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Acute Kidney Injury and Chronic Kidney Diseases

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

Deadline for manuscript submissions: closed (31 January 2022) | Viewed by 67069

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Special Issue Editor

Dr. Hajime Nagasu

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Guest Editor

Department of Nephrology and Hypertension, Kawasaki Medical School, Kawasaki 701-0192, Japan
Interests: chronic kidney diseases; inflammasome; ageing; macrophages; endothelial cells; mitochondria

Special Issue Information

Dear Colleagues,

Chronic kidney disease (CKD) is a progressive loss in kidney function over a period of months or years. It has been known that CKD is not only the risk of kidney failure but also the risk of death. That is the reason why CKD is important health problem in world wide. Many factors, including diabetic status, hypertension, hypoxia and activation of renin-angiotensin system, were involved in the progression of renal disease, and its regulation is difficult. On the other hand acute kindey injury (AKI) is also global health problem. The global or local ischemia contributes to the pathogenesis of AKI. After tubular injury via ischemic stress, Excess inflammation has a pivotal role of progression of kidney injury. To resolve this problem, we have to address on the common pathway to progression of kidney diseases.

Chronic inflammation is one of the most important common pathways to progression of CKD and AKI. Inflammation has been implicated in the pathogenesis of CKD, resulting in disruption of the renal microvasculature, progressive damage to the glomerular capillaries, podocyte and endothelial cell apoptosis, and tubulointerstitial fibrosis. Inflammation also has pivotal role of the AKI to CKD continuum. These facts suggested that we should know about inflammation and innate immune system in all of the kidney diseases.

The topics of special issue address on the inflammation and innate immune system in kidney diseases including AKI and CKD.

Dr. Hajime Nagasu
Guest Editor

Manuscript Submission Information

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Keywords

chronic kidney diseases
acute kidney injury
inflammation
inflammaging
nephritis
innate immune system
macrophages
neutrophils

Published Papers (13 papers)

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Research

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15 pages, 2331 KiB

Open AccessArticle

Investigating the Molecular Mechanisms of Renal Hepcidin Induction and Protection upon Hemoglobin-Induced Acute Kidney Injury

by Laura E. Diepeveen, Gaby Stegemann, Erwin T. Wiegerinck, Rian Roelofs, Myrthe Naber, Olivier Lóreal, Bart Smeets, Frank Thévenod, Dorine W. Swinkels and Rachel P. L. van Swelm

Int. J. Mol. Sci. 2022, 23(3), 1352; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23031352 - 25 Jan 2022

Cited by 3 | Viewed by 2155

Abstract

Hemolysis is known to cause acute kidney injury (AKI). The iron regulatory hormone hepcidin, produced by renal distal tubules, is suggested to exert a renoprotective role during this pathology. We aimed to elucidate the molecular mechanisms of renal hepcidin synthesis and its protection against hemoglobin-induced AKI. In contrast to known hepatic hepcidin induction, incubation of mouse cortical collecting duct (mCCD_cl1) cells with IL-6 or LPS did not induce Hamp1 mRNA expression, whereas iron (FeS) and hemin significantly induced hepcidin synthesis (p < 0.05). Moreover, iron/heme-mediated hepcidin induction in mCCD_cl1 cells was caused by the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway, as indicated by increased nuclear Nrf2 translocation and induced expression of Nrf2 downstream targets GCLM (p < 0.001), NQO1 (p < 0.001), and TXNRD1 (p < 0.005), which could be prevented by the known Nrf2 inhibitor trigonelline. Newly created inducible kidney-specific hepcidin KO mice demonstrated a significant reduction in renal Hamp1 mRNA expression. Phenylhydrazine (PHZ)-induced hemolysis caused renal iron loading and oxidative stress in both wildtype (Wt) and KO mice. PHZ treatment in Wt induced inflammatory markers (IL-6, TNFα) but not Hamp1. However, since PHZ treatment also significantly reduced systemic hepcidin levels in both Wt and KO mice (both p < 0.001), a dissection between the roles of systemic and renal hepcidin could not be made. Combined, the results of our study indicate that there are kidney-specific mechanisms in hepcidin regulation, as indicated by the dominant role of iron and not inflammation as an inducer of renal hepcidin, but also emphasize the complex interplay of various iron regulatory mechanisms during AKI on a local and systemic level. Full article

