed personalized management and intervention.
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Monitores de Presión Sanguínea , Hipotensión/diagnóstico , Diálisis Renal/efectos adversos , Anciano , Presión Sanguínea , Bases de Datos Factuales , Femenino , Humanos , Hipotensión/etiología , Hipotensión/fisiopatología , Modelos Logísticos , Masculino , Persona de Mediana Edad , Pronóstico , Curva ROC , Estudios Retrospectivos , Factores de Riesgo , TaiwánRESUMEN
Studies have demonstrated that a low-protein diet supplemented with ketoanalogs (KAs) could significantly retard progression of renal function in patients with chronic kidney disease (CKD) stages 3-5. However, its effects on endothelial function and serum levels of protein-bound uremic toxins remain elusive. Therefore, this study explored whether a low-protein diet (LPD) supplemented with KAs affects kidney function, endothelial function, and serum uremic toxin levels in a CKD-based cohort. In this retrospective cohort, we enrolled 22 stable CKD stage 3b-4 patients on LPD (0.6-0.8 g/day). Patients were categorized into control (LPD only) and study groups (LPD + KAs 6 tab/day). Serum biochemistry, total/free indoxyl sulfate (TIS/FIS), total/free p-cresyl sulfate (TPCS/FPCS), and flow-mediated dilation (FMD) were measured before and after 6 months of KA supplementation. Before the trial, there were no significant differences in kidney function, FMD, or uremic toxin levels between the control and study groups. When compared with the control group, the paired t-test showed a significant decrease in TIS and FIS (all p < 0.05) and a significant increase in FMD, eGFR, and bicarbonate (all p < 0.05). In multivariate regression analysis, an increase in FMD (p < 0.001) and a decrease in FPCS (p = 0.012) and TIS (p < 0.001) remained persistent findings when adjusted for age, systolic blood pressure (SBP), sodium, albumin, and diastolic blood pressure (DBP). LPD supplemented with KAs significantly preserves kidney function and provides additional benefits on endothelial function and protein-bound uremic toxins in patients with CKD.
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Introduction: Chronic kidney disease (CKD) is a condition defined as a persistent change in kidney structure or function, or both, that compromises human health. Environmental exposure to heavy metals (e.g. cadmium, lead, arsenic and mercury) is common, and high exposure levels are known to cause nephrotoxicity. Micronutrients such as selenium and zinc are positively associated with better kidney function and renal outcomes. This study determined the associations between CKD and heavy metal exposures measured in blood or urine within a community-dwelling population, and assessed whether and how selenium and zinc modified the associations. Method: Data were extracted from 4 cycles of the US National Health and Nutrition Examination Survey (NHANES) database (2011-2012, 2013-2014, 2015-2016 and 2017-2018). Results: Univariate analysis showed that higher quartiles of plasma lead and cadmium concentration were more likely associated with CKD than the lowest quartile, and along with folate, were linked to greater odds of CKD. Conversely, as plasma selenium and serum zinc increased, the odds of CKD decreased. Multivariate analysis had similar results after adjusting for relevant confounders. Higher plasma cadmium quartiles were associated with higher odds of CKD. Associations between higher quartiles of plasma selenium and serum zinc were significantly associated with lower odds of CKD. Conclusion: Elevated blood levels of heavy metals increase CKD, whereas elevated concentrations of plasma selenium and serum zinc decrease CKD. A high serum zinc concentration appears to interact with low-toxicity heavy metals to reduce CKD risk. This study suggests that increased selenium and zinc in the body along with avoidance of heavy metal exposures could protect against CKD.
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Cadmio , Metales Pesados , Encuestas Nutricionales , Insuficiencia Renal Crónica , Selenio , Zinc , Humanos , Selenio/sangre , Insuficiencia Renal Crónica/epidemiología , Insuficiencia Renal Crónica/sangre , Insuficiencia Renal Crónica/inducido químicamente , Insuficiencia Renal Crónica/etiología , Zinc/sangre , Femenino , Masculino , Persona de Mediana Edad , Cadmio/sangre , Cadmio/efectos adversos , Metales Pesados/sangre , Metales Pesados/efectos adversos , Adulto , Plomo/sangre , Exposición a Riesgos Ambientales/efectos adversos , Estados Unidos/epidemiología , Anciano , Mercurio/sangreRESUMEN
Sodium-glucose cotransporter 2 (SGLT2) inhibitors have shown impressive effects in reducing major vascular events in several randomized controlled trials (RCTs). The purpose of this study was to perform a meta-analysis to evaluate the effect of SGLT2 inhibitors on the risk of stroke and its subtypes. All data from prospective RCTs up to 20 October 2020 involving SGLT2 inhibitors that reported stroke events as the primary endpoint or safety in subjects with type 2 diabetes were subjected to meta-analysis. Five eligible RCTs (EMPA-REG, CANVAS, DECLARE-TIMI 58, CREDENCE and VERTIS CV) involving 46,969 participants were included. Pooled analysis of the RCTs showed no significant effect of SGLT2 inhibitors on total stroke [risk ratio (RR) = 0.95; 95% confidence interval (CI) 0.79-1.13, P = 0.585]. Subgroup analysis indicated that SGLT2 inhibitors had no significant effect against fatal stroke, non-fatal stroke, ischemic stroke or transient ischemic attack. When only hemorrhagic stroke was included, SGLT2 inhibitors were associated with a significant 50% reduction compared with placebo (RR = 0.49, 95% CI 0.30-0.82, P = 0.007). This meta-analysis shows that SGLT2 inhibitors have a neutral effect on the risk of stroke and its subtypes but a potential protective effect against hemorrhagic stroke.
