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Molecular Mechanisms of Renal Diseases

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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: closed (28 August 2023) | Viewed by 22940

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Dr. Christos Chatziantoniou

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Guest Editor

Tenon Hospital, 4, rue de la Chine, 75020 Paris, France
Interests: renal diseases; diabetic nephropathy; kidney injury; nephrology; renal disease; biomarkers; renal; endothelial dysfunction; endothelial cells; kidney

Dr. Christos E. Chadjichristos

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Guest Editor

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Dear Colleagues,

Renal fibrosis is a major outcome of kidney diseases, which affect nearly 10% of the population and contribute to the increased number of deaths and the surcharge of the national health systems worldwide. Renal disease can originate from different causes, such as diabetes, hypertension, immune or toxic stimuli. However, it involves common pathological mechanisms, such as chronic inflammation and the development of renal fibrosis, ultimately leading to the impairment of renal function.

Fibrosis initially appears as a normal response to injury, where activated fibroblasts produce high amounts of the extracellular matrix (ECM) in the context of a wound-healing process in order to assist in the repair of the damaged tissue. In the case of a repetitive injury, chronic wound healing leads to an excessive accumulation of ECM, which fails to be resolved by the remodeling mechanisms and leads to organ dysfunction. To understand the mechanisms of renal failure, great attention was paid to pro-inflammatory and pro-fibrotic agents, such as angiotensin II, TGF-β, CTGF, PDGF, and MCP-1.

Despite the fact that drugs targeting some of these mediators are currently used in subgroups of renal patients, no major improvement has been made in specifically targeting the renal disease. The scope of this Special Issue is to assemble original articles or reviews promoting the latest advances on the roles of newly identified mediators of renal dysfunction and emphasize their potential as novel promising therapeutic targets to fight renal disease.

Dr. Christos Chatziantoniou
Dr. Christos E. Chadjichristos
Guest Editors

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Keywords

chronic kidney disease
acute renal failure
fibrosis
tissue repair
inflammation
hypertension
diabetes
IgAN
lupus
TGFb
chemokines
renal biomarkers
renal organoids
nanoparticles
miRNA
tissue-specific drug delivery

Published Papers (12 papers)

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Research

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18 pages, 22847 KiB

Open AccessArticle

Proximal Tubular Lats2 Ablation Exacerbates Ischemia/Reperfusion Injury (IRI)-Induced Renal Maladaptive Repair through the Upregulation of P53

by Chi Zhang, Zhihuang Zheng, Kexin Xu, Guozhe Cheng, Huijuan Wu and Jun Liu

Int. J. Mol. Sci. 2023, 24(20), 15258; https://doi.org/10.3390/ijms242015258 - 17 Oct 2023

Viewed by 949

Abstract

The Hippo pathway mediates renal maladaptive repair after acute kidney injury (AKI), which has been considered a driving force in the progression to chronic kidney disease (CKD). LATS2, a core kinase of the Hippo pathway, exerts non-Hippo-dependent functions in the regulation of the cell cycle and cell fate, providing new insights into AKI and further repair. However, its role remains unknown. Here, we utilized a proximal tubular Lats2 conditional knockout mouse strain (Lats2-CKO) to evaluate the effect of LATS2 deficiency on ischemia/reperfusion-induced AKI-to-CKD transition. Lats2-CKO mice presented with more severe tubular maladaptive repair, inflammatory infiltration, interstitial fibrosis, and apoptosis following AKI. Importantly, we discovered that Lats2 ablation caused the activation of p53, with increased levels of cellular apoptotic molecules (p21, Bax, and cleaved caspase-3), and decreased levels of anti-apoptotic molecules (Bcl-2 and Bcl-xL). Pifithirin-α (p53 inhibitor) effectively attenuated renal fibrosis, inflammation, and apoptosis in Lats2-CKO mice after AKI. Consistently, in vitro Lats2 overexpression decreased p53, p21, Bax and cleaved caspase 3 expression after hypoxia/reoxygenation (H/R) treatment. Of note, the phosphorylation of MDM2, which promotes the ubiquitination degradation of p53, at site Ser186 was decreased in Lats2-CKO kidneys, but increased by Lats2 overexpression in vitro. Therefore, LATS2 deficiency aggravated ischemia/reperfusion injury (IRI)-induced maladaptive repair via regulating the tubular MDM2-p53 axis in AKI-to-CKD transition. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Renal Diseases)

