CRP as a sensitive inflammatory marker is involved in the non-specific inflammatory response of the body. Elevated CRP not only predicts a much higher probability of developing hypertension from normal blood pressure or prehypertension, but in patients with diagnosed hypertension, elevated CRP often indicates poor blood pressure control or the development of hypertensive complications, and in patients with high baseline blood pressure, both systolic and diastolic, CRP is mostly elevated [10]. Several cross-sectional and cohort studies have reported an association between CRP and hypertension, and their studies all support the association between CRP and hypertension, and CRP may serve as a predictor of hypertension [7, 9, 11,12,13]. Savoia et al. [14] found that high levels of CRP upregulate angiotensin receptor expression, promote plasminogen activator inhibitor-1 (PAI-1) production, and activate vascular smooth muscle, promote the release of inflammatory factors, attenuate the response of vascular endothelial cells to diastolic substances, reduce nitric oxide production, and increase vascular resistance. In our study, we found that in the elderly population, blood pressure levels were significantly higher in the group with elevated CRP than in the normal group, and the prevalence of hypertension was higher in the group with elevated CRP than in the normal group, with statistically significant differences (P < 0.05), and logistic regression also showed an independent positive association between elevated CRP and the risk of hypertension (OR = 2.13, 95% CI: 1.14–3.99, P < 0.05). In a study of the effect on the risk of hypertension in the US retired population, which included 2924 participants, logistic regression showed that CRP could be used as a predictor of hypertension in women [15]. In another study of CRP and hypertension in Japanese men [16], 2991 male workers without hypertension were evaluated, and the risk ratio (HR) for the occurrence of hypertensive events was estimated based on the quartiles of CRP, and 579 (19.4%) subjects developed hypertension during the 5-year follow-up period, and the incidence of hypertension increased with increasing levels of CRP, and the HR increased significantly with increasing CRP levels. This may imply that the development of hypertension involves a pathological process in which inflammation is involved and that the inflammatory response may be the direct cause of hypertension.

As we age, our physiological functions gradually decline. In addition to hypertension, the coexistence of various diseases such as coronary heart disease and diabetes is becoming more and more evident in the elderly population. According to a survey conducted by the Journal of the American Medical Family Council in 2013, about 2/3 of American senior citizens have co-morbidities [17]. A large body of evidence suggests that CRP is closely associated with dyslipidemia, diabetes, cardiovascular disease, and metabolic syndrome, and can be used as an indicator for early screening or long-term monitoring to provide some basis for patient prognosis [18,19,20]. CRP acts as a marker of inflammation and numerous studies have shown that CRP is significantly associated with cardiovascular disease. When an inflammatory response is generated, CRP is induced by interleukin 1 (IL-1), interleukin-6 (IL-6) and tumor necrosis factor (T NF-α), mainly by the liver. CRP is often elevated in nonalcoholic fatty liver disease, suggesting that the accumulation of hepatic adipose tissue is associated with enhanced inflammation-mediated oxidative stress. CRP induces a significant increase in the expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), which accelerates the inflammatory response in atherosclerosis. At the same time, high concentrations of CRP can promote thickening of the intima and atherosclerosis, leading to remodeling of hypertensive vessels [21, 22]. In addition, CRP stimulates endothelial cells, megalophils and polymorphonuclear cells to secrete endothelin-1 (ET-1), interleukin-6 (IL-6) and vasoconstrictor peptide, resulting in vasoconstriction [22]. Coronary artery disease was significantly associated with elevated CRP levels in this study, and serum LDL-C was also associated with elevated CRP, with statistically significant differences (P < 0.05). This is consistent with previous research[23]. In addition, CRP has been shown to be an independent predictor of the risk of myocardial infarction, stroke and peripheral vascular disease and can be used to predict future risk in patients with stable and unstable angina [24]. In addition, we found that the prevalence of diabetes was higher in the group with elevated CRP than in the normal group, and although it was not statistically significant, diabetes was positively associated with the development of hypertension (OR = 2.68,95%CI:1.24–5.79, P < 0.05). Studies have concluded that CRP concentrations tend to be higher in patients with type 2 diabetes and that CRP can disrupt insulin homeostasis and increase the risk of disease by blocking the major cascade of downstream insulin signaling [25], and in vitro studies have also shown an association between serum CRP levels and β-cell dysfunction and insulin resistance[26]. In addition, the development of arthritis is undoubtedly an important cause of reduced quality of life in elderly or even elderly patients, and arthritis as an inflammatory condition is closely associated with CRP. For example, patients with rheumatoid arthritis usually have persistently elevated CRP levels, with baseline CRP levels often exceeding 20 mg/L in randomized clinical trials of drugs for rheumatoid arthritis [16], however, retrospective and observational studies have found that many patients with rheumatoid arthritis have normal CRP levels despite exhibiting disease activity, suggesting that CRP levels only reflect signs of disease activity [27, 28].

Obesity as a risk factor for hypertension has become a globally recognized fact, and in this study, BMI was higher in the group with elevated CRP than in the normal group, and although the difference was not statistically significant (P > 0.05), studies have shown that pro-inflammatory proteins such as interleukin 6 (IL-6), which is broken down by adipose tissue in obese individuals, can increase CRP levels in the liver [28]. In 2003, Hotamisligil [29] proposed that obesity is a state of systemic chronic low-grade inflammation induced by different inflammatory factors. CRP, as a relatively sensitive marker of chronic inflammation, reflects the activity and amount of inflammatory factors, and is involved in the pathogenesis of obesity by regulating lipid metabolism, increasing the inflammatory response, decreasing tissue sensitivity to insulin, stimulating insulin secretion, and promoting lipid synthesis, further aggravating obesity [30]. We also found that steroid use was proportionally higher in the group with elevated CRP (p < 0.05). As an inhibitor of hydroxy-methyl-glutaryl coenzyme A reductase, statin not only reduces LDL-C levels, but also decreases inflammation, reduces oxidative stress, and has a protective effect on the cardiovascular system. For example, Rosuvastatin has been shown to be effective not only in improving lipids, but also in lowering CRP levels, reducing vascular inflammatory responses, and improving endothelial cell function, with positive effects on preventing and reducing cardiovascular clinical endpoints [31]. This study also showed that statin use was higher in the group with normal CRP than in the group with elevated CRP, and although not statistically significant, statin use reduced the risk of hypertension (OR = 0.49,95%CI: 0.25–0.94, p < 0.05) and was protective against hypertension. Earlier studies have suggested an association between alcohol consumption and CRP, but the form of the association is uncertain [32]. Our study found a higher proportion of alcohol consumption in the group with elevated CRP (P < 0.05), which is similar to the findings of a recent cohort study of Chinese men aged 50 years and older [33], which showed that compared with never and occasional drinkers (< 1 drink/week), daily (OR = 1.38, 95% CI: 1.24–2.65) and excessive drinkers (weekly ethanol intake ≥ 210 g, OR = 1.57, 95% CI: 1.22–2.02) had a higher risk of elevated CRP and a higher risk of cardiovascular disease, and therefore patients are advised to drink less or even abstain from alcohol.

As a retrospective study with elderly patients, the data were obtained from the electronic medical records of patients attending our hospital, based on the patients' admission, the collection of general data may lack accuracy, thus affecting the interpretation of the results. Furthermore, we included elderly patients, and because co-morbidity is common in elderly patients, it was not possible to set up a healthy population as a control group to assess the relationship between CRP and hypertension. Finally. our study, as a cross-sectional study, was unable to assess the relationship between CRP concentration and the severity of hypertension, with a small sample size, and further prospective analysis is needed in the future.