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Together and Apart: Acute Kidney Injury and Chronic Kidney Disease

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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: 30 June 2024 | Viewed by 4934

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Special Issue Editor

Dr. Jinu Kim

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Guest Editor

1. Department of Anatomy, Jeju National University College of Medicine, Jeju 63243, Republic of Korea
2. Interdisciplinary Graduate Program in Advanced Convergence Technology & Science, Jeju National University, Jeju 63243, Republic of Korea
Interests: acute kidney injury

Special Issue Information

Dear Colleagues,

I am pleased to announce the Special Issue “Together and Apart: Acute Kidney Injury and Chronic Kidney Disease” for the International Journal of Molecular Sciences. For more than 40 years, renal pathophysiologists have classified kidney diseases into two distinct syndromes: acute kidney injury and chronic kidney disease. Although separate conceptual models for both syndromes have been developed to facilitate organized approaches to animal and clinical research during the past decade, recent mechanistic and molecular studies suggest that these syndromes are not distinct entities but rather closely interconnected. This Special Issue will include papers investigating mechanisms underlying the development of chronic kidney disease from acute kidney injury. Furthermore, experimental in vitro and in vivo studies examining potential new approaches to reduce kidney dysfunction and/or tubulointerstitial fibrosis are welcome.

Dr. Jinu Kim
Guest Editor

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.

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Keywords

kidney disease
acute kidney injury
nephrotoxicity
chronic kidney disease
fibrosis
inflammation in vivo model
in vitro model

Published Papers (5 papers)

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Research

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18 pages, 2759 KiB

Open AccessArticle

Loss of SAV1 in Kidney Proximal Tubule Induces Maladaptive Repair after Ischemia and Reperfusion Injury

by Daeun Moon, Babu J. Padanilam, Kwon Moo Park and Jinu Kim

Int. J. Mol. Sci. 2024, 25(9), 4610; https://doi.org/10.3390/ijms25094610 - 23 Apr 2024

Viewed by 274

Abstract

Kidney ischemia and reperfusion injury (IRI) is a significant contributor to acute kidney injury (AKI), characterized by tubular injury and kidney dysfunction. Salvador family WW domain containing protein 1 (SAV1) is a key component of the Hippo pathway and plays a crucial role in the regulation of organ size and tissue regeneration. However, whether SAV1 plays a role in kidney IRI is not investigated. In this study, we investigated the role of SAV1 in kidney injury and regeneration following IRI. A proximal tubule-specific knockout of SAV1 in kidneys (SAV1^ptKO) was generated, and wild-type and SAV1^ptKO mice underwent kidney IRI or sham operation. Plasma creatinine and blood urea nitrogen were measured to assess kidney function. Histological studies, including periodic acid-Schiff staining and immunohistochemistry, were conducted to assess tubular injury, SAV1 expression, and cell proliferation. Western blot analysis was employed to assess the Hippo pathway-related and proliferation-related proteins. SAV1 exhibited faint expression in the proximal tubules and was predominantly expressed in the connecting tubule to the collecting duct. At 48 h after IRI, SAV1^ptKO mice continued to exhibit severe kidney dysfunction, compared to attenuated kidney dysfunction in wild-type mice. Consistent with the functional data, severe tubular damage induced by kidney IRI in the cortex was significantly decreased in wild-type mice at 48 h after IRI but not in SAV1^ptKO mice. Furthermore, 48 h after IRI, the number of Ki67-positive cells in the cortex was significantly higher in wild-type mice than SAV1^ptKO mice. After IRI, activation and expression of Hippo pathway-related proteins were enhanced, with no significant differences observed between wild-type and SAV1^ptKO mice. Notably, at 48 h after IRI, protein kinase B activation (AKT) was significantly enhanced in SAV1^ptKO mice compared to wild-type mice. This study demonstrates that SAV1 deficiency in the kidney proximal tubule worsens the injury and delays kidney regeneration after IRI, potentially through the overactivation of AKT. Full article

