Abstract

Acute kidney injury (AKI) is a condition that develops as a result of a rapid decrease in the glomerular filtration rate, which leads to the accumulation of nitrogenous, including urea and creatinine, and non-nitrogenous metabolic products with electrolytic disorders, impairment of the acid-base balance, and the volume of fluid excreted by the kidneys. Objective: to provide a review of the literature concerning sepsis-associated acute kidney injury. We presented the problems of diagnosis, risk factors, the pathogenesis of sepsis-associated acute kidney injury, as well as to outline terminologically the clinical form of sepsis-associated acute kidney injury: the paradigm shifts from ischemia and vasoconstriction to hyperemia and vasodilation, from acute tubular necrosis to acute tubular apoptosis. Sepsis contributes significantly to the development of AKI: in sepsis, it occurs in 19 % of patients; nevertheless, it is much more frequent in septic shock (45 % of cases), the mortality of individuals with AKI is especially high in non-septic and septic conditions (45 and 73 %, respectively). To effectively diagnose the functional state of the kidneys and conduct nephroprotective therapy, stratification scales for assessing the severity of acute kidney damage are applied, which are based on the determination of plasma creatinine level and urine output: RIFLE (risk, injury, failure, loss of kidney function, and end-stage renal failure), AKIN (Acute Kidney Injury Network), KDIGO (Kidney Disease Improving Global Outcomes); the experts considered KDIGO scale more modern and perfect. It has been found that plasma creatinine is not an early biomarker of AKI that indicates the advisability of using other integral indicators. AKI biomarkers are substances that either participate in the pathological process or witness it allowing diagnose AKI even before an increase in plasma creatinine level. The characteristics of the structure, role of functions of such biomarkers as neutrophil gelatinase-associated lipocalin, cystatin C, interleukin-18, kidney injury molecule-1 and others are given. Intensive care for sepsis-associated acute kidney injury includes the standard therapy corresponding to 2016 Surviving Sepsis Campaign and KDIGO guidelines. Also, the paper focuses on renal replacement therapy (RRT): renal and extrarenal indications for the initiation, factors affecting the initiation of RRT, the timing of initiation, ways of optimization, the timing of RRT discontinuation, recommendations for the dose of RRT, the dose of renal replacement therapy in sepsis-associated AKI, choice of method, advantages and disadvantages of continuous RRT and intermittent hemodialysis, medication support for continuous therapy, the role of hemodialysis machine in the intensive care unit.

Highlights

  • We presented the problems of diagnosis, risk factors, the pathogenesis of sepsis-associated acute kidney injury, as well as to outline terminologically the clinical form of sepsis-associated acute kidney injury: the paradigm shifts from ischemia and vasoconstriction to hyperemia and vasodilation, from acute tubular necrosis to acute

  • Kim S., Kim H.J., Ahn H.S. et al Is plasma neutrophil gelatinase-associated lipocalin a predictive biomarker for acute kidney injury in sepsis patients?

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Summary

НЕВІДКЛАДНИХ СТАНІВ

Приведена концепция стадийного протекания острого повреждения почек (ОПП), которая создает возможность потенциальной преодолимости и обратимости его ранних стадий, в связи с чем большое значение приобретает диагностика для начала своевременного лечения ОПП. Проблема рассмотрена в ключе появления новых данных о диагностике, факторах риска развития, патогенезе ОПП сепсис-ассоциированного генеза; терминологически очерчена его клиническая форма: парадигма смещается от ишемии и вазоконстрикции к гиперемии и вазодилатации, от острого канальцевого некроза к острому канальцевому апоптозу. ОПП сепсис-ассоциированного генеза характеризуется большей тяжестью и более высокой летальностью: ОПП при сепсисе отмечено у 19 % пациентов, при септическом шоке — у 45 %, летальность составляет 73 % при 45 % у несептических пациентов [8,9,10,11,12]. Парадигма перемещается от ишемии и вазоконстрикции к гиперемии и вазодилатации, от острого канальцевого некроза к острому канальцевому апоптозу

Диагностические критерии острого повреждения почек
Интенсивная терапия
Список литературы
Full Text
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