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#34138902   2021/06/17 To Up

Lack of APOL1 in proximal tubules of normal human kidneys and proteinuric APOL1 transgenic mouse kidneys.

The mechanism of pathogenesis associated with APOL1 polymorphisms and risk for non-diabetic chronic kidney disease (CKD) is not fully understood. Prior studies have minimized a causal role for the circulating APOL1 protein, thus efforts to understand kidney pathogenesis have focused on APOL1 expressed in renal cells. Of the kidney cells reported to express APOL1, the proximal tubule expression patterns are inconsistent in published reports, and whether APOL1 is synthesized by the proximal tubule or possibly APOL1 protein in the blood is filtered and reabsorbed by the proximal tubule remains unclear. Using both protein and mRNA in situ methods, the kidney expression pattern of APOL1 was examined in normal human and APOL1 bacterial artificial chromosome transgenic mice with and without proteinuria. APOL1 protein and mRNA was detected in podocytes and endothelial cells, but not in tubular epithelia. In the setting of proteinuria, plasma APOL1 protein did not appear to be filtered or reabsorbed by the proximal tubule. A side-by-side examination of commercial antibodies used in prior studies suggest the original reports of APOL1 in proximal tubules likely reflects antibody non-specificity. As such, APOL1 expression in podocytes and endothelia should remain the focus for mechanistic studies in the APOL1-mediated kidney diseases.
Natalya A Blessing, Zhenzhen Wu, Sethu M Madhavan, Jonathan W Choy, Michelle Chen, Myung K Shin, Maarten Hoek, John R Sedor, John F O'Toole, Leslie A Bruggeman

2710 related Products with: Lack of APOL1 in proximal tubules of normal human kidneys and proteinuric APOL1 transgenic mouse kidneys.

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#33767059   // To Up

Apolipoprotein L1 and mechanisms of kidney disease susceptibility.

Allelic variants in the gene for apolipoprotein L1 (APOL1), found only in individuals of African ancestry, explain a majority of the excess risk of kidney disease in African Americans. However, a clear understanding how the disease-associated APOL1 variants cause kidney injury and the identity of environmental stressors that trigger the injury process have not been determined.
Leslie A Bruggeman, John R Sedor, John F O'Toole

2798 related Products with: Apolipoprotein L1 and mechanisms of kidney disease susceptibility.

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#33576823   2021/02/12 To Up

The spectrum of kidney biopsies in hospitalized patients with COVID-19, acute kidney injury, and/or proteinuria.

We report a multicentric retrospective case series of patients with COVID-19 who developed acute kidney injury and/or proteinuria and underwent a kidney biopsy in the Paris and its metropolitan area. Forty-seven patients (80.9% men) with COVID-19 who underwent a kidney biopsy between March 08 and May 19, 2020 were included. Median age was 63 years IQR [52-69]. Comorbidities included hypertension (66.0%), diabetes mellitus (27.7%), obesity (27.7%), history of chronic kidney (25.5%), cardiac (38.6%) and respiratory (27.3%) diseases. Initial symptoms were fever (85.1%), cough (63.8%), shortness of breath (55.3%), and diarrhea (23.4%). Almost all patients developed acute kidney injury (97.9%) and 63.8% required renal replacement therapy. Kidney biopsy showed two main histopathological patterns, including acute tubular injury in 20 (42.6%) patients, and glomerular injury consisting of collapsing glomerulopathy and focal segmental glomerulosclerosis in 17 (36.2%) patients. Two (4.3%) patients had acute vascular nephropathy, while eight (17%) had alternative diagnosis most likely unrelated to COVID-19. Acute tubular injury occurred almost invariably in the setting of severe forms of COVID-19, whereas patients with glomerular injury had various profiles of COVID-19 severity and collapsing glomerulopathy was only observed in patients harboring a combination of APOL1 risk variants. At last follow-up, 16 of the 30 patients who initially required dialysis were still on dialysis, and 9 died. The present study describes the spectrum of kidney lesions in patients with COVID-19. While acute tubular injury is correlated with COVID-19 severity, the pattern of glomerular injury is intimately associated with the expression of APOL1 risk variants.
Sophie Ferlicot, Matthieu Jamme, François Gaillard, Julie Oniszczuk, Aymeric Couturier, Olivia May, Anne Grünenwald, Aurélie Sannier, Anissa Moktefi, Ophélie Le Monnier, Camille Petit-Hoang, Nadine Maroun, Albane Brodin-Sartorius, Arthur Michon, Hélène Dobosziewicz, Fabrizio Andreelli, Matthieu Guillet, Hassane Izzedine, Christian Richard, Manon Dekeyser, Romain Arrestier, Thomas Sthelé, Edouard Lefèvre, Alexis Mathian, Christophe Legendre, Charlotte Mussini, Marie-Christine Verpont, Nicolas Pallet, Zahir Amoura, Marie Essig, Renaud Snanoudj, Isabelle Brocheriou-Spelle, Hélène François, Xavier Belenfant, Guillaume Geri, Eric Daugas, Vincent Audard, David Buob, Ziad A Massy, Mohamad Zaidan,

