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Molecular Insights into Kidney Injury and Repair
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Molecular Insights into Kidney Injury and Repair

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 July 2025 | Viewed by 8355

Special Issue Editor

Dr. Rossana Franzin

E-Mail Website
Guest Editor
Department of Emergency and Organ Transplantation, University of Bari, 70121 Bari, Italy
Interests: acute kidney injury; renal aging; complement system; renal transplantation; endothelial-to-mesenchymal transition
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Renal disease is defined as a heterogeneous group of disorders affecting kidney structure and function. Acute kidney injury (AKI) is a common clinical syndrome characterized by a sudden decline in loss of kidney function. Different pathogenic mechanisms are related to AKI, such as sepsis, ischemia-reperfusion (I/R) injury, and nephrotoxin exposition. The presence of other pathological conditions, such as diabetes and hypertension, contributes to the transition into chronic kidney disease (CKD). Current knowledge about the kidney repair mechanisms reports the existence of a population of resident stem cells in the kidney, known as ARPCs (Adult Renal Progenitor Cells), which can reestablish a functional tubular epithelium. Renal regeneration can occur by direct proliferation and differentiation of stem progenitors, or by the paracrine pathway, through the release of extracellular vesicles containing miRNAs and regenerative factors. These events could definitely determine the regulation of a pro-regenerative microenvironment. In addition, considerable interest is emerging in the use of organoids, miniature kidney-like structures, which could be a new powerful tool to spotlight the complex inter-cellular interactions and regenerative processes. New insights on the molecular mechanism of action underlying kidney injury and repair would provide early biomarkers to predict clinical outcomes and targeted therapies to prevent injury and delay the progression to chronic kidney disease.

In this Special Issue, we aim to publish original research and reviews that offer new insights into the molecular mechanisms of kidney injury, with special emphasis on renal repair mechanisms.

Dr. Rossana Franzin
Guest Editor

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Keywords

  • kidney injury
  • renal repair
  • acute kidney injury (AKI)
  • chronic kidney disease (CKD)
  • sepsis
  • ischemia-reperfusion (I/R) injury
  • nephrotoxin exposition
  • adult renal progenitor cells

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Published Papers (5 papers)

