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New Insights into Kidney Diseases

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 September 2024 | Viewed by 4335

Special Issue Editor


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Guest Editor
Department of Cardiology and Nephrology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu 514-8507, Mie, Japan
Interests: focal segmental glomerulosclerosis; genetic kidney disease; kidney diseases; nephrotic syndrome; podocyte
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Special Issue Information

Dear Colleagues,

Chronic kidney disease is categorized by the degree of albuminuria/proteinuria and an estimated glomerular filtration rate in urinalysis and blood tests, respectively, and is a lifestyle-related disease that affects one in eight people. It is caused by various causes, such as diabetic nephropathy, chronic glomerulonephritis, and nephrosclerosis. New drug discoveries other than the existing nephroprotective drugs, such as renin-angiotensin-aldosterone system inhibitors and sodium-glucose cotransporter-2 inhibitors, are still under development. Various studies have revealed that podocytes, terminally differentiated cells that exist outside the glomerular basement membrane, are greatly involved in the progression of chronic kidney disease.

The aim of this Special Issue is to gather original research articles and review articles that focus on new insights in kidney diseases. Articles focused on genetic forms of kidney disease are especially encouraged.

Dr. Kan Katayama
Guest Editor

Manuscript Submission Information

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Keywords

  • kidney disease
  • focal segmental glomerulosclerosis
  • genetic kidney disease
  • minimal change disease
  • nephrotic syndrome
  • podocyte

Published Papers (4 papers)

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Research

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11 pages, 2603 KiB  
Article
Keratin Expression in Podocytopathies, ANCA-Associated Vasculitis and IgA Nephropathy
by Paraskevi Pavlakou, Harikleia Gakiopoulou, Sonja Djudjaj, Kostas Palamaris, Maria Stella Trivyza, Kostas Stylianou, Dimitrios S. Goumenos, Evangelos Papachristou and Marios Papasotiriou
Int. J. Mol. Sci. 2024, 25(3), 1805; https://doi.org/10.3390/ijms25031805 - 02 Feb 2024
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Abstract
Keratins are the main components of the cell cytoskeleton of epithelial cells. Epithelial cells under stressful stimuli react by modifying their keratin expression pattern. Glomerular diseases are pathological conditions that may lead to loss of kidney function if not timely diagnosed and treated [...] Read more.
Keratins are the main components of the cell cytoskeleton of epithelial cells. Epithelial cells under stressful stimuli react by modifying their keratin expression pattern. Glomerular diseases are pathological conditions that may lead to loss of kidney function if not timely diagnosed and treated properly. This study aims to examine glomerular and tubular keratin expression in podocytopathies, ANCA-associated vasculitis, and IgA nephropathy and how this expression correlates to clinical outcomes. We included 45 patients with podocytopathies (minimal change disease and focal segmental glomerulosclerosis), ANCA-associated vasculitis, and IgA nephropathy, with or without crescentic lesions, and healthy controls. All tissues were assessed by photon microscopy and immunohistochemistry. Biopsy sections were examined for keratins 7, 8, 18, and 19 expression in the glomerular and tubulointerstitial areas separately. Moreover, we examined how keratin expression was correlated with long-term kidney function outcomes. All four studied keratins had significantly increased glomerular expression in patients with ANCA vasculitis compared to controls and MCD patients. Tubular expression of keratins 7, 8, and 19 was related to kidney outcome in all groups. Patients with crescents had higher expression of all keratins in both glomeruli and tubulointerstitium. The presence of tubular atrophy, interstitial fibrosis, mesangial hyperplasia, and interstitial inflammation did not affect keratin expression. Keratins, an abundant component of renal epithelial cells, have the potential to be featured as a biomarker for kidney function prognosis in patients with glomerular diseases. Full article
(This article belongs to the Special Issue New Insights into Kidney Diseases)
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Review

