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[PMID]:28466968
[Au] Autor:Geard A; Pule GD; Chetcha Chemegni B; Ngo Bitoungui VJ; Kengne AP; Chimusa ER; Wonkam A
[Ad] Endereço:Division of Human Genetics, Department of Pathology, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa.
[Ti] Título:Clinical and genetic predictors of renal dysfunctions in sickle cell anaemia in Cameroon.
[So] Source:Br J Haematol;178(4):629-639, 2017 08.
[Is] ISSN:1365-2141
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Micro-albuminuria and glomerular hyperfiltration are primary indicators of renal dysfunctions in Sickle Cell Disease (SCD), with more severe manifestations previously associated with variants in APOL1 and HMOX1 among African Americans. We have investigated 413 SCD patients from Cameroon. Anthropometric variables, haematological indices, crude albuminuria, albumin-to-creatinine ratio (ACR) and estimated glomerular filtration rate (eGFR) were measured. Patients were genotyped for 3·7 kb alpha-globin gene (HBA1/HBA2) deletion, and for variants in APOL1 (G1/G2; rs60910145, rs73885319, rs71785313) and HMOX1 (rs3074372, rs743811). The median age was 15 years; the majority presented with micro-albuminuria (60·9%; n = 248), and approximately half with glomerular hyperfiltration (49·5%; n = 200). Age, male sex, haemoglobin level, leucocyte count, mean corpuscular volume, blood pressure, body mass index and creatinine levels significantly affected albuminuria and/or eGFR. Co-inheritance of alpha-thalassaemia was protective against macro-albuminuria (P = 0·03). APOL1 G1/G2 risk variants were significantly associated with the ACR (P = 0·01) and borderline with eGFR (P = 0·07). HMOX1 - rs743811 was borderline associated with micro-albuminuria (P = 0·07) and macro-albuminuria (P = 0·06). The results revealed a high proportion of micro-albuminuria and glomerular hyperfiltration among Cameroonian SCD patients, and support the possible use of targeted genetic biomarkers for risks assessment.
[Mh] Termos MeSH primário: Anemia Falciforme/complicações
Insuficiência Renal/etiologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Albuminúria/epidemiologia
Albuminúria/etiologia
Albuminúria/genética
Anemia Falciforme/epidemiologia
Anemia Falciforme/genética
Antropometria/métodos
Apolipoproteína L1
Apolipoproteínas/genética
Camarões/epidemiologia
Criança
Pré-Escolar
Feminino
Deleção de Genes
Predisposição Genética para Doença
Variação Genética
Taxa de Filtração Glomerular/genética
Hemoglobina A Glicada/genética
Heme Oxigenase-1/genética
Seres Humanos
Lipoproteínas HDL/genética
Masculino
Meia-Idade
Estudos Prospectivos
Insuficiência Renal/epidemiologia
Insuficiência Renal/genética
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (APOL1 protein, human); 0 (Apolipoprotein L1); 0 (Apolipoproteins); 0 (Glycated Hemoglobin A); 0 (Lipoproteins, HDL); EC 1.14.14.18 (HMOX1 protein, human); EC 1.14.14.18 (Heme Oxygenase-1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180209
[Lr] Data última revisão:
180209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1111/bjh.14724


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[PMID]:29246831
[Au] Autor:Zhang X; Hong XK; Li SJ; Lai DH; Hide G; Lun ZR; Wen YZ
[Ad] Endereço:Center for Parasitic Organisms, State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-Sen University, Guangzhou 510275, PR China.
[Ti] Título:The effect of normal human serum on the mouse trypanosome Trypanosoma musculi in vitro and in vivo.
[So] Source:Exp Parasitol;184:115-120, 2018 Jan.
