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Article ; Online: The complexity of nicotinamide adenine dinucleotide (NAD), hypoxic, and aryl hydrocarbon receptor cell signaling in chronic kidney disease

Colleen S. Curran / Jeffrey B. Kopp

Journal of Translational Medicine, Vol 21, Iss 1, Pp 1-

2023 Volume 19

Abstract: Abstract Early-stage detection of chronic kidney diseases (CKD) is important to treatment that may slow and occasionally halt CKD progression. CKD of diverse etiologies share similar histologic patterns of glomerulosclerosis, tubular atrophy, and ... ...

Abstract	Abstract Early-stage detection of chronic kidney diseases (CKD) is important to treatment that may slow and occasionally halt CKD progression. CKD of diverse etiologies share similar histologic patterns of glomerulosclerosis, tubular atrophy, and interstitial fibrosis. Macro-vascular disease and micro-vascular disease promote tissue ischemia, contributing to injury. Tissue ischemia promotes hypoxia, and this in turn activates the hypoxia-inducible transcription factors (HIFs). HIF-1α and HIF-2α, share a dimer partner, HIF-1β, with the aryl hydrocarbon receptor (AHR) and are each activated in CKD and associated with kidney cellular nicotinamide adenine dinucleotide (NAD) depletion. The Preiss-Handler, salvage, and de novo pathways regulate NAD biosynthesis and gap-junctions regulate NAD cellular retention. In the Preiss-Handler pathway, niacin forms NAD. Niacin also exhibits crosstalk with HIF and AHR cell signals in the regulation of insulin sensitivity, which is a complication in CKD. Dysregulated enzyme activity in the NAD de novo pathway increases the levels of circulating tryptophan metabolites that activate AHR, resulting in poly-ADP ribose polymerase activation, thrombosis, endothelial dysfunction, and immunosuppression. Therapeutically, metabolites from the NAD salvage pathway increase NAD production and subsequent sirtuin deacetylase activity, resulting in reduced activation of retinoic acid-inducible gene I, p53, NF-κB and SMAD2 but increased activation of FOXO1, PGC-1α, and DNA methyltransferase-1. These post-translational responses may also be initiated through non-coding RNAs (ncRNAs), which are additionally altered in CKD. Nanoparticles traverse biological systems and can penetrate almost all tissues as disease biomarkers and drug delivery carriers. Targeted delivery of non-coding RNAs or NAD metabolites with nanoparticles may enable the development of more effective diagnostics and therapies to treat CKD.
Keywords	Inflammation ; Hypoxia-inducible factor (HIF) ; Glycolysis ; Nicotinamide adenine dinucleotide (NAD) ; Aryl hydrocarbon receptor (AHR) ; Sirtuin ; Medicine ; R
Subject code	610
Language	English
Publishing date	2023-10-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: RAGE pathway activation and function in chronic kidney disease and COVID-19

Colleen S. Curran / Jeffrey B. Kopp

Frontiers in Medicine, Vol

2022 Volume 9

Abstract: The multi-ligand receptor for advanced glycation end-products (RAGE) and its ligands are contributing factors in autoimmunity, cancers, and infectious disease. RAGE activation is increased in chronic kidney disease (CKD) and coronavirus disease 2019 ( ... ...

Abstract	The multi-ligand receptor for advanced glycation end-products (RAGE) and its ligands are contributing factors in autoimmunity, cancers, and infectious disease. RAGE activation is increased in chronic kidney disease (CKD) and coronavirus disease 2019 (COVID-19). CKD may increase the risk of COVID-19 severity and may also develop in the form of long COVID. RAGE is expressed in essentially all kidney cell types. Increased production of RAGE isoforms and RAGE ligands during CKD and COVID-19 promotes RAGE activity. The downstream effects include cellular dysfunction, tissue injury, fibrosis, and inflammation, which in turn contribute to a decline in kidney function, hypertension, thrombotic disorders, and cognitive impairment. In this review, we discuss the forms and mechanisms of RAGE and RAGE ligands in the kidney and COVID-19. Because various small molecules antagonize RAGE activity in animal models, targeting RAGE, its co-receptors, or its ligands may offer novel therapeutic approaches to slowing or halting progressive kidney disease, for which current therapies are often inadequate.
Keywords	receptor for advanced glycation end-products ; macrophage antigen 1 ; S100A8 ; S100A9 ; High-mobility group box 1 ; complement C1q ; Medicine (General) ; R5-920
Subject code	616
Language	English
Publishing date	2022-08-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Glomerular Kidney Diseases in the Single-Cell Era