2627 related Products with: The spectrum of kidney biopsies in hospitalized patients with COVID-19, acute kidney injury, and/or proteinuria.

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#33119586   2020/10/29 To Up

Schistosoma mansoni infection as a trigger to collapsing glomerulopathy in a patient with high-risk APOL1 genotype.

Schistosoma mansoni schistosomiasis (SM) remains a public health problem in Brazil. Renal involvement is classically manifested as a glomerulopathy, most often membranoproliferative glomerulonephritis or focal and segmental glomerulosclerosis. We report a case of collapsing glomerulopathy (CG) associated with SM and high-risk APOL1 genotype (HRG).
Precil D Neves, Ramaiane A Bridi, Janaína A Ramalho, Lectícia B Jorge, Elieser H Watanabe, Andreia Watanabe, Luis Yu, Viktoria Woronik, Rafaela B Pinheiro, Leonardo A Testagrossa, Lívia B Cavalcante, Denise M Malheiros, Cristiane B Dias, Luiz F Onuchic

2961 related Products with: Schistosoma mansoni infection as a trigger to collapsing glomerulopathy in a patient with high-risk APOL1 genotype.

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#32889430   2020/08/20 To Up

The Trypanosoma Brucei KIFC1 Kinesin Ensures the Fast Antibody Clearance Required for Parasite Infectivity.

Human innate immunity to Trypanosoma brucei involves the trypanosome C-terminal kinesin TbKIFC1, which transports internalized trypanolytic factor apolipoprotein L1 (APOL1) within the parasite. We show that TbKIFC1 preferentially associates with cholesterol-containing membranes and is indispensable for mammalian infectivity. Knockdown of TbKIFC1 did not affect trypanosome growth in vitro but rendered the parasites unable to infect mice unless antibody synthesis was compromised. Surface clearance of Variant Surface Glycoprotein (VSG)-antibody complexes was far slower in these cells, which were more susceptible to capture by macrophages. This phenotype was not due to defects in VSG expression or trafficking but to decreased VSG mobility in a less fluid, stiffer surface membrane. This change can be attributed to increased cholesterol level in the surface membrane in TbKIFC1 knockdown cells. Clearance of surface-bound antibodies by T. brucei is therefore essential for infectivity and depends on high membrane fluidity maintained by the cholesterol-trafficking activity of TbKIFC1.
Laurence Lecordier, Sophie Uzureau, Gilles Vanwalleghem, Magali Deleu, Jean-Marc Crowet, Paul Barry, Barry Moran, Paul Voorheis, Andra-Cristina Dumitru, Yoshiki Yamaryo-Botté, Marc Dieu, Patricia Tebabi, Benoit Vanhollebeke, Laurence Lins, Cyrille Y Botté, David Alsteens, Yves Dufrêne, David Pérez-Morga, Derek P Nolan, Etienne Pays

1399 related Products with: The Trypanosoma Brucei KIFC1 Kinesin Ensures the Fast Antibody Clearance Required for Parasite Infectivity.