[Is] ISSN:1090-2449
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Trypanosoma musculi, a common blood flagellate found in mice, is similar in morphology and life cycle to the rat trypanosome T. lewisi. Both species belong to the subgenus Herpetosoma, and as T. lewisi has recently been shown to be a zoonotic pathogen, there is concern that T. musculi could also be potentially infective to humans. To test this hypothesis, a well-established method, the normal human serum (NHS) incubation test, was carried out which distinguishes human and non-human infective trypanosomes. We found that T. musculi could grow in 0.31% NHS in vitro, and even kept their infectivity to mice after incubation with 10% NHS for 24 h. In in vivo experiments, T. musculi were only slightly affected by NHS injection, confirming that it was less sensitive to the NHS than T. b. brucei, but more sensitive than T. lewisi. This resistance probably does not rely on a restricted uptake of ApoL-1. Due to this partial resistance, we cannot definitively confirm that T. musculi has the potential for infection to humans. As resistance is less than that of T. lewisi, our data suggest that it is unlikely to be a zoonotic pathogen although we would advise caution in the case of immunocompromised people such as AIDS and cancer patients.
[Mh] Termos MeSH primário: Hospedeiro Imunocomprometido/imunologia
Soro/imunologia
Trypanosoma/imunologia
Tripanossomíase/imunologia
[Mh] Termos MeSH secundário: Adulto
Animais
Apolipoproteína L1/genética
Apolipoproteína L1/imunologia
Apolipoproteína L1/metabolismo
Western Blotting
DNA de Protozoário/química
DNA de Protozoário/isolamento & purificação
DNA Ribossômico/química
Eletroforese em Gel de Poliacrilamida
Endocitose/imunologia
Haplótipos
Seres Humanos
Hospedeiro Imunocomprometido/genética
Camundongos
Parasitemia/imunologia
Parasitemia/parasitologia
Reação em Cadeia da Polimerase
RNA Ribossômico 18S/genética
Ratos
Ratos Sprague-Dawley
Alinhamento de Sequência
Trypanosoma/genética
Tripanossomíase/genética
Tripanossomíase/parasitologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apolipoprotein L1); 0 (DNA, Protozoan); 0 (DNA, Ribosomal); 0 (RNA, Ribosomal, 18S)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180205
[Lr] Data última revisão:
180205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171217
[St] Status:MEDLINE


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[PMID]:29236630
[Au] Autor:Cohen SD; Kopp JB; Kimmel PL
[Ad] Endereço:From the Division of Renal Diseases and Hypertension, Department of Medicine, George Washington University, Washington, DC (S.D.C., P.L.K.); and the National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD (J.B.K., P.L.K.).
[Ti] Título:Kidney Diseases Associated with Human Immunodeficiency Virus Infection.
[So] Source:N Engl J Med;377(24):2363-2374, 2017 Dec 14.
[Is] ISSN:1533-4406
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Nefropatia Associada a AIDS
Antirretrovirais/uso terapêutico
[Mh] Termos MeSH secundário: Nefropatia Associada a AIDS/diagnóstico
Nefropatia Associada a AIDS/tratamento farmacológico
Nefropatia Associada a AIDS/etiologia
Nefropatia Associada a AIDS/genética
Antirretrovirais/efeitos adversos
Apolipoproteína L1/genética
Infecções por HIV/tratamento farmacológico
Seres Humanos
Falência Renal Crônica/cirurgia
Transplante de Rim
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (APOL1 protein, human); 0 (Anti-Retroviral Agents); 0 (Apolipoprotein L1)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171220
[Lr] Data última revisão:
171220
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171214
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMra1508467


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[PMID]:29059176
[Au] Autor:Ahouty B; Koffi M; Ilboudo H; Simo G; Matovu E; Mulindwa J; Hertz-Fowler C; Bucheton B; Sidibé I; Jamonneau V; MacLeod A; Noyes H; N'Guetta SP; TrypanoGEN Research Group as members of The H3Africa Consortium
[Ad] Endereço:Laboratoire de Génétique, Félix Houphouët Boigny University, Abidjan, Côte d'Ivoire.
[Ti] Título:Candidate genes-based investigation of susceptibility to Human African Trypanosomiasis in Côte d'Ivoire.
[So] Source:PLoS Negl Trop Dis;11(10):e0005992, 2017 Oct.
