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Pharmaceuticals
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Pharmacotherapy of Kidney Diseases
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Pharmacotherapy of Kidney Diseases

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Pharmacology".

Deadline for manuscript submissions: closed (31 August 2023) | Viewed by 6076

Special Issue Editors

Dr. Beatriz Suárez-Álvarez

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Guest Editor
Translational Immunology Laboratory, Instituto de Investigación Sanitaria del Principado de Asturias, Oviedo, Spain
Interests: kidney disease; immunology; epigenetics; new targets; nanoparticles
Dr. María Laura Saiz Álvarez

E-Mail Website
Guest Editor
Translational Immunology Laboratory, Instituto de Investigación Sanitaria del Principado de Asturias, Oviedo, Spain
Interests: AKI; CKD; kidney ischemia reperfusion; mouse models of kidney disease; nanoparticles; UPR; leukocyte extravasation; endothelial damage; cardiorenal axis
Prof. Dr. Marco Filice

E-Mail Website
Guest Editor
Nanobiotechnology for Life Sciences Group, Department of Chemistry in Pharmaceutical Sciences, Faculty of Pharmacy, Universidad Complutense de Madrid (UCM), Plaza Ramón y Cajal s/n, E-28040 Madrid, Spain
Interests: nanobiotechnology; medicinal chemistry; multimodal molecular imaging; theranosis; nanoparticles; cancer; kidney and cardiovascular diseases
Special Issues, Collections and Topics in MDPI journals
Dr. Stefanie Steiger

E-Mail Website
Guest Editor
Division of Nephrology, Department of Medicine IV, Hospital of the Ludwig-Maximilians-University Munich, Munich, Germany
Interests: acute kidney injury; tissue repair; fibrosis; kidney stones and crystal biology; hyperuricemia; inflammation; infection; immune-cell activation and plasticity
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Kidney diseases are a series of pathologies that impair the kidneys’ ability to properly filter blood and remove waste products. The most common type of kidney disease is chronic kidney disease (CKD)—a progressive condition that affects >10% of the general population worldwide, amounting to more than 800 million individuals. Indeed, by 2040, CKD will become the fifth leading cause of death worldwide; however, there is no cure for this condition, and current treatments just rely on relieving symptoms and strategies to prevent disease progression. Other diseases that affect the kidneys include acute kidney injury, stones, infections, cysts, cancer and rare autoimmune (Alport syndrome, Fabry disease, membranous nephropathy, atypical hemolytic uremic syndrome) or metabolic diseases (cystinosis, distal renal tubular acidosis). Of note, many of the aforementioned diseases may end up in kidney failure which requires lifelong dialysis or kidney transplantation with long-term immunosuppressant treatments and complications thereof. Consequently, kidney diseases have a severe impact on patients’ quality of life, which also experience an increased risk of cardiovascular morbidity and premature mortality. In addition, all the required medical attention implies an immense healthcare and economic burden. Therefore, enhanced efforts for the better prevention and treatment of kidney diseases are urgently needed. Recent progress in our understanding of the pathophysiology of these conditions, together with the development of novel therapeutic agents thanks to the advancement of technology, should support improvements in the pharmacotherapy of kidney disease. This Special Issue aims to highlight the latest findings in the field of kidney disease therapies. We seek studies that explore any conditions related to kidney disease in its different manifestations, using basic science but also clinical and population-based approaches with an eye towards the development of treatment strategies.

Dr. Beatriz Suárez-Álvarez
Dr. María Laura Saiz Álvarez
Prof. Dr. Marco Filice
Dr. Stefanie Steiger
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. Pharmaceuticals is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). 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

  • nanotherapy
  • cell death
  • inflammation
  • fibrosis
  • epigenetic drugs
  • inhibitors
  • nephroprotective agents
  • SGLT2 inhibitors
  • anti-ischemic therapy
  • anti-diabetic drugs

Published Papers (4 papers)

