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Kidney Diseases: From Molecular Basis to Therapy

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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: closed (15 April 2024) | Viewed by 10269

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Special Issue Editor

Dr. Jana Reiterová

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Guest Editor

Department of Nephrology, First Faculty of Medicine, Charles University, 128 08 Prague, Czech Republic
Interests: hereditary kidney diseases

Special Issue Information

Dear Colleagues,

Chronic kidney disease (CKD), defined as the presence of abnormalities of kidney function or structure lasting at least three months, is an epidemic health issue that requires global attention. The global rise in the incidence of CKD has been accompanied by a general increase in human longevity, as well as an increase in the traditional and non-traditional risk factors for the disease. CKD is associated with significant comorbidity and mortality, being responsible for enormous healthcare costs.

Intensive research in this area includes the investigation of cellular communication, phenotype changes (including those related to senescent phenotypes), novel mediators of kidney injury, epigenetic mechanisms, activation of signaling pathways, among others, illustrating the complexity of this field. Strategies to target resident glomerular or tubular damage, as well as immune cells, have been proposed to ameliorate disease progression or even revert kidney damage. Despite all the available data, the translation of new research into novel therapies in CKD is greatly lagging behind other disciplines.

We invite you to submit novel research about molecular and cellular mechanisms involved in kidney injury.

Dr. Jana Reiterová
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.

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

chronic kidney disease
molecular mechanisms
oxidative stress
inflammation

Published Papers (6 papers)

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Research

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12 pages, 1497 KiB

Open AccessArticle

Long-Term Effects of Tolvaptan in Autosomal Dominant Polycystic Kidney Disease: Predictors of Treatment Response and Safety over 6 Years of Continuous Therapy

by Mai Yamazaki, Haruna Kawano, Miho Miyoshi, Tomoki Kimura, Keiji Takahashi, Satoru Muto and Shigeo Horie

Int. J. Mol. Sci. 2024, 25(4), 2088; https://doi.org/10.3390/ijms25042088 - 8 Feb 2024

Viewed by 1352

Abstract

Tolvaptan, an oral vasopressin V2 receptor antagonist, reduces renal volume expansion and loss of renal function in patients with autosomal dominant polycystic kidney disease (ADPKD). Data for predictive factors indicating patients more likely to benefit from long-term tolvaptan are lacking. Data were retrospectively collected from 55 patients on tolvaptan for 6 years. Changes in renal function, progression of renal dysfunction (estimated glomerular filtration rate [eGFR], 1-year change in eGFR [ΔeGFR/year]), and renal volume (total kidney volume [TKV], percentage 1-year change in TKV [ΔTKV%/year]) were evaluated at 3-years pre-tolvaptan, at baseline, and at 6 years. In 76.4% of patients, ΔeGFR/year improved at 6 years. The average 6-year ΔeGFR/year (range) minus baseline ΔeGFR/year: 3.024 (−8.77–20.58 mL/min/1.73 m²). The increase in TKV was reduced for the first 3 years. A higher BMI was associated with less of an improvement in ΔeGFR (p = 0.027), and family history was associated with more of an improvement in ΔeGFR (p = 0.044). Hypernatremia was generally mild; 3 patients had moderate-to-severe hyponatremia due to prolonged, excessive water intake in response to water diuresis—a side effect of tolvaptan. Family history of ADPKD and baseline BMI were contributing factors for ΔeGFR/year improvement on tolvaptan. Hyponatremia should be monitored with long-term tolvaptan administration. Full article

(This article belongs to the Special Issue Kidney Diseases: From Molecular Basis to Therapy)

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18 pages, 2961 KiB

Open AccessArticle

Long-Term Effects of Suramin on Renal Function in Streptozotocin-Induced Diabetes in Rats

by Gabriela Chyła-Danił, Kornelia Sałaga-Zaleska, Ewelina Kreft, Olaf Stumski, Aleksandra Krzesińska, Monika Sakowicz-Burkiewicz, Agnieszka Kuchta and Maciej Jankowski

Int. J. Mol. Sci. 2023, 24(19), 14671; https://doi.org/10.3390/ijms241914671 - 28 Sep 2023