[Is] ISSN:1935-2735
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human African Trypanosomiasis (HAT) or sleeping sickness is a Neglected Tropical Disease. Long regarded as an invariably fatal disease, there is increasing evidence that infection by T. b. gambiense can result in a wide range of clinical outcomes, including latent infections, which are long lasting infections with no parasites detectable by microscopy. The determinants of this clinical diversity are not well understood but could be due in part to parasite or host genetic diversity in multiple genes, or their interactions. A candidate gene association study was conducted in Côte d'Ivoire using a case-control design which included a total of 233 subjects (100 active HAT cases, 100 controls and 33 latent infections). All three possible pairwise comparisons between the three phenotypes were tested using 96 SNPs in16 candidate genes (IL1, IL4, IL4R, IL6, IL8, IL10, IL12, IL12R, TNFA, INFG, MIF, APOL1, HPR, CFH, HLA-A and HLA-G). Data from 77 SNPs passed quality control. There were suggestive associations at three loci in IL6 and TNFA in the comparison between active cases and controls, one SNP in each of APOL1, MIF and IL6 in the comparison between latent infections and active cases and seven SNP in IL4, HLA-G and TNFA between latent infections and controls. No associations remained significant after Bonferroni correction, but the Benjamini Hochberg false discovery rate test indicated that there were strong probabilities that at least some of the associations were genuine. The excess of associations with latent infections despite the small number of samples available suggests that these subjects form a distinct genetic cluster different from active HAT cases and controls, although no clustering by phenotype was observed by principle component analysis. This underlines the complexity of the interactions existing between host genetic polymorphisms and parasite diversity.
[Mh] Termos MeSH primário: Estudos de Associação Genética
Predisposição Genética para Doença
Tripanossomíase Africana/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Idoso de 80 Anos ou mais
Apolipoproteína L1
Apolipoproteínas/genética
Estudos de Casos e Controles
Criança
Costa do Marfim/epidemiologia
Feminino
Seres Humanos
Interleucina-4/genética
Interleucina-6/genética
Oxirredutases Intramoleculares/genética
Lipoproteínas HDL/genética
Fatores Inibidores da Migração de Macrófagos/genética
Masculino
Meia-Idade
Fenótipo
Polimorfismo de Nucleotídeo Único
Análise de Componente Principal
Trypanosoma brucei gambiense
Tripanossomíase Africana/epidemiologia
Tripanossomíase Africana/parasitologia
Fator de Necrose Tumoral alfa/genética
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (APOL1 protein, human); 0 (Apolipoprotein L1); 0 (Apolipoproteins); 0 (IL4 protein, human); 0 (IL6 protein, human); 0 (Interleukin-6); 0 (Lipoproteins, HDL); 0 (Macrophage Migration-Inhibitory Factors); 0 (Tumor Necrosis Factor-alpha); 207137-56-2 (Interleukin-4); EC 5.3.- (Intramolecular Oxidoreductases); EC 5.3.2.1 (MIF protein, human)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171024
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pntd.0005992


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[PMID]:28784698
[Au] Autor:Jotwani V; Atta MG; Estrella MM
[Ad] Endereço:Kidney Health Research Collaborative, Department of Medicine, University of California, San Francisco, California.
[Ti] Título:Kidney Disease in HIV: Moving beyond HIV-Associated Nephropathy.
[So] Source:J Am Soc Nephrol;28(11):3142-3154, 2017 Nov.
[Is] ISSN:1533-3450
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In developed countries, remarkable advances in antiretroviral therapy have transformed HIV infection into a chronic condition. As a result, HIV-associated nephropathy, the classic HIV-driven kidney lesion among individuals of African descent, has largely disappeared in these regions. However, HIV-positive blacks continue to have much higher rates of ESRD than HIV-positive whites, which could be attributed to the renal risk variants. Additionally, HIV-positive individuals face adverse consequences beyond HIV itself, including traditional risk factors for CKD and nephrotoxic effects of antiretroviral therapy. Concerns for nephrotoxicity also extend to HIV-negative individuals using tenofovir disoproxil fumarate-based pre-exposure prophylaxis for the prevention of HIV infection. Therefore, CKD remains an important comorbid condition in the HIV-positive population and an emerging concern among HIV-negative persons receiving pre-exposure prophylaxis. With the improved longevity of HIV-positive individuals, a kidney transplant has become a viable option for many who have progressed to ESRD. Herein, we review the growing knowledge regarding the renal risk variants in the context of HIV infection, antiretroviral therapy-related nephrotoxicity, and developments in kidney transplantation among HIV-positive individuals.