Khun Zaw Latt / Jurgen Heymann / Teruhiko Yoshida / Jeffrey B. Kopp

Frontiers in Medicine, Vol

2021 Volume 8

Abstract: Recent advances in single-cell technology have enabled investigation of genomic profiles and molecular crosstalk among individual cells obtained from tissues and biofluids at unprecedented resolution. Glomerular diseases, either primary or secondary to ... ...

Abstract	Recent advances in single-cell technology have enabled investigation of genomic profiles and molecular crosstalk among individual cells obtained from tissues and biofluids at unprecedented resolution. Glomerular diseases, either primary or secondary to systemic diseases, often manifest elements of inflammation and of innate and adaptive immune responses. Application of single-cell methods have revealed cellular signatures of inflammation, cellular injury, and fibrosis. From these signatures, potential therapeutic targets can be inferred and in theory, this approach might facilitate identification of precision therapeutics for these diseases. Single-cell analyses of urine samples and skin lesions from patients with lupus nephritis and of urine samples from patients with diabetic nephropathy and focal segmental glomerulosclerosis have presented potential novel approaches for the diagnosis and monitoring of disease activity. These single-cell approaches, in contrast to kidney biopsy, are non-invasive and could be repeated multiple times as needed.
Keywords	glomerular diseases ; single cell genomics ; precision medicine ; immunity and inflammation ; urine biomarkers ; Medicine (General) ; R5-920
Subject code	610
Language	English
Publishing date	2021-10-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: COVID-19 Usurps Host Regulatory Networks

Colleen S. Curran / Donna R. Rivera / Jeffrey B. Kopp

Frontiers in Pharmacology, Vol

2020 Volume 11

Abstract: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection causes coronavirus disease 2019 (COVID-19). SARS-CoV-2 binds the angiotensin-converting enzyme 2 (ACE2) on the cell surface and this complex is internalized. ACE2 serves as an ... ...

Abstract	Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection causes coronavirus disease 2019 (COVID-19). SARS-CoV-2 binds the angiotensin-converting enzyme 2 (ACE2) on the cell surface and this complex is internalized. ACE2 serves as an endogenous inhibitor of inflammatory signals associated with four major regulator systems: the renin-angiotensin-aldosterone system (RAAS), the complement system, the coagulation cascade, and the kallikrein-kinin system (KKS). Understanding the pathophysiological effects of SARS-CoV-2 on these pathways is needed, particularly given the current lack of proven, effective treatments. The vasoconstrictive, prothrombotic and pro-inflammatory conditions induced by SARS-CoV-2 can be ascribed, at least in part, to the activation of these intersecting physiological networks. Moreover, patients with immune deficiencies, hypertension, diabetes, coronary heart disease, and kidney disease often have altered activation of these pathways, either due to underlying disease or to medications, and may be more susceptible to SARS-CoV-2 infection. Certain characteristic COVID-associated skin, sensory, and central nervous system manifestations may also be linked to viral activation of the RAAS, complement, coagulation, and KKS pathways. Pharmacological interventions that target molecules along these pathways may be useful in mitigating symptoms and preventing organ or tissue damage. While effective anti-viral therapies are critically needed, further study of these pathways may identify effective adjunctive treatments and patients most likely to benefit.
Keywords	SARS-CoV-2 ; renin-angiotensin-aldosterone system ; COVID-19 ; pharmacotherapy ; angiotensin II ; bradykinin ; Therapeutics. Pharmacology ; RM1-950 ; covid19
Subject code	610 ; 570
Language	English
Publishing date	2020-08-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Efficacy of Xanthine Oxidase Inhibitors in Lowering Serum Uric Acid in Chronic Kidney Disease

Yoojin Lee / Jennifer Hwang / Shaan H. Desai / Xiaobai Li / Christopher Jenkins / Jeffrey B. Kopp / Cheryl A. Winkler / Sung Kweon Cho

Journal of Clinical Medicine, Vol 11, Iss 2468, p

A Systematic Review and Meta-Analysis

2022 Volume 2468

Abstract: Objective: Current guidelines for gout recommend a treat-to-target approach with serum uric acid (SUA). However, there is little evidence for the dose-dependent effects of urate-lowering therapy (ULT). Herein, we analyzed the reported SUA-lowering effect ...