(This article belongs to the Special Issue Acute Kidney Injury and Chronic Kidney Diseases)

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23 pages, 4011 KiB

Open AccessArticle

Pro-Inflammatory Serum Amyloid a Stimulates Renal Dysfunction and Enhances Atherosclerosis in Apo E-Deficient Mice

by Antony Gao, Sameesh Gupta, Han Shi, Yuyang Liu, Angie L. Schroder, Paul K. Witting and Gulfam Ahmad

Int. J. Mol. Sci. 2021, 22(22), 12582; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222212582 - 22 Nov 2021

Cited by 3 | Viewed by 2165

Abstract

Acute serum amyloid A (SAA) is an apolipoprotein that mediates pro-inflammatory and pro-atherogenic pathways. SAA-mediated signalling is diverse and includes canonical and acute immunoregulatory pathways in a range of cell types and organs. This study aimed to further elucidate the roles for SAA in the pathogenesis of vascular and renal dysfunction. Two groups of male ApoE-deficient mice were administered SAA (100 µL, 120 µg/mL) or vehicle control (100 µL PBS) and monitored for 4 or 16 weeks after SAA treatment; tissue was harvested for biochemical and histological analyses at each time point. Under these conditions, SAA administration induced crosstalk between NF-κB and Nrf2 transcriptional factors, leading to downstream induction of pro-inflammatory mediators and antioxidant response elements 4 weeks after SAA administration, respectively. SAA treatment stimulated an upregulation of renal IFN-γ with a concomitant increase in renal levels of p38 MAPK and matrix metalloproteinase (MMP) activities, which is linked to tissue fibrosis. In the kidney of SAA-treated mice, the immunolocalisation of inducible nitric oxide synthase (iNOS) was markedly increased, and this was localised to the parietal epithelial cells lining Bowman’s space within glomeruli, which led to progressive renal fibrosis. Assessment of aortic root lesion at the study endpoint revealed accelerated atherosclerosis formation; animals treated with SAA also showed evidence of a thinned fibrous cap as judged by diffuse collagen staining. Together, this suggests that SAA elicits early renal dysfunction through promoting the IFN-γ-iNOS-p38 MAPK axis that manifests as the fibrosis of renal tissue and enhanced cardiovascular disease. Full article

(This article belongs to the Special Issue Acute Kidney Injury and Chronic Kidney Diseases)

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11 pages, 1226 KiB

Open AccessArticle

Quinacrine Ameliorates Cisplatin-Induced Renal Toxicity via Modulation of Sirtuin-1 Pathway

by Nada F. Abo El-Magd, Hasnaa Ali Ebrahim, Mohamed El-Sherbiny and Nada H. Eisa

Int. J. Mol. Sci. 2021, 22(19), 10660; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms221910660 - 01 Oct 2021

Cited by 11 | Viewed by 2183

Abstract

Renal toxicity is a serious side effect that hinders the use of cisplatin, a commonly used and effective chemotherapeutic agent. Meanwhile, quinacrine is an FDA approved drug that has been stated for its anti-inflammatory effect. Thus, we investigated the ameliorative effect of quinacrine against cisplatin-induced renal toxicity. Single intraperitoneal (i.p.) 10 mg/kg cisplatin administration induced renal injury in rats. Our results showed that 10 mg/kg/day quinacrine decreased the mortality rate of rats from 46.15% (cisplatin group) to 12.5%, and significantly decreased renal tissue fibrosis, relative kidney to body weight ratio, serum creatinine and urea levels compared with the cisplatin group. Indeed, quinacrine significantly decreased renal malondialdehyde concentration and increased renal total antioxidant capacity, compared with the cisplatin group. Furthermore, quinacrine caused significant upregulation of renal sirtuin-1 (SIRT-1) with significant downregulation of intercellular adhesion molecule-1 (ICAM-1) and tumor necrosis factor-α (TNF-α). Moreover, quinacrine significantly blocked cisplatin-induced apoptosis, which was made evident by downregulating renal apoptotic proteins (BAX and p53) and upregulating the renal anti-apoptotic protein BCL2, compared with the cisplatin group. In conclusion, this study demonstrates, for the first time, that quinacrine alleviates cisplatin-induced renal toxicity via upregulating SIRT-1, downregulating inflammatory markers (ICAM-1 and TNF-α), reducing oxidative stress, and inhibiting apoptosis. Full article

