Kidney Inflammation, Injury and Regeneration

Abstract

Damage to kidney cells can occur due to a variety of ischemic and toxic insults and leads to inflammation and cell death, which can result in acute kidney injury (AKI). Inflammation plays a key role in the injury of renal cells, as well as subsequent cellular regeneration processes. However, persistent chronic inflammation may trigger renal fibrosis. The investigation of the molecular mechanisms involved in each individual injury is currently insufficiently elucidated. Whereas the kidney has a remarkable capacity for regeneration after injury and may completely recover depending on the type of renal lesions, the options for clinical intervention are restricted to fluid management and extracorporeal kidney support. AKI is still associated with high morbidity and mortality incidence rates, and it also bears an elevated risk of subsequent chronic kidney disease. Therefore, the development of novel therapies to improve renal regeneration capacity after AKI, to preserve renal function, and to prevent AKI is urgently needed. In this context, we wanted to offer a forum for the publication of new results on renal inflammation, injury and regeneration, as well as for the review and discussion of existing studies from this interesting research field.This Special Issue covers research articles that investigated the molecular mechanisms of inflammation [1-3] and injury [4,5] during different renal pathologies and renal regeneration [6], diagnostics using new biomarkers [7-9], and the effects of different stimuli like medication or bacterial components on isolated renal cells or in vivo models [10][11][12], all of which were summarized in a very simplified manner. Furthermore, this Special Issue contains important reviews that dealt with the current knowledge of cell death and regeneration [13,14], inflammation [15][16][17][18], and the molecular mechanisms of kidney diseases [19][20][21][22]. In addition, the potential of cell-based therapy approaches that use mesenchymal stromal/stem cells (MSCs) or their derivates is summarized [23][24][25]. This edition is complemented by a series of reviews that deal with the current data situation on other very specific topics like diabetes and diabetic nephropathy [26][27][28], as well as new therapeutic targets [29].In this Special Issue, twelve original research articles are presented that dealt with different questions and the research models used within. The findings of Mocker and co-workers demonstrate that renal chemerin expression, a chemoattractant adipokine, is associated with processes of inflammation and fibrosis during renal damage [2]. The protection of kidney function by attenuating induced renal inflammation was shown with the use of Farnesiferol B, an agonist of a receptor that is expressed by renal tubular epithelial cells [1]. The xanthin oxidase inhibitor febuxostat is shown to exert anti-inflammatory action and protect against diabetic nephropathy development [3]. Kidney injury leading to focal segmental glomerulosclerosis was shown by variants in the collagen 4A5 g...

Toll-Like Receptor as a Potential Biomarker in Renal Diseases

“…The authors indicate that acute kidney injury accounts for up to 15% of the reasons for admission to hospital and occurs in as much as 50% of patients treated in intensive care units [180]. Therefore, it is argued that AKI is still associated with high morbidity and mortality [181]. There are many causes of AKI, including acute ischemia, analgesic nephropathy, sepsis, and severe glomerulopathies.…”

The Off-Target Effects, Electrolyte and Mineral Disorders of SGLT2i

“…Sodium concentrations in the skin and muscles are reportedly positively correlated with the risk of cardiovascular diseases and blood pressure in chronic kidney disease [27]. Impaired sodium-hydrogen exchange has been demonstrated to have deleterious effects on cardiomyocytes by the increased intracellular concentration of sodium [22,41].…”

“…In mice models, SGLT2i proved to be effective in lowering the release of inflammatory cytokines [ 24 ]. Human studies are still limited, however, in a cohort of fifteen diabetic patients, empagliflozin increased anti-inflammatory cytokines IL-10 [ 27 ].…”

“…a cohort of fifteen diabetic patients, empagliflozin increased anti-inflammatory cytokines IL-10[27].…”

Protective Effect of Gynura Bicolor Alcohol Extracts on Rat Kidney Epithelial NRK-52E Cells Induced by Tert-Butyl Hydroperoxide

“…Once renal dysfunction occurs, it causes multiple pathologies. A variety of ischemic conditions, oxidative stress, bacterial infection, sepsis, and toxicity can lead to kidney cell damage and death, which can result in acute kidney injury (AKI) [15,16]. In addition to AKI, diabetic complications, hypertension, obesity, and autoimmunity lead to chronic kidney disease (CKD).…”