Viewed by 886

Abstract

In short-term diabetes (3 weeks), suramin, a drug used clinically, affects renal function and the expression of vascular endothelial growth factor A (VEGF-A), which may be involved in the pathogenesis of diabetic nephropathy, the main cause of end-stage renal disease. In the present study, we evaluated the long-term (11 weeks) effects of suramin (10 mg/kg, i.p., once-weekly) in diabetic rats. Concentrations of VEGF-A, albumin, soluble adhesive molecules (sICAM-1, sVCAM-1), nucleosomes, and thrombin–antithrombin complex (TAT) were measured by ELISA, total protein was measured using a biuret reagent. Glomerular expression of VEGF-A was evaluated by Western blot, mRNA for VEGF-A receptors in the renal cortex by RT-PCR. The vasoreactivity of the interlobar arteries to acetylcholine was assessed by wire myography. Long-term diabetes led to an increased concentration of VEGF-A, TAT, and urinary excretion of total protein and albumin, and a decrease in the concentration of sVCAM-1. We have shown that suramin in diabetes reduces total urinary protein excretion and restores the relaxing properties of acetylcholine relaxation properties to non-diabetic levels. Suramin had no effect on glomerular expression VEGF-A expression and specific receptors, and on sICAM-1 and nucleosomes concentrations in diabetic rats. In conclusion, the long-term effect of suramin on the kidneys in diabetes, expressed in the reduction of proteinuria and the restoration of endothelium-dependent relaxation of the renal arteries, can be considered as potentially contributing to the reduction/slowing down of the development of diabetic nephropathy. Full article

(This article belongs to the Special Issue Kidney Diseases: From Molecular Basis to Therapy)

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14 pages, 6085 KiB

Open AccessArticle

Mild Chronic Kidney Disease Associated with Low Bone Formation and Decrease in Phosphate Transporters and Signaling Pathways Gene Expression

by Evdokia Bogdanova, Airat Sadykov, Galina Ivanova, Irina Zubina, Olga Beresneva, Natalia Semenova, Olga Galkina, Marina Parastaeva, Vladimir Sharoyko and Vladimir Dobronravov

Int. J. Mol. Sci. 2023, 24(8), 7270; https://doi.org/10.3390/ijms24087270 - 14 Apr 2023

Cited by 2 | Viewed by 1627

Abstract

The initial phases of molecular and cellular maladaptive bone responses in early chronic kidney disease (CKD) remain mostly unknown. We induced mild CKD in spontaneously hypertensive rats (SHR) by either causing arterial hypertension lasting six months (sham-operated rats, SO6) or in its’ combination with 3/4 nephrectomy lasting two and six months (Nx2 and Nx6, respectively). Sham-operated SHRs (SO2) and Wistar Kyoto rats (WKY2) with a two-month follow-up served as controls. Animals were fed standard chow containing 0.6% phosphate. Upon follow-up completion in each animal, we measured creatinine clearance, urine albumin-to-creatinine ratio, renal interstitial fibrosis, inorganic phosphate (Pi) exchange, intact parathyroid hormone (PTH), fibroblast growth factor 23 (FGF23), Klotho, Dickkopf-1, sclerostin, and assessed bone response by static histomorphometry and gene expression profiles. The mild CKD groups had no increase in renal Pi excretion, FGF23, or PTH levels. Serum Pi, Dickkopf-1, and sclerostin were higher in Nx6. A decrease in trabecular bone area and osteocyte number was obvious in SO6. Nx2 and Nx6 had additionally lower osteoblast numbers. The decline in eroded perimeter, a resorption index, was only apparent in Nx6. Significant downregulation of genes related to Pi transport, MAPK, WNT, and BMP signaling accompanied histological alterations in Nx2 and Nx6. We found an association between mild CKD and histological and molecular features suggesting lower bone turnover, which occurred at normal levels of systemic Pi-regulating factors. Full article

(This article belongs to the Special Issue Kidney Diseases: From Molecular Basis to Therapy)

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18 pages, 6115 KiB

Open AccessArticle

Metabolomic Profiling of Plasma, Urine, and Saliva of Kidney Transplantation Recipients

by Hitoshi Iwamoto, Masaaki Okihara, Isao Akashi, Yu Kihara, Osamu Konno, Shigeyuki Kawachi, Makoto Sunamura and Masahiro Sugimoto

Int. J. Mol. Sci. 2022, 23(22), 13938; https://doi.org/10.3390/ijms232213938 - 11 Nov 2022

