Your browser doesn't support javascript.
Mostrar: 20 | 50 | 100
Resultados 1 - 20 de 9.109
Filtrar
1.
Medicine (Baltimore) ; 98(42): e17588, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31626129

RESUMO

In 2014/2015, tyrosine kinase inhibitors (TKIs) were introduced as a secondary treatment for refractory differentiated thyroid cancer (DTC) in Japan. While renal dysfunction is an adverse event of TKI, data on this adverse event in TKI-treated DTC remains insufficient. Here, we investigated renal function in patients undergoing TKI treatment for DTC and evaluated the efficacy of dose reduction/withdrawal for cases of renal dysfunction.A total of 73 cases of radioactive iodine-refractory DTC treated with sorafenib (n = 22) or lenvatinib (n = 51) were included. Patient data evaluated were TKI treatment period, estimated glomerular filtration rate (eGFR) before and after TKI therapy, incidence and degree (maximum value at time of TKI treatment) of proteinuria, and albumin levels before and after TKI therapy were compared.The mean ΔeGFR was -6.75% with lenvatinib and +5.90% with sorafenib. It was not significant (P = .15). The mean Δalbumin was -8.90% and -5.85% with lenvatinib and sorafenib, respectively; there was no significant difference between the lenvatinib and sorafenib groups (P = .77). According to our program of TKI dose reduction and withdrawal, all patients except 2 with diabetes were successfully continuing treatment.Overall, the present results demonstrated that renal function is negatively affected by long-term TKI treatment for RAI-refractory DTC. However, heightened proteinuria, decreased eGFR and albumin levels, and significant but apparently reversible renal dysfunction were more frequent with lenvatinib than sorafenib.


Assuntos
Taxa de Filtração Glomerular/fisiologia , Radioisótopos do Iodo/uso terapêutico , Nefropatias/etiologia , Compostos de Fenilureia/uso terapêutico , Proteínas Tirosina Quinases/antagonistas & inibidores , Quinolinas/uso terapêutico , Sorafenibe/uso terapêutico , Neoplasias da Glândula Tireoide/terapia , Idoso , Substituição de Medicamentos , Feminino , Seguimentos , Humanos , Nefropatias/fisiopatologia , Masculino , Pessoa de Meia-Idade , Inibidores de Proteínas Quinases/uso terapêutico , Tolerância a Radiação , Estudos Retrospectivos , Neoplasias da Glândula Tireoide/complicações , Neoplasias da Glândula Tireoide/diagnóstico , Tomografia Computadorizada por Raios X , Resultado do Tratamento
2.
Zhonghua Nei Ke Za Zhi ; 58(10): 758-762, 2019 Oct 01.
Artigo em Chinês | MEDLINE | ID: mdl-31594174

RESUMO

Objective: To investigate the clinical characteristics of polyarteritis nodosa (PAN) patients with renal involvement. Methods: PAN patients admitted to the department of rheumatology, department of pediatrics, department of nephrology, general internal medicine department and department of vascular surgery at Peking Union Medical College Hospital from June 2012 to August 2018 were enrolled in this study and were divided into two groups according to renal involvement or not. The clinical characteristics were analyzed. Results: A total of 94 PAN patients were finally enrolled and 57 (60.64%) presented kidney manifestation. The mean age of onset was (37.76±17.40) years old and the interval from onset to diagnosis was 10 (0 to 240) months. Forty patients were misdiagnosed once or more times. In patients with renal involvement, 9 cases suffered from renal ischemia or infarction, 31 with microscopic haematuria, 26 with proteinuria, renal artery or its branch involved in 17 cases, renal vein thrombosis in 1 case, 4 cases with pyeloureterectasis, one case with renal fascia thickening, 33 cases with impaired renal function (serum creatinine>84 µmol/L) including creatinine>140 µmol/L in 10 patients. Renal artery branch stenosis was the most common presentation [9 cases (52.94%)] of renal vascular involvement, other abnormalities including nodular dilatation [4 cases (23.53%)], occlusion [3 cases (17.65%)]. There were significant differences (P<0.05) in the PAN patients with and without renal involvement in the following: age of onset [(33.72±16.13) years vs. (43.97±17.66) years, t(2)=2.901, P=0.005], weight loss(≥4kg since PAN onset) [25(43.86%) vs. 7(18.92%), χ(2)=6.216, P=0.013], elevation of diastolic blood pressure [22(38.60%) vs. 7(18.92%), χ(2)=4.072, P=0.044], acromegaly gangrene [18(31.58%) vs. 21(56.76%), χ(2)=5.859, P=0.015], and gastrointestinal artery involvement [20(35.09%) vs. 6(1.22%), χ(2)=3.993, P=0.046]. Laboratory parameters and the application of glucocorticoid and cyclophosphamide therapies were similar in two groups (all P>0.05). Conclusion: Young PAN patients are more likely to be associated with renal involvement, especially gastrointestinal arteries.