(This article belongs to the Special Issue Acute Kidney Injury and Chronic Kidney Diseases)

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14 pages, 4698 KiB

Open AccessArticle

Endothelial Dysfunction Accelerates Impairment of Mitochondrial Function in Ageing Kidneys via Inflammasome Activation

by Yoshihisa Wada, Reina Umeno, Hajime Nagasu, Megumi Kondo, Atsuyuki Tokuyama, Hiroyuki Kadoya, Kengo Kidokoro, Shun’ichiro Taniguchi, Masafumi Takahashi, Tamaki Sasaki and Naoki Kashihara

Int. J. Mol. Sci. 2021, 22(17), 9269; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22179269 - 27 Aug 2021

Cited by 2 | Viewed by 2642

Abstract

Chronic kidney disease is a common problem in the elderly and is associated with increased mortality. We have reported on the role of nitric oxide, which is generated from endothelial nitric oxide synthase (eNOS), in the progression of aged kidneys. To elucidate the role of endothelial dysfunction and the lack of an eNOS-NO pathway in ageing kidneys, we conducted experiments using eNOS and ASC-deficient mice. C57B/6 J mice (wild type (WT)), eNOS knockout (eNOS KO), and ASC knockout (ASC KO) mice were used in the present study. Then, eNOS/ASC double-knockout (eNOS/ASC DKO) mice were generated by crossing eNOS KO and ASC KO mice. These mice were sacrificed at 17−19 months old. The Masson positive area and the KIM-1 positive area tended to increase in eNOS KO mice, compared with WT mice, but not eNOS/ASC DKO mice. The COX-positive area was significantly reduced in eNOS KO mice, compared with WT and eNOS/ASC DKO mice. To determine whether inflammasomes were activated in infiltrating macrophages, the double staining of IL-18 and F4/80 was performed. IL-18 and F4/80 were found to be co-localised in the tubulointerstitial areas. Inflammasomes play a pivotal role in inflammaging in ageing kidneys. Furthermore, inflammasome activation may accelerate cellular senescence via mitochondrial dysfunction. The importance of endothelial function as a regulatory mechanism suggests that protection of endothelial function may be a potential therapeutic target. Full article

(This article belongs to the Special Issue Acute Kidney Injury and Chronic Kidney Diseases)

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21 pages, 11964 KiB

Open AccessArticle

CRKL, AIFM3, AIF, BCL2, and UBASH3A during Human Kidney Development

by Mirela Lozic, Luka Minarik, Anita Racetin, Natalija Filipovic, Mirna Saraga Babic and Katarina Vukojevic

Int. J. Mol. Sci. 2021, 22(17), 9183; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22179183 - 25 Aug 2021

Cited by 5 | Viewed by 2167

Abstract

We aimed to investigate the spatio-temporal expression of possible CAKUT candidate genes CRKL, AIFM3, and UBASH3A, as well as AIF and BCL2 during human kidney development. Human fetal kidney tissue was stained with antibodies and analyzed by fluorescence microscopy and RT-PCR. Quantification of positive cells was assessed by calculation of area percentage and counting cells in nephron structures. Results showed statistically significant differences in the temporal expression patterns of the examined markers, depending on the investigated developmental stage. Limited but strong expression of CRKL was seen in developing kidneys, with increasing expression up to the period where the majority of nephrons are formed. Results also lead us to conclude that AIFM3 and AIF are important for promoting cell survival, but only AIFM3 is considered a CAKUT candidate gene due to the lack of AIF in nephron developmental structures. Our findings imply great importance of AIFM3 in energy production in nephrogenesis and tubular maturation. UBASH3A raw scores showed greater immunoreactivity in developing structures than mature ones which would point to a meaningful role in nephrogenesis. The fact that mRNA and proteins of CRKL, UBASH3A, and AIFM3 were detected in all phases of kidney development implies their role as renal development control genes. Full article

(This article belongs to the Special Issue Acute Kidney Injury and Chronic Kidney Diseases)

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Review

Jump to: Research

17 pages, 2162 KiB

Open AccessReview

Indoleamine 2,3 Dioxygenase 1—The Potential Link between the Innate Immunity and the Ischemia-Reperfusion-Induced Acute Kidney Injury?

