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Cardiovascular Consequence of Acute Kidney Injury, Chronic Kidney Disease and...
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Cardiovascular Consequence of Acute Kidney Injury, Chronic Kidney Disease and AKI-to-CKD Transition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 June 2021) | Viewed by 12605

Special Issue Editors

Dr. Md Abdul Hye Khan

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Guest Editor
Department of Pharmacology & Toxicology, The Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, USA
Dr. John D. Imig

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Guest Editor
Department of Pharmacology & Toxicology, The Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, USA
Dr. Michael M Yeboah

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Guest Editor
Department of Medicine; Division of Nephrology; The Medical College of Wisconsin; 8701 Watertown Plank Road, Milwaukee, WI 53226, USA

Special Issue Information

Over the past 20 years, there has been an increased appreciation of the long-term sequelae of acute kidney injury (AKI) and the potential development of chronic kidney disease (CKD). Several pathophysiologic features have been proposed to describe AKI to CKD progression, including maladaptive alterations in tubular, interstitial, inflammatory, and vascular cells. These alterations likely interact to culminate in the progression to hypertension and CKD. The objective of this Research Topic is to highlight several renal vascular and epithelial mechanisms that contribute to AKI and CKD, and particularly to the AKI to salt-sensitive hypertension and CKD transition. Currently, an effective intervention for these disorders is still lacking, and this is particularly true for AKI and its long-term cardiovascular and renal effects. Principally, therapeutic strategies targeting the AKI and the consequent cardiovascular and renal complications can be divided into those reducing the severity of AKI or promoting the regenerative process towards beneficially adaptive repair pathways. The Research Topic has a broad interest in renal and cardiovascular pathology covering AKI, CKD, hypertension, and cardiovascular diseases. Research publications will span cell signaling, animal studies, disease pathology studies, renal hemodynamics, excretory functions, and renal epithelial transport studies associated with AKI, CKD, and AKI to salt-sensitive hypertension and CKD transition. The Research Topic will present current progress on pathophysiology and therapeutic development for AKI, CKD, and also intervening development of salt-sensitive hypertension and CKD following AKI.

Dr. Md Abdul Hye Khan
Dr. John D. Imig
Dr. Michael M Yeboah
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • kidney disease
  • acute kidney injury
  • chronic kidney diseases
  • salt sensitivity
  • hypertension
  • renal vascular
  • renal epithelia

Published Papers (3 papers)

