Acute-on-Chronic Inflammation and Patients’ Risk for Renal Support in Critically Ill Patients

Hypertension (HTN) and heart failure (HF) can chronically activate the renin-angiotensin-aldosterone system, a mechanism designed to maintain hemodynamic stability by reabsorption of water and electrolytes. Additionally, this system activates the sympathetic nervous system to increase vagal tone. When these patients face acute illness requiring hospitalization, the acute stressor or pathogen also activates the sympathetic nervous system. The combination of activation of both systems puts patients at increased risk of organ failure, specifically renal failure. With early recognition of renal insult, organ damage can be reversed. C-reactive protein (CRP) and D-dimer are commonly used to measure acute inflammation. These biomarkers can alert critical care nurses to excessive inflammation in patients with underlying HTN and HF, enabling nurses to make informed decisions to intervene at the earliest sign of renal failure. This retrospective study of adult SARS-CoV-2 patients in an intensive care unit setting sought to examine the relationship of CRP, D-dimer, and the need for eventual renal support in patients with HF and HTN. Of the sample (n + 189), mean age was 62 (SD = 14.0), and most (70.9%) were male. Thirty-nine patients (20.6%) required renal support. Of the cases requiring renal support, 21 (53.8%) had a history of prior renal disease ( P < 0.001, r = 0.351). History of HTN was significantly correlated with requirement for renal support ( P = 0.010, r = 0.187). D-dimer ( P = 0.038, η = 1.0) and CRP ( P = 0.018, η = 0.924) were also significant. Survival was significantly worse in the renal support group ( P < 0.001, r = −0.310). D-dimer and CRP were correlated with more severe illness and need for renal support. Study findings have implications for future validation research of chronic inflammation and risk for renal support during acute severe illness.