by Anna Krupa, Mikolaj M. Krupa and Krystyna Pawlak

Int. J. Mol. Sci. 2022, 23(11), 6176; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23116176 - 31 May 2022

Cited by 4 | Viewed by 2007

Abstract

Ischemia-reperfusion injury (IRI) is of the most common causes of acute kidney injury (AKI); nevertheless, the mechanisms responsible for both early kidney injury and the reparative phase are not fully recognised. The inflammatory response following ischemia is characterised by the crosstalk between cells belonging to the innate immune system—dendritic cells (DCs), macrophages, neutrophils, natural killer (NK) cells, and renal tubular epithelial cells (RTECs). A tough inflammatory response can damage the renal tissue; it may also have a protective effect leading to the repair after IRI. Indoleamine 2,3 dioxygenase 1 (IDO1), the principal enzyme of the kynurenine pathway (KP), has a broad spectrum of immunological activity from stimulation to immunosuppressive activity in inflamed areas. IDO1 expression occurs in cells of the innate immunity and RTECs during IRI, resulting in local tryptophan (TRP) depletion and generation of kynurenines, and both of these mechanisms contribute to the immunosuppressive effect. Nonetheless, it is unknown if the above mechanism can play a harmful or preventive role in IRI-induced AKI. Despite the scarcity of literature in this field, the current review attempts to present a possible role of IDO1 activation in the regulation of the innate immune system in IRI-induced AKI. Full article

(This article belongs to the Special Issue Acute Kidney Injury and Chronic Kidney Diseases)

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16 pages, 709 KiB

Open AccessReview

Uric Acid and Oxidative Stress—Relationship with Cardiovascular, Metabolic, and Renal Impairment

by Mihai-Emil Gherghina, Ileana Peride, Mirela Tiglis, Tiberiu Paul Neagu, Andrei Niculae and Ionel Alexandru Checherita

Int. J. Mol. Sci. 2022, 23(6), 3188; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23063188 - 16 Mar 2022

Cited by 87 | Viewed by 10101

Abstract

Background: The connection between uric acid (UA) and renal impairment is well known due to the urate capacity to precipitate within the tubules or extra-renal system. Emerging studies allege a new hypothesis concerning UA and renal impairment involving a pro-inflammatory status, endothelial dysfunction, and excessive activation of renin–angiotensin–aldosterone system (RAAS). Additionally, hyperuricemia associated with oxidative stress is incriminated in DNA damage, oxidations, inflammatory cytokine production, and even cell apoptosis. There is also increasing evidence regarding the association of hyperuricemia with chronic kidney disease (CKD), cardiovascular disease, and metabolic syndrome or diabetes mellitus. Conclusions: Important aspects need to be clarified regarding hyperuricemia predisposition to oxidative stress and its effects in order to initiate the proper treatment to determine the optimal maintenance of UA level, improving patients’ long-term prognosis and their quality of life. Full article

(This article belongs to the Special Issue Acute Kidney Injury and Chronic Kidney Diseases)

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20 pages, 1702 KiB

Open AccessReview

The Role of Centrosome Distal Appendage Proteins (DAPs) in Nephronophthisis and Ciliogenesis

by Fatma Mansour, Felix J. Boivin, Iman B. Shaheed, Markus Schueler and Kai M. Schmidt-Ott

Int. J. Mol. Sci. 2021, 22(22), 12253; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222212253 - 12 Nov 2021

Cited by 6 | Viewed by 3418

Abstract

The primary cilium is found in most mammalian cells and plays a functional role in tissue homeostasis and organ development by modulating key signaling pathways. Ciliopathies are a group of genetically heterogeneous disorders resulting from defects in cilia development and function. Patients with ciliopathic disorders exhibit a range of phenotypes that include nephronophthisis (NPHP), a progressive tubulointerstitial kidney disease that commonly results in end-stage renal disease (ESRD). In recent years, distal appendages (DAPs), which radially project from the distal end of the mother centriole, have been shown to play a vital role in primary ciliary vesicle docking and the initiation of ciliogenesis. Mutations in the genes encoding these proteins can result in either a complete loss of the primary cilium, abnormal ciliary formation, or defective ciliary signaling. DAPs deficiency in humans or mice commonly results in NPHP. In this review, we outline recent advances in our understanding of the molecular functions of DAPs and how they participate in nephronophthisis development. Full article