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Research

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13 pages, 5045 KiB  
Article
Kidney-Targeted Epoxyeicosatrienoic Acid Analog, EET-F01, Reduces Inflammation, Oxidative Stress, and Cisplatin-Induced Nephrotoxicity
by John D. Imig, Md Abdul Hye Khan, Anna Burkhan, Guan Chen, Adeniyi Michael Adebesin and John R. Falck
Int. J. Mol. Sci. 2021, 22(6), 2793; https://doi.org/10.3390/ijms22062793 - 10 Mar 2021
Cited by 12 | Viewed by 2551
Abstract
Although epoxyeicosatrienoic acid (EET) analogs have performed well in several acute and chronic kidney disease models, targeted delivery of EET analogs to the kidney can be reasonably expected to reduce the level of drug needed to achieve a therapeutic effect and obviate possible [...] Read more.
Although epoxyeicosatrienoic acid (EET) analogs have performed well in several acute and chronic kidney disease models, targeted delivery of EET analogs to the kidney can be reasonably expected to reduce the level of drug needed to achieve a therapeutic effect and obviate possible side effects. For EET analog kidney-targeted delivery, we conjugated a stable EET analog to folic acid via a PEG-diamine linker. Next, we compared the kidney targeted EET analog, EET-F01, to a well-studied EET analog, EET-A. EET-A or EET-F01 was infused i.v. and plasma and kidney tissue collected. EET-A was detected in the plasma but was undetectable in the kidney. On the other hand, EET-F01 was detected in the plasma and kidney. Experiments were conducted to compare the efficacy of EET-F01 and EET-A for decreasing cisplatin nephrotoxicity. Cisplatin was administered to WKY rats treated with vehicle, EET-A (10 mg/kg i.p.) or EET-F01 (20 mg/kg or 2 mg/kg i.p.). Cisplatin increased kidney injury markers, viz., blood urea nitrogen (BUN), N-acetyl-β-(D)-glucosaminidase (NAG), kidney injury molecule-1 (KIM-1), and thiobarbituric acid reactive substances (TBARS). EET-F01 was as effective as EET-A in decreasing BUN, NAG, KIM-1, TBARS, and renal histological injury caused by cisplatin. Despite its almost 2×-greater molecular weight compared with EET-A, EET-F01 was comparably effective in decreasing renal injury at a 10-fold w/w lower dose. EET-F01 decreased cisplatin nephrotoxicity by reducing oxidative stress and inflammation. These data demonstrate that EET-F01 targets the kidney, allows for a lower effective dose, and combats cisplatin nephrotoxicity. In conclusion, we have developed a kidney targeted EET analog, EET-F01, that demonstrates excellent potential as a therapeutic for kidney diseases. Full article
(This article belongs to the Special Issue Cardiovascular Consequence of Acute Kidney Injury, Chronic Kidney Disease and AKI-to-CKD Transition)
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17 pages, 1567 KiB  
Article
Empagliflozin Inhibits Basal and IL-1β-Mediated MCP-1/CCL2 and Endothelin-1 Expression in Human Proximal Tubular Cells
by Markus Pirklbauer, Maximilian Bernd, Lisa Fuchs, Petra Staudinger, Ulrike Corazza, Johannes Leierer, Gert Mayer and Herbert Schramek
Int. J. Mol. Sci. 2020, 21(21), 8189; https://doi.org/10.3390/ijms21218189 - 1 Nov 2020
Cited by 18 | Viewed by 2953
Abstract
SGLT2 inhibitors (SGLT2i) slow the progression of chronic kidney disease; however, evidence for the underlying molecular mechanisms is scarce. We investigated SGLT2i-mediated effects on differential gene expression in two independent human proximal tubular cell (HPTC) lines (HK-2 and RPTEC/TERT1) at the mRNA and [...] Read more.
SGLT2 inhibitors (SGLT2i) slow the progression of chronic kidney disease; however, evidence for the underlying molecular mechanisms is scarce. We investigated SGLT2i-mediated effects on differential gene expression in two independent human proximal tubular cell (HPTC) lines (HK-2 and RPTEC/TERT1) at the mRNA and protein levels under normoglycemic conditions, utilizing IL-1β as a pro-inflammatory mediator. Microarray hybridization identified 259 genes that were uniformly upregulated by IL-1β (10 mg/mL) and downregulated by empagliflozin (Empa) (500 nM) after 24 h of stimulation in two independent HPTC lines (n = 2, each). The functional annotation of these genes identified eight pathway clusters. Among 12 genes annotated to the highest ranked cluster (enrichment score, 3.51), monocyte chemoattractant protein-1/CC-chemokine ligand 2 (MCP-1/CCL2) and endothelin-1 (ET-1) were selected for verification at mRNA and protein levels based on their established involvement in the early pathogenesis of chronic kidney disease: IL-1β upregulated basal MCP-1/CCL2 (15- and 19-fold) and ET-1 (3- and 8-fold) mRNA expression, while Empa downregulated basal MCP-1/CCL2 (0.6- and 0.5-fold) and ET-1 (0.3- and 0.2-fold) mRNA expression as early as 1 h after stimulation and for at least 24 h in HK-2 and RPTEC/TERT1 cells, respectively. The co-administration of Empa inhibited IL-1β-mediated MCP-1/CCL2 (0.2-fold, each) and ET-1 (0.2-fold, each) mRNA expression as early as 1 h after ligand stimulation and for at least 24 h in both HPTC lines, respectively. This inhibitory effect of Empa on basal and IL-1β-mediated MCP-1/CCL2 and ET-1 mRNA expression was corroborated at the protein level. Our study presents novel evidence for the interference of SGLT2 inhibition with tubular inflammatory response mechanisms under normoglycemic conditions that might account for SGLT2i-mediated nephroprotection. Full article
(This article belongs to the Special Issue Cardiovascular Consequence of Acute Kidney Injury, Chronic Kidney Disease and AKI-to-CKD Transition)
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Review

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12 pages, 2842 KiB  
Review
Factors Affecting the Progression of Infection-Related Glomerulonephritis to Chronic Kidney Disease
by Takashi Oda and Nobuyuki Yoshizawa
Int. J. Mol. Sci. 2021, 22(2), 905; https://doi.org/10.3390/ijms22020905 - 18 Jan 2021
Cited by 15 | Viewed by 6606
Abstract
Acute glomerulonephritis (AGN) triggered by infection is still one of the major causes of acute kidney injury. During the previous two decades, there has been a major paradigm shift in the epidemiology of AGN. The incidence of poststreptococcal acute glomerulonephritis (PSAGN), which develops [...] Read more.
Acute glomerulonephritis (AGN) triggered by infection is still one of the major causes of acute kidney injury. During the previous two decades, there has been a major paradigm shift in the epidemiology of AGN. The incidence of poststreptococcal acute glomerulonephritis (PSAGN), which develops after the cure of group A Streptococcus infection in children has decreased, whereas adult AGN cases have been increasing, and those associated with nonstreptococcal infections, particularly infections by Staphylococcus, are now as common as PSAGN. In adult AGN patients, particularly older patients with comorbidities, infections are usually ongoing at the time when glomerulonephritis is diagnosed; thus, the term “infection-related glomerulonephritis (IRGN)” has recently been popularly used instead of “post-infectious AGN”. The prognosis of children with PSAGN is generally considered excellent compared with that of adult IRGN cases. However, long-term epidemiological analysis demonstrated that an episode of PSAGN in childhood is a strong risk factor for chronic kidney disease (CKD), even after the complete remission of PSAGN. Although the precise mechanism of the transition from IRGN to CKD remains unknown, its clarification is important as it will lead to the prevention of CKD. In this review, we therefore focus on the possible factors that may contribute to the progression of IRGN into CKD. Four factors, namely, persistent infection, genetic background of the host’s complement system, tubulointerstitial changes, and pre-existing histological damage, are discussed. Full article
(This article belongs to the Special Issue Cardiovascular Consequence of Acute Kidney Injury, Chronic Kidney Disease and AKI-to-CKD Transition)
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