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Diabetes Mellitus Tipo 2/tratamiento farmacológico , Accidente Cerebrovascular Hemorrágico/tratamiento farmacológico , Inhibidores del Cotransportador de Sodio-Glucosa 2/uso terapéutico , Transportador 2 de Sodio-Glucosa/genética , Diabetes Mellitus Tipo 2/complicaciones , Diabetes Mellitus Tipo 2/genética , Diabetes Mellitus Tipo 2/patología , Accidente Cerebrovascular Hemorrágico/genética , Accidente Cerebrovascular Hemorrágico/patología , Accidente Cerebrovascular Hemorrágico/prevención & control , Humanos , Ensayos Clínicos Controlados Aleatorios como Asunto , Medición de Riesgo , Inhibidores del Cotransportador de Sodio-Glucosa 2/efectos adversosRESUMEN
Pulse wave velocity (PWV) is a non-invasive test for assessing arterial stiffness, and brachial-ankle PWV has been used as an index of peripheral arterial stiffness. This study aimed to investigate the association between the PWV value and severity of diabetic retinopathy (DR). 846 patients with type 2 diabetes (T2DM) consecutively underwent brachial-ankle PWV, and the degree of PWV was defined by tertile. The severity of DR was categorized as no diabetic retinopathy (NDR), non-proliferative diabetic retinopathy (NPDR) or proliferative diabetic retinopathy (PDR) based on the Early Treatment Diabetic Retinopathy Study Scale. Multinomial logistic regression analyses were utilized not only to explore the association between the degree of PWV and severity of DR but also to examine the association of a high-tertile PWV with PDR. PWV levels, diabetes duration and blood pressure were all significantly higher in subjects with NPDR or PDR as compared with individuals with NDR. In the univariate analysis, the highest tertile of PWV (>19.6 m/s) was significantly associated with both NPDR (p<0.001) and PDR (p<0.001) as compared with NDR. After adjusting for confounding factors, the highest tertile of PWV remained significantly associated with PDR (p=0.005), but not with NPDR (p=0.107). Furthermore, the highest tertile of PWV was more significantly associated with PDR (OR=6.15, 95%CI 1.38 to 27.38) as compared with the lowest tertile. In our study, an increasing degree of PWV was positively associated with the severity of DR. High PWV was strongly associated with the risk of severe DR, especially PDR.
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Arteria Braquial/fisiopatología , Diabetes Mellitus Tipo 2/complicaciones , Retinopatía Diabética/fisiopatología , Análisis de la Onda del Pulso , Rigidez Vascular/fisiología , Adulto , Anciano , Anciano de 80 o más Años , Presión Sanguínea , Estudios Transversales , Retinopatía Diabética/clasificación , Femenino , Humanos , Masculino , Persona de Mediana Edad , Gravedad del Paciente , Curva ROCRESUMEN
Elderly patients with type 2 diabetes (T2DM) are more prone to developing diabetic kidney disease (DKD). Patients with DKD can develop albuminuria, and some studies have suggested an association between metabolic syndrome and albuminuria. The prevalence of both metabolic syndrome and albuminuria increases with age. We evaluated the association of these risk factors with worsening renal function and albuminuria progression in 460 T2DM patients with a mean age of 72 years. During the 5-year follow-up period, progression of albuminuria and worsening of renal function were observed in 97 (21.2%) and 23 (5.1%) patients, respectively. After adjusting for confounding factors, the group with metabolic syndrome had a higher multivariable-adjusted hazard ratio (HR) for worsening renal function (P = 0.038) and albuminuria progression (P = 0.039) than the group without metabolic syndrome. When patients were divided into four groups according to the presence of metabolic syndrome and/or albuminuria, the HR gradually increased. The group with both albuminuria and metabolic syndrome exhibited the highest cumulative incidence of worsening renal function (P = 0.003). When we redefined metabolic syndrome to exclude the blood pressure (BP) component, similar results were obtained. We concluded that the presence of metabolic syndrome independently predicts the progression of renal disease in elderly patients with T2DM. The use of both metabolic syndrome and albuminuria provides a better risk stratification model for DKD progression than albuminuria alone.