(This article belongs to the Special Issue Acute Kidney Injury and Chronic Kidney Diseases)

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22 pages, 2367 KiB

Open AccessReview

The Role of Mitochondria in Acute Kidney Injury and Chronic Kidney Disease and Its Therapeutic Potential

by Xiaoqin Zhang, Ewud Agborbesong and Xiaogang Li

Int. J. Mol. Sci. 2021, 22(20), 11253; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222011253 - 19 Oct 2021

Cited by 70 | Viewed by 8039

Abstract

Mitochondria are heterogeneous and highly dynamic organelles, playing critical roles in adenosine triphosphate (ATP) synthesis, metabolic modulation, reactive oxygen species (ROS) generation, and cell differentiation and death. Mitochondrial dysfunction has been recognized as a contributor in many diseases. The kidney is an organ enriched in mitochondria and with high energy demand in the human body. Recent studies have been focusing on how mitochondrial dysfunction contributes to the pathogenesis of different forms of kidney diseases, including acute kidney injury (AKI) and chronic kidney disease (CKD). AKI has been linked to an increased risk of developing CKD. AKI and CKD have a broad clinical syndrome and a substantial impact on morbidity and mortality, encompassing various etiologies and representing important challenges for global public health. Renal mitochondrial disorders are a common feature of diverse forms of AKI and CKD, which result from defects in mitochondrial structure, dynamics, and biogenesis as well as crosstalk of mitochondria with other organelles. Persistent dysregulation of mitochondrial homeostasis in AKI and CKD affects diverse cellular pathways, leading to an increase in renal microvascular loss, oxidative stress, apoptosis, and eventually renal failure. It is important to understand the cellular and molecular events that govern mitochondria functions and pathophysiology in AKI and CKD, which should facilitate the development of novel therapeutic strategies. This review provides an overview of the molecular insights of the mitochondria and the specific pathogenic mechanisms of mitochondrial dysfunction in the progression of AKI, CKD, and AKI to CKD transition. We also discuss the possible beneficial effects of mitochondrial-targeted therapeutic agents for the treatment of mitochondrial dysfunction-mediated AKI and CKD, which may translate into therapeutic options to ameliorate renal injury and delay the progression of these kidney diseases. Full article

(This article belongs to the Special Issue Acute Kidney Injury and Chronic Kidney Diseases)

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27 pages, 1053 KiB

Open AccessReview

Adipose-Derived Stem/Stromal Cells in Kidney Transplantation: Status Quo and Future Perspectives

by Gabriele Storti, Evaldo Favi, Francesca Albanesi, Bong-Sung Kim and Valerio Cervelli

Int. J. Mol. Sci. 2021, 22(20), 11188; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222011188 - 17 Oct 2021

Cited by 7 | Viewed by 2557

Abstract

Kidney transplantation (KT) is the gold standard treatment of end-stage renal disease. Despite progressive advances in organ preservation, surgical technique, intensive care, and immunosuppression, long-term allograft survival has not significantly improved. Among the many peri-operative complications that can jeopardize transplant outcomes, ischemia–reperfusion injury (IRI) deserves special consideration as it is associated with delayed graft function, acute rejection, and premature transplant loss. Over the years, several strategies have been proposed to mitigate the impact of IRI and favor tolerance, with rather disappointing results. There is mounting evidence that adipose stem/stromal cells (ASCs) possess specific characteristics that could help prevent, reduce, or reverse IRI. Immunomodulating and tolerogenic properties have also been suggested, thus leading to the development of ASC-based prophylactic and therapeutic strategies in pre-clinical and clinical models of renal IRI and allograft rejection. ASCs are copious, easy to harvest, and readily expandable in culture. Furthermore, ASCs can secrete extracellular vesicles (EV) which may act as powerful mediators of tissue repair and tolerance. In the present review, we discuss the current knowledge on the mechanisms of action and therapeutic opportunities offered by ASCs and ASC-derived EVs in the KT setting. Most relevant pre-clinical and clinical studies as well as actual limitations and future perspective are highlighted. Full article

(This article belongs to the Special Issue Acute Kidney Injury and Chronic Kidney Diseases)