Assuntos
Arterite/diagnóstico , Nefropatias/etiologia , Rim/fisiopatologia , Poliarterite Nodosa/diagnóstico , Adulto , Idoso , Ciclofosfamida/uso terapêutico , Gastroenteropatias , Glomerulonefrite/diagnóstico , Glucocorticoides/uso terapêutico , Humanos , Infarto , Nefropatias/fisiopatologia , Pessoa de Meia-Idade , Poliarterite Nodosa/complicações , Poliarterite Nodosa/tratamento farmacológico , Adulto Jovem
3.
Adv Exp Med Biol ; 1165: 165-194, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31399966

RESUMO

The main cellular constituents in glomerular mesangium are mesangial cells, which account for approximately 30-40% of the total cells in the glomerulus. Together with the mesangial matrix, mesangial cells form the glomerular basement membrane (GBM) in the glomerulus, whose main function is to perform the filtration. Under the pathologic conditions, mesangial cells are activated, leading to hyperproliferation and excess extracellular matrix (ECM). Moreover, mesangial cells also secrete several kinds of inflammatory cytokines, adhesion molecules, chemokines, and enzymes, all of which participate in the process of renal glomerular fibrosis. During the past years, researchers have revealed the roles of mesangial cells and the associated signal pathways involved in renal fibrosis. In this section, we will discuss how mesangial cells are activated and its contributions to renal fibrosis, as well as the molecular mechanisms and novel anti-fibrotic agents. Full understanding of the contributions of mesangial cells to renal fibrosis will benefit the clinical drug developing.


Assuntos
Mesângio Glomerular/citologia , Nefropatias/fisiopatologia , Células Mesangiais/citologia , Moléculas de Adesão Celular , Quimiocinas , Citocinas , Matriz Extracelular , Fibrose , Humanos , Rim/patologia , Glomérulos Renais
4.
Adv Exp Med Biol ; 1165: 233-252, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31399968

RESUMO

The renal tubules are the major component of the kidney and are vulnerable to a variety of injuries including ischemia, proteinuria, toxins, and metabolic disorders. It has long been believed that tubules are the victim of injury. In this review, we shift this concept to renal tubules as a driving force in the progression of kidney disease. In response to injury, tubular epithelial cells (TECs) can synthesize and secrete varieties of bioactive molecules that drive interstitial inflammation and fibrosis. Innate immune-sensing receptors on the TECs also aggravate immune responses. Necroinflammation, an auto-amplification loop between tubular cell death and interstitial inflammation, leads to the exacerbation of renal injury. Furthermore, TECs also play an active role in progressive renal injury via mechanisms associated with the conversion into collagen-producing fibroblast phenotype, cell cycle arrest at both G1/S and G2/M checkpoints, and metabolic disorder. Thus, a better understanding the mechanisms by which tubular injury drives AKI and CKD is necessary for the development of therapeutics to halt the progression of CKD.