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Research

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14 pages, 1568 KiB  
Article
Markers of Kidney Injury: Proenkephalin A and Uromodulin, but Not Dickkopf-3, Are Elevated in Patients After Hematopoietic Stem Cell Transplantation
by Aleksandra Kaszyńska, Małgorzata Kępska-Dzilińska, Ewa Karakulska-Prystupiuk, Agnieszka Tomaszewska, Grzegorz Władysław Basak, Marcin Żórawski, Zuzanna Jakubowska and Jolanta Małyszko
Int. J. Mol. Sci. 2025, 26(8), 3581; https://doi.org/10.3390/ijms26083581 - 10 Apr 2025
Viewed by 264
Abstract
Kidney injury encompasses a broad spectrum of structural and functional abnormalities, directly associated with stem cell transplantation. Acute kidney injury and chronic kidney disease represent perilous complications of hematopoietic stem cell transplantation (HSCT), with an elevated risk of mortality and progression to end-stage [...] Read more.
Kidney injury encompasses a broad spectrum of structural and functional abnormalities, directly associated with stem cell transplantation. Acute kidney injury and chronic kidney disease represent perilous complications of hematopoietic stem cell transplantation (HSCT), with an elevated risk of mortality and progression to end-stage renal disease. The early detection of these complications is, therefore, paramount, and research is increasingly focused on the identification of novel biomarkers of kidney damage. Recently, proenkephalin (PENK), a monomeric peptide that is freely filtered by the glomerulus and thus reflects glomerular filtration very well, has been shown to be an additional useful predictor of the occurrence of acute kidney injury and heart failure. Dickkopf-3 (DKK3) is a glycoprotein secreted by the renal tubular epithelium in response to stress and has been implicated in the development of interstitial fibrosis. It has therefore been evaluated primarily as a marker of fibrosis in chronic kidney disease (CKD), but may also help predict the development of acute kiney injury. Uromodulin is regarded as a renal marker. Previous studies have examined the potential of PENK, DKK-3 and uromodulin as a biomarker in individuals with preserved renal function. However, the urinary levels of PENK, DKK-3 and uromodulin in patients following HSCT have not yet been established. The objective of the present study was to assess urinary PENK, DKK-3, and uromodulin concentrations in patients who had been under ambulatory care of the Hematology, Transplantation and Internal Medicine Department for a minimum of three months following HSCT, and to investigate their correlations with kidney function, as reflected by serum creatinine and eGFR. The study population comprised 80 patients who had undergone allogeneic HSCT for various reasons, primarily hematological malignancies such as acute leukemias and lymphomas. In addition, 32 healthy volunteers were included in order to establish normal ranges for the biomarkers of interest. Urine concentrations of proenkephalin, DKK-3, and uromodulin were evaluated using a commercially available sandwich ELISA immunoassay. Demographic and clinical data were retrieved from the patients’ records. Statistical analyses were conducted using XLSLAT 2022 (Lumivero, Denver, CO, USA) and STATISTICAv13.0 (StatSoft, Tulsa, OH, USA). The results showed that PENK and DKK-3 levels were significantly higher in patients after HSCT compared to healthy volunteers. Furthermore, when patients were divided according to kidney function (below and over 60 mL/min/1.72 m2), it was found that the concentration of PENK and DKK-3 were significantly higher in 23 patients with CKD stage 3 relative to patients with eGFR over 60 mL min 1.72 m2. In univariate correlations, PENK demonstrated an inverse relationship with eGFR (r: −0.21, p < 0.05), while DKK-3 exhibited no significant correlation with creatinine or eGFR.Patients following allogeneic HSCT, despite having normal or near-normal kidney function, exhibited evidence of kidney injury. However, further research is necessary to ascertain the clinical utility of the novel biomarker. Full article
(This article belongs to the Special Issue Molecular Insights into Kidney Injury and Repair)
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14 pages, 2090 KiB  
Article
Enrichment of RedoxifibromiR miR-21-5p in Plasma Exosomes of Hypertensive Patients with Renal Injury
by Olga Martinez-Arroyo, Ana Flores-Chova, Marta Mendez-Debaets, Sergio Martinez-Hervas, Fernando Martinez, Maria J. Forner, Josep Redon, Ana Ortega and Raquel Cortes
Int. J. Mol. Sci. 2025, 26(2), 590; https://doi.org/10.3390/ijms26020590 - 12 Jan 2025
Viewed by 856
Abstract
Several microRNAs (miRNAs) emerged as powerful regulators of fibrotic processes, “fibromiRs”, and can also influence the expression of genes responsible for the generation of reactive oxygen species, “redoximiRs”. We aimed to investigate whether plasma exosomes from hypertensive and diabetes patients are enriched in [...] Read more.
Several microRNAs (miRNAs) emerged as powerful regulators of fibrotic processes, “fibromiRs”, and can also influence the expression of genes responsible for the generation of reactive oxygen species, “redoximiRs”. We aimed to investigate whether plasma exosomes from hypertensive and diabetes patients are enriched in fibromiRs and redoximiRs using deep sequencing technology and their association with relevant signalling pathways implicated in oxidative stress and fibrogenesis by GO terms and KEGG pathways. RNA-Seq analysis from P-EXO identified 31 differentially expressed (DE) miRNAs in patients compared to controls, of which 77% are biofluid specific. The majority of the exosomal DE miRNAs were identified as fibromiRs (55%) or redoximiRs (26%). One of the most representative miRNAs identified was miR-21-5p, of which levels in P-EXO were increased by 3.83-fold change (p < 0.0001) in hypertensive patients with albuminuria and were highly associated (r Spearman = 0.64, p < 0.0001). In addition, P-EXO miR-21-5p had a high accuracy in discriminating renal damage (AUC = 0.82, p < 0.0001). Bioinformatic analysis revealed that miR-21-5p regulates key pathways in the context of organ fibrosis, such as chemokine, Ras, and MAPK signalling. Additionally, in vitro studies showed an increase in P-EXO miR-21-5p levels after TGF-β1 damage and oxidative stress. This novel study found an enrichment of fibromiRs and redoximiRs in P-EXO from hypertensive/diabetic patients with renal dysfunction. miR-21-5p, such as a RedoxifibromiR, has a significant accuracy for discriminating renal damage and is closely related with relevant signalling pathways implicated in fibrogenesis in podocytes. Full article
(This article belongs to the Special Issue Molecular Insights into Kidney Injury and Repair)
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27 pages, 17389 KiB  
Article
Nmnat1 Deficiency Causes Mitoribosome Excess in Diabetic Nephropathy Mediated by Transcriptional Repressor HIC1
by Kazuhiro Hasegawa, Masanori Tamaki, Yusuke Sakamaki and Shu Wakino
Int. J. Mol. Sci. 2024, 25(12), 6384; https://doi.org/10.3390/ijms25126384 - 9 Jun 2024
Cited by 1 | Viewed by 2010
Abstract
Nicotinamide adenine dinucleotide (NAD) is involved in renal physiology and is synthesized by nicotinamide mononucleotide adenylyltransferase (NMNAT). NMNAT exists as three isoforms, namely, NMNAT1, NMNAT2, and NMNAT3, encoded by Nmnat1, Nmnat2, and Nmnat3, respectively. In diabetic nephropathy (DN), NAD levels [...] Read more.
Nicotinamide adenine dinucleotide (NAD) is involved in renal physiology and is synthesized by nicotinamide mononucleotide adenylyltransferase (NMNAT). NMNAT exists as three isoforms, namely, NMNAT1, NMNAT2, and NMNAT3, encoded by Nmnat1, Nmnat2, and Nmnat3, respectively. In diabetic nephropathy (DN), NAD levels decrease, aggravating renal fibrosis. Conversely, sodium–glucose cotransporter-2 inhibitors increase NAD levels, mitigating renal fibrosis. In this regard, renal NAD synthesis has recently gained attention. However, the renal role of Nmnat in DN remains uncertain. Therefore, we investigated the role of Nmnat by establishing genetically engineered mice. Among the three isoforms, NMNAT1 levels were markedly reduced in the proximal tubules (PTs) of db/db mice. We examined the phenotypic changes in PT-specific Nmnat1 conditional knockout (CKO) mice. In CKO mice, Nmnat1 expression in PTs was downregulated when the tubules exhibited albuminuria, peritubular type IV collagen deposition, and mitochondrial ribosome (mitoribosome) excess. In CKO mice, Nmnat1 deficiency-induced mitoribosome excess hindered mitoribosomal translation of mitochondrial inner membrane-associated oxidative phosphorylation complex I (CI), CIII, CIV, and CV proteins and mitoribosomal dysfunction. Furthermore, the expression of hypermethylated in cancer 1, a transcription repressor, was downregulated in CKO mice, causing mitoribosome excess. Nmnat1 overexpression preserved mitoribosomal function, suggesting its protective role in DN. Full article
(This article belongs to the Special Issue Molecular Insights into Kidney Injury and Repair)
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Review

