Renal is of Latin origin and is more difficult and obscure than kidney, which is of Middle English origin, and therefore the latter is more acceptable; injury, as opposed to failure, better reflects the pathophysiological nature of the disease and, moreover, some injuries do not necessarily reach the point of renal failure.
Such linguistic details may seem trivial compared to the clinical issues that need to be addressed. However, Farley SJ points out that precise nomenclature is the first step to accurate definition.
Definition and diagnosis
There is no single standard: more than 30;
The most widely accepted of these is the definition used in the PICARD study: a rise in creatinine ≥0.5 mg/dl when baseline blood creatinine is <1.5 mg/dl represents new-onset AKI/ARF; a rise in creatinine ≥1.0 mg/dl when baseline blood creatinine is >1.5 mg/dl but <5.0 mg/dl represents AKI/ARF on the basis of chronic kidney disease ( AKI/ARF on chronic kidney disease, A on C).
In 2002, the second meeting of ADQI proposed the RIFLE classification criteria for AKI/ARF, which classified AKI/ARF into three levels: Risk, Injury, Failure and two prognostic levels: Loss of renal function (Loss), End stage renal disease (ESRD). The RIFLE criteria are currently one of the most commonly used criteria for the diagnosis of AKI/ARF. The specific graded diagnostic criteria are shown in Table 1.
In 2004, expert members from ASN, ISN and NFK, ADQI, and the European Society of Intensive Care Medicine (ESICM) convened in Ieenza, Italy, to establish the Acute Kidney Injury Network (AKIN), and the first meeting of AKIN was held in Amsterdam in September 2005, which revised the diagnostic and grading criteria for AKI based on RIFLE.
AKI is defined (diagnostic criteria) as 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 ≥ 0.3 mg/dl (≥ 26.4 umol/l), or an increase of ≥ 50% (up to 1.5 times the baseline value), or a urine output < 0.5 ml/kg/h for more than 6 hours. AKI was also classified into stages 1, 2 and 3, corresponding to Risk, Injury and Failure of RIFLE criteria, respectively.
The main differences between AKI staging and RIFLE are
The L and E levels have been removed because they are not relevant to the severity of AKI and are prognostic judgments;
The GFR criterion was removed, as it is difficult and unreliable to evaluate GFR in an acute state, and the relative change in blood creatinine can reflect the change in GFR;
An absolute increase in Scr >26.4umol/L (0.3mg/dl) can be used as a diagnostic basis for AKI stage 1.
New diagnostic markers
Blood creatinine and urine volume are currently the only reliable tests, and these two indicators are also the current basis for AKI staging. However, blood creatinine is not a sensitive indicator, and the physiology of blood creatinine metabolism and distribution shows that blood creatinine not only reflects GFR, but is also influenced by the combined effects of its distribution and excretion. Urine output is more susceptible to non-renal factors such as volume status and medications.
There are many studies on early diagnostic markers of AKI. The main ones are Cystatin C, KIM-1, NGAL, IL-18, Cyr61, etc. The current basic research and a few clinical studies indicate that these markers may have better sensitivity and may differentiate the etiology of AKI. However, all these markers are still in the research stage and are still some distance away from clinical application. Blood creatinine and urine volume are still the most reliable diagnostic indicators at present.
In addition, there is a lack of international research on biomarkers for acute glomerular disease causing AKI and acute interstitial nephritis (especially drug-induced AIN).
Prevention and treatment
Primary prevention: is a clinical measure to reduce the incidence of AKI in patients with pre-existing or no chronic kidney disease (CKD) without evidence of acute kidney injury (AKI). the fourth meeting of ADQI was held in Vicenza, Italy in 2004, and the following clinical recommendations and guidelines were given after discussion at the meeting.
(1) Avoid the use of nephrotoxic drugs whenever possible;
(2) Early aggressive fluid supplementation may reduce the nephrotoxicity of myoglobinuria and prevent ARF/AKI (grade D); controlled studies have failed to confirm the effectiveness of mannitol with alkalinized urine;
(3) When contrast agents are required, non-ionic isotonic contrast agents should be used in high-risk patients (diabetes mellitus with renal insufficiency). Intravenous input of isotonic fluids reduces the incidence of contrast nephropathy (CIN) (Class I, B), and isotonic sodium bicarbonate solution is superior to isotonic saline (Class II, C), but oral administration is less effective (Class C);
(4) Colloidal solution is not superior to crystalloid solution in the prevention of ARF/AKI in critically ill patients (Class A);
(5) Timely and effective ICU resuscitation can reduce the incidence of ARF/AKI.
Secondary prevention: It refers to the prevention of additional secondary injury in the case of an original primary kidney injury. It is difficult to distinguish between primary and secondary injury when the initial injury progresses, and the goal of prevention is to prevent the second strike of the initial injury and to change the natural outcome of the initial injury, which is also the treatment we routinely talk about in clinical practice. ADQI clinical recommendations and guidelines are as follows.
(1) Hypotension (SAP > 80 mmHg) must be avoided, cardiac output, mean arterial pressure and intravascular volume must be supported to maintain renal perfusion and facilitate recovery of renal function, and norepinephrine is preferred when vasopressors are needed to reverse systemic vasodilation (e.g., septic shock);
(2) Drugs that selectively alter renal blood flow, which have not been shown to alter the natural consequences of ARF, include dopamine, ANP, BNP, etc.
Renal replacement therapy (RRT) is the mainstay of treatment for severe AKI and mimics RRT in established end-stage renal disease (ESRD), but patients with AKI are more hemodynamically unstable, more catabolic, and require more intensive nutritional therapy and fluid intake, all of which require different treatment modalities. These require different treatment modalities.
Furthermore, AKI is not only about short-term mortality, but also about maximizing renal function, and how RRT is performed has a direct impact on patient prognosis. The choice of dialysis timing, dialysis dose, and dialysis modality remains the focus of current AKI clinical research.