Assuntos
Células Epiteliais/patologia , Nefropatias/fisiopatologia , Túbulos Renais/citologia , Pontos de Checagem do Ciclo Celular , Fibrose , Humanos , Imunidade Inata , Rim/patologia
5.
Adv Exp Med Biol ; 1165: 253-283, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31399969

RESUMO

Renal fibrosis is characterized by excessive deposition of extracellular matrix (ECM), leading to destruction of normal kidney architecture and loss of renal function. The activation of α-smooth muscle actin-positive myofibroblasts plays a key role in this process. After kidney injury, profibrotic factors are secreted by injured tubular epithelia and infiltrated inflammatory cells to promote complex cascades of signaling events leading to myofibroblastic activation, proliferation, and ECM production. The origins of myofibroblasts remain controversial, and possibilities include resident fibroblasts, pericytes, bone marrow-derived cells, and endothelial cells. Recent evidence supports the existence of localized fibrogenic niches, which provides a specialized tissue microenvironment for myofibroblastic activation and expansion. Myofibroblasts often undergo epigenetic modifications, leading to their sustained activation and resistance to apoptosis. In this chapter, we discuss the origins, heterogeneity, and activation of myofibroblasts in diseased kidneys. We also highlight novel strategies for the treatment of patients with fibrotic kidney diseases.


Assuntos
Nefropatias/fisiopatologia , Miofibroblastos/citologia , Linhagem da Célula , Matriz Extracelular , Fibrose , Humanos , Rim/patologia
6.
Adv Exp Med Biol ; 1165: 285-303, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31399970

RESUMO

Monocytes/macrophages are highly involved in the process of renal injury, repair and fibrosis in many aspects of experimental and human renal diseases. Monocyte-derived macrophages, characterized by high heterogeneity and plasticity, are recruited, activated, and polarized in the whole process of renal fibrotic diseases in response to local microenvironment. As classically activated M1 or CD11b+/Ly6Chigh macrophages accelerate renal injury by producing pro-inflammatory factors like tumor necrosis factor-alpha (TNFα) and interleukins, alternatively activated M2 or CD11b+/Ly6Cintermediate macrophages may contribute to kidney repair by exerting anti-inflammation and wound healing functions. However, uncontrolled M2 macrophages or CD11b+/Ly6Clow macrophages promote renal fibrosis via paracrine effects or direct transition to myofibroblast-like cells via the process of macrophage-to-myofibroblast transition (MMT). In this regard, therapeutic strategies targeting monocyte/macrophage recruitment, activation, and polarization should be emphasized in the treatment of renal fibrosis.


Assuntos
Nefropatias/fisiopatologia , Macrófagos/citologia , Diferenciação Celular , Fibrose , Humanos , Rim/patologia , Monócitos , Miofibroblastos/citologia
7.
Adv Exp Med Biol ; 1165: 365-380, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31399974

RESUMO

CCN2, also known as connective tissue growth factor (CTGF), is one of important members of the CCN family. Generally, CTGF expresses at low levels in normal adult kidney, while increases significantly in various kidney diseases, playing an important role in the development of glomerular and tubulointerstitial fibrosis in progressive kidney diseases. CTGF is involved in cell proliferation, migration, and differentiation and can promote the progression of fibrosis directly or act as a downstream factor of transforming growth factor ß (TGF-ß). CTGF also regulates the expression and activity of TGF-ß and bone morphogenetic protein (BMP), thereby playing an important role in the process of kidney repair. In patients with chronic kidney disease, elevated plasma CTGF is an independent risk factor for progression to end-stage renal disease and is closely related to glomerular filtration rate. Therefore, CTGF may be a potential biological marker of kidney fibrosis, but more clinical studies are needed to confirm this view. This section briefly describes the role and molecular mechanisms of CTGF in renal fibrosis and also discusses the potential value of targeting CCN2 for the treatment of renal fibrosis.