Abstract	Objective: Current guidelines for gout recommend a treat-to-target approach with serum uric acid (SUA). However, there is little evidence for the dose-dependent effects of urate-lowering therapy (ULT). Herein, we analyzed the reported SUA-lowering effect and SUA target achievement differences for various doses of xanthine oxidase inhibitors. Methods: Approved ULT drugs were selected from the FDA Drug Database. We included prospective randomized controlled trials of ULT drugs from ClinicalTrials.gov, articles published in the journal “Drugs”, and Embase, a literature database. A meta-analysis was performed to determine the ability of different ULT drugs and doses to lower and maintain a target SUA < 6 mg/dL. Results: We identified 35 trials including 8172 patients with a baseline SUA of 8.92 mg/dL. The allopurinol, febuxostat, and topiroxostat showed dose-proportional SUA-lowering responses. Compared with allopurinol 300 mg daily, febuxostat 80 mg daily and 120 mg daily more effectively maintained SUA < 6 mg/dL. Conclusion: Allopurinol, febuxostat, and topiroxostat showed dose-proportional ability to lower and achieve a target SUA < 6 mg/dL. Significance and Innovations. We showed dose-dependent SUA lowering effects of allopurinol, febuxostat, and topiroxostat. Febuxostat is effective at ULT compared to allopurinol and could be potentially offered as an alternative agent when patients (1) have CKD, (2) have the human leukocyte antigen HLA-B*5801 allele, and (3) become refractory to allopurinol. Gradual allopurinol dose increase with a lower starting dose is needed in CKD.
Keywords	dose-proportional response ; meta-analysis ; urate-lowering therapeutics ; Medicine ; R
Subject code	610
Language	English
Publishing date	2022-04-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Taming the fire of nephrotoxic botanicals

Francesca Holden / Vanisha Amin / Dominic Kuek / Jeffrey B Kopp / Bruce M Hendry / Qi-He Xu

World Journal of Traditional Chinese Medicine, Vol 5, Iss 3, Pp 151-

2019 Volume 163

Abstract: Criteria for diagnosing nephropathy and urothelial neoplasms induced by botanicals containing aristolochic acids (AAs) are well established. Highlights of recent research on AAs include mechanisms of AA intrarenal transport and metabolism and vigorous ... ...

Abstract	Criteria for diagnosing nephropathy and urothelial neoplasms induced by botanicals containing aristolochic acids (AAs) are well established. Highlights of recent research on AAs include mechanisms of AA intrarenal transport and metabolism and vigorous debate on whether AAs may also cause liver cancers. Many other botanicals may also cause renal injury, but a generalized framework for diagnosing botanical-induced kidney injury (BIKI) is lacking. Based on what we have learnt about the wide spectrum of phenotypes of BIKI attributed to AAs and a recently published standardized phenotypic framework of drug-induced kidney disease, we propose that BIKI may be categorized into six phenotypes (acute kidney injury, tubular dysfunction, glomerular disorders, nephrolithiasis, chronic kidney disease, and neoplasms) and four mechanistic types (A, predictable; B, idiosyncratic; C, chronic; and D, delayed). We call for international cooperation assembling a task force to develop, refine, and regularly appraise an online BIKI database, documenting botanical use, phenotypes, mechanisms, and levels of evidence. Once established, such a database may be linked with electronic patient records and pharmacovigilance channels to generate alerts, guide clinical decision-making, direct future research, and support evidence-based regulation of herbal medicines and education of healthcare professionals and the public. Finally, to prevent BIKI, we propose that a proactive approach integrating the triad of botanicals, users, and stakeholders will be needed.
Keywords	Adverse effects ; database ; herbal ; kidney ; mechanisms ; phenotypes ; prevention ; Medicine (General) ; R5-920
Subject code	610
Language	English
Publishing date	2019-01-01T00:00:00Z
Publisher	Wolters Kluwer Medknow Publications
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: APOL1 variant alleles associate with reduced risk for opportunistic infections in HIV infection