[Mh] Termos MeSH primário: Infecções por HIV/complicações
Insuficiência Renal Crônica/etiologia
[Mh] Termos MeSH secundário: Nefropatia Associada a AIDS/etiologia
Antirretrovirais/efeitos adversos
Apolipoproteína L1
Apolipoproteínas/genética
Infecções por HIV/tratamento farmacológico
Seres Humanos
Transplante de Rim
Lipoproteínas HDL/genética
Insuficiência Renal Crônica/genética
Insuficiência Renal Crônica/cirurgia
Fatores de Risco
Tenofovir/efeitos adversos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (APOL1 protein, human); 0 (Anti-Retroviral Agents); 0 (Apolipoprotein L1); 0 (Apolipoproteins); 0 (Lipoproteins, HDL); 99YXE507IL (Tenofovir)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170809
[St] Status:MEDLINE
[do] DOI:10.1681/ASN.2017040468


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[PMID]:28732083
[Au] Autor:Stanifer JW; Karia F; Maro V; Kilonzo K; Qin X; Patel UD; Hauser ER
[Ad] Endereço:Department of Medicine, Duke University; Durham, NC United States of America.
[Ti] Título:APOL1 risk alleles among individuals with CKD in Northern Tanzania: A pilot study.
[So] Source:PLoS One;12(7):e0181811, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: In sub-Saharan Africa, approximately 100 million people have CKD, yet genetic risk factors are not well-understood. Despite the potential importance of understanding APOL1 risk allele status among individuals with CKD, little genetic research has been conducted. Therefore, we conducted a pilot study evaluating the feasibility of and willingness to participate in genetic research on kidney disease, and we estimated APOL1 risk allele frequencies among individuals with CKD. METHODS: In 2014, we conducted a community-based field study evaluating CKD epidemiology in northern Tanzania. We assessed for CKD using urine albumin and serum creatinine to estimate GFR. We invited participants with CKD to enroll in an additional genetic study. We obtained dried-blood spots on filter cards, from which we extracted DNA using sterile punch biopsies. We genotyped for two single nucleotide polymorphisms (SNPs) defining the APOL1 G1 risk allele and an insertion/deletion polymorphism defining the G2 risk allele. Genotyping was performed in duplicate. RESULTS: We enrolled 481 participant, 57 (12%) of whom had CKD. Among these, enrollment for genotyping was high (n = 48; 84%). We extracted a median of 19.4 ng of DNA from each dried-blood spot sample, and we genotyped the two APOL1 G1 SNPs and the APOL1 G2 polymorphism. Genotyping quality was high, with all duplicated samples showing perfect concordance. The frequency of APOL1 risk variants ranged from 7.0% to 11.0%, which was similar to previously-reported frequencies from the general population of northern Tanzania (p>0.2). DISCUSSION: In individuals with CKD from northern Tanzania, we demonstrated feasibility of genotyping APOL1 risk alleles. We successfully genotyped three risk variants from DNA extracted from filter cards, and we demonstrated a high enrollment for participation. In this population, more extensive genetic studies of kidney disease may be well-received and will be feasible.
[Mh] Termos MeSH primário: Apolipoproteínas/genética
Predisposição Genética para Doença/genética
Lipoproteínas HDL/genética
Polimorfismo de Nucleotídeo Único/genética
Insuficiência Renal Crônica/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Alelos
Apolipoproteína L1
Estudos Transversais
Feminino
Frequência do Gene/genética
Genótipo
Seres Humanos
Masculino
Meia-Idade
Projetos Piloto
Fatores de Risco
Tanzânia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (APOL1 protein, human); 0 (Apolipoprotein L1); 0 (Apolipoproteins); 0 (Lipoproteins, HDL)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170722
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181811


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[PMID]:28699644
[Au] Autor:Kormann R; Jannot AS; Narjoz C; Ribeil JA; Manceau S; Delville M; Joste V; Prié D; Pouchot J; Thervet E; Courbebaisse M; Arlet JB
[Ad] Endereço:Physiology Department, Georges Pompidou European Hospital, Assistance Publique-Hôpitaux de Paris, Paris, France.