Assuntos
Fator de Crescimento do Tecido Conjuntivo/fisiologia , Nefropatias/fisiopatologia , Rim/patologia , Fibrose , Humanos , Fator de Crescimento Transformador beta
8.
Adv Exp Med Biol ; 1165: 381-406, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31399975

RESUMO

Renal inflammation is the initial, healthy response to renal injury. However, prolonged inflammation promotes the fibrosis process, which leads to chronic pathology and eventually end-stage kidney disease. There are two major sources of inflammatory cells: first, bone marrow-derived leukocytes that include neutrophils, macrophages, fibrocytes and mast cells, and second, locally activated kidney cells such as mesangial cells, podocytes, tubular epithelial cells, endothelial cells and fibroblasts. These activated cells produce many profibrotic cytokines and growth factors that cause accumulation and activation of myofibroblasts, and enhance the production of the extracellular matrix. In particular, activated macrophages are key mediators that drive acute inflammation into chronic kidney disease. They produce large amounts of profibrotic factors and modify the microenvironment via a paracrine effect, and they also transdifferentiate to myofibroblasts directly, although the origin of myofibroblasts in the fibrosing kidney remains controversial. Collectively, understanding inflammatory cell functions and mechanisms during renal fibrosis is paramount to improving diagnosis and treatment of chronic kidney disease.


Assuntos
Mediadores da Inflamação/fisiologia , Nefropatias/fisiopatologia , Rim/patologia , Transdiferenciação Celular , Fibrose , Humanos , Leucócitos/citologia , Macrófagos/citologia , Miofibroblastos/citologia
9.
Adv Exp Med Biol ; 1165: 501-524, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31399982

RESUMO

Mitochondria are important organelles in eukaryotic cells and perform a variety of biosynthetic and metabolic functions. Many human diseases are closely related to mitochondrial dysfunction. Kidney is an organ with high-energy requirements, which is distributed with a large number of mitochondria. Mitochondrial dysfunction plays a crucial role in the pathogenesis of kidney disease, and studies have shown that mitochondrial dysfunction is involved in the physiological process of renal fibrosis. This review introduced the biogenesis and pathophysiology of mitochondria, illustrated the involvement of mitochondrial dysfunction in renal fibrosis based on various kinds of cells, and finally summarized the latest mitochondria-targeted therapies.


Assuntos
Nefropatias/fisiopatologia , Rim/patologia , Mitocôndrias/patologia , Fibrose , Humanos
10.
Adv Exp Med Biol ; 1165: 525-541, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31399983

RESUMO

Since the lipid nephrotoxicity hypothesis was proposed in 1982, increasing evidence has supported the hypothesis that lipid abnormalities contributed to the progression of glomerulosclerosis. In this chapter, we will discuss the general promises of the original hypothesis, focusing especially on the role of lipids and metabolic inflammation accompanying CKD in renal fibrosis and potential new strategies of prevention.


Assuntos
Nefropatias/fisiopatologia , Transtornos do Metabolismo dos Lipídeos/fisiopatologia , Progressão da Doença , Fibrose , Humanos , Inflamação , Lipídeos
11.
Adv Exp Med Biol ; 1155: 497-505, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31468426

RESUMO

Taurine (2-aminoethanesulfonic acid) is a sulfur-containing organic acid possessing several important effects, including antioxidant and anti-inflammatory ones. Exposure to ionizing radiation generates free radicals and reactive oxygen species (ROS) in irradiated cells, and free radical generation leads to oxidative stress. It is known that radiation nephropathy includes an inflammation-based process in which ROS and cytokines are responsible. Different doses of explored radiation can cause apoptosis, inflammation and a profound oxidative stress in kidneys. Oxidative stress is involved in renal injury after exposure to both ionizing radiation and inflammation. In this review, we describe the protective effect of taurine against several kidney diseases and the potential effects of taurine in the mitigation of radiation nephropathy. We also report that X-irradiation decreased the expression of taurine and TauT in the kidney. Taurine administration suppressed the decrease in the expression of taurine and TauT in the kidney after radiation exposure. Taurine might contribute to the mitigation of kidney injury induced by radiation.


