keyword
https://read.qxmd.com/read/38496548/hiv-1-nef-acts-in-synergy-with-apol1-g1-to-induce-nephrocyte-cell-death-in-a-new-drosophila-model-of-hiv-related-kidney-diseases
#1
Jun-Yi Zhu, Yulong Fu, Joyce van de Leemput, Ying Yu, Jinliang Li, Patricio E Ray, Zhe Han
BACKGROUND: People carrying two APOL1 risk alleles (RA) G1 or G2 are at greater risk of developing HIV-associated nephropathy (HIVAN). Studies in transgenic mice showed that the expression of HIV-1 genes in podocytes, and nef in particular, led to HIVAN. However, it remains unclear whether APOL1-RA and HIV-1 Nef interact to induce podocyte cell death. METHOD: We generated transgenic (Tg) flies that express APOL1-G1 (derived from a child with HIVAN) and HIV-1 nef specifically in the nephrocytes, the fly equivalent of mammalian podocytes, and assessed their individual and combined effects on the nephrocyte filtration structure and function...
March 10, 2024: bioRxiv
https://read.qxmd.com/read/38415700/apol1-nephropathy-a-population-genetics-success-story
#2
JOURNAL ARTICLE
Orly Tabachnikov, Karl Skorecki, Etty Kruzel-Davila
PURPOSE OF REVIEW: More than a decade ago, apolipoprotein L1 (APOL1) risk alleles designated G1 and G2, were discovered to be causally associated with markedly increased risk for progressive kidney disease in individuals of recent African ancestry. Gratifying progress has been made during the intervening years, extending to the development and clinical testing of genomically precise small molecule therapy accompanied by emergence of RNA medicine platforms and clinical testing within just over a decade...
February 29, 2024: Current Opinion in Nephrology and Hypertension
https://read.qxmd.com/read/38345208/-the-highlights-in-nephrology-in-2023
#3
JOURNAL ARTICLE
Mickaël Bobot, Sandrine Lemoine
This article aims to summarize the “Quoi de neuf en néphrologie?” session held at the 2023 SFNDT Congress in Liège and sessions focused on updates regarding IgA nephropathy (NIgA) and ANCA-associated vasculitis. The agenda for the nephrology “Quoi de neuf en néphrologie?” session this year was to review key publications from non-nephrology journals, discussing topics such as nephroprotection, treatment of glomerulopathies (IgA and APOL1), clinical trials on arterial hypertension, urinary lithiasis, and other areas of renal physiology, including glomerular filtration rate estimation...
February 12, 2024: Néphrologie & Thérapeutique
https://read.qxmd.com/read/38341125/apol1-nephropathy-risk-variants-through-the-life-course-a-review
#4
REVIEW
Ai Itoku, Jaya Isaac, Scott Wilson, Kimberly Reidy, Frederick Kaskel
Two variant alleles of the gene APOL1, known as risk variants (RVs), are a major contributor to kidney disease burden in those of African descent. The APOL1 protein contributes to innate immunity and may protect against trypanosoma, human immunodeficiency virus, salmonella, and leishmaniasis. However, the effects of carrying one or more RVs contribute to a variety of disease processes starting as early as in utero and can be exacerbated by other factors (or "second hits"). Indeed, these genetic variations interact with environmental exposures, infections, and systemic disease to modify health outcomes across one's lifespan...
February 8, 2024: American Journal of Kidney Diseases
https://read.qxmd.com/read/38273026/the-changing-landscape-of-hiv-associated-kidney-disease
#5
REVIEW
Nina E Diana, Saraladevi Naicker
The HIV epidemic has devastated millions of people globally, with approximately 40 million deaths since its start. The availability of antiretroviral therapy (ART) has transformed the prognosis of millions of individuals infected with HIV such that a diagnosis of HIV infection no longer automatically confers death. However, morbidity and mortality remain substantial among people living with HIV. HIV can directly infect the kidney to cause HIV-associated nephropathy (HIVAN) - a disease characterized by podocyte and tubular damage and associated with an increased risk of kidney failure...