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13 pages, 281 KiB

Open AccessArticle

Association between Human Leukocyte Antigen and End-Stage Renal Disease in Patients from Transylvania, Romania

by Luminita-Ioana Iancu Loga, Lucia Dican, Alin Dan Chiorean, Vlad Florin Chelaru, Florin Ioan Elec, Cristina Sorina Catana, Monica Mihaela Marta, Roxana Liana Lucaciu, Adriana Corina Hangan, Cosmina Ioana Bondor, Mihaela Laura Vica and Horea Vladi Matei

Int. J. Mol. Sci. 2023, 24(17), 13383; https://doi.org/10.3390/ijms241713383 - 29 Aug 2023

Cited by 1 | Viewed by 808

Abstract

End-stage renal disease (ESRD) is the final stage of chronic kidney disease. This study explored the association between human leukocyte antigen (HLA) and ESRD. The interaction between genetic and environmental factors may also play a role in the development of ESRD. The study included 2392 ESRD patients who were awaiting renal transplantation. Blood samples were genotyped by SSOP and SSP-PCR methods. Multivariate logistic regression analysis showed that HLA-A*11 (p = 0.027), HLA-A*34 (p = 0.017), HLA-A*69 (p = 0.012), HLA-B*41 (p < 0.001), HLA-B*50 (p = 0.004), HLA-DRB1*10 (p = 0.027), and HLA-DRB1*14 (p = 0.004) were positively associated with ESRD (OR > 1); HLA-DRB1*07 (p < 0.001), HLA-DRB1*08 (p = 0.005), and HLA-DRB1*13 (p < 0.001) were protective against ESRD (OR < 1); and the three-locus haplotype HLA-A*02–B*41–DRB1*03, containing one susceptible allele, was strongly associated with ESRD (p < 0.001, OR = 3.15). In conclusion, this retrospective analysis of HLA typing in patients with ESRD of various etiologies suggests that molecular data on the HLA polymorphism should be collected in order to identify high-risk ESRD patients and to improve graft survival after kidney transplantation. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Renal Diseases)

15 pages, 12292 KiB

Open AccessArticle

The Role of Gender Differences and Menopause in Obesity-Related Renal Disease, Renal Inflammation and Lipotoxicity

by Aaron Afonso-Alí, Esteban Porrini, Silvia Teixido-Trujillo, José Antonio Pérez-Pérez, Sergio Luis-Lima, Nieves Guadalupe Acosta-González, Irene Sosa-Paz, Laura Díaz-Martín, Covadonga Rodríguez-González and Ana Elena Rodríguez-Rodríguez

Int. J. Mol. Sci. 2023, 24(16), 12984; https://doi.org/10.3390/ijms241612984 - 19 Aug 2023

Viewed by 1288

Abstract

The pathogenesis of obesity-related-renal disease is unknown. Menopause can promote renal disease in obese women, but this interaction is unclear. In a previous study, we observed that obese male and female mice developed albuminuria, hyperfiltration, and glomerulomegaly, and these changes were more severe in those obese ovariectomized females. In this study, we also evaluated renal inflammation and lipotoxicity in that animal model. For six months, 43 males and 36 females C57BL6/J mice were randomized to standard diet (SD) or high fat diet (HFD). A group of female animals on SD or HFD was ovariectomized to simulate menopause. We evaluated cytokines: NF-κβ p65, IL-1β, MCP-1, TNF-α, total lipid content, lipid classes, and fatty acid profile in total lipid and individual lipid classes in renal tissue and urine. We found that obese males and females showed higher NF-kβ p-65, TNF-α and MCP-1 in renal tissue, and obese females ovariectomized had higher IL-1β and TNF-α compared with not-ovariectomized. Also, obese animals showed lower proinflammatory and higher anti-inflammatory fatty acids in kidney total lipids, while obese females ovariectomized had a more exacerbated pattern. In brief, obesity induces inflammation and an unbalanced lipidic profile in renal tissue. This pattern seems to be enhanced in obesity after menopause. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Renal Diseases)