[Ti] Título:Roles of APOL1 G1 and G2 variants in sickle cell disease patients: kidney is the main target.
[So] Source:Br J Haematol;179(2):323-335, 2017 Oct.
[Is] ISSN:1365-2141
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In African-American patients with sickle cell disease (SCD), APOL1 G1 and G2 variants are associated with increased risk of sickle cell nephropathy (SCN). To determine the role of APOL1 variants in SCD patients living in Europe, we genotyped 152 SCD patients [aged 30·4 (24·3-36·4) years], mainly of Sub-Saharan African ancestry, for APOL1 G1 and G2 and for variants of four genes with kidney tropism (GSTM1, GSTT1, GSTP1, and HMOX1). Homozygous or double-heterozygous APOL G1 and G2 genotypes were strongly associated with end stage renal disease (P = 0·003) and worse Kidney Disease: Improving Global Outcomes stages (P = 0·001). Further, these genotypes were associated in an age-dependent manner with lower estimated glomerular filtration rate (eGFR, P = 0·008), proteinuria (P = 0·009) and albuminuria (P < 0·001) but not with other SCD complications. Compared to APOL1 G1/wild type (WT), the APOL1 G2/WT genotype was associated with a lower eGFR (P = 0·04) in an age-dependent manner, suggesting that the G2/WT patients are likely to have worse kidney prognosis. Other genes variants analysed were not associated with SCN or other SCD complications. Our data indicate that APOL1 screening should be considered for the management of SCD patients, including those of non-African-American origin, as those with homozygous or double heterozygous variants are clearly at higher risk of SCN.
[Mh] Termos MeSH primário: Albuminúria
Anemia Falciforme
Apolipoproteínas/genética
Variação Genética
Heterozigoto
Homozigoto
Rim/fisiopatologia
Lipoproteínas HDL/genética
[Mh] Termos MeSH secundário: Adulto
Afroamericanos
Albuminúria/genética
Albuminúria/fisiopatologia
Anemia Falciforme/genética
Anemia Falciforme/fisiopatologia
Apolipoproteína L1
Feminino
Taxa de Filtração Glomerular
Glutationa S-Transferase pi/genética
Glutationa Transferase/genética
Heme Oxigenase-1/genética
Seres Humanos
Masculino
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (APOL1 protein, human); 0 (Apolipoprotein L1); 0 (Apolipoproteins); 0 (Lipoproteins, HDL); EC 1.14.14.18 (HMOX1 protein, human); EC 1.14.14.18 (Heme Oxygenase-1); EC 2.5.1.- (glutathione S-transferase T1); EC 2.5.1.18 (GSTP1 protein, human); EC 2.5.1.18 (Glutathione S-Transferase pi); EC 2.5.1.18 (Glutathione Transferase); EC 2.5.1.18 (glutathione S-transferase M1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170713
[St] Status:MEDLINE
[do] DOI:10.1111/bjh.14842


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[PMID]:28696248
[Au] Autor:Granado D; Müller D; Krausel V; Kruzel-Davila E; Schuberth C; Eschborn M; Wedlich-Söldner R; Skorecki K; Pavenstädt H; Michgehl U; Weide T
[Ad] Endereço:Department of Internal Medicine D and.
[Ti] Título:Intracellular APOL1 Risk Variants Cause Cytotoxicity Accompanied by Energy Depletion.
[So] Source:J Am Soc Nephrol;28(11):3227-3238, 2017 Nov.
[Is] ISSN:1533-3450
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Population genetic approaches have uncovered a strong association between kidney diseases and two sequence variants of the gene, called risk variant G1 and variant G2, compared with the nonrisk G0 allele. However, the mechanism whereby these variants lead to disease manifestation and, in particular, whether this involves an intracellular or extracellular pool of APOL1 remains unclear. Herein, we show a predominantly intracellular localization of APOL1 G0 and the renal risk variants, which localized to membranes of the endoplasmic reticulum in podocyte cell lines. This localization did not depend on the N-terminal signal peptide that mediates APOL1 secretion into the circulation. Additionally, a fraction of these proteins localized to structures surrounding mitochondria. overexpression of G1 or G2 lacking the signal peptide inhibited cell viability, triggered phosphorylation of stress-induced kinases, increased the phosphorylation of AMP-activated protein kinase, reduced intracellular potassium levels, and reduced mitochondrial respiration rates. These findings indicate that functions at intracellular membranes, specifically those of the endoplasmic reticulum and mitochondria, are crucial factors in APOL1 renal risk variant-mediated cell injury.