January 25, 2024: Nature Reviews. Nephrology
https://read.qxmd.com/read/38246019/association-of-normal-and-mutated-apol1-g2-rs60910145-alleles-with-scd-body-mass-index-and-renal-function-biomarkers-and-indices
#6
JOURNAL ARTICLE
Abazar Mahmoud Ismail, Bakri Mohammed Nour, Adam Dawoud Abakar, Babiker Saad Almugadam, Hisham N Altayb, Rania TagEsir Ahmed, Mubarak Elsaeed Mustafa Elkarsany
PURPOSE OF THE STUDY: The current study aimed to detect the frequency of normal and mutated APOL1 alleles in sickle cell disease (SCD) patients and test their relation with Microalbuminuria, Creatinine, Urea, Glomerular Filtration Rate (GFR), and Body Mass Index (BMI). PATIENTS AND METHODS: The study included 156 SCD subjects. Serum Creatinine (mg/dl) and Urea (mg/dl) as well as Microalbuminuria (mg/l) level were measured by using Biosystems kit (Biosystems, Barcelona, Spain) and Mindary BA88A semi-automated biochemistry analyzer...
September 29, 2023: Current Research in Translational Medicine
https://read.qxmd.com/read/38041817/apolipoproteins-l1-and-l3-control-mitochondrial-membrane-dynamics
#7
JOURNAL ARTICLE
Laurence Lecordier, Paul Heo, Jonas H Graversen, Dorle Hennig, Maria Kløjgaard Skytthe, Alexandre Cornet d'Elzius, Frédéric Pincet, David Pérez-Morga, Etienne Pays
Apolipoproteins L1 and L3 (APOLs) are associated at the Golgi with the membrane fission factors phosphatidylinositol 4-kinase-IIIB (PI4KB) and non-muscular myosin 2A. Either APOL1 C-terminal truncation (APOL1Δ) or APOL3 deletion (APOL3-KO [knockout]) reduces PI4KB activity and triggers actomyosin reorganization. We report that APOL3, but not APOL1, controls PI4KB activity through interaction with PI4KB and neuronal calcium sensor-1 or calneuron-1. Both APOLs are present in Golgi-derived autophagy-related protein 9A vesicles, which are involved in PI4KB trafficking...
December 1, 2023: Cell Reports
https://read.qxmd.com/read/38036523/strong-protective-effect-of-the-apol1-p-n264k-variant-against-g2-associated-focal-segmental-glomerulosclerosis-and-kidney-disease
#8
JOURNAL ARTICLE
Yask Gupta, David J Friedman, Michelle T McNulty, Atlas Khan, Brandon Lane, Chen Wang, Juntao Ke, Gina Jin, Benjamin Wooden, Andrea L Knob, Tze Y Lim, Gerald B Appel, Kinsie Huggins, Lili Liu, Adele Mitrotti, Megan C Stangl, Andrew Bomback, Rik Westland, Monica Bodria, Maddalena Marasa, Ning Shang, David J Cohen, Russell J Crew, William Morello, Pietro Canetta, Jai Radhakrishnan, Jeremiah Martino, Qingxue Liu, Wendy K Chung, Angelica Espinoza, Yuan Luo, Wei-Qi Wei, Qiping Feng, Chunhua Weng, Yilu Fang, Iftikhar J Kullo, Mohammadreza Naderian, Nita Limdi, Marguerite R Irvin, Hemant Tiwari, Sumit Mohan, Maya Rao, Geoffrey K Dube, Ninad S Chaudhary, Orlando M Gutiérrez, Suzanne E Judd, Mary Cushman, Leslie A Lange, Ethan M Lange, Daniel L Bivona, Miguel Verbitsky, Cheryl A Winkler, Jeffrey B Kopp, Dominick Santoriello, Ibrahim Batal, Sérgio Veloso Brant Pinheiro, Eduardo Araújo Oliveira, Ana Cristina Simoes E Silva, Isabella Pisani, Enrico Fiaccadori, Fangming Lin, Loreto Gesualdo, Antonio Amoroso, Gian Marco Ghiggeri, Vivette D D'Agati, Riccardo Magistroni, Eimear E Kenny, Ruth J F Loos, Giovanni Montini, Friedhelm Hildebrandt, Dirk S Paul, Slavé Petrovski, David B Goldstein, Matthias Kretzler, Rasheed Gbadegesin, Ali G Gharavi, Krzysztof Kiryluk, Matthew G Sampson, Martin R Pollak, Simone Sanna-Cherchi
African Americans have a significantly higher risk of developing chronic kidney disease, especially focal segmental glomerulosclerosis -, than European Americans. Two coding variants (G1 and G2) in the APOL1 gene play a major role in this disparity. While 13% of African Americans carry the high-risk recessive genotypes, only a fraction of these individuals develops FSGS or kidney failure, indicating the involvement of additional disease modifiers. Here, we show that the presence of the APOL1 p.N264K missense variant, when co-inherited with the G2 APOL1 risk allele, substantially reduces the penetrance of the G1G2 and G2G2 high-risk genotypes by rendering these genotypes low-risk...
