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1.
Clin Nephrol ; 93(3): 111-122, 2020 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-32017699

RESUMO

The global burden of chronic kidney disease (CKD) is rapidly increasing with a projection of becoming the 5th most common cause of years of life lost globally by 2040. Aggravatingly, CKD is a major cause of catastrophic health expenditure. The costs of dialysis and transplantation consume up to 3% of the annual healthcare budget in high-income countries. Crucially, however, the onset and progression of CKD is often preventable. In 2020, the World Kidney Day campaign highlights the importance of preventive interventions - be it primary, secondary or tertiary. This complementing article focuses on outlining and analyzing measures that can be implemented in every country to promote and advance CKD prevention. Primary prevention of kidney disease should focus on the modification of risk factors and addressing structural abnormalities of the kidney and urinary tracts, as well as exposure to environmental risk factors and nephrotoxins. In persons with pre-existing kidney disease, secondary prevention, including blood pressure optimization and glycemic control, should be the main goal of education and clinical interventions. In patients with advanced CKD, management of co-morbidities such as uremia and cardiovascular disease is a highly recommended preventative intervention to avoid or delay dialysis or kidney transplantation. Political efforts are needed to proliferate the preventive approach. While national policies and strategies for non-communicable diseases might be present in a country, specific policies directed toward education and awareness about CKD screening, management, and treatment are often lacking. Hence, there is an urgent need to increase the awareness of the importance of preventive measures throughout populations, professionals, and policy makers.

3.
J Ren Care ; 46(1): 4-12, 2020 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-32052938

RESUMO

The global burden of chronic kidney disease (CKD) is increasing with a projection of becoming the fifth leading cause of years of life lost globally by 2040. CKD is a major cause of catastrophic health expenditure. The costs of dialysis and transplantation consume up to 3% of the entire annual healthcare budget in high-income countries. Crucially, however, both the onset and progression of CKD is potentially preventable. In 2020, the World Kidney Day campaign highlights the importance of preventive interventions-be it primary, i.e. to prevent de novo CKD, or secondary or tertiary, i.e. prevention of worsening early CKD or progression of more advanced CKD to end-stage kidney disease, respectively. Primary prevention should focus on the modification of CKD risk factors and address the structural abnormalities of the kidney and urinary tracts, and exposure to environmental risk factors and nephrotoxins. In persons with pre-existing kidney disease, secondary prevention, including blood pressure optimization, glycemic control and avoiding high-protein high-sodium diet should be the main goal of education and clinical interventions. In patients with moderate to advanced CKD, the management of comorbidities such as uremia and cardiovascular disease along with low-protein diet are among the recommended preventative interventions to avoid or delay dialysis or kidney transplantation. Whereas national policies and strategies for noncommunicable diseases may exist in a country, specific policies directed toward education and awareness about CKD screening, prevention and treatment are often lacking. There is an urgent need to increase awareness for preventive measures throughout populations, professionals and policy makers.

6.
Artigo em Inglês | MEDLINE | ID: mdl-31927516

RESUMO

Background Urate in its crystal form is a known danger-associated molecular pattern, which after its internalization activates cells of the innate immune system. However, by inducing lipid raft sequestration and clustering of membrane-bound proteins with immunoreceptor tyrosine-based activation motifs, urate crystals can also activate cells of the innate immune system without previous internalization. Also, urate crystals trigger T-cell receptor signal transduction and induce T-cell proliferation. In this study, we evaluated whether urate crystals can also initiate B-cell receptor (BCR) signal transduction and promote B-cell proliferation. Methods B cells were isolated from the blood of 10 individuals and cultured with or without urate at a concentration of 10 mg/dL, at which crystallization occurs. Phosphorylated Igα (CD79A) and c-Myc were assessed by Western blotting and B-cell proliferation with BrdU assay. Results Urate increased the level of phosphorylated Igα, a component of the BCR complex. Phosphorylation of Igα is the very proximal event in BCR signal transduction. Also, urate increased the expression of c-Myc, an essential transcription factor for BCR-induced B-cell proliferation. Finally, urate induces B-cell proliferation. Conclusions Urate crystals trigger BCR signal transduction and induce B-cell proliferation. The clinical significance of urate-induced B-cell activation remains to be elucidated.