Assuntos
Nefropatias/tratamento farmacológico , Lesões por Radiação/tratamento farmacológico , Taurina/farmacologia , Humanos , Rim/efeitos dos fármacos , Rim/efeitos da radiação , Nefropatias/fisiopatologia , Glicoproteínas de Membrana/metabolismo , Proteínas de Membrana Transportadoras/metabolismo , Estresse Oxidativo , Radiação Ionizante , Espécies Reativas de Oxigênio
12.
Methodist Debakey Cardiovasc J ; 15(2): 158-159, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31384382

RESUMO

This column is supplied by Benjamin J. Lee, MD, MAS, an assistant professor of clinical medicine at both the Houston Methodist Institute for Academic Medicine and Weill Cornell Medical College. After earning his medical degree at Harvard Medical School, Dr. Lee completed a residency in internal medicine at the University of California, San Francisco (UCSF). He subsequently completed a nephrology fellowship at UCSF while simultaneously obtaining a Master of Advanced Study in clinical research from the UCSF Department of Epidemiology and Biostatistics. Dr. Lee is a Fellow of the American Society of Nephrology, a Certified Hypertension Specialist through the American Hypertension Specialist Certification Program, and a member of the American Society of Transplantation. He maintains his clinical practice with the Houston Kidney Consultants.


Assuntos
Cianose/etiologia , Cardiopatias Congênitas/complicações , Nefropatias/etiologia , Rim/fisiopatologia , Cianose/diagnóstico , Cianose/fisiopatologia , Cardiopatias Congênitas/diagnóstico , Cardiopatias Congênitas/tratamento farmacológico , Cardiopatias Congênitas/fisiopatologia , Humanos , Rim/efeitos dos fármacos , Rim/patologia , Nefropatias/diagnóstico , Nefropatias/tratamento farmacológico , Nefropatias/fisiopatologia , Prognóstico , Fatores de Risco
13.
Internist (Berl) ; 60(9): 903-911, 2019 Sep.
Artigo em Alemão | MEDLINE | ID: mdl-31375850

RESUMO

BACKGROUND: Inhibitors of sodium-glucose cotransporters type 2 (SGLT-2) are a class of oral antidiabetic drugs with a novel specific mode of action in the kidneys. OBJECTIVE: The effects of SGLT-2 inhibitors on cardiovascular (CV) and renal endpoints in outcome trials with type 2 diabetes patients. MATERIAL AND METHODS: Differential analysis and interpretation of the results of outcome trials with the SGLT-2 inhibitors empagliflozin, canagliflozin and dapagliflozin in type 2 diabetes mellitus. RESULTS: In the EMPA-REG OUTCOME trial, empagliflozin demonstrated a significant reduction in major cardiac adverse events (MACE), hospitalization for heart failure (HHI), renal endpoints, CV and total mortality vs. placebo in >7000 patients with type 2 diabetes and established CV disease over 3.1 years. In the CANVAS program, canagliflozin demonstrated a significant reduction of MACE, HHI and renal endpoints vs. placebo in >10,000 patients with type 2 diabetes and high CV risk over 2.4 years. In the CREDENCE trial, canagliflozin demonstrated a significant reduction of a combined renal endpoint and CV endpoints vs. placebo in >4000 patients with type 2 diabetes and established kidney disease with albuminuria over 2.6 years. In the DECLARE-TIMI 58 trial, dapagliflozin demonstrated a significant reduction in a combined endpoint of CV death and HHI vs. placebo in >17,000 patients with type 2 diabetes and established CV disease or with multiple CV risk factors over 3.1 years. CONCLUSION: Outcome trials with SGLT-2 inhibitors have collectively demonstrated cardioprotective and nephroprotective effects in patients with type 2 diabetes and high CV risk. The use of SGLT-2 inhibitors is recommended in current guidelines and consensus statements as primary combination partners for metformin in patients with type 2 diabetes and established CV disease, high CV risk, heart failure or kidney disease.