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Albuminuria/epidemiología , Diabetes Mellitus Tipo 2/epidemiología , Nefropatías Diabéticas/epidemiología , Síndrome Metabólico/epidemiología , Anciano , Anciano de 80 o más Años , Comorbilidad , Diabetes Mellitus Tipo 2/sangre , Progresión de la Enfermedad , Femenino , Humanos , Incidencia , Estimación de Kaplan-Meier , Masculino , Persona de Mediana Edad , Prevalencia , Medición de Riesgo/métodos , Medición de Riesgo/estadística & datos numéricos , Factores de Riesgo , Taiwán/epidemiologíaRESUMEN
The origin and fate of renal myofibroblasts is not clear after acute kidney injury (AKI). Here, we demonstrate that myofibroblasts were activated from quiescent pericytes (qPericytes) and the cell numbers increased after ischemia/reperfusion injury-induced AKI (IRI-AKI). Myofibroblasts underwent apoptosis during renal recovery but one-fifth of them survived in the recovered kidneys on day 28 after IRI-AKI and their cell numbers increased again after day 56. Microarray data showed the distinctive gene expression patterns of qPericytes, activated pericytes (aPericytes, myofibroblasts), and inactivated pericytes (iPericytes) isolated from kidneys before, on day 7, and on day 28 after IRI-AKI. Hypermethylation of the Acta2 repressor Ybx2 during IRI-AKI resulted in epigenetic modification of iPericytes to promote the transition to chronic kidney disease (CKD) and aggravated fibrogenesis induced by a second AKI induced by adenine. Mechanistically, transforming growth factor-ß1 decreased the binding of YBX2 to the promoter of Acta2 and induced Ybx2 hypermethylation, thereby increasing α-smooth muscle actin expression in aPericytes. Demethylation by 5-azacytidine recovered the microvascular stabilizing function of aPericytes, reversed the profibrotic property of iPericytes, prevented AKI-CKD transition, and attenuated fibrogenesis induced by a second adenine-AKI. In conclusion, intervention to erase hypermethylation of pericytes after AKI provides a strategy to stop the transition to CKD.
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Lesión Renal Aguda/metabolismo , Metilación de ADN , Pericitos/metabolismo , Insuficiencia Renal Crónica/metabolismo , Daño por Reperfusión/metabolismo , Lesión Renal Aguda/complicaciones , Lesión Renal Aguda/genética , Lesión Renal Aguda/patología , Animales , Ratones , Ratones Transgénicos , Análisis de Secuencia por Matrices de Oligonucleótidos , Pericitos/patología , Insuficiencia Renal Crónica/etiología , Insuficiencia Renal Crónica/genética , Insuficiencia Renal Crónica/patología , Daño por Reperfusión/complicaciones , Daño por Reperfusión/genética , Daño por Reperfusión/patologíaRESUMEN
BACKGROUND: While metabolic syndrome can independently predict the development of diabetic kidney disease (DKD) in patients with type 2 diabetes, the risk factors for DKD progression have rarely been discussed. The purpose of this study is to evaluate the association between metabolic syndrome and the progression of DKD in patients with type 2 diabetes. MATERIAL AND METHODS: This retrospective observational cohort study lasted approximately five years. We defined metabolic syndrome using the criteria of the National Cholesterol Education Program Adult Treatment Panel III with the Asian definition of obesity. The progression of DKD was demonstrated by either the progression of albuminuria or worsening renal function. Progression of albuminuria was defined by the transition from normoalbuminuria (<30â¯mg/g) to microalbuminuria (30-300â¯mg/g) or from micro- to macroalbuminuria (>300â¯mg/g). Worsening renal function was defined by a reduction of eGFR to 50% of the baseline or the doubling of serum creatinine. We adopted multivariate Cox-regression analysis to determine the risk factors associated with DKD progression. RESULTS: This study consisted of 935 type 2 diabetic patients with a mean age of 64.62â¯years. We found progression of albuminuria in 172 patients (18.4%) and worsened renal function in 41 patients (4.4%). After Cox regression analysis, the multivariable-adjusted HR for the progression of albuminuria and worsened renal function was 1.65 (95% C.I.:1.07-2.53 Pâ¯=â¯0.022) and 2.62 (95% C.I.:1.01-6.79 Pâ¯=â¯0.047) respectively, for those with metabolic syndrome compared to those without metabolic syndrome. CONCLUSION: The presence of metabolic syndrome independently predicts DKD progression in patients with type 2 diabetes.
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Diabetes Mellitus Tipo 2/sangre , Nefropatías Diabéticas/etiología , Síndrome Metabólico/complicaciones , Adulto , Anciano , Anciano de 80 o más Años , Estudios de Cohortes , Nefropatías Diabéticas/patología , Femenino , Humanos , Masculino , Síndrome Metabólico/patología , Persona de Mediana Edad , Estudios Retrospectivos , Factores de Riesgo , Adulto JovenRESUMEN
Acute kidney injury is a common complication following cardiac surgery. Even small increases in creatinine levels are associated with increases in morbidity and mortality. Numerous factors such as hemolysis can contribute to the development of acute kidney injury after cardiac surgery. We present a rare case of severe hemolysis related to cardiopulmonary bypass resulting in kidney injury and requiring dialysis. The patient's renal function gradually recovered when hemolysis was improved. After follow-up for 3 months, his creatinine levels returned to normal. We discussed the pathogenesis of this hemolysis-related kidney dysfunction, the causes of hemolysis during cardiac surgery, and a new treatment option.