8.
Biomolecules ; 9(12)2019 Dec 05.
Artigo em Inglês | MEDLINE | ID: mdl-31817562

RESUMO

Along with infections, ultrafiltration failure due to the toxicity of glucose-containing peritoneal dialysis (PD) solutions is the Achilles' heel of PD method. Triggered by the protective effect of general control nonderepressible-2 (GCN-2) kinase activation against high-glucose conditions in other cell types, we evaluated whether the same occurs in human peritoneal mesothelial cells. We activated GCN-2 kinase with halofuginone or tryptophanol, and assessed the impact of this intervention on glucose transporter-1, glucose transporter-3, and sodium-glucose cotransporter-1, glucose influx, reactive oxygen species (ROS), and the events that result in glucotoxicity. These involve the inhibition of glyceraldehyde 3-phosphate dehydrogenase and the diversion of upstream glycolytic products to the aldose pathway (assessed by D-sorbitol), the lipid synthesis pathway (assessed by protein kinase C activity), the hexosamine pathway (determined by O-linked ß-N-acetyl glucosamine-modified proteins), and the advanced glycation end products generation pathway (assessed by methylglyoxal). Then, we examined the production of the profibrotic transforming growth factor-ß1 (TGF-ß1), the pro-inflammatory interleukin-8 (IL-8). Cell apoptosis was assessed by cleaved caspase-3, and mesothelial to mesenchymal transition (MMT) was evaluated by α-smooth muscle actin protein. High-glucose conditions increased glucose transporters, glucose influx, ROS, all the high-glucose-induced harmful pathways, TGF-ß1 and IL-8, cell apoptosis, and MMT. Halofuginone and tryptophanol inhibited all of the above high glucose-induced alterations, indicating that activation of GCN-2 kinase ameliorates glucotoxicity in human peritoneal mesothelial cells, preserves their integrity, and prevents MMT. Whether such a strategy could be applied in the clinic to avoid ultrafiltration failure in PD patients remains to be investigated.

9.
Int J Mol Sci ; 20(22)2019 Nov 16.
Artigo em Inglês | MEDLINE | ID: mdl-31744097

RESUMO

Encapsulating peritoneal sclerosis (EPS) is a life-threatening complication of long-term peritoneal dialysis (PD), which may even occur after patients have switched to hemodialysis (HD) or undergone kidney transplantation. The incidence of EPS varies across the globe and increases with PD vintage. Causative factors are the chronic exposure to bioincompatible PD solutions, which cause long-term modifications of the peritoneum, a high peritoneal transporter status involving high glucose concentrations, peritonitis episodes, and smoldering peritoneal inflammation. Additional potential causes are predisposing genetic factors and some medications. Clinical symptoms comprise signs of intestinal obstruction and a high peritoneal transporter status with incipient ultrafiltration failure. In radiological, macro-, and microscopic studies, a massively fibrotic and calcified peritoneum enclosed the intestine and parietal wall in such cases. Empirical treatments commonly used are corticosteroids and tamoxifen, which has fibrinolytic properties. Immunosuppressants like azathioprine, mycophenolate mofetil, or mTOR inhibitors may also help with reducing inflammation, fibrin deposition, and collagen synthesis and maturation. In animal studies, N-acetylcysteine, colchicine, rosiglitazone, thalidomide, and renin-angiotensin system (RAS) inhibitors yielded promising results. Surgical treatment has mainly been performed in severe cases of intestinal obstruction, with varying results. Mortality rates are still 25-55% in adults and about 14% in children. To reduce the incidence of EPS and improve the outcome of this devastating complication of chronic PD, vigorous consideration of the risk factors, early diagnosis, and timely discontinuation of PD and therapeutic interventions are mandatory, even though these are merely based on empirical evidence.

