How to diagnose and manage septic acute kidney injury? Split diagnosis is not advisable!

Acute kidney injury (AKI) is a clinical syndrome caused by a sudden drop in glomerular filtration rate due to various reasons in a short period of time, accumulation of nitrogenous substances in the body, and rapid development of water, electrolyte, acid-base balance and systemic complications. With the increasing aging of society, irregular use of drugs, increase in difficult surgeries and invasive examinations, its incidence rate has been rising in a straight line. Among them, septic acute kidney injury (SAKI) is more harmful and can easily cause irreversible damage to patients' important organs such as the heart, brain, and lungs, threatening the patient's life. Therefore, medical staff should pay more attention to SAKI.

The pathogenesis of SAKI is complex and its specific mechanism has not yet been elucidated. It is currently believed that the pathogenesis of SAKI mainly involves abnormal systemic and renal hemodynamics, immune and inflammatory-mediated damage, and tubular cell apoptosis. Epidemiological surveys and studies have found that elderly people and women are more likely to develop SAKI. In addition, chronic kidney disease, diabetes, heart failure, malignant tumors, and liver disease can increase the susceptibility to SAKI. Therefore, clinical attention should be paid to this high-risk population.

01SAKI diagnosis is not independent and must meet the dual diagnostic criteria of sepsis and AKI

The diagnosis of SAKI is not independent and cannot be diagnosed separately. It must meet the dual diagnostic criteria of sepsis and AKI. In the diagnosis of sepsis, the Sequential Organ Failure Assessment Scale score due to infection factors proposed by the 2016 Sepsis-3 guidelines must be met, and sepsis can be diagnosed if the change is ≥2 hours. In the diagnosis of AKI, according to the Global Kidney Disease Outcomes Improvement Organization standard, the absolute increase in serum creatinine within 48 hours is ≥26.5 μmol/L, or the serum creatinine increases by 1.5 times the baseline value within 1 week, or the 6-hour urine volume is <0.5 ml/(kg·h), then AKI can be diagnosed. In addition, while meeting the above two diagnostic criteria at the same time, it should be noted that AKI must be secondary to sepsis.

Serum creatinine and urine volume are not specific as diagnostic markers and cannot help to make a clear diagnosis in time. However, studies have shown that urinary neutrophil gelatinase-associated lipocalin and activating transcription factor 3 in urinary exosomes can be used for early diagnosis of SAKI to a certain extent.

In addition, ultrasound angiography can also be used to detect renal microperfusion at an early stage. Studies have shown that its early diagnosis rate can reach more than 80%, which can reflect renal function damage earlier.

02Three treatment methods for SAKI

Because the mechanism of sepsis-induced AKI has not been fully elucidated, there is currently no single effective treatment to improve the development of SAKI. The main treatment methods are as follows.

(1) Continuous renal replacement therapy (CRRT): CRRT refers to a group of extracorporeal blood purification treatment technologies, which is a general term for all continuous and slow water and solute removal treatment methods. Its modes include SCUF, CWHD, CVVH, and CVVHDF. At present, CRRT is routinely used in clinical treatment of SAKI. In addition, there are some experimental treatment methods, such as paired plasma filtration adsorption, selective cell adsorption device, and hemoperfusion of polymyxin B solidified adsorption column.

(2) Fluid resuscitation: The type of fluid resuscitation is based on the recommendations of the 2012 Sepsis Guidelines. Crystalloid fluids can be used for early fluid resuscitation of patients with severe sepsis and septic shock, and hydroxyethyl starch should be used with caution.

(3) Drug treatment: Currently, the commonly used drugs include alkaline phosphatase, which can dephosphorylate and inactivate endotoxins, thereby improving endogenous immune responses. Erythropoietin is a multifunctional cytoprotective hormone that has anti-inflammatory, antioxidant, anti-apoptotic and erythropoietic effects in a variety of tissues. Erythrocyte receptor agonists mainly produce renal protection by inhibiting inflammatory responses. In addition, antibiotics or targeted molecular and cell therapy drugs can also be used, which can be applied in combination with the actual clinical situation of the patient.

In conclusion, SAKI is a special type of AKI. Due to its unique and complex pathophysiological mechanism, our understanding of it is still insufficient. Therefore, clinicians still need to pay enough attention to it and have sufficient knowledge about it in order to better prevent and treat the disease.

References:

[1] Yan Wenyan, Mao Huijuan. Advances in diagnosis and treatment of septic acute kidney injury[J]. Journal of Clinical Nephrology, 2016, 16(02): 120-123.