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Research

15 pages, 3618 KiB  
Article
Protective Role of Betulinic Acid against Cisplatin-Induced Nephrotoxicity and Its Antibacterial Potential toward Uropathogenic Bacteria
by Fatemah A. Alherz, Engy Elekhnawy, Hend Mostafa Selim, Thanaa A. El-Masry, Aya H. El-Kadem, Ismail A. Hussein and Walaa A. Negm
Pharmaceuticals 2023, 16(8), 1180; https://doi.org/10.3390/ph16081180 - 18 Aug 2023
Viewed by 1034
Abstract
Acute kidney injury (AKI) is one of the major side effects of cisplatin, a remarkable anticancer agent. Therefore, there is a growing need to find an agent that could mitigate cisplatin-induced nephrotoxicity. Betulinic acid (BA) is a natural compound isolated from Silene succulenta [...] Read more.
Acute kidney injury (AKI) is one of the major side effects of cisplatin, a remarkable anticancer agent. Therefore, there is a growing need to find an agent that could mitigate cisplatin-induced nephrotoxicity. Betulinic acid (BA) is a natural compound isolated from Silene succulenta Forssk for the first time, with miraculous biological activities and no reports of its effect on the nephrotoxicity induced by cisplatin. Mice received BA orally with doses of 30 and 50 mg/kg before the intraperitoneal injection of cisplatin. Betulinic acid was found to decrease serum levels of creatinine and tissue levels of NGAL and kidney injury molecule (KIM-1) and improve the histological changes in the kidney. In addition, BA decreased the oxidative stress marker malondialdehyde (MDA), increased superoxide dismutase (SOD) antioxidative activity and suppressed the intensity of IL-1B and NFкB immuno-staining. Interestingly, betulinic acid enhanced autophagy by increasing beclin 1, ATG5, and LC3II and decreasing p62 expressions. Thus, our findings suggest betulinic acid as a potential agent that may protect from acute kidney injury by targeting inflammation, oxidative stress, and autophagy processes. Novel drugs are needed to combat the spreading of multidrug resistance between pathogenic bacteria, especially uropathogenic isolates. So, we elucidated the antibacterial properties of BA on Pseudomonas aeruginosa, Escherichia coli, Proteus mirabilis, and Klebsiella pneumoniae. Betulinic acid had minimum inhibitory concentration values (128 to 512 µg/mL). In addition, it adversely affected the membrane integrity of the tested isolates. Accordingly, betulinic acid should be clinically investigated in the future for urinary tract diseases. Full article
(This article belongs to the Special Issue Pharmacotherapy of Kidney Diseases)
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23 pages, 11582 KiB  
Article
Evaluation of Cisplatin-Induced Acute Renal Failure Amelioration Using Fondaparinux and Alteplase
by Mohamed S. Abdel-Bakky, Anas S. A. Aldakhili, Hussein M. Ali, Ali Y. Babiker, Ahmad H. Alhowail and Salman A. A. Mohammed
Pharmaceuticals 2023, 16(7), 910; https://doi.org/10.3390/ph16070910 - 21 Jun 2023
Viewed by 1130
Abstract
Acute renal failure (ARF) is a deleterious condition with increased mortality or healthcare costs or dialysis-dependent end-stage renal disease. The study aims to compare prophylaxis with fondaparinux (Fund) vs. treatment with alteplase (Alt) in ameliorating cisplatin (Cis)-induced ARF. Sixty male mice were equally [...] Read more.
Acute renal failure (ARF) is a deleterious condition with increased mortality or healthcare costs or dialysis-dependent end-stage renal disease. The study aims to compare prophylaxis with fondaparinux (Fund) vs. treatment with alteplase (Alt) in ameliorating cisplatin (Cis)-induced ARF. Sixty male mice were equally divided randomly into six groups of control, Cis, Alt, and Cis + Alt groups receiving normal saline for 10 days. All four groups except for the control received Cis (30 mg/kg, i.p.) on day 7, and 6 h later, both the Alt groups received Alt (0.9 mg/kg, i.v.). The animal groups Fund and Fund + Cis received Fund (5 mg/kg, i.p.) for 10 days, and the Fund + Cis group on day 7 received Cis. All the animal groups were euthanized 72 h after the Cis dose. The Fund + Cis group showed significantly increased expression levels of platelet count, retinoid X receptor alpha (RXR-α) and phosphorylated Akt (p-Akt) in addition to decreased levels of urea, blood urea nitrogen (BUN), uric acid, white blood cells (WBCs), red blood cells (RBCs), relative kidney body weight, kidney injury score, glucose, prothrombin (PT), A Disintegrin And Metalloproteinases-10 (ADAM10), extracellular matrix deposition, protease-activated receptor 2 (PAR-2), and fibrinogen expression when compared to the Cis-only group. Meanwhile, the Cis + Alt group showed increased caspase-3 expression in addition to decreased levels of urea, BUN, uric acid, WBCs, RBCs, glucose, platelet count and PT expression with a marked decrease in PAR-2 protein expression compared to the Cis group. The creatinine levels for both the Fund + Cis and Cis + Alt groups were found to be comparable to those of the Cis-only group. The results demonstrate that the coagulation system’s activation through the stimulation of PAR-2 and fibrinogen due to Cis-induced ADAM10 protein expression mediated the apoptotic pathway, as indicated by caspase-3 expression through the p-Akt pathway. This is normally accompanied by the loss of RXR-α distal and proximal tubules as lipid droplets. When the animals were pre-treated with the anticoagulant, Fund, the previous deleterious effect was halted while the fibrinolytic agent, Alt, most of the time failed to treat Cis-induced toxicity. Full article
(This article belongs to the Special Issue Pharmacotherapy of Kidney Diseases)