10.
J Hypertens ; 37(11): 2200-2208, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31584899

RESUMO

OBJECTIVES: Hemodialysis patients have premature arterial stiffness, and the relationship between pulse wave velocity (PWV) and blood pressure (BP) may be different than in other hypertensives. Previous studies in such patients showed that when BP decrease is accompanied by PWV decrease the survival is improved. This study examines the prognostic role of the mean BP (MBP)-PWV association for cardiovascular outcomes and all-cause mortality in hemodialysis. METHODS: A total of 242 hemodialysis patients underwent 48-h ambulatory BP monitoring with Mobil-O-Graph-NG and were followed for 33.17 ±â€Š19.68 months. The within-individual MBP-PWV association (MBP, dependent and PWV independent variable) was evaluated using the ß-coefficient value from simple linear regression analysis for each patient. The primary end-point was first occurrence of all-cause death, nonfatal myocardial infarction or nonfatal stroke. Secondary end-points were all-cause mortality, cardiovascular mortality and a combination of cardiovascular events. RESULTS: Higher quartiles of ß-coefficients (indicating strong within-individual association of MBP with PWV) were related to greater cumulative freedom from the primary end-point (50.8, 60.0, 70.0 and 80.3% for quartiles 1-4, respectively; log-rank P = 0.001), better overall survival (60.7, 61.7, 73.3, 86.9%; log-rank P = 0.002) and better cardiovascular survival (78.7, 75.0, 81.7, 91.8% for quartiles 1-4; log-rank P = 0.044). The future risks of the primary end-point, all-cause and cardiovascular mortality and the combined outcome were progressively increasing with lower quartiles of ß-coefficients, indicating patients with weak MBP-PWV association (hazard ratios for all-cause mortality 3.395; 95% confidence interval: 1.524-7.563, P = 0.003 for quartile 1 vs. quartile 4). CONCLUSION: Weaker within-individual MBP-PWV association, based on ABPM recordings, is associated with higher risk of death and cardiovascular events in hemodialysis. These findings support that arterial stiffness insensitive to BP changes is the underlying factor for adverse outcomes in these individuals.

11.
Biology (Basel) ; 8(4)2019 Sep 30.
Artigo em Inglês | MEDLINE | ID: mdl-31574983

RESUMO

During hibernation, repeated cycles of ischemia-reperfusion (I-R) leave vital organs without injury. Studying this phenomenon may reveal pathways applicable to improving outcomes in I-R injury-induced human diseases. We evaluated whether the H2S-nuclear factor erythroid 2-like 2 (Nrf2)-antioxidant proteins axis protects renal proximal tubular epithelial cells (RPTECs) of the native hibernator, the Syrian hamster, from reperfusion-induced cell death. To imitate I-R, the hamsters', and control mice's RPTECs were subjected to warm anoxia, washed, and then subjected to reoxygenation in fresh culture medium. Whenever required, the H2S-producing enzymes inhibitor aminooxyacetate or the lipid peroxidation inhibitor α-tocopherol were used. A handmade H2S detection methylene blue assay, a reactive oxygen species (ROS) detection kit, a LDH release cytotoxicity assay kit, and western blotting were used. Reoxygenation upregulated the H2S-producing enzymes cystathionine beta-synthase, cystathionine γ-lyase, and 3-mercaptopyruvate sulfurtransferase in the hamster, but not in mouse RPTECs. As a result, H2S production increased only in the hamster RPTECs under reoxygenation conditions. Nrf2 expression followed the alterations of H2S production leading to an enhanced level of the antioxidant enzymes superoxide dismutase 3 and glutathione reductase, and anti-ferroptotic proteins ferritin H and cystine-glutamate antiporter. The upregulated antioxidant enzymes and anti-ferroptotic proteins controlled ROS production and rescued hamster RPTECs from reoxygenation-induced, lipid peroxidation-mediated cell death. In conclusion, in RPTECs of the native hibernator Syrian hamster, reoxygenation activates the H2S-Nrf2-antioxidant proteins axis, which rescues cells from reoxygenation-induced cell death. Further studies may reveal that the therapeutic activation of this axis in non-hibernating species, including humans, may be beneficial in I-R injury-induced diseases.