November 30, 2023: Nature Communications
https://read.qxmd.com/read/37927001/local-inflammation-but-not-kidney-cell-infection-associated-with-high-apol1-expression-in-covid-associated-nephropathy
#9
JOURNAL ARTICLE
Jane K Nguyen, Zhenzhen Wu, Jose Agudelo, Leal C Herlitz, Aaron W Miller, Leslie A Bruggeman
No abstract text is available yet for this article.
November 6, 2023: Kidney360
https://read.qxmd.com/read/37925499/a-snare-protective-pool-antagonizes-apol1-renal-toxicity-in-drosophila-nephrocytes
#10
JOURNAL ARTICLE
Jin-Gu Lee, Yulong Fu, Jun-Yi Zhu, Pei Wen, Joyce van de Leemput, Patricio E Ray, Zhe Han
BACKGROUND: People of Sub-Saharan African ancestry are at higher risk of developing chronic kidney disease (CKD), attributed to the Apolipoprotein L1 (APOL1) gene risk alleles (RA) G1 and G2. The underlying mechanisms by which the APOL1-RA precipitate CKD remain elusive, hindering the development of potential treatments. RESULTS: Using a Drosophila genetic modifier screen, we found that SNARE proteins (Syx7, Ykt6, and Syb) play an important role in preventing APOL1 cytotoxicity...
November 4, 2023: Cell & Bioscience
https://read.qxmd.com/read/37901695/viral-glomerulopathy
#11
REVIEW
Margaret Deoliveira, Hridyesh Sikri, Samuel Mon-Wei Yu, John Cijiang He
BACKGROUND: The association between viral infections and glomerular diseases, commonly known as "viral glomerulopathies," has been described in various clinical scenarios for decades. Despite advancements in diagnostic tools, it remains challenging to establish a causative link fully. SUMMARY: Data from mouse models have substantiated clinical observations and implicate direct viral infection in the pathogenesis of viral glomerulopathy, particularly in human immunodeficiency virus-associated nephropathy...
2023: Glomerular diseases
https://read.qxmd.com/read/37577628/strong-protective-effect-of-the-apol1-p-n264k-variant-against-g2-associated-focal-segmental-glomerulosclerosis-and-kidney-disease
#12
Yask Gupta, David J Friedman, Michelle McNulty, Atlas Khan, Brandon Lane, Chen Wang, Juntao Ke, Gina Jin, Benjamin Wooden, Andrea L Knob, Tze Y Lim, Gerald B Appel, Kinsie Huggins, Lili Liu, Adele Mitrotti, Megan C Stangl, Andrew Bomback, Rik Westland, Monica Bodria, Maddalena Marasa, Ning Shang, David J Cohen, Russell J Crew, William Morello, Pietro Canetta, Jai Radhakrishnan, Jeremiah Martino, Qingxue Liu, Wendy K Chung, Angelica Espinoza, Yuan Luo, Wei-Qi Wei, Qiping Feng, Chunhua Weng, Yilu Fang, Iftikhar J Kullo, Mohammadreza Naderian, Nita Limdi, Marguerite R Irvin, Hemant Tiwari, Sumit Mohan, Maya Rao, Geoffrey Dube, Ninad S Chaudhary, Orlando M Gutiérrez, Suzanne E Judd, Mary Cushman, Leslie A Lange, Ethan M Lange, Daniel L Bivona, Miguel Verbitsky, Cheryl A Winkler, Jeffrey B Kopp, Dominick Santoriello, Ibrahim Batal, Sérgio Veloso Brant Pinheiro, Eduardo Araújo Oliveira, Ana Cristina Simoes E Silva, Isabella Pisani, Enrico Fiaccadori, Fangming Lin, Loreto Gesualdo, Antonio Amoroso, Gian Marco Ghiggeri, Vivette D D'Agati, Riccardo Magistroni, Eimear E Kenny, Ruth J F Loos, Giovanni Montini, Friedhelm Hildebrandt, Dirk S Paul, Slavé Petrovski, David B Goldstein, Matthias Kretzler, Rasheed Gbadegesin, Ali G Gharavi, Krzysztof Kiryluk, Matthew G Sampson, Martin R Pollak, Simone Sanna-Cherchi
Black Americans have a significantly higher risk of developing chronic kidney disease (CKD), especially focal segmental glomerulosclerosis (FSGS), than European Americans. Two coding variants (G1 and G2) in the APOL1 gene play a major role in this disparity. While 13% of Black Americans carry the high-risk recessive genotypes, only a fraction of these individuals develops FSGS or kidney failure, indicating the involvement of additional disease modifiers. Here, we show that the presence of the APOL1 p.N264K missense variant, when co-inherited with the G2 APOL1 risk allele, substantially reduces the penetrance of the G1G2 and G2G2 high-risk genotypes by rendering these genotypes low-risk...