Ping An / Efe Sezgin / Gregory D. Kirk / Priya Duggal / Elizabeth Binns-Roemer / George Nelson / Sophie Limou / Mark L. Van Natta / Douglas A. Jabs / Michelle Estrella / Jeffrey B. Kopp / Cheryl A. Winkler

Communications Biology, Vol 4, Iss 1, Pp 1-

2021 Volume 8

Abstract: An et al. determine the presence of variants of the innate immune factor APOL1 in four cohorts of HIV-positive patients. The study suggests that APOL1 might confer carriers of two variant alleles protection from HIV related opportunistic infections, ... ...

Abstract	An et al. determine the presence of variants of the innate immune factor APOL1 in four cohorts of HIV-positive patients. The study suggests that APOL1 might confer carriers of two variant alleles protection from HIV related opportunistic infections, especially fungal infections.
Keywords	Biology (General) ; QH301-705.5
Language	English
Publishing date	2021-03-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Observations from the emergency management of dialysis patients evacuated from the US Virgin Islands to Puerto Rico following hurricane Irma

Guillermo J. Avilés Mendoza / Kristen P. Finne / Francisco Torre Leon / Lisandro Montalvo Burke / Jessica Cabrera-Marquez / Ana M. Mercado Casillas / Grasiela Malave / Christopher Brown / Jeffrey Kelman / Jeffrey B. Kopp

BMC Health Services Research, Vol 21, Iss 1, Pp 1-

2021 Volume 10

Abstract: Abstract Two category 5 hurricanes, Irma and Maria, arrived in the Caribbean in September 2017 in rapid succession. On September 6, Irma devastated the islands of St. Thomas and St. John, in the Virgin Islands of the United States (USVI). Most medical ... ...

Abstract	Abstract Two category 5 hurricanes, Irma and Maria, arrived in the Caribbean in September 2017 in rapid succession. On September 6, Irma devastated the islands of St. Thomas and St. John, in the Virgin Islands of the United States (USVI). Most medical infrastructure was damaged, including hemodialysis facilities, paralyzing dialysis operations. After Irma’s landfall, Puerto Rico served as a safehaven for thousands of displaced and repatriated persons from the impacted islands. These included a cohort of 129 hemodialysis patients evacuated from St. Thomas, USVI to San Juan, Puerto Rico from September 9−11, 2017. The hemodialysis patients arrived first at hotels in San Juan and were then transferred to a Special Needs Shelter, run by the Commonwealth of Puerto Rico and located in the Puerto Rico Convention Center. With the imminent arrival of Hurricane Maria, most patients were evacuated on September 19 to a special needs shelter on the campus of the Florida International University, in Miami, Florida. While in San Juan, hemodialysis treatments were provided by local nephrologists working with local hemodialysis centers. Here, we describe the challenges and the emergency management actions taken to ensure continuity of care, including providing dialysis, general medical care, shelter, food and transportation for USVI dialysis patients during their stay in San Juan, Puerto Rico. We describe here the experiences of federal and host state/territorial officials in the special needs shelter, in the context of the state/territorial and federal response to disasters, in order to provide ideas about challenges, solutions, and approaches to coordinating care for dialysis patients evacuated from a disaster.
Keywords	Disaster response ; Special needs population ; Access and functional needs ; Disaster shelters ; End-stage renal disease ; dialysis ; Public aspects of medicine ; RA1-1270
Language	English
Publishing date	2021-11-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Variant APOL1 protein in plasma associates with larger particles in humans and mouse models of kidney injury.

PLoS ONE, Vol 17, Iss 10, p e

2022 Volume 0276649

Abstract: Background Genetic variants in apolipoprotein L1 (APOL1), a protein that protects humans from infection with African trypanosomes, explain a substantial proportion of the excess risk of chronic kidney disease affecting individuals with sub-Saharan ... ...