12.
Hypertension ; 74(4): 998-1004, 2019 10.
Artigo em Inglês | MEDLINE | ID: mdl-31401878

RESUMO

The International Society of Peritoneal Dialysis recommends that adequate blood pressure (BP) assessment among patients on peritoneal dialysis should at least include measurements performed once-weekly at home and at each visit at clinic. However, the quality of evidence to support this guidance is suboptimal. Using ambulatory daytime BP as reference standard, we explored the diagnostic performance of clinic and home BP recordings in a cohort of 81 stable patients receiving peritoneal dialysis. BP was recorded using 3 different methodologies: (1) triplicate automated clinic BP recordings after a 5-minute seated rest with the validated monitor HEM 705 CP (Omron Healthcare); (2) 1-week averaged home BP recorded with a validated automated monitor on awaking and at bedtime; and (3) ambulatory BP monitoring with the Mobil-O-Graph device (IEM, Germany). The area under the curve of receiver operating characteristic curves in detection of ambulatory daytime systolic BP (SBP) ≥135 mm Hg was similar for clinic [area under the curve, 0.859; 95% CI, 0.776-0.941] and home SBP (area under the curve, 0.895; 95% CI, 0.815-0.976). In Bland-Altman analysis, clinic SBP overestimated daytime ambulatory SBP by 5.02 mm Hg with 95% limits of agreement ranging from -17.92 to 27.96 mm Hg. Similarly, home SBP overestimated daytime ambulatory SBP by 4.23 mm Hg, again with wide 95% limits of agreement (-16.05 to 24.51 mm Hg). These results show that 1-week averaged home SBP is of at least similar accuracy with standardized clinic SBP in diagnosing hypertension confirmed by ambulatory BP monitoring among patients on peritoneal dialysis.


Assuntos
Monitorização Ambulatorial da Pressão Arterial/métodos , Pressão Sanguínea/fisiologia , Hipertensão/diagnóstico , Falência Renal Crônica/fisiopatologia , Diálise Peritoneal , Adulto , Idoso , Feminino , Humanos , Hipertensão/fisiopatologia , Falência Renal Crônica/terapia , Masculino , Pessoa de Meia-Idade
13.
Clin Exp Hypertens ; : 1-7, 2019 Aug 03.
Artigo em Inglês | MEDLINE | ID: mdl-31379216

RESUMO

Background: Aortic-to-brachial pulse pressure (PP) amplification is a novel biomarker that prognosticates the cardiovascular risk above and beyond central aortic and brachial blood pressure. This phenomenon is modulated by left ventricular contractility and chronotrophy, large-artery stiffness and reflecting properties of microcirculation. However, the relative importance of these parameters as hemodynamic determinant of PP amplification remains elusive. Methods: A total of 88 consecutive drug-naïve hypertensives underwent a non-invasive assessment of central and peripheral hemodynamics via impedance cardiography and pulse wave analysis. Participants were classified into tertiles according to the magnitude of PP amplification. Hemodynamic determinants of low PP amplification were explored in univariate and multivariate regression analysis. Results: Compared with the high tertile, patients within the low PP amplification tertile were older and more commonly female and had lower height, weight and heart rate. Augmentation index (AIx) and systemic vascular resistance index (SVRI) were higher among patients within the low PP amplification tertile, whereas aortic pulse wave velocity (PWV) did not differ among groups. In multivariate analysis, higher AIx (OR: 1.27; 95% CI: 1.09-1.48) and higher SVRI were independently associated with higher odds for low PP amplification, whereas higher heart rate was the only parameter related to lower odds for low PP amplification (OR: 0.84; 95% CI: 0.71-0.99). Conclusion: This study shows that among newly-diagnosed drug-naïve hypertensives, elevated wave reflections and systemic vascular resistance are stronger determinants of PP amplification than aortic stiffness.