Assuntos
Canagliflozina/uso terapêutico , Doenças Cardiovasculares/fisiopatologia , Diabetes Mellitus Tipo 2/tratamento farmacológico , Diabetes Mellitus Tipo 2/terapia , Nefropatias/fisiopatologia , Inibidores do Transportador 2 de Sódio-Glicose/uso terapêutico , Glicemia/efeitos dos fármacos , Glicemia/metabolismo , Canagliflozina/efeitos adversos , Diabetes Mellitus Tipo 2/metabolismo , Humanos , Hipoglicemiantes/uso terapêutico , Guias de Prática Clínica como Assunto , Transportador 2 de Glucose-Sódio/efeitos dos fármacos , Transportador 2 de Glucose-Sódio/metabolismo , Inibidores do Transportador 2 de Sódio-Glicose/efeitos adversos , Resultado do Tratamento
14.
Physiol Rev ; 99(4): 1819-1875, 2019 10 01.
Artigo em Inglês | MEDLINE | ID: mdl-31434538

RESUMO

Metabolomics uses advanced analytical chemistry techniques to enable the high-throughput characterization of metabolites from cells, organs, tissues, or biofluids. The rapid growth in metabolomics is leading to a renewed interest in metabolism and the role that small molecule metabolites play in many biological processes. As a result, traditional views of metabolites as being simply the "bricks and mortar" of cells or just the fuel for cellular energetics are being upended. Indeed, metabolites appear to have much more varied and far more important roles as signaling molecules, immune modulators, endogenous toxins, and environmental sensors. This review explores how metabolomics is yielding important new insights into a number of important biological and physiological processes. In particular, a major focus is on illustrating how metabolomics and discoveries made through metabolomics are improving our understanding of both normal physiology and the pathophysiology of many diseases. These discoveries are yielding new insights into how metabolites influence organ function, immune function, nutrient sensing, and gut physiology. Collectively, this work is leading to a much more unified and system-wide perspective of biology wherein metabolites, proteins, and genes are understood to interact synergistically to modify the actions and functions of organelles, organs, and organisms.


Assuntos
Metabolismo Energético , Metaboloma , Metabolômica/métodos , Animais , Biomarcadores/metabolismo , Doenças Cardiovasculares/metabolismo , Doenças Cardiovasculares/fisiopatologia , Humanos , Nefropatias/metabolismo , Nefropatias/fisiopatologia , Erros Inatos do Metabolismo/metabolismo , Erros Inatos do Metabolismo/fisiopatologia , Neoplasias/metabolismo , Neoplasias/fisiopatologia , Fluxo de Trabalho
15.
Intern Med ; 58(13): 1885-1889, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31257276

RESUMO

Intravascular large B-cell lymphoma (IVLBCL) frequently involves the hepatobiliary system, but its clinical course and pathophysiology are still not fully known. We herein describe a case of IVLBCL mimicking acute hepatobiliary infection. An 85-year-old woman was admitted because of fever and epigastric pain, and she was diagnosed to have acute acalculous cholecystitis based on gallbladder wall thickening with fluid collection. The gallbladder swelling regressed within several days, and areas of intrahepatic hypoperfusion appeared. Inflammation continued despite treatment with antibiotics, and she died within 21 days. An autopsy examination revealed IVLBCL. IVLBCL can present as acute cholecystitis with an improvement in the imaging findings and the presence of a subsequent liver mass.


Assuntos
Nefropatias/terapia , Hepatopatias/terapia , Linfoma Difuso de Grandes Células B/diagnóstico , Linfoma Difuso de Grandes Células B/mortalidade , Linfoma Difuso de Grandes Células B/terapia , Idoso de 80 Anos ou mais , Evolução Fatal , Feminino , Humanos , Nefropatias/diagnóstico , Nefropatias/fisiopatologia , Hepatopatias/diagnóstico , Hepatopatias/microbiologia , Hepatopatias/fisiopatologia , Linfoma Difuso de Grandes Células B/fisiopatologia
16.
Physiol Rev ; 99(3): 1575-1653, 2019 07 01.
Artigo em Inglês | MEDLINE | ID: mdl-31215303

RESUMO

The identification of genes causing inherited kidney diseases yielded crucial insights in the molecular basis of disease and improved our understanding of physiological processes that operate in the kidney. Monogenic kidney disorders are caused by mutations in genes coding for a large variety of proteins including receptors, channels and transporters, enzymes, transcription factors, and structural components, operating in specialized cell types that perform highly regulated homeostatic functions. Common variants in some of these genes are also associated with complex traits, as evidenced by genome-wide association studies in the general population. In this review, we discuss how the molecular genetics of inherited disorders affecting different tubular segments of the nephron improved our understanding of various transport processes and of their involvement in homeostasis, while providing novel therapeutic targets. These include inherited disorders causing a dysfunction of the proximal tubule (renal Fanconi syndrome), with emphasis on epithelial differentiation and receptor-mediated endocytosis, or affecting the reabsorption of glucose, the handling of uric acid, and the reabsorption of sodium, calcium, and magnesium along the kidney tubule.


