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Kidney Diseases: Molecular Pathogenesis and Therapeutic Strategies—2nd Edition
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Kidney Diseases: Molecular Pathogenesis and Therapeutic Strategies—2nd Edition

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: 20 February 2025 | Viewed by 4805

Special Issue Editor

Dr. Gábor Kökény

E-Mail Website
Guest Editor
Semmelweis Egyetem, Budapest, Hungary
Interests: kidney fibrosis; glomerulosclerosis; diabetic nephropathy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The number of patients with chronic kidney disease is growing exponentially worldwide, affecting up to 14% of the adult population. A wide range of damaging factors (e.g., immunological causes, hypertension, diabetes mellitus, and acute kidney injury) cause inflammation and scarring in the kidney. Due to the high prevalence of chronic kidney disease and its progression to renal failure regardless of the etiology, it is important to better understand the underlying pathomechanisms.

Unraveling new molecular pathways that participate in disease progression is essential in order to develop better therapeutic strategies. This Special Issue aims to present some novel experimental and clinical aspects of kidney disease pathogenesis and treatment.

Dr. Gábor Kökény
Guest Editor

Manuscript Submission Information

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Keywords

  • kidney fibrosis
  • chronic kidney disease
  • gene expression
  • acute kidney injury
  • inflammation

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Related Special Issue

Published Papers (4 papers)

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Research

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11 pages, 687 KiB  
Article
Prediction of Successful Liberation from Continuous Renal Replacement Therapy Using a Novel Biomarker in Patients with Acute Kidney Injury after Cardiac Surgery—An Observational Trial
by Johanna Tichy, Andrea Hausmann, Johannes Lanzerstorfer, Sylvia Ryz, Ludwig Wagner, Andrea Lassnigg and Martin H. Bernardi
Int. J. Mol. Sci. 2024, 25(20), 10873; https://doi.org/10.3390/ijms252010873 - 10 Oct 2024
Viewed by 398
Abstract
An acute kidney injury (AKI) is the most common complication following cardiac surgery, and can lead to the initiation of continuous renal replacement therapy (CRRT). However, there is still insufficient evidence for when patients should be liberated from CRRT. Proenkephalin A 119–159 (PENK) [...] Read more.
An acute kidney injury (AKI) is the most common complication following cardiac surgery, and can lead to the initiation of continuous renal replacement therapy (CRRT). However, there is still insufficient evidence for when patients should be liberated from CRRT. Proenkephalin A 119–159 (PENK) is a novel biomarker that reflects kidney function independently of other factors. This study investigated whether PENK could guide successful liberation from CRRT. Therefore, we performed a prospective, observational, single-center study at the Medical University of Vienna between July 2022 and May 2023, which included adult patients who underwent cardiac surgery for a cardiopulmonary bypass; patients on preoperative RRT were excluded. The PENK levels were measured at the time of AKI diagnosis and at the initiation of and liberation from CRRT, and were subsequently compared to determine whether the patients were successfully liberated from CRRT. We screened 61 patients with postoperative AKI; 20 patients experienced a progression of AKI requiring CRRT. The patients who were successfully liberated from CRRT had mean PENK levels of 113 ± 95.4 pmol/L, while the patients who were unsuccessfully liberated from CRRT had mean PENK levels of 290 ± 175 pmol/L (p = 0.018). For the prediction of the successful liberation from CRRT, we found an area under the curve of 0.798 (95% CI, 0.599–0.997) with an optimal threshold value of 126.7 pmol/L for PENK (Youden Index = 0.53, 95% CI, 0.10–0.76) at the time of CRRT liberation (sensitivity = 0.64, specificity = 0.89). In conclusion, PENK is a novel biomarker that has the potential to predict the successful liberation from CRRT for patients with AKI after cardiac surgery. Full article
(This article belongs to the Special Issue Kidney Diseases: Molecular Pathogenesis and Therapeutic Strategies—2nd Edition)
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17 pages, 1613 KiB  
Article
The Relationship between Vascular Biomarkers (Serum Endocan and Endothelin-1), NT-proBNP, and Renal Function in Chronic Kidney Disease, IgA Nephropathy: A Cross-Sectional Study
by Balázs Sági, Tibor Vas, Csenge Gál, Zoltán Horváth-Szalai, Tamás Kőszegi, Judit Nagy, Botond Csiky and Tibor József Kovács
Int. J. Mol. Sci. 2024, 25(19), 10552; https://doi.org/10.3390/ijms251910552 - 30 Sep 2024
Viewed by 406
Abstract
IgA nephropathy (IgAN) is the most common primary glomerular disease. Endothelin-1 (ET-1) is one of the strongest vasoconstrictor materials in the blood. The N-terminal prohormone of brain natriuretic peptide (NT-proBNP) is associated with renal function and poor outcomes in chronic kidney disease (CKD). [...] Read more.
IgA nephropathy (IgAN) is the most common primary glomerular disease. Endothelin-1 (ET-1) is one of the strongest vasoconstrictor materials in the blood. The N-terminal prohormone of brain natriuretic peptide (NT-proBNP) is associated with renal function and poor outcomes in chronic kidney disease (CKD). Serum endocan is a biomarker associated with proinflammatory cytokines, and the increase in the serum level plays a critical role in inflammatory, proliferative, and neovascularization processes and is associated with poor cardiovascular outcomes in patients with CKD too. Identifying high-risk patients using biomarkers could help to optimize their treatment. Ninety patients with biopsy-confirmed IgAN were included in the study (50 males/40 females, mean age: 54.9 ± 14.4 years). Serum endocan, ET-1, and NT-proBNP were measured by enzyme-linked immunosorbent assay kits. Echocardiography was performed, and carotid-femoral pulse wave velocity (cfPWV) was measured by SphygmoCor in this cross-sectional study. Patients were divided into two groups based on serum endocan median level (cut-off: 44 ug/L). There was significantly higher aorta systolic blood pressure (SBPao) (p = 0.013), NT-proBNP (p = 0.028), albumin/creatinine ratio (p = 0.036), and uric acid (p = 0.045) in the case of the higher endocan group compared to the lower. There was also significantly higher SBPao (p = 0.037) and NT-proBNP (p = 0.038) in the case of higher endothelin-1 (ET-1) levels compared to the lower (cut-off: 231 pg/mL) group by the two-sample t-test. Then, we divided the patients into two groups based on the eGFR (CKD 1–2 vs. CKD 3–5). The levels of serum endocan, NT-proBNP, cfPWV, SBPao, left ventricular mass index (LVMI), uric acid, and albuminuria were significantly higher in the CKD 3–5 group compared to the CKD 1–2 group. The serum endocan and NT-proBNP levels were significantly higher in the diastolic dysfunction group (p = 0.047, p = 0.015). There was a significant increase in serum endocan levels (CKD 1 vs. CKD 5; p = 0.008) with decreasing renal function. In IgAN, vascular biomarkers (endocan, ET-1) may play a role in endothelial dysfunction through vascular damage and elevation of SBPao. Serum endocan, ET-1, and NT-proBNP biomarkers may help to identify IgAN patients at high risk. Full article
(This article belongs to the Special Issue Kidney Diseases: Molecular Pathogenesis and Therapeutic Strategies—2nd Edition)
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13 pages, 3509 KiB  
Article
Association between PD-L1 Expression and the Prognosis and Clinicopathologic Features of Non-Clear Cell Renal Cell Carcinoma
by Magdalena Chrabańska, Nikola Szweda-Gandor, Magdalena Rynkiewicz, Dominik Hraboš and Bogna Drozdzowska
Int. J. Mol. Sci. 2024, 25(7), 3916; https://doi.org/10.3390/ijms25073916 - 31 Mar 2024
Viewed by 1322
Abstract
PD-L1 is one of the two programmed cell death 1 (PD-1) ligands and a part of an immune checkpoint system (PD-1/PD-L1) with widespread clinical application. The aim of this study was to investigate PD-L1 expression and its association with clinicopathological and prognostic significance [...] Read more.
PD-L1 is one of the two programmed cell death 1 (PD-1) ligands and a part of an immune checkpoint system (PD-1/PD-L1) with widespread clinical application. The aim of this study was to investigate PD-L1 expression and its association with clinicopathological and prognostic significance in non-clear cell renal cell carcinoma (non-ccRCC) patients. A total of 41 papillary (pRCC) and 20 chromophobe (chRCC) RCC tumors were examined for PD-L1 expression by immunohistochemistry in the cancer cells and tumor-infiltrating mononuclear cells (TIMCs). PD-L1 positivity was detected in 36.6% pRCC and 85.0% chRCC cancer cells, while PD-L1 positivity was observed in 73.2% pRCC and 50.0% chRCC TIMCs. PD-L1 positivity in both pRCC and chRCC tumor cells was not correlated with any of the examined clinicopathological features, while PD-L1 positivity in TIMCs was associated with the age of patients with pRCC. During follow-up, the death was documented among 6 patients with pRCC. Papillary RCC patients with PD-L1-positive tumor cells were significantly associated with an increased risk of death compared with patients with PD-L1-negative cancer cells. A similar trend was observed when comparing PD-L1 expression in TIMCs. However, no differences in overall survival for PD-L1-positive pRCC patients with compared to PD-L1-negative patients were observed in tumor cells or TIMCs. Full article
(This article belongs to the Special Issue Kidney Diseases: Molecular Pathogenesis and Therapeutic Strategies—2nd Edition)
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Review