14.
Nutrients ; 11(8)2019 Aug 15.
Artigo em Inglês | MEDLINE | ID: mdl-31443225

RESUMO

Increased serum levels of uric acid have been associated with the onset and development of chronic kidney disease (CKD), cardiovascular disease, and mortality, through several molecular pathogenetic mechanisms, such as inflammation and oxidative stress. Oxidative stress is present even in the early stages of CKD, progresses parallelly with the deterioration of kidney function, and is even more exacerbated in end-stage renal disease patients undergoing maintenance hemodialysis. Although acting in the plasma as an antioxidant, once uric acid enters the intracellular environment; it behaves as a powerful pro-oxidant. Exogenous intake of antioxidants has been repeatedly shown to prevent inflammation, atherosclerosis and oxidative stress in CKD patients. Moreover, certain antioxidants have been proposed to exert uric acid-lowering properties. This review aims to present the available data regarding the effects of antioxidant supplements on both oxidative stress and uric acid serum levels, in a population particularly susceptible to oxidative damage such as CKD patients.

15.
Int J Mol Sci ; 20(15)2019 Jul 29.
Artigo em Inglês | MEDLINE | ID: mdl-31362427

RESUMO

Amplification of oxidative stress is present since the early stages of chronic kidney disease (CKD), holding a key position in the pathogenesis of renal failure. Induction of renal pro-oxidant enzymes with excess generation of reactive oxygen species (ROS) and accumulation of dityrosine-containing protein products produced during oxidative stress (advanced oxidation protein products-AOPPs) have been directly linked to podocyte damage, proteinuria, and the development of focal segmental glomerulosclerosis (FSGS) as well as tubulointerstitial fibrosis. Vascular oxidative stress is considered to play a critical role in CKD progression, and ROS are potential mediators of the impaired myogenic responses of afferent renal arterioles in CKD and impaired renal autoregulation. Both oxidative stress and inflammation are CKD hallmarks. Oxidative stress promotes inflammation via formation of proinflammatory oxidized lipids or AOPPs, whereas activation of nuclear factor κB transcription factor in the pro-oxidant milieu promotes the expression of proinflammatory cytokines and recruitment of proinflammatory cells. Accumulating evidence implicates oxidative stress in various clinical models of CKD, including diabetic nephropathy, IgA nephropathy, polycystic kidney disease as well as the cardiorenal syndrome. The scope of this review is to tackle the issue of oxidative stress in CKD in a holistic manner so as to provide a future framework for potential interventions.


Assuntos
Estresse Oxidativo , Insuficiência Renal Crônica/etiologia , Insuficiência Renal Crônica/metabolismo , Albuminúria/etiologia , Albuminúria/metabolismo , Animais , Biomarcadores , Gerenciamento Clínico , Modelos Animais de Doenças , Progressão da Doença , Fibrose , Humanos , Glomérulos Renais/metabolismo , Glomérulos Renais/patologia , Microvasos/metabolismo , Microvasos/patologia , Insuficiência Renal Crônica/diagnóstico , Insuficiência Renal Crônica/terapia
16.
Biomed Rep ; 1(1): 1-5, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-31258898

