Acute kidney injury is most common in middle-aged and elderly people, with rapid clinical onset, rapid disease progression and high mortality.
Acute kidney injury (AKI) is a sudden (within 48 hours) decline in renal function caused by an injury that results in structural or functional changes in the kidney, as evidenced by an absolute increase in blood creatinine (Scr) of ≥26.4 μmol/L, or an increase of ≥50%, or a 6-hour urine output.
Injury
Scr rises or exceeds 2 times its original value, urine output 50%, >12 hours.
Failure
Scr rises or exceeds 3 times its original value, urine output 75%, >24 hours or Scr ≥332 μmol/L. Acute increase ≥44 μmol/L or no urine >12 hours.
Loss of renal function
Persistent renal failure > 4 weeks.
End-stage renal disease
Persistent renal failure >3 months.
The incidence of ARF has been reported in the West as 1-25%. And from 1992 to 2002, the rate increased by 11% per year, and the mortality rate was as high as 60%-70%, and the mortality rate of those who underwent renal replacement therapy was 50%, mainly related to the timing of replacement. Statistics show that for every 44 μmol/L increase in Scr, the risk of death increases by 6.5 times and the length of hospital stay increases by 3.5 days. Thirteen to 28% of surviving AKI patients enter end-stage renal disease within 3 years and are dependent on dialysis treatment for survival.
Prevention and treatment response.
Considerable difficulty exists in the treatment of AKI and remains dominated by evidence-based supportive therapy, including replacement therapy. There is no clinically recognized drug therapy with proven efficacy, because early treatment is limited by early diagnosis, and some of the best times for treatment are already missed when there is a significant change in Scr. Secondly, there are many causes of AKI, and treatment measures for different causes are different.
Therefore, it is important to pay more attention to early prevention, which mainly includes the following aspects.
Primary prevention.
(1) Avoid the use of nephrotoxic drugs as much as possible;
(2) Early and active fluid supplementation can reduce the nephrotoxicity of myoglobinuria and prevent AKI.
(3) When contrast agents are required, non-ionic isotonic contrast agents should be used in high-risk patients. Intravenous input of isotonic fluids reduces the incidence of contrast nephropathy. Isotonic sodium bicarbonate is superior to isotonic saline.
(4) Colloid fluid is not superior to crystalloid for AKI prophylaxis in critically ill patients;
(5) Timely and effective ICU resuscitation can reduce the incidence of AKI/ARF.
Secondary prevention.
(1) Hypotension (SAP>80 mmHg) must be avoided to support cardiac output, mean arterial pressure and intravascular volume to maintain renal perfusion and facilitate renal function recovery. When vasopressors are needed to reverse all-out vasodilation (e.g., septic shock), norepinephrine is preferred.
(2) Drugs that selectively improve renal blood flow have not been shown to alter the consequences of AKI.
(3) Renal replacement therapy (CRRT) is the mainstay of treatment for severe AKI. However, due to hemodynamic instability and more vigorous catabolism in patients with AKI, enhanced nutritional support and timely adjustment of dialysis modality and dialysis dose are required.