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29 pages, 3330 KiB  
Review
Targeting Macrophages: Therapeutic Approaches in Diabetic Kidney Disease
by Da-Wei Lin, Tsung-Ming Yang, Cheng Ho, Ya-Hsueh Shih, Chun-Liang Lin and Yung-Chien Hsu
Int. J. Mol. Sci. 2024, 25(8), 4350; https://doi.org/10.3390/ijms25084350 - 15 Apr 2024
Cited by 1 | Viewed by 2094
Abstract
Diabetes is not solely a metabolic disorder but also involves inflammatory processes. The immune response it incites is a primary contributor to damage in target organs. Research indicates that during the initial phases of diabetic nephropathy, macrophages infiltrate the kidneys alongside lymphocytes, initiating [...] Read more.
Diabetes is not solely a metabolic disorder but also involves inflammatory processes. The immune response it incites is a primary contributor to damage in target organs. Research indicates that during the initial phases of diabetic nephropathy, macrophages infiltrate the kidneys alongside lymphocytes, initiating a cascade of inflammatory reactions. The interplay between macrophages and other renal cells is pivotal in the advancement of kidney disease within a hyperglycemic milieu. While M1 macrophages react to the inflammatory stimuli induced by elevated glucose levels early in the disease progression, their subsequent transition to M2 macrophages, which possess anti-inflammatory and tissue repair properties, also contributes to fibrosis in the later stages of nephropathy by transforming into myofibroblasts. Comprehending the diverse functions of macrophages in diabetic kidney disease and regulating their activity could offer therapeutic benefits for managing this condition. Full article
(This article belongs to the Special Issue Kidney Diseases: Molecular Pathogenesis and Therapeutic Strategies—2nd Edition)
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