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9 pages, 583 KiB  
Communication
Maintenance of Potent Cellular and Humoral Immune Responses in Long-Term Hemodialysis Patients after 1273-mRNA SARS-CoV-2 Vaccination
by Maria Gonzalez-Perez, Jana Baranda, Marcos J. Berges-Buxeda, Patricia Conde, Mayte Pérez-Olmeda, Daniel Lozano-Ojalvo, Carmen Cámara, Maria del Rosario Llópez-Carratalá, Emilio Gonzalez-Parra, Pilar Portolés, Alberto Ortiz, Jose Portoles and Jordi Ochando
Pharmaceuticals 2023, 16(4), 574; https://doi.org/10.3390/ph16040574 - 11 Apr 2023
Cited by 2 | Viewed by 1448
Abstract
Continuous evaluation of the coronavirus disease 2019 (COVID-19) vaccine effectiveness in hemodialysis (HD) patients is critical in this immunocompromised patient group with higher mortality rates due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. The response towards vaccination in HD patients has [...] Read more.
Continuous evaluation of the coronavirus disease 2019 (COVID-19) vaccine effectiveness in hemodialysis (HD) patients is critical in this immunocompromised patient group with higher mortality rates due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. The response towards vaccination in HD patients has been studied weeks after their first and second SARS-CoV-2 vaccination dose administration, but no further studies have been developed in a long-term manner, especially including both the humoral and cellular immune response. Longitudinal studies that monitor the immune response to COVID-19 vaccination in individuals undergoing HD are therefore necessary to prioritize vaccination strategies and minimize the pathogenic effects of SARS-CoV-2 in this high-risk group of patients. We followed up HD patients and healthy volunteers (HV) and monitored their humoral and cellular immune response three months after the second (V2+3M) and after the third vaccination dose (V3+3M), taking into consideration previous COVID-19 infections. Our cellular immunity results show that, while HD patients and HV individuals secrete comparable levels of IFN-γ and IL-2 in ex vivo stimulated whole blood at V2+3M in both naïve and COVID-19-recovered individuals, HD patients secrete higher levels of IFN-γ and IL-2 than HV at V3+3M. This is mainly due to a decay in the cellular immune response in HV individuals after the third dose. In contrast, our humoral immunity results show similar IgG binding antibody units (BAU) between HD patients and HV individuals at V3+3M, independently of their previous infection status. Overall, our results indicate that HD patients maintain strong cellular and humoral immune responses after repeated 1273-mRNA SARS-CoV-2 vaccinations over time. The data also highlights significant differences between cellular and humoral immunity after SARS-CoV-2 vaccination, which emphasizes the importance of monitoring both arms of the immune response in the immunocompromised population. Full article
(This article belongs to the Special Issue Pharmacotherapy of Kidney Diseases)
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22 pages, 7665 KiB  
Article
Intermedin Alleviates Vascular Calcification in CKD through Sirtuin 3-Mediated Inhibition of Mitochondrial Oxidative Stress
by Shi-Meng Liu, Ya-Rong Zhang, Yao Chen, Deng-Ren Ji, Jie Zhao, Su Fu, Mo-Zhi Jia, Yan-Rong Yu, Chao-Shu Tang, Wei Huang, Ye-Bo Zhou and Yong-Fen Qi
Pharmaceuticals 2022, 15(10), 1224; https://doi.org/10.3390/ph15101224 - 02 Oct 2022
Cited by 2 | Viewed by 1831
Abstract
Vascular calcification (VC) is a common pathophysiological process of chronic kidney disease (CKD). Sirtuin 3 (Sirt3), a major NAD+-dependent protein deacetylase predominantly in mitochondria, is involved in the pathogenesis of VC. We previously reported that intermedin (IMD) could protect against VC. [...] Read more.
Vascular calcification (VC) is a common pathophysiological process of chronic kidney disease (CKD). Sirtuin 3 (Sirt3), a major NAD+-dependent protein deacetylase predominantly in mitochondria, is involved in the pathogenesis of VC. We previously reported that intermedin (IMD) could protect against VC. In this study, we investigated whether IMD attenuates VC by Sirt3-mediated inhibition of mitochondrial oxidative stress. A rat VC with CKD model was induced by the 5/6 nephrectomy plus vitamin D3. Vascular smooth muscle cell (VSMC) calcification was induced by CaCl2 and β-glycerophosphate. IMD1-53 treatment attenuated VC in vitro and in vivo, rescued the depressed mitochondrial membrane potential (MMP) level and decreased mitochondrial ROS levels in calcified VSMCs. IMD1-53 treatment recovered the reduced protein level of Sirt3 in calcified rat aortas and VSMCs. Inhibition of VSMC calcification by IMD1-53 disappeared when the cells were Sirt3 absent or pretreated with the Sirt3 inhibitor 3-TYP. Furthermore, 3-TYP pretreatment blocked IMD1-53-mediated restoration of the MMP level and inhibition of mitochondrial oxidative stress in calcified VSMCs. The attenuation of VSMC calcification by IMD1-53 through upregulation of Sirt3 might be achieved through activation of the IMD receptor and post-receptor signaling pathway AMPK, as indicated by pretreatment with an IMD receptor antagonist or AMPK inhibitor blocking the inhibition of VSMC calcification and upregulation of Sirt3 by IMD1-53. AMPK inhibitor treatment reversed the effects of IMD1-53 on restoring the MMP level and inhibiting mitochondrial oxidative stress in calcified VSMCs. In conclusion, IMD attenuates VC by improving mitochondrial function and inhibiting mitochondrial oxidative stress through upregulating Sirt3. Full article
(This article belongs to the Special Issue Pharmacotherapy of Kidney Diseases)
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