Cited by 5 | Viewed by 1613

Abstract

Kidney biopsy is commonly used to diagnose kidney transplant dysfunction after transplantation. Therefore, the development of minimally invasive and quantitative methods to evaluate kidney function in transplant recipients is necessary. Here, we used capillary electrophoresis-mass spectrometry to analyze the biofluids collected from transplant recipients with impaired (Group I, n = 31) and stable (Group S, n = 19) kidney function and from donors (Group D, n = 9). Metabolomics analyses identified and quantified 97 metabolites in plasma, 133 metabolites in urine, and 108 metabolites in saliva. Multivariate analyses revealed apparent differences in the metabolomic profiles of the three groups. In plasma samples, arginine biosynthesis and purine metabolism between the I and S Groups differed. In addition, considerable differences in metabolomic profiles were observed between samples collected from participants with T cell-mediated rejection (TCR), antibody-mediated rejection, and other kidney disorders (KD). The metabolomic profiles in the three types of biofluids showed different patterns between TCR and KD, wherein 3-indoxyl sulfate showed a significant increase in TCR consistently in both plasma and urine samples. These results suggest that each biofluid has different metabolite features to evaluate kidney function after transplantation and that 3-indoxyl sulfate could predict acute rejection. Full article

(This article belongs to the Special Issue Kidney Diseases: From Molecular Basis to Therapy)

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Review

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15 pages, 2294 KiB

Open AccessReview

Mechanosensitive Cation Channel Piezo1 Is Involved in Renal Fibrosis Induction

by Marta Drobnik, Jakub Smólski, Łukasz Grądalski, Szymon Niemirka, Ewelina Młynarska, Jacek Rysz and Beata Franczyk

Int. J. Mol. Sci. 2024, 25(3), 1718; https://doi.org/10.3390/ijms25031718 - 31 Jan 2024

Cited by 1 | Viewed by 1295

Abstract

Renal fibrosis, the result of different pathological processes, impairs kidney function and architecture, and usually leads to renal failure development. Piezo1 is a mechanosensitive cation channel highly expressed in kidneys. Activation of Piezo1 by mechanical stimuli increases cations influx into the cell with slight preference of calcium ions. Two different models of Piezo1 activation are considered: force through lipid and force through filament. Expression of Piezo1 on mRNA and protein levels was confirmed within the kidney. Their capacity is increased in the fibrotic kidney. The pharmacological tools for Piezo1 research comprise selective activators of the channels (Yoda1 and Jedi1/2) as well as non-selective inhibitors (spider peptide toxin) GsMTx4. Piezo1 is hypothesized to be the upstream element responsible for the activation of integrin. This pathway (calcium/calpain2/integrin beta1) is suggested to participate in profibrotic response induced by mechanical stimuli. Administration of the Piezo1 unspecific inhibitor or activators to unilateral ureter obstruction (UUO) mice or animals with folic acid-induced fibrosis modulates extracellular matrix deposition and influences kidney function. All in all, according to the recent data Piezo1 plays an important role in kidney fibrosis development. This channel has been selected as the target for pharmacotherapy of renal fibrosis. Full article

(This article belongs to the Special Issue Kidney Diseases: From Molecular Basis to Therapy)

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25 pages, 1035 KiB

Open AccessReview

MicroRNAs Associated with Chronic Kidney Disease in the General Population and High-Risk Subgroups—A Systematic Review

by Dipuo D. Motshwari, Don M. Matshazi, Rajiv T. Erasmus, Andre P. Kengne, Tandi E. Matsha and Cindy George

Int. J. Mol. Sci. 2023, 24(2), 1792; https://doi.org/10.3390/ijms24021792 - 16 Jan 2023

Cited by 7 | Viewed by 2526

Abstract

The potential utility of microRNAs (miRNAs) as diagnostic or prognostic biomarkers, as well as therapeutic targets, for chronic kidney disease (CKD) has been advocated. However, studies evaluating the expression profile of the same miRNA signatures in CKD report contradictory findings. This review aimed to characterize miRNAs associated with CKD and/or measures of kidney function and kidney damage in the general population, and also in high-risk subgroups, including people with hypertension (HTN), diabetes mellitus (DM) and human immunodeficiency virus (HIV) infection. Medline via PubMed, Scopus, Web of Science, and EBSCOhost databases were searched to identify relevant studies published in English or French languages on or before 30 September 2022. A total of 75 studies fulfilled the eligibility criteria: CKD (n = 18), diabetic kidney disease (DKD) (n = 51) and HTN-associated CKD (n = 6), with no study reporting on miRNA profiles in people with HIV-associated nephropathy. In individuals with CKD, miR-126 and miR-223 were consistently downregulated, whilst in DKD, miR-21 and miR-29b were consistently upregulated and miR-30e and let-7a were consistently downregulated in at least three studies. These findings suggest that these miRNAs may be involved in the pathogenesis of CKD and therefore invites further research to explore their clinical utility for CKD prevention and control. Full article

(This article belongs to the Special Issue Kidney Diseases: From Molecular Basis to Therapy)

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