[Mh] Termos MeSH primário: Apolipoproteínas
Metabolismo Energético
Lipoproteínas HDL
[Mh] Termos MeSH secundário: Apolipoproteína L1
Apolipoproteínas/análise
Apolipoproteínas/genética
Apolipoproteínas/fisiologia
Células Cultivadas
Retículo Endoplasmático/química
Variação Genética
Seres Humanos
Lipoproteínas HDL/análise
Lipoproteínas HDL/genética
Lipoproteínas HDL/fisiologia
Membranas Mitocondriais/química
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (APOL1 protein, human); 0 (Apolipoprotein L1); 0 (Apolipoproteins); 0 (Lipoproteins, HDL)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170712
[St] Status:MEDLINE
[do] DOI:10.1681/ASN.2016111220


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[PMID]:28650456
[Au] Autor:Hayek SS; Koh KH; Grams ME; Wei C; Ko YA; Li J; Samelko B; Lee H; Dande RR; Lee HW; Hahm E; Peev V; Tracy M; Tardi NJ; Gupta V; Altintas MM; Garborcauskas G; Stojanovic N; Winkler CA; Lipkowitz MS; Tin A; Inker LA; Levey AS; Zeier M; Freedman BI; Kopp JB; Skorecki K; Coresh J; Quyyumi AA; Sever S; Reiser J
[Ad] Endereço:Emory Clinical Cardiovascular Research Institute, Division of Cardiology, Emory University School of Medicine, Atlanta, Georgia, USA.
[Ti] Título:A tripartite complex of suPAR, APOL1 risk variants and α ß integrin on podocytes mediates chronic kidney disease.
[So] Source:Nat Med;23(8):945-953, 2017 Aug.
[Is] ISSN:1546-170X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Soluble urokinase plasminogen activator receptor (suPAR) independently predicts chronic kidney disease (CKD) incidence and progression. Apolipoprotein L1 (APOL1) gene variants G1 and G2, but not the reference allele (G0), are associated with an increased risk of CKD in individuals of recent African ancestry. Here we show in two large, unrelated cohorts that decline in kidney function associated with APOL1 risk variants was dependent on plasma suPAR levels: APOL1-related risk was attenuated in patients with lower suPAR, and strengthened in those with higher suPAR levels. Mechanistically, surface plasmon resonance studies identified high-affinity interactions between suPAR, APOL1 and α ß integrin, whereby APOL1 protein variants G1 and G2 exhibited higher affinity for suPAR-activated avb3 integrin than APOL1 G0. APOL1 G1 or G2 augments α ß integrin activation and causes proteinuria in mice in a suPAR-dependent manner. The synergy of circulating factor suPAR and APOL1 G1 or G2 on α ß integrin activation is a mechanism for CKD.
[Mh] Termos MeSH primário: Apolipoproteínas/genética
Integrina alfaVbeta3/metabolismo
Lipoproteínas HDL/genética
Podócitos/metabolismo
Proteinúria/genética
Receptores de Ativador de Plasminogênio Tipo Uroquinase/metabolismo
Insuficiência Renal Crônica/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Afroamericanos
Idoso
Alelos
Animais
Apolipoproteína L1
Apolipoproteínas/metabolismo
Estudos de Coortes
Feminino
Predisposição Genética para Doença
Genótipo
Seres Humanos
Lipoproteínas HDL/metabolismo
Masculino
Camundongos
Meia-Idade
Proteinúria/metabolismo
Insuficiência Renal Crônica/metabolismo
Ressonância de Plasmônio de Superfície
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (APOL1 protein, human); 0 (Apolipoprotein L1); 0 (Apolipoproteins); 0 (Integrin alphaVbeta3); 0 (Lipoproteins, HDL); 0 (Receptors, Urokinase Plasminogen Activator)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170627
[St] Status:MEDLINE
[do] DOI:10.1038/nm.4362


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[PMID]:28572159
[Au] Autor:Chen TK; Appel LJ; Grams ME; Tin A; Choi MJ; Lipkowitz MS; Winkler CA; Estrella MM
[Ad] Endereço:From the Divisions of Nephrology (T.K.C., M.E.G., M.J.C.) and General Internal Medicine (L.J.A.), Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD; Welch Center for Prevention, Epidemiology, and Clinical Research, Johns Hopkins Medical Institutions, Baltimore, MD (L
[Ti] Título: Risk Variants and Cardiovascular Disease: Results From the AASK (African American Study of Kidney Disease and Hypertension).