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22 pages, 2573 KiB

Open AccessArticle

The Angiogenesis Inhibitor Isthmin-1 (ISM1) Is Overexpressed in Experimental Models of Glomerulopathy and Impairs the Viability of Podocytes

by Virgilia Sahiri, Jonathan Caron, Elena Roger, Christophe Desterke, Khalil Ghachem, Inna Mohamadou, Justine Serre, Niki Prakoura, Soraya Fellahi, Sandrine Placier, Sahil Adriouch, Lu Zhang, Christos E. Chadjichristos, Christos Chatziantoniou, Hans Kristian Lorenzo and Jean-Jacques Boffa

Int. J. Mol. Sci. 2023, 24(3), 2723; https://doi.org/10.3390/ijms24032723 - 01 Feb 2023

Cited by 1 | Viewed by 1798

Abstract

Focal segmental glomerulosclerosis (FSGS) is a major cause of end-stage renal disease and remains without specific treatment. To identify new events during FSGS progression, we used an experimental model of FSGS associated with nephroangiosclerosis in rats injected with L-NAME (N_ω-nitro-L-arginine methyl ester). After transcriptomic analysis we focused our study on the role of Isthmin-1 (ISM1, an anti-angiogenic protein involved in endothelial cell apoptosis. We studied the renal expression of ISM1 in L-NAME rats and other models of proteinuria, particularly at the glomerular level. In the L-NAME model, withdrawal of the stimulus partially restored basal ISM1 levels, along with an improvement in renal function. In other four animal models of proteinuria, ISM1 was overexpressed and localized in podocytes while the renal function was degraded. Together these facts suggest that the glomerular expression of ISM1 correlates directly with the progression-recovery of the disease. Further in vitro experiments demonstrated that ISM1 co-localized with its receptors GRP78 and integrin αvβ5 on podocytes. Treatment of human podocytes with low doses of recombinant ISM1 decreased cell viability and induced caspase activation. Stronger ISM1 stimuli in podocytes dropped mitochondrial membrane potential and induced nuclear translocation of apoptosis-inducing factor (AIF). Our results suggest that ISM1 participates in the progression of glomerular diseases and promotes podocyte apoptosis in two different complementary ways: one caspase-dependent and one caspase-independent associated with mitochondrial destabilization. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Renal Diseases)

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13 pages, 11260 KiB

Open AccessArticle

Antifibrotic Soluble Thy-1 Correlates with Renal Dysfunction in Chronic Kidney Disease

by Anja Saalbach, Ulf Anderegg, Ralph Wendt, Joachim Beige, Anette Bachmann, Nora Klöting, Matthias Blüher, Ming-Zhi Zhang, Raymond C. Harris, Michael Stumvoll, Anke Tönjes and Thomas Ebert

Int. J. Mol. Sci. 2023, 24(3), 1896; https://doi.org/10.3390/ijms24031896 - 18 Jan 2023

Cited by 1 | Viewed by 1412

Abstract

Kidney fibrosis is a major culprit in the development and progression of chronic kidney disease (CKD), ultimately leading to the irreversible loss of organ function. Thymocyte differentiation antigen-1 (Thy-1) controls many core functions of fibroblasts relevant to fibrogenesis but is also found in a soluble form (sThy-1) in serum and urine. We investigated the association of sThy-1 with clinical parameters in patients with CKD receiving hemodialysis treatment compared to individuals with a preserved renal function. Furthermore, Thy-1 tissue expression was detected in a mouse model of diabetic CKD (eNOS^−/−; db/db) and non-diabetic control mice (eNOS^−/−). Serum and urinary sThy-1 concentrations significantly increased with deteriorating renal function, independent of the presence of diabetes. Serum creatinine is the major, independent, and inverse predictor of serum sThy-1 levels. Moreover, sThy-1 is not only predicted by markers of renal function but is also itself an independent and strong predictor of markers of renal function, i.e., serum creatinine. Mice with severe diabetic CKD show increased Thy-1 mRNA and protein expression in the kidney compared to control animals, as well as elevated urinary sThy-1 levels. Pro-fibrotic mediators, such as interleukin (IL)-4, IL-13, IL-6 and transforming growth factor β, increase Thy-1 gene expression and release of sThy-1 from fibroblasts. Our data underline the role of Thy-1 in the control of kidney fibrosis in CKD and raise the opportunity that Thy-1 may function as a renal antifibrotic factor. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Renal Diseases)