(This article belongs to the Special Issue Together and Apart: Acute Kidney Injury and Chronic Kidney Disease)

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13 pages, 2189 KiB

Open AccessArticle

Acute Kidney Injury and BK Polyomavirus in Urine Sediment Cells

by Sahra Pajenda, Daniela Anna Gerges, Raimundo Freire, Ludwig Wagner, Zsofia Hevesi, Monika Aiad, Michael Eder, Alice Schmidt, Wolfgang Winnicki and Farsad Alexander Eskandary

Int. J. Mol. Sci. 2023, 24(24), 17511; https://doi.org/10.3390/ijms242417511 - 15 Dec 2023

Cited by 1 | Viewed by 754

Abstract

Polyomaviruses are widespread, with BK viruses being most common in humans who require immunosuppression due to allotransplantation. Infection with BK polyomavirus (BKV) may manifest as BK virus-associated nephropathy and hemorrhagic cystitis. Established diagnostic methods include the detection of polyomavirus in urine and blood by PCR and in tissue biopsies via immunohistochemistry. In this study, 79 patients with pathological renal retention parameters and acute kidney injury (AKI) were screened for BK polyomavirus replication by RNA extraction, reverse transcription, and virus-specific qPCR in urine sediment cells. A short fragment of the VP2 coding region was the target of qPCR amplification; patients with (n = 31) and without (n = 48) a history of renal transplantation were included. Urine sediment cell immunofluorescence staining for VP1 BK polyomavirus protein was performed using confocal microscopy. In 22 patients with acute renal injury, urinary sediment cells from 11 participants with kidney transplantation (KTX) and from 11 non-kidney transplanted patients (nonKTX) were positive for BK virus replication. BK virus copies were found more frequently in patients with AKI stage III (n = 14). Higher copy numbers were detected in KTX patients having experienced BK polyoma-nephropathy (BKPyVAN) in the past or diagnosed recently by histology (5.6 × 10⁹–3.1 × 10¹⁰). One patient developed BK viremia following delayed graft function (DGF) with BK virus-positive urine sediment. In nonKTX patients with BK copies, decoy cells were absent; however, positive staining of cells was found with epithelial morphology. Decoy cells were only found in KTX patients with BKPyVAN. In AKI, damage to the tubular epithelium itself may render the epithelial cells more permissive for polyoma replication. This non-invasive diagnostic approach to assess BK polyomavirus replication in urine sediment cells has the potential to identify KTX patients at risk for viremia and BKPyVAN during AKI. This method might serve as a valuable screening tool for close monitoring and tailored immunosuppression decisions. Full article

(This article belongs to the Special Issue Together and Apart: Acute Kidney Injury and Chronic Kidney Disease)

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15 pages, 3226 KiB

Open AccessArticle

Metalloporphyrins Reduce Proteinuria in Podocyte Immune Injury: The Role of Metal and Porphyrin Moieties

by Elias A. Lianos, Gia Nghi Phung, Michelle Foster, Jianping Zhou and Mukut Sharma

Int. J. Mol. Sci. 2023, 24(16), 12777; https://doi.org/10.3390/ijms241612777 - 14 Aug 2023