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17 pages, 846 KiB  
Review
SGLT2 Inhibitors in Kidney Diseases—A Narrative Review
by Agata Gajewska, Jakub Wasiak, Natalia Sapeda, Ewelina Młynarska, Jacek Rysz and Beata Franczyk
Int. J. Mol. Sci. 2024, 25(9), 4959; https://doi.org/10.3390/ijms25094959 - 01 May 2024
Viewed by 332
Abstract
Some of the most common conditions affecting people are kidney diseases. Among them, we distinguish chronic kidney disease and acute kidney injury. Both entities pose serious health risks, so new drugs are still being sought to treat and prevent them. In recent years, [...] Read more.
Some of the most common conditions affecting people are kidney diseases. Among them, we distinguish chronic kidney disease and acute kidney injury. Both entities pose serious health risks, so new drugs are still being sought to treat and prevent them. In recent years, such a role has begun to be assigned to sodium-glucose cotransporter-2 (SGLT2) inhibitors. They increase the amount of glucose excreted in the urine. For this reason, they are currently used as a first-line drug in type 2 diabetes mellitus. Due to their demonstrated cardioprotective effect, they are also used in heart failure treatment. As for the renal effects of SGLT2 inhibitors, they reduce intraglomerular pressure and decrease albuminuria. This results in a slower decline in glomelular filtration rate (GFR) in patients with kidney disease. In addition, these drugs have anti-inflammatory and antifibrotic effects. In the following article, we review the evidence for the effectiveness of this group of drugs in kidney disease and their nephroprotective effect. Further research is still needed, but meta-analyses indicate SGLT2 inhibitors' efficacy in kidney disease, especially the one caused by diabetes. Development of new drugs and clinical trials on specific patient subgroups will further refine their nephroprotective effects. Full article
(This article belongs to the Special Issue New Insights into Kidney Diseases)
16 pages, 2235 KiB  
Review
Autosomal Dominant Polycystic Kidney Disease: Extrarenal Involvement
by Matteo Righini, Raul Mancini, Marco Busutti and Andrea Buscaroli
Int. J. Mol. Sci. 2024, 25(5), 2554; https://doi.org/10.3390/ijms25052554 - 22 Feb 2024
Viewed by 821
Abstract
Autosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary kidney disorder, but kidneys are not the only organs involved in this systemic disorder. Individuals with the condition may display additional manifestations beyond the renal system, involving the liver, pancreas, and brain [...] Read more.
Autosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary kidney disorder, but kidneys are not the only organs involved in this systemic disorder. Individuals with the condition may display additional manifestations beyond the renal system, involving the liver, pancreas, and brain in the context of cystic manifestations, while involving the vascular system, gastrointestinal tract, bones, and cardiac valves in the context of non-cystic manifestations. Despite kidney involvement remaining the main feature of the disease, thanks to longer survival, early diagnosis, and better management of kidney-related problems, a new wave of complications must be faced by clinicians who treated patients with ADPKD. Involvement of the liver represents the most prevalent extrarenal manifestation and has growing importance in the symptom burden and quality of life. Vascular abnormalities are a key factor for patients’ life expectancy and there is still debate whether to screen or not to screen all patients. Arterial hypertension is often the earliest onset symptom among ADPKD patients, leading to frequent cardiovascular complications. Although cardiac valvular abnormalities are a frequent complication, they rarely lead to relevant problems in the clinical history of polycystic patients. One of the newest relevant aspects concerns bone disorders that can exert a considerable influence on the clinical course of these patients. This review aims to provide the “state of the art” among the extrarenal manifestation of ADPKD. Full article
(This article belongs to the Special Issue New Insights into Kidney Diseases)
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16 pages, 1136 KiB  
Review
Autosomal Dominant Polycystic Kidney Disease: Is There a Role for Autophagy?
by Claudio Ponticelli, Gabriella Moroni and Francesco Reggiani
Int. J. Mol. Sci. 2023, 24(19), 14666; https://doi.org/10.3390/ijms241914666 - 28 Sep 2023
Cited by 1 | Viewed by 1476
Abstract
Autosomal-Dominant Polycystic Kidney Disease (ADPKD) is a monogenic disorder initiated by mutations in either PKD1 or PKD2 genes, responsible for encoding polycystin 1 and polycystin 2, respectively. These proteins are primarily located within the primary cilia. The disease follows an inexorable progression, leading [...] Read more.
Autosomal-Dominant Polycystic Kidney Disease (ADPKD) is a monogenic disorder initiated by mutations in either PKD1 or PKD2 genes, responsible for encoding polycystin 1 and polycystin 2, respectively. These proteins are primarily located within the primary cilia. The disease follows an inexorable progression, leading most patients to severe renal failure around the age of 50, and extra-renal complications are frequent. A cure for ADPKD remains elusive, but some measures can be employed to manage symptoms and slow cyst growth. Tolvaptan, a vasopressin V2 receptor antagonist, is the only drug that has been proven to attenuate ADPKD progression. Recently, autophagy, a cellular recycling system that facilitates the breakdown and reuse of aged or damaged cellular components, has emerged as a potential contributor to the pathogenesis of ADPKD. However, the precise role of autophagy in ADPKD remains a subject of investigation, displaying a potentially twofold impact. On the one hand, impaired autophagy may promote cyst formation by inducing apoptosis, while on the other hand, excessive autophagy may lead to fibrosis through epithelial to mesenchymal transition. Promising results of autophagy inducers have been observed in preclinical studies. Clinical trials are warranted to thoroughly assess the long-term safety and efficacy of a combination of autophagy inducers with metabolic and/or aquaferetic drugs. This research aims to shed light on the complex involvement of autophagy in ADPKD, explore the regulation of autophagy in disease progression, and highlight the potential of combination therapies as a promising avenue for future investigations. Full article
(This article belongs to the Special Issue New Insights into Kidney Diseases)
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