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18 pages, 10242 KiB

Open AccessArticle

Liver Graft Proteomics Reveals Potential Incipient Mechanisms behind Early Renal Dysfunction after Liver Transplantation

by Åsa Norén, Mihai Oltean, Styrbjörn Friman, Antonio Molinaro, Johan Mölne, Carina Sihlbom, Gustaf Herlenius and Annika Thorsell

Int. J. Mol. Sci. 2022, 23(19), 11929; https://doi.org/10.3390/ijms231911929 - 08 Oct 2022

Cited by 3 | Viewed by 1540

Abstract

Acute kidney injury (AKI) is frequent after liver transplantation (LT) and correlates with later development of chronic kidney disease. Its etiology is multifactorial and combines pre-, intra-, and postoperative factors. Additionally, the liver graft itself seems an important element in the development of AKI, yet the detailed mechanisms remain unclear. We hypothesized that grafts of LT recipients developing significant early AKI may show distinct proteomic alterations, and we set out to identify proteome differences between LT recipients developing moderate or severe AKI (n = 7) and LT recipients without early renal injury (n = 7). Liver biopsies obtained one hour after reperfusion were assessed histologically and using quantitative proteomics. Several cytokines and serum amyloid A2 (SAA2) were analyzed in serum samples obtained preoperatively, 2–4 h, and 20–24 h after graft reperfusion, respectively. LT induced mild histological alterations without significant differences between groups but uniformly altered liver function tests peaking on postoperative day 1, with a trend towards more severe alterations in patients developing AKI. Global quantitative proteomic analysis revealed 136 proteins differing significantly in their expression levels (p < 0.05, FC 20%): 80 proteins had higher and 56 had lower levels in the AKI group. Most of these proteins were related to immune and inflammatory responses, host defense, and neutrophil degranulation. No differences between the studied pro- and anti-inflammatory cytokines or SAA2 between groups were found at any moment. Our results suggest that grafts of LT patients who develop early AKI reveal a distinct proteome dominated by an early yet prominent activation of the innate immunity. These findings support the hypothesis that AKI after LT may be favored by certain graft characteristics. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Renal Diseases)

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11 pages, 3877 KiB

Open AccessCommunication

Differences of Uric Acid Transporters Carrying Extracellular Vesicles in the Urine from Uric Acid and Calcium Stone Formers and Non-Stone Formers

by Zhijian Lin, Muthuvel Jayachandran, Zejfa Haskic, Sanjay Kumar and John C. Lieske

Int. J. Mol. Sci. 2022, 23(17), 10010; https://doi.org/10.3390/ijms231710010 - 02 Sep 2022

Cited by 2 | Viewed by 1813

Abstract

Background: Low urine pH and volume are established risk factors for uric acid (UA) stone disease (UASD). Renal tubular epithelial cells exposed to an acidic pH and/or UA crystals can shed extracellular vesicles (EVs) into the tubular fluid, and these EVs may be a pathogenic biomarker of UASD. Methods: Urinary EVs bearing UA transporters (SLC2A9, SLC17A3, SLC22A12, SLC5A8, ABCG2, and ZNF365) were quantified in urine from UA stone formers (UASFs), calcium stone formers (CSFs), and age-/sex-matched non-stone formers (NSFs) using a standardized and published method of digital flow cytometry. Results: Urinary pH was lower (p < 0.05) and serum and urinary UA were greater (p < 0.05) in UASFs compared with NSFs. Urinary EVs carrying SLC17A3 and SLC5A8 were lower (p < 0.05) in UASFs compared with NSFs. Urinary EVs bearing SLC2A9, SLC22A12, SLC5A8, ABCG2, and ZNF365 were lower (p < 0.05) in CSFs than UASFs, while excretion of SLC17A3-bearing EVs did not differ between groups. Conclusion: EVs bearing specific UA transporters might contribute to the pathogenesis of UASD and represent non-invasive pathogenic biomarkers for calcium and UA stone risk. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Renal Diseases)

