Recently, neutrophil/lymphocyte ratio (NLR) has been proved to be a useful indicator of inflammation and cardiovascular risk. Brachial-ankle pulse wave velocity is an indicator for early atherosclerotic changes. It is unknown whether NLR differs in subtypes of hypertension, and little research has been performed on the relationship between NLR and arteriosclerosis in subtypes of hypertension. The purpose of this article was to investigate their relationship. A total of 217 consecutive patients with hypertension and 132 persons without hypertension were included. All hypertension patients were divided into three groups according to office blood pressure. Brachial-ankle pulse wave velocity was elevated in patients with isolated systolic hypertension, isolated diastolic hypertension, and systolic and diastolic hypertension compared with normotensive controls. NLR in patients with isolated systolic hypertension and systolic and diastolic hypertension were higher than in normotensive controls. Correlation analysis revealed a positive correlation between NLR and brachial-ankle pulse wave velocity.Multivariate linear regression analysis showed that NLR was an effective indicator for brachial-ankle pulse wave velocity.
The crosstalk between the heart and kidney is carried out through various bidirectional pathways. Cardiorenal syndrome (CRS) is a pathological condition in which acute or chronic dysfunction in the heart or kidneys induces acute or chronic dysfunction of the other organ. Complex hemodynamic factors and biochemical and hormonal pathways contribute to the development of CRS. In addition to playing a critical role in generating metabolic energy in eukaryotic cells and serving as signaling hubs during several vital processes, mitochondria rapidly sense and respond to a wide range of stress stimuli in the external environment. Impaired adaptive responses ultimately lead to mitochondrial dysfunction, inducing cell death and tissue damage. Subsequently, these changes result in organ failure and trigger a vicious cycle. In vitro and animal studies have identified an important role of mitochondrial dysfunction in heart failure (HF) and chronic kidney disease (CKD). Maintaining mitochondrial homeostasis may be a promising therapeutic strategy to interrupt the vicious cycle between HF and acute kidney injury (AKI)/CKD. In this review, we hypothesize that mitochondrial dysfunction may also play a central role in the development and progression of CRS. We first focus on the role of mitochondrial dysfunction in the pathophysiology of HF and AKI/CKD, then discuss the current research evidence supporting that mitochondrial dysfunction is involved in various types of CRS.
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