Acute kidney injury (AKI) affects about half of patients admitted to the intensive care unit (ICU), and worsens their short- and long-term outcomes. Apparently self-limiting AKI episodes initiate a progression toward chronic kidney disease (CKD) through cellular and molecular mechanisms that are yet to be explained. In particular, persistent AKI, defined in 2016 by the Acute Dialysis Quality Initiative as an AKI which lasts more than 48 h from its onset, has been correlated with higher morbidity and mortality, and with a higher progression to acute kidney disease (AKD) and CKD than transient AKI (i.e. AKI with a reversal within 48 h). This classification has been also used in the setting of solid organ transplantation, demonstrating similar outcomes. Due to its incidence and poor prognosis and because prompt interventions seem to change its course, persistent AKI should be recognized early and followed-up also after its recovery. However, while AKI and CKD are well-described syndromes, persistent AKI and AKD are relatively new entities. The purpose of this review is to highlight the key phases of persistent AKI in ICU patients in terms of both clinical and mechanistic features in order to offer to clinicians and researchers an updated basis from which to start improving patients' care and direct future research.
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http://dx.doi.org/10.1093/ckj/sfad107 | DOI Listing |
JPEN J Parenter Enteral Nutr
January 2025
The University of Queensland, Brisbane, Australia.
Background: Advanced glycation end-products (AGEs) can enter patients' circulation through exogenous sources, such as enteral nutrition formulae. Circulating AGEs, specifically carboxymethyllysine, can promote insulin resistance and activation of pro-inflammatory pathways leading to oxidative stress, cell death, and organ failure. Suboptimal kidney function increases the risk of elevated circulating AGEs because levels are controlled through urinary excretion.
View Article and Find Full Text PDFCase Rep Crit Care
January 2025
Department of Anesthesiology and Intensive Care Medicine, Kreiskliniken Günzburg-Krumbach, Krumbach, Germany.
Drug-induced rhabdomyolysis has become increasingly prevalent due to the rising use of medications such as statins, antidepressants, and antipsychotics. These can lead to muscle cell destruction and the release of myoglobin, potentially causing kidney damage. Recent advancements include the use of CytoSorb hemoadsorption as a promising therapy to remove myoglobin and other potentially toxic substances from the bloodstream.
View Article and Find Full Text PDFBiomolecules
January 2025
Department of Urology, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Acute kidney injury (AKI) and chronic kidney disease (CKD) represent two frequently observed clinical conditions. AKI is characterized by an abrupt decrease in glomerular filtration rate (GFR), generally associated with elevated serum creatinine (sCr), blood urea nitrogen (BUN), and electrolyte imbalances. This condition usually persists for approximately a week, causing a transient reduction in kidney function.
View Article and Find Full Text PDFCureus
December 2024
Biotechnology, Shri Venkateshwara University, Gajraula, IND.
Sepsis-associated acute kidney injury (S-AKI) is a critical complication that significantly contributes to the morbidity and mortality of sepsis patients. This narrative review explores the complex and multifactorial pathophysiology of S-AKI, which involves hemodynamic alterations, microcirculatory dysfunction, endothelial damage, inflammatory responses, oxidative stress, and direct tubular injury. Conventional perspectives linking S-AKI primarily to reduced renal blood flow are now being reconsidered, with growing insights highlighting the significance of microcirculatory dysfunction and endothelial activation as key contributors.
View Article and Find Full Text PDFFront Nephrol
January 2025
Department of Nephrology, Nephrology Vanderbilt Institute for Global Health (VIGH), Nashville, TN, United States.
Introduction: Antiretroviral therapy (ART) increases the life expectancy of persons living with HIV (PLWH), but not without potentially serious adverse effects. Tenofovir disoproxil fumarate (TDF) can cause nephrotoxicity, manifesting as acute kidney injury (AKI) that may persist after treatment discontinuation. Kidney injury biomarkers such as kidney injury molecule-1 (KIM-1), retinol-binding protein-4 (RBP-4), interleukin-18 (IL-18), and neutrophil gelatinase-associated lipocalin (NGAL) can aid early diagnosis and predict TDF-associated nephrotoxicity.
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