[So] Source:Arterioscler Thromb Vasc Biol;37(9):1765-1769, 2017 Sep.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Among African Americans, the apolipoprotein L1 ( ) risk variants have been associated with various types of kidney disease and chronic kidney disease progression. We aimed to determine whether these same risk variants also confer an increased risk for cardiovascular disease. APPROACH AND RESULTS: In a cohort of African Americans with hypertension-attributed chronic kidney disease followed for up to 12 years, we used Cox proportional hazards models to estimate the relative hazard of a composite cardiovascular disease outcome (cardiovascular death or hospitalization for myocardial infarction, cardiac revascularization procedure, heart failure, or stroke) for the high- (2 risk variants) versus low-risk (0-1 risk variant) genotypes. We adjusted for age, sex, ancestry, smoking, heart disease history, body mass index, cholesterol, randomized treatment groups, and baseline and longitudinal estimated glomerular filtration rate, systolic blood pressure, and proteinuria. Among 693 participants with genotyping available (23% high risk), the high-risk group had lower mean estimated glomerular filtration rate (44.7 versus 50.1 mL/min per 1.73 m ) and greater proteinuria (median 0.19 versus 0.06) compared with the low-risk group at baseline. There was no significant association between genotypes and the composite cardiovascular disease outcome in both unadjusted (hazard ratio=1.23; 95% confidence interval: 0.83-1.81) and fully adjusted (hazard ratio=1.16; 95% confidence interval: 0.77-1.76) models; however, in using an additive model, high-risk variants were associated with increased cardiovascular mortality. CONCLUSIONS: Among African Americans with hypertension-attributed chronic kidney disease, risk variants were not associated with an overall risk for cardiovascular disease although some signals for cardiovascular mortality were noted.
[Mh] Termos MeSH primário: Afroamericanos/genética
Apolipoproteínas/genética
Variação Genética
Insuficiência Cardíaca/genética
Hipertensão/genética
Lipoproteínas HDL/genética
Infarto do Miocárdio/genética
Insuficiência Renal Crônica/genética
Acidente Vascular Cerebral/genética
[Mh] Termos MeSH secundário: Adulto
Apolipoproteína L1
Distribuição de Qui-Quadrado
Progressão da Doença
Feminino
Estudos de Associação Genética
Predisposição Genética para Doença
Insuficiência Cardíaca/etnologia
Insuficiência Cardíaca/mortalidade
Insuficiência Cardíaca/terapia
Hospitalização
Seres Humanos
Hipertensão/etnologia
Hipertensão/mortalidade
Incidência
Estimativa de Kaplan-Meier
Masculino
Meia-Idade
Infarto do Miocárdio/etnologia
Infarto do Miocárdio/mortalidade
Infarto do Miocárdio/terapia
Revascularização Miocárdica
Fenótipo
Prognóstico
Modelos de Riscos Proporcionais
Insuficiência Renal Crônica/etnologia
Insuficiência Renal Crônica/mortalidade
Medição de Risco
Fatores de Risco
Acidente Vascular Cerebral/etnologia
Acidente Vascular Cerebral/mortalidade
Acidente Vascular Cerebral/terapia
Fatores de Tempo
Estados Unidos/epidemiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (APOL1 protein, human); 0 (Apolipoprotein L1); 0 (Apolipoproteins); 0 (Lipoproteins, HDL)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170603
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.309384



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