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16 pages, 5074 KiB

Open AccessArticle

TMAO Suppresses Megalin Expression and Albumin Uptake in Human Proximal Tubular Cells Via PI3K and ERK Signaling

by Stefania Kapetanaki, Ashok Kumar Kumawat, Katarina Persson and Isak Demirel

Int. J. Mol. Sci. 2022, 23(16), 8856; https://doi.org/10.3390/ijms23168856 - 09 Aug 2022

Cited by 3 | Viewed by 2054

Abstract

Trimethylamine-N-oxide (TMAO) is a uremic toxin, which has been associated with chronic kidney disease (CKD). Renal tubular epithelial cells play a central role in the pathophysiology of CKD. Megalin is an albumin-binding surface receptor on tubular epithelial cells, which is indispensable for urine protein reabsorption. To date, no studies have investigated the effect of TMAO on megalin expression and the functional properties of human tubular epithelial cells. The aim of this study was first to identify the functional effect of TMAO on human renal proximal tubular cells and second, to unravel the effects of TMAO on megalin-cubilin receptor expression. We found through global gene expression analysis that TMAO was associated with kidney disease. The microarray analysis also showed that megalin expression was suppressed by TMAO, which was also validated at the gene and protein level. High glucose and TMAO was shown to downregulate megalin expression and albumin uptake similarly. We also found that TMAO suppressed megalin expression via PI3K and ERK signaling. Furthermore, we showed that candesartan, dapagliflozin and enalaprilat counteracted the suppressive effect of TMAO on megalin expression. Our results may further help us unravel the role of TMAO in CKD development and to identify new therapeutic targets to counteract TMAOs effects. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Renal Diseases)

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12 pages, 2477 KiB

Open AccessArticle

by Xuejing Zhu, Dan Gao, Vittorio Albertazzi, Jianyong Zhong, Li-Jun Ma, Liping Du, Yu Shyr, Valentina Kon, Hai-Chun Yang and Agnes B. Fogo

Int. J. Mol. Sci. 2022, 23(11), 6018; https://doi.org/10.3390/ijms23116018 - 27 May 2022

Cited by 1 | Viewed by 1434

Abstract

We previously found that short-term treatment (week 8 to 12 after injury) with high-dose angiotensin receptor blocker (ARB) induced the regression of existing glomerulosclerosis in 5/6 nephrectomy rats. We therefore assessed the effects of long-term intervention with ARB vs. nonspecific antihypertensives in this study. Adult rats underwent 5/6 nephrectomy and renal biopsy 8 weeks later. The rats were then divided into three groups with equivalent renal function and glomerular sclerosis and treated with high-dose losartan (ARB), nonspecific antihypertensive triple-therapy (TRX), or left untreated (Control) until week 30. We found that blood pressure, serum creatinine levels, and glomerulosclerosis were lower at sacrifice in ARB and TRX vs. Control. Only ARB reduced proteinuria and maintained the density of WT-1-positive podocytes. Glomerular tufts showed more double-positive cells for CD44, a marker of activated parietal epithelial cells, and synaptopodin after ARB vs. TRX or Control. ARB treatment reduced aldosterone levels. ARB-treated rats had significantly improved survival when compared with TRX or Control. We conclude that both long-term ARB and triple-therapy ameliorate progression, but do not sustain the regression of glomerulosclerosis. ARB resulted in the superior preservation of podocyte integrity and decreased proteinuria and aldosterone, linked to increased survival in the uremic environment. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Renal Diseases)

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Review

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19 pages, 2696 KiB

Open AccessReview

Pathophysiology and Main Molecular Mechanisms of Urinary Stone Formation and Recurrence

by Flavia Tamborino, Rossella Cicchetti, Marco Mascitti, Giulio Litterio, Angelo Orsini, Simone Ferretti, Martina Basconi, Antonio De Palma, Matteo Ferro, Michele Marchioni and Luigi Schips