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23 pages, 2834 KiB

Open AccessReview

Chronic Kidney Disease: Strategies to Retard Progression

by Ming-Tso Yan, Chia-Ter Chao and Shih-Hua Lin

Int. J. Mol. Sci. 2021, 22(18), 10084; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms221810084 - 18 Sep 2021

Cited by 36 | Viewed by 16193

Abstract

Chronic kidney disease (CKD), defined as the presence of irreversible structural or functional kidney damages, increases the risk of poor outcomes due to its association with multiple complications, including altered mineral metabolism, anemia, metabolic acidosis, and increased cardiovascular events. The mainstay of treatments for CKD lies in the prevention of the development and progression of CKD as well as its complications. Due to the heterogeneous origins and the uncertainty in the pathogenesis of CKD, efficacious therapies for CKD remain challenging. In this review, we focus on the following four themes: first, a summary of the known factors that contribute to CKD development and progression, with an emphasis on avoiding acute kidney injury (AKI); second, an etiology-based treatment strategy for retarding CKD, including the approaches for the common and under-recognized ones; and third, the recommended approaches for ameliorating CKD complications, and the final section discusses the novel agents for counteracting CKD progression. Full article

(This article belongs to the Special Issue Acute Kidney Injury and Chronic Kidney Diseases)

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11 pages, 1243 KiB

Open AccessReview

Acute Kidney Injury in COVID-19

by Marta Głowacka, Sara Lipka, Ewelina Młynarska, Beata Franczyk and Jacek Rysz

Int. J. Mol. Sci. 2021, 22(15), 8081; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22158081 - 28 Jul 2021

Cited by 30 | Viewed by 4995

Abstract

COVID-19 is mainly considered a respiratory illness, but since SARS-CoV-2 uses the angiotensin converting enzyme 2 receptor (ACE2) to enter human cells, the kidney is also a target of the viral infection. Acute kidney injury (AKI) is the most alarming condition in COVID-19 patients. Recent studies have confirmed the direct entry of SARS-CoV-2 into the renal cells, namely podocytes and proximal tubular cells, but this is not the only pathomechanism of kidney damage. Hypovolemia, cytokine storm and collapsing glomerulopathy also play an important role. An increasing number of papers suggest a strong association between AKI development and higher mortality in COVID-19 patients, hence our interest in the matter. Although knowledge about the role of kidneys in SARS-CoV-2 infection is changing dynamically and is yet to be fully investigated, we present an insight into the possible pathomechanisms of AKI in COVID-19, its clinical features, risk factors, impact on hospitalization and possible ways for its management via renal replacement therapy. Full article

(This article belongs to the Special Issue Acute Kidney Injury and Chronic Kidney Diseases)

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26 pages, 23931 KiB

Open AccessReview

Biomarkers and Mechanisms of Oxidative Stress—Last 20 Years of Research with an Emphasis on Kidney Damage and Renal Transplantation

by Karol Tejchman, Katarzyna Kotfis and Jerzy Sieńko

Int. J. Mol. Sci. 2021, 22(15), 8010; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22158010 - 27 Jul 2021

Cited by 42 | Viewed by 5696

Abstract

Oxidative stress is an imbalance between pro- and antioxidants that adversely influences the organism in various mechanisms and on many levels. Oxidative damage occurring concomitantly in many cellular structures may cause a deterioration of function, including apoptosis and necrosis. The damage leaves a molecular “footprint”, which can be detected by specific methodology, using certain oxidative stress biomarkers. There is an intimate relationship between oxidative stress, inflammation, and functional impairment, resulting in various diseases affecting the entire human body. In the current narrative review, we strengthen the connection between oxidative stress mechanisms and their active compounds, emphasizing kidney damage and renal transplantation. An analysis of reactive oxygen species (ROS), antioxidants, products of peroxidation, and finally signaling pathways gives a lot of promising data that potentially will modify cell responses on many levels, including gene expression. Oxidative damage, stress, and ROS are still intensively exploited research subjects. We discuss compounds mentioned earlier as biomarkers of oxidative stress and present their role documented during the last 20 years of research. The following keywords and MeSH terms were used in the search: oxidative stress, kidney, transplantation, ischemia-reperfusion injury, IRI, biomarkers, peroxidation, and treatment. Full article

(This article belongs to the Special Issue Acute Kidney Injury and Chronic Kidney Diseases)

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