Assuntos
Nefropatias/genética , Nefropatias/fisiopatologia , Rim/fisiologia , Rim/fisiopatologia , Animais , Humanos , Doenças Raras
17.
Urologiia ; (2): 103-107, 2019 Jun.
Artigo em Russo | MEDLINE | ID: mdl-31162910

RESUMO

The results of recent studies on the mechanisms of kidney damage are presented in the review of literature. The role of the immune system in the occurrence, development and outcome of damage to the epithelium of the renal tubules, as well as molecular, genetic and metabolic changes which determine the extent and consequences of renal trauma are described in details. The mechanisms of restoration of the renal parenchyma and the development of fibrosis following the cessation of injury are given.


Assuntos
Nefropatias/fisiopatologia , Túbulos Renais/fisiopatologia , Rim/fisiopatologia , Urotélio/fisiopatologia , Fibrose/fisiopatologia , Humanos , Rim/lesões , Nefropatias/etiologia , Túbulos Renais/lesões , Urotélio/lesões
18.
Lakartidningen ; 1162019 May 28.
Artigo em Sueco | MEDLINE | ID: mdl-31192397

RESUMO

Shrunken Pore Syndrome was defined in 2015 and is characterised by the glomerular filtration of 5-40 kDa molecules being selectively decreased compared to that of molecules <0.2 kDa, e.g. water and creatinine. The diagnose is based upon identification of a decreased eGFRcystatin C/eGFRcreatinine ratio, and ratios -< 0.6 or 0.7 have most often been used to identify the diagnose. The mortality is strongly increased in all investigated populations and increases progressively with a decrease in the eGFRcystatin C/eGFRcreatinine ratio used to identify the syndrome. The prevalence of the syndrome varies with the eGFRcystatin C/eGFRcreatinine ratio used for diagnosis, but when a ratio of 0.6 is used, the prevalence has varied between 2 and 8%. The pathophysiology might be the accumulation of atherosclerosis-promoting proteins occurring in patients with the syndrome. The syndrome might explain the superiority of eGFRcystatin C over eGFRcreatinine in identifying high-risk kidney patients.


Assuntos
Taxa de Filtração Glomerular/fisiologia , Nefropatias , Biomarcadores/sangue , Creatinina/sangue , Cistatina C/sangue , Humanos , Nefropatias/diagnóstico , Nefropatias/epidemiologia , Nefropatias/mortalidade , Nefropatias/fisiopatologia , Síndrome
19.
Medicine (Baltimore) ; 98(20): e15453, 2019 May.
Artigo em Inglês | MEDLINE | ID: mdl-31096441

RESUMO

Preoperative renal dysfunction is associated with mortality in patients who undergo coronary artery bypass graft and valve surgery. However, the role of preoperative renal dysfunction in type A aortic dissection (TAAD) remains unclear. This study aimed to evaluate the impact of preoperative renal dysfunction on the outcome of surgical intervention in patients with TAAD.We retrospectively studied the outcomes of 159 patients with TAAD who were treated at a tertiary referral hospital between 2005 and 2010. The demographics and surgical details of patients were analyzed according to their renal function. Risk factors for outcomes were analyzed using multivariable logistic regression. Thirty-two of the patients (20.1%) had preoperative serum creatinine of 1.5 mg/dL or more. The multivariable logistic regression model revealed independent risk factors of in-hospital mortality to be renal dysfunction (odds ratio [OR], 3.79; 95% confidence interval [CI], 1.64-8.77), preoperative shock (OR, 8.75; 95% CI, 2.83-27.02), and bypass time (OR, 1.008; 95% CI, 1.003-1.013). In addition, patients with renal dysfunction exhibited a lower 90-day survival rate than did patients without the condition (P of log-rank test = .005).Preoperative renal dysfunction may have a critical role in the surgical outcomes of patients with TAAD. Additional large-scale investigations are warranted.


