BackgroundPatients with acute myocardial infarction (AMI) complicated by acute kidney injury (AKI) tend to have a poor prognosis. However, the exact mechanism of the co‐occurrence of the two diseases is unknown. Therefore, this study aims to determine the risk factors for severe AKI in patients with AMI.MethodsA total of 2022 patients were included in the Medical Information Mart for Intensive Care. Variables were identified via univariate logistic regression, and the variables were corrected via multivariate logistic regression. Restricted cubic splines were used to examine the risks associated with the variables. The Kaplan–Meier method was used to compare the risk of severe AKI among the patients.ResultsPatients with severe AKI had a higher in‐hospital mortality rate (28.6% vs. 9.0%, P < 0.001) and a longer duration of intensive care (6.5 days vs. 2.9 days, P < 0.001). In patients with AMI, the mean systolic blood pressure (SBP); international normalized ratio (INR); the levels of blood urea nitrogen (BUN), glucose, and calcium; and a history of liver disease were found to be the independent risk factors for developing severe AKI after their admission. Increased levels of BUN and blood glucose and a high INR increased the risk of severe AKI; however, increased levels of calcium decreased the risk; SBP presented a U‐shaped curve relationship.ConclusionsPatients with severe AKI have a poor prognosis following an episode of AMI. Furthermore, in patients with AMI, SBP; INR; a history of liver disease; and the levels of BUN, glucose, and calcium are the independent risk factors for developing severe AKI after their admission.

Sepsis‐induced myocardial dysfunction (SIMD) is the leading cause of death in patients with sepsis in the intensive care units. The main manifestations of SIMD are systolic and diastolic dysfunctions of the myocardium. Despite our initial understanding of the SIMD over the past three decades, the incidence and mortality of SIMD remain high. This may be attributed to the large degree of heterogeneity among the initiating factors, disease processes, and host states involved in SIMD. Previously, organ dysfunction caused by sepsis was thought to be an impairment brought about by an excessive inflammatory response. However, many recent studies have shown that SIMD is a consequence of a combination of factors shaped by the inflammatory responses between the pathogen and the host. In this article, we review the mechanisms of the inflammatory responses and potential novel therapeutic strategies in SIMD.

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