RESUMO

Chronic antibody-mediated rejection remains a major cause of late graft loss. Regarding cellular alloimmunity, the immunosuppressive properties of indoleamine 2,3-dioxygenase (IDO) have been well investigated; however, little is known of its effects on humoral alloimmunity. Therefore, the present study aimed to evaluate the effects of IDO on humoral alloimmunity. We developed a method for the induction of humoral alloimmunity in a one-way mixed lymphocyte reaction (MLR), which was measured with an antibody-mediated complement-dependent cytotoxicity assay using resting cells, which are similar to the stimulator cells of the aforementioned MLR. In parallel, cellular alloimmunity was assessed in two-way MLRs. The IDO inhibitor 1-methyl-DL-tryptophan was used for evaluating the role of IDO. In order to investigate whether the pathways known to serve a role in the effects of IDO on T cells are applied in humoral alloimmunity, the general control nonderepressible-2 (GCN-2) kinase activator tryptophanol and the aryl hydrocarbon receptor (AhR) inhibitor CH223191 were employed. The IDO inhibitor was revealed to increased cellular autoimmunity, but was decreased by the GCN-2 kinase activator. Unexpectedly, the AhR inhibitor decreased cellular alloimmunity. In addition, the IDO inhibitor was observed to suppress humoral alloimmunity, which may occur in manners independent of GCN-2 kinase AhR. The present study proposed that IDO may decrease humoral alloimmunity in primary human peripheral blood mononuclear cells via pathways that differ to those associated with its effect on T cells.

17.
Medicina (Kaunas) ; 55(8)2019 Jul 26.
Artigo em Inglês | MEDLINE | ID: mdl-31357502

RESUMO

Background and Objectives: The defects in the CLDN16 gene are a cause of primary hypomagnesemia (FHHNC), which is characterized by massive renal magnesium wasting, resulting in nephrocalcinosis and renal failure. The mutations occur throughout the gene's coding region and can impact on intracellular trafficking of the protein or its paracellular pore forming function. To gain more understanding about the mechanisms by which CLDN16 mutations can induce FHHNC, we performed an in-depth computational analysis of the CLDN16 gene and protein, focusing specifically on the prediction of the latter's subcellular localization. Materials and Methods: The complete nucleotide or amino acid sequence of CLDN16 in FASTA format was entered and processed in 14 databases. Results: One CpG island was identified. Twenty five promoters/enhancers were predicted. The CLDN16 interactome was found to consist of 20 genes, mainly involved in kidney diseases. No signal peptide cleavage site was identified. A probability of export to mitochondria equal to 0.9740 and a cleavable mitochondrial localization signal in the N terminal of the CLDN16 protein were predicted. The secondary structure prediction was visualized. Νo phosphorylation sites were identified within the CLDN16 protein region by applying DISPHOS to the functional class of transport. The KnotProt database did not predict any knot or slipknot in the protein structure of CLDN16. Seven putative miRNA binding sites within the 3'-UTR region of CLDN16 were identified. Conclusions: This is the first study to identify mitochondria as a probable cytoplasmic compartment for CLDN16 localization, thus providing new insights into the protein's intracellular transport. The results relative to the CLDN16 interactome underline its role in renal pathophysiology and highlight the functional dependence of CLDNs-10, 14, 16, 19. The predictions pertaining to the miRNAs, promoters/enhancers and CpG islands of the CLDN16 gene indicate a strict regulation of its expression both transcriptionally and post-transcriptionally.


Assuntos
Claudinas/análise , Claudinas/genética , Biologia Computacional/métodos , Mitocôndrias/genética , Humanos , Hipercalciúria/genética , Nefrocalcinose/genética , Regiões Promotoras Genéticas/genética , Erros Inatos do Transporte Tubular Renal/genética , Análise de Sequência de Proteína/métodos
19.
Int Urol Nephrol ; 51(7): 1249-1260, 2019 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-31161521

