Published online Jul 6, 2020. doi: 10.12998/wjcc.v8.i13.2738
Peer-review started: February 27, 2020
First decision: April 21, 2020
Revised: May 25, 2020
Accepted: June 9, 2020
Article in press: June 9, 2020
Published online: July 6, 2020
Processing time: 131 Days and 0.1 Hours
As a common disease in the intensive care unit (ICU), sepsis refers to a condition that the immune function is affected by inflammatory cells and then involves related multiple organ dysfunction. The disease is uncontrollable and persistent, and there are more new cases and deaths worldwide every year, which have been increasing. Sepsis is usually caused by severe trauma, suppuration, and other infectious conditions. Its severe conditions cause toxins and pathogenic bacteria to rapidly spread from the infected site to blood circulation, finally resulting in systemic infection.
Continuous renal replacement therapy (CRRT) is a continuous and slow blood purification treatment that removes retained water and solute in an adsorptive, convective, and dispersive blood purification mode with extracorporeal circulation. This therapy removes serum pro- and anti-inflammatory mediators and helps the recovery of body immune function in patients. Prostaglandin E (PGE) pharmacologically affects vasodilation and platelet aggregation, so as to protect vascular endothelium, improve microcirculation, and greatly restore the physiological functions of damaged kidneys.
This study aimed to investigate the effects of PGE combined with CRRT on urinary augmenter of liver regeneration (ALR), urinary Na+/H+ exchanger 3 (NHE3), and serum inflammatory cytokines in patients with septic acute kidney injury (SAKI).
Enrolled patients were treated with comprehensive medical treatment such as fluid resuscitation, anti-infective shock, and nutritional support. A bedside hemofiltration apparatus was used for CRRT, adjusted to the continuous veno-venous hemofiltration mode. The flow range was between 20-50 mL/(kg·h) for treatment over 12-24 h each time, and the blood flow was controlled to 200-220 mL/min. The patients were anticoagulated with low molecular heparin, and treated for 5 consecutive days. Patients in the experimental group were additionally treated with PGE, and the mixed solution (20 μg of PGE + 100 mL of normal saline) of standard dose was slowly and intravenously dripped twice per day. They were treated for 7 consecutive days.
Before treatment, urinary ALR, urinary NHE3, blood urea nitrogen (BUN), serum creatinine (SCr), CD3+ T lymphocytes, CD4+ T lymphocytes, and CD4+/CD8+ T lymphocyte ratio in the control and experimental groups were approximately the same (P > 0.05). After treatment, urinary ALR and NHE3 decreased, while BUN, SCr, CD3+ T lymphocytes, CD4+ T lymphocytes, and CD4+/CD8+ T lymphocyte ratio increased in all subjects. Urinary ALR, urinary NHE3, BUN, and SCr in the experimental group were lower than those in the control group, while CD3+ T lymphocytes, CD4+ T lymphocytes, and CD4+/CD8+ T lymphocyte ratio were higher than those in the control group (P < 0.05). After treatment, the levels of tumor necrosis factor-α, interleukin-18, and hs-CRP in the experimental group were lower than those in the control group (P < 0.05). The time for urine volume recovery and ICU treatment in the experimental group was significantly shorter than that in the control group (P < 0.05), although there was no statistically significant difference in hospital stays between the two groups (P > 0.05). The total incidence of adverse reactions did not differ statistically between the two groups (P > 0.05). The 28-d survival rate in the experimental group (80.33%) was significantly higher than that in the control group (66.04%).
PGE combined with CRRT is clinically effective for treating SAKI, and the combination therapy can significantly improve renal function and reduce inflammatory responses.
Since inflammatory responses are a critical factor during sepsis progression, the clearance of inflammatory mediators in vivo is an important direction for the prevention and treatment of SAKI.