Cited by 1 | Viewed by 835

Abstract

Depending on their central metal atom, metalloporphyrins (MPs) can attenuate or exacerbate the severity of immune-mediated kidney injury, and this has been attributed to the induction or inhibition of heme oxygenase (HO) activity, particularly the inducible isoform (HO-1) of this enzyme. The role of central metal or porphyrin moieties in determining the efficacy of MPs to attenuate injury, as well as mechanisms underlying this effect, have not been assessed. Using an antibody-mediated complement-dependent model of injury directed against rat visceral glomerular epithelial cells (podocytes) and two MPs (FePPIX, CoPPIX) that induce both HO-1 expression and HO enzymatic activity in vivo but differ in their chelated metal, we assessed their efficacy in reducing albuminuria. Podocyte injury was induced using rabbit immune serum raised against the rat podocyte antigen, Fx1A, and containing an anti-Fx1A antibody that activates complement at sites of binding. FePPIX or CoPPIX were injected intraperitoneally (5 mg/kg) 24 h before administration of the anti-Fx1A serum and on days 1, 3, 6, and 10 thereafter. Upon completion of urine collection on day 14, the kidney cortex was obtained for histopathology and isolation of glomeruli, from which total protein extracts were obtained. Target proteins were analyzed by capillary-based separation and immunodetection (Western blot analysis). Both MPs had comparable efficacy in reducing albuminuria in males, but the efficacy of CoPPIX was superior in female rats. The metal-free protoporphyrin, PPIX, had minimal or no effect on urine albumin excretion. CoPPIX was also the most potent MP in inducing glomerular HO-1, reducing complement deposition, and preserving the expression of the complement regulatory protein (CRP) CD55 but not that of CD59, the expression of which was reduced by both MPs. These observations demonstrate that the metal moiety of HO-1-inducing MPs plays an important role in reducing proteinuria via mechanisms involving reduced complement deposition and independently of an effect on CRPs. Full article

(This article belongs to the Special Issue Together and Apart: Acute Kidney Injury and Chronic Kidney Disease)

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Review

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23 pages, 1069 KiB

Open AccessReview

Therapeutic Effect of Natural Products and Dietary Supplements on Aflatoxin-Induced Nephropathy

by Ebenezer Ofori-Attah, Mai Hashimoto, Mayu Oki and Daisuke Kadowaki

Int. J. Mol. Sci. 2024, 25(5), 2849; https://doi.org/10.3390/ijms25052849 - 01 Mar 2024

Viewed by 1130

Abstract

Aflatoxins are harmful natural contaminants found in foods and are known to be hepatotoxic. However, recent studies have linked chronic consumption of aflatoxins to nephrotoxicity in both animals and humans. Here, we conducted a systematic review of active compounds, crude extracts, herbal formulations, and probiotics against aflatoxin-induced renal dysfunction, highlighting their mechanisms of action in both in vitro and in vivo studies. The natural products and dietary supplements discussed in this study alleviated aflatoxin-induced renal oxidative stress, inflammation, tissue damage, and markers of renal function, mostly in animal models. Therefore, the information provided in this review may improve the management of kidney disease associated with aflatoxin exposure and potentially aid in animal feed supplementation. However, future research is warranted to translate the outcomes of this study into clinical use in kidney patients. Full article

(This article belongs to the Special Issue Together and Apart: Acute Kidney Injury and Chronic Kidney Disease)

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29 pages, 2527 KiB

Open AccessReview

The AKI-to-CKD Transition: The Role of Uremic Toxins

by Camille André, Sandra Bodeau, Saïd Kamel, Youssef Bennis and Pauline Caillard

Int. J. Mol. Sci. 2023, 24(22), 16152; https://doi.org/10.3390/ijms242216152 - 10 Nov 2023

Cited by 1 | Viewed by 1387

Abstract

After acute kidney injury (AKI), renal function continues to deteriorate in some patients. In a pro-inflammatory and profibrotic environment, the proximal tubules are subject to maladaptive repair. In the AKI-to-CKD transition, impaired recovery from AKI reduces tubular and glomerular filtration and leads to chronic kidney disease (CKD). Reduced kidney secretion capacity is characterized by the plasma accumulation of biologically active molecules, referred to as uremic toxins (UTs). These toxins have a role in the development of neurological, cardiovascular, bone, and renal complications of CKD. However, UTs might also cause CKD as well as be the consequence. Recent studies have shown that these molecules accumulate early in AKI and contribute to the establishment of this pro-inflammatory and profibrotic environment in the kidney. The objective of the present work was to review the mechanisms of UT toxicity that potentially contribute to the AKI-to-CKD transition in each renal compartment. Full article

(This article belongs to the Special Issue Together and Apart: Acute Kidney Injury and Chronic Kidney Disease)

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