RESUMO

PURPOSE: Patients with end-stage renal disease (ESRD) seem to have a negative attitude towards physical activity, which is mainly favored by the lack of counseling provided by the medical and nursing staff. The aim of this study was to investigate the attitudes of both ESRD patients and medical staff on the participation and promotion of physical activity and identify the obstacles that discourage patients' involvement in intervention programs. STUDY DESIGN: Subjective assessment questionnaires and the International Physical Activity Questionnaire were administrated to hemodialysis patients and medical staff, to investigate the association between patient's barriers to physical activity, the total intensity level of physical activity, and attitudes of both ESRD patients and medical staff on the participation and promotion of physical activity. RESULTS: A total of 103 ESRD patients (61 men, 59.2%), 20 nephrologists (12 men, 60.0%), and 72 nurses (61 women, 84.7%) participated in the study. Most commonly reported patient's barriers were fatigue on dialysis (97.4%) and non-dialysis days (55.1%). Healthcare staff showed positive attitude towards renal rehabilitation exercise programs. However, most of physicians (85.0%) and nurses (83.3%) did not have previous experience with interventional exercise rehabilitation programs. Binary logistic regression revealed significant association between patients' inactivity, demographic data, and barriers towards physical activity, such as fatigue and pain in dialysis and non-dialysis days (p < 0.05), family's and physician's concern (p < 0.05), too many medical problems (p < 0.05), the fear of getting hurt (p = 0.01), and unwillingness for exercise (p < 0.05). Interestingly, healthcare staff's negative attitudes toward patient's physical activity seem to be strongly associated with patient's inactivity status. CONCLUSION: Healthcare staff negative attitudes and multiple related barriers especially fatigue on dialysis and non-dialysis days, towards ESRD patient's physical activity, suppress desire for exercise and active patients' status, leading them to abstain from it.


Assuntos
Atitude do Pessoal de Saúde , Atitude Frente a Saúde , Terapia por Exercício , Exercício , Falência Renal Crônica , Participação do Paciente/psicologia , Diálise Renal , Adulto , Aconselhamento , Exercício/fisiologia , Exercício/psicologia , Terapia por Exercício/métodos , Terapia por Exercício/psicologia , Fadiga/etiologia , Fadiga/psicologia , Feminino , Humanos , Falência Renal Crônica/psicologia , Falência Renal Crônica/reabilitação , Falência Renal Crônica/terapia , Masculino , Pessoa de Meia-Idade , Nefrologistas/psicologia , Recursos Humanos de Enfermagem/psicologia , Diálise Renal/efeitos adversos , Diálise Renal/métodos , Diálise Renal/psicologia , Comportamento Sedentário
20.
Semin Dial ; 32(5): 463-466, 2019 09.
Artigo em Inglês | MEDLINE | ID: mdl-31044475

RESUMO

During the last two decades, oxidative stress (OS) has emerged as a novel risk factor for a variety of adverse events, including atherosclerosis and mortality in chronic kidney disease (CKD) patients. Increased OS occurs even in early stages of the disease, progresses with deterioration of renal function and is further aggravated by hemodialysis (HD), due to the bioincompatibility of the method. Compared to HD, peritoneal dialysis (PD) is a more biocompatible dialysis modality, characterized by a significantly reduced, but still high, OS status. The culprit for OS in PD is mainly the composition of PD solutions (low pH, lactate buffer, increased osmolarity and high glucose concentration). After heat sterilization of PD solutions, formation of glucose degradation products (GDPs) and advanced glycation end-products (AGEs) trigger inflammation and enhance OS. Chronic exposure of the peritoneum to this toxic, hyperglycemic environment leads to OS-derived morphologic damage of peritoneal cells, loss of ultrafiltration capacity and decreased technique survival. Moreover, OS is linked with peritonitis, loss of residual renal function, inflammation, atherosclerosis, cardiovascular (CV) disease, and increased mortality. To ameliorate OS status in PD, a multitargeted approach is necessary that includes use of neutral pH, low GDP, low lactate and iso-ismolar PD solutions, strict glycemic control, optimal volume management and, probably supplementation with antioxidants, N-acetylcysteine being the most promising among them.

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