Genetic Susceptibility to Acute Kidney Injury

Abstract

Acute kidney injury (AKI) is a widely held concern related to a substantial burden of morbidity, mortality and expenditure in the healthcare system. AKI is not a simple illness but a complex conglomeration of syndromes that often occurs as part of other syndromes in its wide clinical spectrum of the disease. Genetic factors have been suggested as potentially responsible for its susceptibility and severity. As there is no current cure nor an effective treatment other than generally accepted supportive measures and renal replacement therapy, updated knowledge of the genetic implications may serve as a strategic tactic to counteract its dire consequences. Further understanding of the genetics that predispose AKI may shed light on novel approaches for the prevention and treatment of this condition. This review attempts to address the role of key genes in the appearance and development of AKI, providing not only a comprehensive update of the intertwined process involved but also identifying specific markers that could serve as precise targets for further AKI therapies.

A nomogram for predicting the mortality of patients with type 2 diabetes mellitus complicated with acute kidney injury in the intensive care unit

“…Diabetes increases the risk of acute kidney injury (AKI), which can sometimes be regarded as an acute complication of diabetes [4]. AKI is a sudden renal dysfunction syndrome with a high incidence rate and mortality, is common in patients with critical illness and cardiac surgery and is associated with genetic susceptibilities [5][6][7]. Studies have found that AKI affects more than 13 million people per year, 80% of patients live in the developing world, and AKI contributes to 1.7 million deaths annually [8,9].…”

Nanodrugs alleviate acute kidney injury: Manipulate RONS at kidney

“…In addition, the rodents are basically genetically identical or inbred animals in AKI in order to reduce experimental influence factors and improve data stability [ 248 ]. Patients with AKI have high diverse genetic diversity [ [249] , [250] , [251] ], which may affect the efficacy of nanodrugs. Moreover, current animal models of AKI do not reflect the complete characteristics of clinical AKI patients.…”

Diagnosis, pathophysiology and preventive strategies for cardiac surgery-associated acute kidney injury: a narrative review

“…A number of studies have suggested the role of genetic polymorphisms in the development of CSA-AKI. Polymorphisms of angiotensinogen, apolipoprotein E (APOE), angiotensin-converting enzyme (ACE), endothelial nitric oxide synthase (eNOS), erythropoietin, interleukin-6 (IL-6), interleukin-10 (IL-10), catechol-O-methyltransferase (COMT), GRM7 | LMCD1—AS1 loci and BBS9, transducer and activator of transcription 3 (STAT3), and macrophage migration inhibitory factor (MIF) genes have been proven to be associated with a higher risk of AKI after cardiac surgery [ 100 ]. However, some studies have denied a correlation between some of these gene polymorphisms and CSA-AKI [ 101 , 102 ].…”