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#32764142   2020/08/06 To Up

Apolipoprotein L1-Specific Antibodies Detect Endogenous APOL1 inside the Endoplasmic Reticulum and on the Plasma Membrane of Podocytes.

APOL1 is found in human kidney podocytes and endothelia. Variants G1 and G2 of the gene account for the high frequency of nondiabetic CKD among African Americans. Proposed mechanisms of kidney podocyte cytotoxicity resulting from variant overexpression implicate different subcellular compartments. It is unclear where endogenous podocyte APOL1 resides, because previous immunolocalization studies utilized overexpressed protein or commercially available antibodies that crossreact with APOL2. This study describes and distinguishes the locations of both APOLs.
Suzie J Scales, Nidhi Gupta, Ann M De Mazière, George Posthuma, Cecilia P Chiu, Andrew A Pierce, Kathy Hötzel, Jianhua Tao, Oded Foreman, Georgios Koukos, Francesca Oltrabella, Judith Klumperman, WeiYu Lin, Andrew S Peterson

1388 related Products with: Apolipoprotein L1-Specific Antibodies Detect Endogenous APOL1 inside the Endoplasmic Reticulum and on the Plasma Membrane of Podocytes.

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#32764138   2020/08/06 To Up

Domain-Specific Antibodies Reveal Differences in the Membrane Topologies of Apolipoprotein L1 in Serum and Podocytes.

Circulating APOL1 lyses trypanosomes, protecting against human sleeping sickness. Two common African gene variants of , G1 and G2, protect against infection by species of trypanosomes that resist wild-type APOL1. At the same time, the protection predisposes humans to CKD, an elegant example of balanced polymorphism. However, the exact mechanism of APOL1-mediated podocyte damage is not clear, including APOL1's subcellular localization, topology, and whether the damage is related to trypanolysis.
Nidhi Gupta, Xinhua Wang, Xiaohui Wen, Paul Moran, Maciej Paluch, Philip E Hass, Amy Heidersbach, Benjamin Haley, Daniel Kirchhofer, Randall J Brezski, Andrew S Peterson, Suzie J Scales

2032 related Products with: Domain-Specific Antibodies Reveal Differences in the Membrane Topologies of Apolipoprotein L1 in Serum and Podocytes.

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#32668317   2020/07/12 To Up

COVID-19-Related Collapsing Glomerulopathy in a Kidney Transplant Recipient.

We report a case of a kidney transplant recipient who presented with acute kidney injury and nephrotic-range proteinuria in a context of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Kidney biopsy revealed collapsing glomerulopathy. Droplet-based digital polymerase chain reaction did not detect the presence of SARS-CoV-2 RNA in the biopsy fragment, and the virus was barely detectable in plasma at the time of the biopsy. SARS-CoV-2 RNAemia peaked several days later, followed by a seroconversion despite the absence of circulating CD19-positive lymphocytes at admission due to rituximab-based treatment of antibody-mediated rejection 3 months earlier. Genotyping for the 2 risk alleles of the apolipoprotein L1 (APOL1) gene revealed that the donor carried the low-risk G0/G2 genotype. This case illustrates that coronavirus disease 2019 infection may promote a collapsing glomerulopathy in kidney allografts with a low-risk APOL1 genotype in the absence of detectable SARS-CoV-2 RNA in the kidney and that podocyte injury may precede SARS-CoV-2 RNAemia.
Hélène Lazareth, Hélène Péré, Yannick Binois, Melchior Chabannes, Juliet Schurder, Thomas Bruneau, Alexandre Karras, Eric Thervet, Marion Rabant, David Veyer, Nicolas Pallet

2359 related Products with: COVID-19-Related Collapsing Glomerulopathy in a Kidney Transplant Recipient.

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