August 4, 2023: medRxiv
https://read.qxmd.com/read/37511514/towards-the-definition-of-the-molecular-hallmarks-of-idiopathic-membranous-nephropathy-in-serum-proteome-a-dia-pasef-approach
#13
JOURNAL ARTICLE
Paolo Previtali, Lisa Pagani, Giulia Risca, Giulia Capitoli, Eleonora Bossi, Glenda Oliveira, Isabella Piga, Antonella Radice, Barbara Trezzi, Renato Alberto Sinico, Fulvio Magni, Clizia Chinello
Idiopathic membranous nephropathy (IMN) is a pathologically defined disorder of the glomerulus, primarily responsible for nephrotic syndromes (NS) in nondiabetic adults. The underlying molecular mechanisms are still not completely clarified. To explore possible molecular and functional signatures, an optimised mass spectrometry (MS) method based on next-generation data-independent acquisition combined with ion-mobility was applied to serum of patients affected by IMN (n = 15) or by other glomerulopathies (PN) (n = 15)...
July 21, 2023: International Journal of Molecular Sciences
https://read.qxmd.com/read/37485073/successful-treatment-of-covid-19-associated-collapsing-glomerulopathy-22-months-of-follow-up
#14
Pulkit Gandhi, Caoimhe Sorcha Dowling, Anjali Satoskar, Ankur Shah
The term COVAN (COVID-19-associated nephropathy) has been used to describe collapsing focal segmental glomerulosclerosis (FSGS) in individuals who have been infected with the SARS-CoV-2. This helps differentiate it from the majority of cases of acute kidney injury in COVID-19 patients, which are typically caused by acute tubular injury. The exact pathophysiology is unclear but is proposed to involve pro-inflammatory cytokines such as type 1 interferons, which are thought to increase expression of the APOL1 gene in glomerular epithelial cells...
2023: Clinical Nephrology. Case Studies
https://read.qxmd.com/read/37274308/covid-19-and-glomerular-diseases
#15
REVIEW
Nattawat Klomjit, Ladan Zand, Lynn D Cornell, Mariam Priya Alexander
COVID-19 is a systemic disease, and the kidney is one of the target organs of infection. Kidney injury is common and can occur in up to 40% of patients. Several glomerular diseases have been reported in association with COVID-19. Some are likely related to COVID-19 whereas many are likely coincidental. Glomerular diseases that are frequently reported in COVID-19 and have a plausible mechanistic explanation are likely to be related to COVID-19. In contrast, glomerular diseases that are seldom reported and have no known plausible mechanism, are likely to be unrelated...
June 2023: KI Reports
https://read.qxmd.com/read/37261508/the-metabolic-effects-of-apol1-in-humans
#16
REVIEW
María M Adeva-Andany, Raquel Funcasta-Calderón, Carlos Fernández-Fernández, Eva Ameneiros-Rodríguez, Matilde Vila-Altesor, Elvira Castro-Quintela
Harboring apolipoprotein L1 (APOL1) variants coded by the G1 or G2 alleles of the APOL1 gene increases the risk for collapsing glomerulopathy, focal segmental glomerulosclerosis, albuminuria, chronic kidney disease, and accelerated kidney function decline towards end-stage kidney disease. However, most subjects carrying APOL1 variants do not develop the kidney phenotype unless a second clinical condition adds to the genotype, indicating that modifying factors modulate the genotype-phenotype correlation. Subjects with an APOL1 high-risk genotype are more likely to develop essential hypertension or obesity, suggesting that carriers of APOL1 risk variants experience more pronounced insulin resistance compared to noncarriers...