Int. J. Mol. Sci. 2024, 25(5), 3075; https://doi.org/10.3390/ijms25053075 - 06 Mar 2024

Viewed by 1089

Abstract

Kidney stone disease (KSD) is one of the most common urological diseases. The incidence of kidney stones has increased dramatically in the last few decades. Kidney stones are mineral deposits in the calyces or the pelvis, free or attached to the renal papillae. They contain crystals and organic components, and they are made when urine is supersaturated with minerals. Calcium-containing stones are the most common, with calcium oxalate as the main component of most stones. However, many of these form on a calcium phosphate matrix called Randall’s plaque, which is found on the surface of the kidney papilla. The etiology is multifactorial, and the recurrence rate is as high as 50% within 5 years after the first stone onset. There is a great need for recurrence prevention that requires a better understanding of the mechanisms involved in stone formation to facilitate the development of more effective drugs. This review aims to understand the pathophysiology and the main molecular mechanisms known to date to prevent recurrences, which requires behavioral and nutritional interventions, as well as pharmacological treatments that are specific to the type of stone. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Renal Diseases)

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16 pages, 1623 KiB

Open AccessReview

Burn-Induced Acute Kidney Injury–Two-Lane Road: From Molecular to Clinical Aspects

by Andrei Niculae, Ileana Peride, Mirela Tiglis, Evgeni Sharkov, Tiberiu Paul Neagu, Ioan Lascar and Ionel Alexandru Checherita

Int. J. Mol. Sci. 2022, 23(15), 8712; https://doi.org/10.3390/ijms23158712 - 05 Aug 2022

Cited by 10 | Viewed by 5075

Abstract

Severe burn injuries lead to acute kidney injury (AKI) development, increasing the mortality risk up to 28–100%. In addition, there is an increase in hospitalization days and complications appearance. Various factors are responsible for acute or late AKI debut, like hypovolemia, important inflammatory response, excessive load of denatured proteins, sepsis, and severe organic dysfunction. The main measure to improve the prognosis of these patients is rapidly recognizing this condition and reversing the underlying events. For this reason, different renal biomarkers have been studied over the years for early identification of burn-induced AKI, like neutrophil gelatinase-associated lipocalin (NGAL), cystatin C, kidney injury molecule-1 (KIM-1), tissue inhibitor of metalloproteinase-2 (TIMP-2), interleukin-18 (IL-18), and insulin-like growth factor-binding protein 7 (IGFBP7). The fundamental purpose of these studies is to find a way to recognize and prevent acute renal injury progression early in order to decrease the risk of mortality and chronic kidney disease (CKD) onset. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Renal Diseases)

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18 pages, 1810 KiB

Open AccessReview

Lymphangiogenesis and Lymphatic Barrier Dysfunction in Renal Fibrosis

by Jing Liu and Chen Yu

Int. J. Mol. Sci. 2022, 23(13), 6970; https://doi.org/10.3390/ijms23136970 - 23 Jun 2022

Cited by 7 | Viewed by 2604

Abstract

As an integral part of the vascular system, the lymphatic vasculature is essential for tissue fluid homeostasis, nutritional lipid assimilation and immune regulation. The composition of the lymphatic vasculature includes fluid-absorbing initial lymphatic vessels (LVs), transporting collecting vessels and anti-regurgitation valves. Although, in recent decades, research has drastically enlightened our view of LVs, investigations of initial LVs, also known as lymphatic capillaries, have been stagnant due to technical limitations. In the kidney, the lymphatic vasculature mainly presents in the cortex, keeping the local balance of fluid, solutes and immune cells. The contribution of renal LVs to various forms of pathology, especially chronic kidney diseases, has been addressed in previous studies, however with diverging and inconclusive results. In this review, we discuss the most recent advances in the proliferation and permeability of lymphatic capillaries as well as their influencing factors. Novel technologies to visualize and measure LVs function are described. Then, we highlight the role of the lymphatic network in renal fibrosis and the crosstalk between kidney and other organs, such as gut and heart. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Renal Diseases)

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