Assuntos
Aneurisma Dissecante/cirurgia , Nefropatias/diagnóstico , Nefropatias/fisiopatologia , Rim/fisiopatologia , Adulto , Idoso , Aneurisma Dissecante/mortalidade , Aneurisma Dissecante/fisiopatologia , Ponte de Artéria Coronária/mortalidade , Creatinina/sangue , Feminino , Mortalidade Hospitalar , Humanos , Nefropatias/mortalidade , Masculino , Pessoa de Meia-Idade , Complicações Pós-Operatórias/etiologia , Período Pré-Operatório , Prognóstico , Estudos Retrospectivos , Fatores de Risco , Taxa de Sobrevida , Resultado do Tratamento
20.
Sao Paulo Med J ; 137(1): 39-44, 2019 May 08.
Artigo em Inglês | MEDLINE | ID: mdl-31116269

RESUMO

BACKGROUND: Up to 5% of familial Mediterranean fever (FMF) cases are unresponsive to colchicine, through resistance, side effects and toxicity. Anakinra is an alternative treatment for FMF patients whose disease remains uncontrolled with colchicine. We aimed to evaluate anti-interleukin-1 treatment regarding clinical findings, laboratory parameters and quality of life (QoL) among FMF patients presenting resistance and toxicity towards colchicine. DESIGN AND SETTING: Descriptive observational study at the rheumatology clinic, Adnan Menderes University Medical School, Aydin, Turkey. METHODS: Among the patients included, age, sex, MEFV genotypes, acute-phase reactants, hepatic/renal function tests, average colchicine dose, disease duration, attack frequency, attack duration, disease severity, proteinuria, amyloidosis and QoL were evaluated. Colchicine resistance was defined as > 6 typical episodes/year or > 3 per 4-6 months. Kolmogorov-Smirnov, Friedman and two-way analysis of variance tests were used for statistical analyses. RESULTS: Between 2015 and 2017, 14 FMF patients receiving anakinra were enrolled. The mean colchicine dose was 1.7 ± 0.3 mg/day before use of anakinra. Ten patients were attack-free after treatment, while three showed reductions of at least 50% in attack frequency, attack duration and disease severity. Proteinuria levels in all patients with renal amyloidosis decreased after treatment. QoL among patients with renal amyloidosis differed significantly from QoL among non-amyloidosis patients. Mean visual analogue scale scores significantly improved in both groups after use of anakinra. CONCLUSIONS: Use of anakinra reduced attack frequency and proteinuria and acute-phase reactant levels, and improved QoL, with only a few uncomplicated side effects among colchicine-resistant or intolerant FMF patients. Injection-site reactions of severity insufficient to require discontinuation of treatment were seen.


Assuntos
Antirreumáticos/uso terapêutico , Colchicina/uso terapêutico , Resistência a Medicamentos/efeitos dos fármacos , Febre Familiar do Mediterrâneo/tratamento farmacológico , Proteína Antagonista do Receptor de Interleucina 1/uso terapêutico , Interleucina-1/antagonistas & inibidores , Qualidade de Vida , Adulto , Amiloidose/tratamento farmacológico , Amiloidose/fisiopatologia , Análise de Variância , Sedimentação Sanguínea , Febre Familiar do Mediterrâneo/fisiopatologia , Feminino , Humanos , Nefropatias/tratamento farmacológico , Nefropatias/fisiopatologia , Masculino , Pessoa de Meia-Idade , Proteinúria/urina , Valores de Referência , Reprodutibilidade dos Testes , Estudos Retrospectivos , Índice de Gravidade de Doença , Estatísticas não Paramétricas , Fatores de Tempo , Resultado do Tratamento , Turquia , Escala Visual Analógica
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA