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Renal Lesions and Nephrotoxicity
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Renal Lesions and Nephrotoxicity

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Toxicology".

Deadline for manuscript submissions: closed (31 January 2023) | Viewed by 15287

Special Issue Editor

Dr. Egor Yu. Plotnikov

E-Mail Website
Guest Editor
A.N. Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, 119991 Moscow, Russia
Interests: acute kidney injury; renal progenitor cells; mitochondria; mesenchymal stromal cells; inflammation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The incidence of acute and chronic renal lesions remains increasing all over the world. Accurate and fast recognition of renal damage, as well as an understanding of the pathophysiological mechanisms of kidney injury and nephrotoxicity, is of great importance for the development of effective therapeutic interventions. We need to develop adequate diagnostics for recognition of AKI and nephrotoxicity before the point of no return is passed.

The key scientific problem addressed in this Issue is to determine molecular mechanisms of renal lesions and nephrotoxicity in various pathologies of genesis (sepsis, ischemia, nephrotoxic compounds) as well as age-associated. The solution to this problem will allow target universal pathways of kidney disease progression. Insight of basic mechanisms of kidney dysfunction will allow creating effective methods of diagnosis for nephrotoxicity as well as approaches for nephroprotective therapy.

In this topic, we would like to assemble cutting-edge views on the mechanisms of acute kidney injury and chronic kidney disease, nephrotoxicity of drugs, and environmental agents. We will also welcome the analysis of nephrotoxicity in nephrogenesis and regeneration of the kidneys after injury, to evaluate the possibilities of approaches for the treatment of kidney pathologies. We strive to review the latest achievements in the field of molecular biology, kidney physiology.

Dr. Egor Yu. Plotnikov
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

  • acute kidney injury
  • chronic kidney disease
  • renal inflammation
  • renal tubular epithelial cells
  • biomarkers
  • fibrosis
  • aging
  • diabetes
  • proteinuria
  • therapeutics

Published Papers (6 papers)

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Editorial

Jump to: Research, Review

3 pages, 162 KiB  
Editorial
Renal Lesions and Nephrotoxicity: Contemporary Challenges and Future Directions
by Egor Plotnikov
Int. J. Mol. Sci. 2023, 24(8), 7015; https://doi.org/10.3390/ijms24087015 - 10 Apr 2023
Viewed by 695
Abstract
Renal lesions and nephrotoxicity are major challenges for researchers and patients alike [...] Full article
(This article belongs to the Special Issue Renal Lesions and Nephrotoxicity)

Research

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13 pages, 3078 KiB  
Article
Pyruvate Kinase M2: A New Biomarker for the Early Detection of Diabetes-Induced Nephropathy
by Yeon Su Park, Joo Hee Han, Jae Hyeon Park, Ji Soo Choi, Seung Hyeon Kim and Hyung Sik Kim
Int. J. Mol. Sci. 2023, 24(3), 2683; https://doi.org/10.3390/ijms24032683 - 31 Jan 2023
Cited by 2 | Viewed by 2133
Abstract
Diabetic nephropathy (DN) is a common complication of diabetes. DN progresses to end-stage renal disease, which has a high mortality rate. Current research is focused on identifying non-invasive potential biomarkers in the early stage of DN. We previously indicated that pyruvate kinase M2 [...] Read more.
Diabetic nephropathy (DN) is a common complication of diabetes. DN progresses to end-stage renal disease, which has a high mortality rate. Current research is focused on identifying non-invasive potential biomarkers in the early stage of DN. We previously indicated that pyruvate kinase M2 (PKM2) is excreted in the urine of rats after cisplatin-induced acute kidney injury (AKI). However, it has not been reported whether PKM2 can be used as a biomarker to diagnose DN. Therefore, we try to compare whether the protein PKM2 can be detected in the urine samples from diabetic patients as shown in the results of DN models. In this study, high-fat diet (HFD)-induced Zucker diabetic fatty (ZDF) rats were used for DN phenotyping. After 19 weeks of receiving a HFD, the DN model’s blood glucose, blood urea nitrogen, and serum creatinine levels were significantly increased; severe tubular and glomerular damages were also noted. The following protein-based biomarkers were increased in the urine of these models: kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL), and PKM2. PKM2 had the earliest detection rate. In the urine samples of patients, PKM2 protein was highly detected in the urine of diabetic patients but was not excreted in the urine of normal subjects. Therefore, PKM2 was selected as the new biomarker for the early diagnosis of DN. Our results reflect current knowledge on the role of PKM2 in DN. Full article
(This article belongs to the Special Issue Renal Lesions and Nephrotoxicity)
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17 pages, 3096 KiB  
Article
Age-Associated Loss in Renal Nestin-Positive Progenitor Cells
by Marina I. Buyan, Nadezda V. Andrianova, Vasily A. Popkov, Ljubava D. Zorova, Irina B. Pevzner, Denis N. Silachev, Dmitry B. Zorov and Egor Y. Plotnikov
Int. J. Mol. Sci. 2022, 23(19), 11015; https://doi.org/10.3390/ijms231911015 - 20 Sep 2022
Cited by 3 | Viewed by 2122
Abstract
The decrease in the number of resident progenitor cells with age was shown for several organs. Such a loss is associated with a decline in regenerative capacity and a greater vulnerability of organs to injury. However, experiments evaluating the number of progenitor cells [...] Read more.
The decrease in the number of resident progenitor cells with age was shown for several organs. Such a loss is associated with a decline in regenerative capacity and a greater vulnerability of organs to injury. However, experiments evaluating the number of progenitor cells in the kidney during aging have not been performed until recently. Our study tried to address the change in the number of renal progenitor cells with age. Experiments were carried out on young and old transgenic nestin-green fluorescent protein (GFP) reporter mice, since nestin is suggested to be one of the markers of progenitor cells. We found that nestin+ cells in kidney tissue were located in the putative niches of resident renal progenitor cells. Evaluation of the amount of nestin+ cells in the kidneys of different ages revealed a multifold decrease in the levels of nestin+ cells in old mice. In vitro experiments on primary cultures of renal tubular cells showed that all cells including nestin+ cells from old mice had a lower proliferation rate. Moreover, the resistance to damaging factors was reduced in cells obtained from old mice. Our data indicate the loss of resident progenitor cells in kidneys and a decrease in renal cells proliferative capacity with aging. Full article
(This article belongs to the Special Issue Renal Lesions and Nephrotoxicity)
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9 pages, 975 KiB  
Article
Fast Tacrolimus Metabolism Does Not Promote Post-Transplant Diabetes Mellitus after Kidney Transplantation
by Ulrich Jehn, Nathalie Wiedmer, Göran Ramin Boeckel, Hermann Pavenstädt, Gerold Thölking and Stefan Reuter
Int. J. Mol. Sci. 2022, 23(16), 9131; https://doi.org/10.3390/ijms23169131 - 15 Aug 2022
Cited by 4 | Viewed by 1321
Abstract
Post-transplant diabetes mellitus (PTDM) after kidney transplantation induced by tacrolimus is an important issue. Fast tacrolimus metabolism, which can be estimated by concentration-to-dose (C/D) ratio, is associated with increased nephrotoxicity and unfavorable outcomes after kidney transplantation. Herein, we elucidate whether fast tacrolimus metabolism [...] Read more.
Post-transplant diabetes mellitus (PTDM) after kidney transplantation induced by tacrolimus is an important issue. Fast tacrolimus metabolism, which can be estimated by concentration-to-dose (C/D) ratio, is associated with increased nephrotoxicity and unfavorable outcomes after kidney transplantation. Herein, we elucidate whether fast tacrolimus metabolism also increases the risk for PTDM. Data from 596 non-diabetic patients treated with tacrolimus-based immunosuppression at the time of kidney transplantation between 2007 and 2015 were retrospectively analyzed. The median follow-up time after kidney transplantation was 4.7 years (IQR 4.2 years). Our analysis was complemented by experimental modeling of fast and slow tacrolimus metabolism kinetics in cultured insulin-producing pancreatic cells (INS-1 cells). During the follow-up period, 117 (19.6%) patients developed PTDM. Of all patients, 210 (35.2%) were classified as fast metabolizers (C/D ratio < 1.05 ng/mL × 1/mg). Fast tacrolimus metabolizers did not have a higher incidence of PTDM than slow tacrolimus metabolizers (p = 0.496). Consistent with this, insulin secretion and the viability of tacrolimus-treated INS-1 cells exposed to 12 h of tacrolimus concentrations analogous to the serum profiles of fast or slow tacrolimus metabolizers or to continuous exposure did not differ (p = 0.286). In conclusion, fast tacrolimus metabolism is not associated with increased incidence of PTDM after kidney transplantation, either in vitro or in vivo. A short period of incubation of INS-1 cells with tacrolimus using different concentration profiles led to comparable effects on cell viability and insulin secretion in vitro. Consistent with this, in our patient, collective fast Tac metabolizers did not show a higher PTDM incidence compared to slow metabolizers. Full article
(This article belongs to the Special Issue Renal Lesions and Nephrotoxicity)
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14 pages, 8732 KiB  
Article
Renal Injuries after Cardiac Arrest: A Morphological Ultrastructural Study
by Maria Tsivilika, Dimitrios Kavvadas, Sofia Karachrysafi, Katerina Kotzampassi, Vasilis Grosomanidis, Eleni Doumaki, Soultana Meditskou, Antonia Sioga and Theodora Papamitsou
Int. J. Mol. Sci. 2022, 23(11), 6147; https://doi.org/10.3390/ijms23116147 - 30 May 2022
Cited by 3 | Viewed by 2464
Abstract
Background: This study aims to investigate the probable lesions and injuries induced in the renal tissue after a cardiac arrest. The renal ischemia–reperfusion model in cardiac arrest describes the effects of ischemia in the kidneys, alongside a whole-body ischemia–reperfusion injury. This protocol excludes [...] Read more.
Background: This study aims to investigate the probable lesions and injuries induced in the renal tissue after a cardiac arrest. The renal ischemia–reperfusion model in cardiac arrest describes the effects of ischemia in the kidneys, alongside a whole-body ischemia–reperfusion injury. This protocol excludes ischemic conditions caused by surgical vascular manipulation, venous injury or venous congestion. Methods: For the experimental study, 24 swine were subjected to cardiac arrest. Seven minutes later, the cardiopulmonary resuscitation technique was performed for 5 min. Afterwards, advanced life support was provided. The resuscitated swine consisted one group and the non-resuscitated the other. Tissue samples were obtained from both groups for light and electron microscopy evaluation. Results: Tissue lesions were observed in the tubules, parallel to destruction of the microvilli, reduction in the basal membrane invaginations, enlarged mitochondria, cellular vacuolization, cellular apoptosis and disorganization. In addition, fusion of the podocytes, destruction of the Bowman’s capsule parietal epithelium and abnormal peripheral urinary space was observed. The damage appeared more extensive in the non-resuscitated swine group. Conclusions: Acute kidney injury is not the leading cause of death after cardiac arrest. However, evidence suggests that the kidney damage after a cardiac arrest should be highly considered in the prognosis of the patients’ health outcome. Full article
(This article belongs to the Special Issue Renal Lesions and Nephrotoxicity)
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Review

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16 pages, 581 KiB  
Review
Rhabdomyolysis-Induced AKI (RIAKI) Including the Role of COVID-19
by Ewelina Młynarska, Julia Krzemińska, Magdalena Wronka, Beata Franczyk and Jacek Rysz
Int. J. Mol. Sci. 2022, 23(15), 8215; https://doi.org/10.3390/ijms23158215 - 26 Jul 2022
Cited by 14 | Viewed by 5786
Abstract
Rhabdomyolysis is a compound disease that may be induced by many factors, both congenital and acquired. Statin therapy is considered one of the most common acquired factors. However, recent scientific reports suggest that serious complications such as rhabdomyolysis are rarely observed. Researchers suggest [...] Read more.
Rhabdomyolysis is a compound disease that may be induced by many factors, both congenital and acquired. Statin therapy is considered one of the most common acquired factors. However, recent scientific reports suggest that serious complications such as rhabdomyolysis are rarely observed. Researchers suggest that, in many cases, side effects that occur with statin therapy, including muscle pain, can be avoided with lower-dose statin therapy or in combination therapy with other drugs. One of the most recent agents discovered to contribute to rhabdomyolysis is COVID-19 disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Rhabdomyolysis is defined as a damage to striated muscle cells with escape of intracellular substances into the bloodstream. These substances, including myoglobin, creatine kinase (CK), potassium, and uridine acid, are markers of muscle damage and early complications of rhabdomyolysis. Symptoms may be helpful in establishing the diagnosis. However, in almost 50% of patients, they do not occur. Therefore, the diagnosis is confirmed by serum CK levels five times higher than the upper limit of normal. One of the late complications of this condition is acute kidney injury (AKI), which is immediately life-threatening and has a high mortality rate among patients. Therefore, the prompt detection and treatment of rhabdomyolysis is important. Markers of muscle damage, such as CK, lactate dehydrogenase (LDH), myoglobin, troponins, and aspartate aminotransferase (AST), are important in diagnosis. Treatment of rhabdomyolysis is mainly based on early, aggressive fluid resuscitation. However, therapeutic interventions, such as urinary alkalinization with sodium bicarbonate or the administration of mannitol or furosemide, have not proven to be beneficial. In some patients who develop AKI in the course of rhabdomyolysis, renal replacement therapy (RRT) is required. Full article
(This article belongs to the Special Issue Renal Lesions and Nephrotoxicity)
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