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24 pages, 8337 KiB  
Review
Podocyte Death in Diabetic Kidney Disease: Potential Molecular Mechanisms and Therapeutic Targets
by Suye Zhong, Na Wang and Chun Zhang
Int. J. Mol. Sci. 2024, 25(16), 9035; https://doi.org/10.3390/ijms25169035 - 20 Aug 2024
Cited by 1 | Viewed by 2955
Abstract
Cell deaths maintain the normal function of tissues and organs. In pathological conditions, the abnormal activation or disruption of cell death often leads to pathophysiological effects. Diabetic kidney disease (DKD), a significant microvascular complication of diabetes, is linked to high mortality and morbidity [...] Read more.
Cell deaths maintain the normal function of tissues and organs. In pathological conditions, the abnormal activation or disruption of cell death often leads to pathophysiological effects. Diabetic kidney disease (DKD), a significant microvascular complication of diabetes, is linked to high mortality and morbidity rates, imposing a substantial burden on global healthcare systems and economies. Loss and detachment of podocytes are key pathological changes in the progression of DKD. This review explores the potential mechanisms of apoptosis, necrosis, autophagy, pyroptosis, ferroptosis, cuproptosis, and podoptosis in podocytes, focusing on how different cell death modes contribute to the progression of DKD. It recognizes the limitations of current research and presents the latest basic and clinical research studies targeting podocyte death pathways in DKD. Lastly, it focuses on the future of targeting podocyte cell death to treat DKD, with the intention of inspiring further research and the development of therapeutic strategies. Full article
(This article belongs to the Special Issue Molecular Insights into Kidney Injury and Repair)
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Other

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14 pages, 5862 KiB  
Case Report
Multisystemic Beryllium Disease: An Exceptional Case Revealed by a Urinary Tract Granulomatosis
by Lucas Jacobs, Maxime Taghavi, Jennifer Fallas, Caroline Geers, Mark Libertalis, Julie Smet, Joëlle Nortier and Maria do Carmo Filomena Mesquita
Int. J. Mol. Sci. 2024, 25(15), 8166; https://doi.org/10.3390/ijms25158166 - 26 Jul 2024
Viewed by 1510
Abstract
Chronic beryllium disease (CBD), or berylliosis, is an interstitial lung disease caused by the chronic inhalation of finely particulate beryllium, frequently mistaken for sarcoidosis. It is rarely associated with skin nodular lesions, asymptomatic granulomatous hepatitis or calcium nephrolithiasis. To date, it has never [...] Read more.
Chronic beryllium disease (CBD), or berylliosis, is an interstitial lung disease caused by the chronic inhalation of finely particulate beryllium, frequently mistaken for sarcoidosis. It is rarely associated with skin nodular lesions, asymptomatic granulomatous hepatitis or calcium nephrolithiasis. To date, it has never been reported as a diffused multi-organ granulomatous disease. A 60-year-old Pakistani man, a former excavation worker with ancient history of suspected sarcoidosis, underwent a left nephroureterectomy for suspected papillary kidney carcinoma. The histopathological analysis showed a benign non-necrotic granulomatous infiltration of the renal pelvis and ureter. Six months later, he suffered from two consecutive episodes of acute kidney failure. Bladder biopsies found similar noncaseous granulomatosis and kidney biopsies showed interstitial nephritis. Known for suspected asthma, sleep apnea, and usual interstitial pneumonia, the patient would regularly consult for episodes of pyrexia, chills, nocturnal coughing, and wheezing. As kidney function gradually worsened, he ultimately started hemodialysis and was transferred to our facility. A positive blood beryllium lymphocyte proliferation test confirmed the diagnosis of CBD. This original report is the first description of multi-organ berylliosis with diffused urothelial granulomatosis and pseudo-tumor. The patient’s pulmonary disease is minimal compared with renal and urinary tract involvement, eventually responsible for end-stage kidney disease. Berylliosis usually responds to glucocorticoids. This case report highlights the importance of evoking the diagnosis of CBD in the presence of any granulomatosis, even extra-thoracic, especially if associated with pulmonary symptoms, however atypical. Full article
(This article belongs to the Special Issue Molecular Insights into Kidney Injury and Repair)
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