Molecular Mechanisms of the Acute Kidney Injury to Chronic Kidney Disease Transition: An Updated View

Abstract

Increasing evidence has demonstrated the bidirectional link between acute kidney injury (AKI) and chronic kidney disease (CKD) such that, in the clinical setting, the new concept of a unified syndrome has been proposed. The pathophysiological reasons, along with the cellular and molecular mechanisms, behind the ability of a single, acute, apparently self-limiting event to drive chronic kidney disease progression are yet to be explained. This acute injury could promote progression to chronic disease through different pathways involving the endothelium, the inflammatory response and the development of fibrosis. The interplay among endothelial cells, macrophages and other immune cells, pericytes and fibroblasts often converge in the tubular epithelial cells that play a central role. Recent evidence has strengthened this concept by demonstrating that injured tubules respond to acute tubular necrosis through two main mechanisms: The polyploidization of tubular cells and the proliferation of a small population of self-renewing renal progenitors. This alternative pathophysiological interpretation could better characterize functional recovery after AKI.

Kidney disease and all-cause mortality in patients with COVID-19 hospitalized in Genoa, Northern Italy

“…As a matter of fact, one-third of CKD patients developed AKI during hospitalization and about half of AKI patients had a history of CKD. These data are coherent with the evidence, derived from both experimental and clinical studies, supporting the link between AKI and CKD, representing reciprocal risk factors [21,22].…”

Kidney Inflammation, Injury and Regeneration

“…This Special Issue covers research articles that investigated the molecular mechanisms of inflammation [1][2][3] and injury [4,5] during different renal pathologies and renal regeneration [6], diagnostics using new biomarkers [7][8][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].…”

Kidney Organoids and Tubuloids

“…The origin of pathogenic myofibroblasts is debated, and suspected sources include pericytes and interstitial fibroblasts. Episodes of AKI increase the risk of CKD, but also vice versa [ 13 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 ].…”