June 1, 2023: Pflügers Archiv: European Journal of Physiology
https://read.qxmd.com/read/37090576/apol1-kidney-risk-variants-in-glomerular-diseases-modeled-in-transgenic-mice
#17
Teruhiko Yoshida, Khun Zaw Latt, Briana A Santo, Shashi Shrivastav, Yongmei Zhao, Paride Fenaroli, Joon-Yong Chung, Stephen M Hewitt, Vincent M Tutino, Pinaki Sarder, Avi Z Rosenberg, Cheryl A Winkler, Jeffrey B Kopp
APOL1 high-risk variants partially explain the high kidney disease prevalence among African ancestry individuals. Many mechanisms have been reported in cell culture models, but few have been demonstrated in mouse models. Here we characterize two models: (1) HIV-associated nephropathy (HIVAN) Tg26 mice crossed with bacterial artificial chromosome (BAC)/APOL1 transgenic mice and (2) interferon-γ administered to BAC/APOL1 mice. Both models showed exacerbated glomerular disease in APOL1-G1 compared to APOL1-G0 mice...
March 27, 2023: bioRxiv
https://read.qxmd.com/read/37024977/coronavirus-disease-2019-associated-nephropathy-in-an-african-american-patient-a-case-report-and-review-of-the%C3%A2-literature
#18
REVIEW
Vijaypal S Dhillon, Ahmad Alkashash, Karolina Viquez-Beita
BACKGROUND: Acute kidney injury is now recognized as a common complication of coronavirus disease 2019, affecting up to 46% of patients, with acute tubular injury as the most common etiology. Recently, we have seen an increase in cases of collapsing glomerulonephritis in patients with coronavirus disease 2019, also known as coronavirus disease 2019-associated nephropathy. It has been noted to be seen with a higher incidence in African American patients who are carriers of the APOL1 variant allele...
April 7, 2023: Journal of Medical Case Reports
https://read.qxmd.com/read/36816427/hiv-associated-nephropathy-in-2022
#19
REVIEW
Frederick Berro Rivera, Marie Francesca Mapua Ansay, Jem Marie Golbin, Pia Gabrielle I Alfonso, Gerard Francis E Mangubat, Rajiv Hans Solita Menghrajani, Siena Placino, Marianne Katharina Vicera Taliño, Deogracias Villa De Luna, Nicolo Cabrera, Carlo Nemesio Trinidad, Amir Kazory
BACKGROUND: HIV-associated nephropathy (HIVAN) is a renal parenchymal disease that occurs exclusively in people living with HIV. It is a serious kidney condition that may possibly lead to end-stage kidney disease, particularly in the HIV-1 seropositive patients. SUMMARY: The African-American population has increased susceptibility to this comorbidity due to a strong association found in the APOL1 gene, specifically two missense mutations in the G1 allele and a frameshift deletion in the G2 allele, although a "second-hit" event is postulated to have a role in the development of HIVAN...
2023: Glomerular diseases
https://read.qxmd.com/read/36763808/kidney-disease-progression-in-membranous-nephropathy-among-black-participants-with-high-risk-apol1-genotype
#20
JOURNAL ARTICLE
Dhruti P Chen, Candace D Henderson, Jaeline Anguiano, Claudia P Aiello, Mary M Collie, Vanessa Moreno, Yichun Hu, Susan L Hogan, Ronald J Falk
BACKGROUND: Disparity in CKD progression among Black individuals persists in glomerular diseases. Genetic variants in the Apolipoprotein L1 (APOL1) gene in the Black population contribute to kidney disease, but the influence in membranous nephropathy remains unknown. METHODS: Longitudinally followed participants enrolled in the Glomerular Disease Collaborative Network or Cure Glomerulonephropathy Network were included if they had DNA or genotyping available for APOL1 (Black participants with membranous nephropathy) or had membranous nephropathy but were not Black...
January 18, 2023: Clinical Journal of the American Society of Nephrology: CJASN
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