Abstract	Background Genetic variants in apolipoprotein L1 (APOL1), a protein that protects humans from infection with African trypanosomes, explain a substantial proportion of the excess risk of chronic kidney disease affecting individuals with sub-Saharan ancestry. The mechanisms by which risk variants damage kidney cells remain incompletely understood. In preclinical models, APOL1 expressed in podocytes can lead to significant kidney injury. In humans, studies in kidney transplant suggest that the effects of APOL1 variants are predominantly driven by donor genotype. Less attention has been paid to a possible role for circulating APOL1 in kidney injury. Methods Using liquid chromatography-tandem mass spectrometry, the concentrations of APOL1 were measured in plasma and urine from participants in the Seattle Kidney Study. Asymmetric flow field-flow fractionation was used to evaluate the size of APOL1-containing lipoprotein particles in plasma. Transgenic mice that express wild-type or risk variant APOL1 from an albumin promoter were treated to cause kidney injury and evaluated for renal disease and pathology. Results In human participants, urine concentrations of APOL1 were correlated with plasma concentrations and reduced kidney function. Risk variant APOL1 was enriched in larger particles. In mice, circulating risk variant APOL1-G1 promoted kidney damage and reduced podocyte density without renal expression of APOL1. Conclusions These results suggest that plasma APOL1 is dynamic and contributes to the progression of kidney disease in humans, which may have implications for treatment of APOL1-associated kidney disease and for kidney transplantation.
Keywords	Medicine ; R ; Science ; Q
Subject code	616
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Podocytes degrade endocytosed albumin primarily in lysosomes.

John M Carson / Kayo Okamura / Hidefumi Wakashin / Kim McFann / Evgenia Dobrinskikh / Jeffrey B Kopp / Judith Blaine

PLoS ONE, Vol 9, Iss 6, p e

2014 Volume 99771

Abstract: Albuminuria is a strong, independent predictor of chronic kidney disease progression. We hypothesize that podocyte processing of albumin via the lysosome may be an important determinant of podocyte injury and loss. A human urine derived podocyte-like ... ...

Abstract	Albuminuria is a strong, independent predictor of chronic kidney disease progression. We hypothesize that podocyte processing of albumin via the lysosome may be an important determinant of podocyte injury and loss. A human urine derived podocyte-like epithelial cell (HUPEC) line was used for in vitro experiments. Albumin uptake was quantified by Western blot after loading HUPECs with fluorescein-labeled (FITC) albumin. Co-localization of albumin with lysosomes was determined by confocal microscopy. Albumin degradation was measured by quantifying FITC-albumin abundance in HUPEC lysates by Western blot. Degradation experiments were repeated using HUPECs treated with chloroquine, a lysosome inhibitor, or MG-132, a proteasome inhibitor. Lysosome activity was measured by fluorescence recovery after photo bleaching (FRAP). Cytokine production was measured by ELISA. Cell death was determined by trypan blue staining. In vivo, staining with lysosome-associated membrane protein-1 (LAMP-1) was performed on tissue from a Denys-Drash trangenic mouse model of nephrotic syndrome. HUPECs endocytosed albumin, which co-localized with lysosomes. Choloroquine, but not MG-132, inhibited albumin degradation, indicating that degradation occurs in lysosomes. Cathepsin B activity, measured by FRAP, significantly decreased in HUPECs exposed to albumin (12.5% of activity in controls) and chloroquine (12.8%), and declined further with exposure to albumin plus chloroquine (8.2%, p<0.05). Cytokine production and cell death were significantly increased in HUPECs exposed to albumin and chloroquine alone, and these effects were potentiated by exposure to albumin plus chloroquine. Compared to wild-type mice, glomerular staining of LAMP-1 was significantly increased in Denys-Drash mice and appeared to be most prominent in podocytes. These data suggest lysosomes are involved in the processing of endocytosed albumin in podocytes, and lysosomal dysfunction may contribute to podocyte injury and glomerulosclerosis in albuminuric diseases. Modifiers ...
Keywords	Medicine ; R ; Science ; Q
Subject code	571
Language	English
Publishing date	2014-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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