Acute Kidney Injury Consensus Released, Please Keep 43 Suggestions!

In clinical work, contrast agents and other nephrotoxic drugs are one of the main causes of acute kidney injury (AKI) and chronic kidney disease (CKD). However, there is currently no effective treatment. Therefore, the prevention and risk prediction of drug-related AKI is an important work in clinical practice.

On January 5, 2022, the Taiwan AKI Working Group released the latest consensus on drug-related AKI, managing drug-related AKI from five aspects, namely: ① contrast media nephropathy; ② risk prediction; ③ prevention; ④ treatment and follow-up management; ⑤ medication management after AKI recovery.

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Contrast Nephropathy

1. If there are other options, it is recommended not to inject a contrast agent (not rated);

2. Isotonic or hypotonic nonionic iodinated contrast media is preferred, and isotonic contrast media is better than hypotonic contrast media; if contrast media AKI occurs, the former has a better protective effect on the kidneys (1B);

3. Before the injection of contrast agent, it is recommended to instill isotonic saline or sodium bicarbonate solution intravenously (1A);

4. Routine oral or intravenous N-acetylcysteine is not recommended to prevent AKI caused by contrast media (1A);

5. Routine, prophylactic, intermittent hemodialysis or hemofiltration is not recommended to prevent contrast-induced AKI (2C);

6. Potential benefit of high-dose statins, ischemic preconditioning, and vasodilators for the prevention of contrast-induced AKI (not rated);

7. Other novel antioxidants (quercetin, febuxostat, recombinant Klotho protein) may hold promise for the prevention of contrast-induced AKI (not rated).

Risk prediction

1. Biomarkers such as kidney injury molecule-1, β2 microglobulin, Clusterin, and cystatin C are promising for early detection and intervention of AKI (not graded);

2. When using warfarin, it is necessary to assess the risk of AKI, including age and risk factors such as diabetes, heart failure, hypertension, and nephrotic syndrome (1A);

3. For patients with estimated glomerular filtration rate (eGFR) >30 mL/min/1.73 m2, new oral anticoagulants may be better than warfarin because the former can reduce the risk of AKI (1A);

4. There has not been a systematic review or meta-analysis to suggest that the prognosis of AKI due to different etiologies is different (not rated).

prevention

1. AKI can be identified and intervened early through an electronic AKI alert system (not rated);

2. The 5R/6R method can evaluate the potential risk of AKI occurrence of drugs, which are risk, identification, response, renal support, rehabilitation, and research (not rated);

3. A systematic review shows that the use of computerized decision support systems to assist in drug prescription management reduces the risk of death and the risk of adverse events, whether life-threatening or not (1A);

4. Clinicians should pay attention to the risk of AKI when using vancomycin and piperacillin-tazobactam (not rated);

5. Serum concentrations of vancomycin need to be monitored in patients receiving vancomycin therapy (not rated);

6. If the vancomycin concentration exceeds 15ng/mL, the physician should be vigilant because the risk of AKI is high (1C);

7. For high-risk patients, teicoplanin is recommended instead of vancomycin (1C);

8. Lipid-based amphotericin B reduces nephrotoxicity compared to conventional amphotericin B (not rated).

Treatment and follow-up management

1. In the event of drug-related AKI, the risk-benefit ratio should be carefully considered before dose reduction or discontinuation of the drug; for some dose-related nephrotoxic drugs, dose reduction may be sufficient to reduce damage, but for others, Types of nephrotoxic drugs often require discontinuation (not rated);

2. The underlying etiology of AKI patients needs to be evaluated, and the renal function of the patients should be accurately measured; the serum creatinine level and urine output of the patients should be checked daily; the drug adjustment should also be based on the creatinine clearance rate and urine test results (not rated);

3. Hemodynamics, volume status, and renal perfusion need to be reassessed; complications of AKI, such as fluid overload, acidosis, and hyperkalemia, need to be paid attention to, and the need for renal replacement therapy (RRT) should be assessed. If the cause of AKI is unclear, a nephrologist should be consulted (not rated);

4. Regular monitoring of urinary creatinine clearance in patients with AKI is required (not rated);

5. It is recommended not to use eGFR to assess renal function in patients with AKI. It is recommended to assess serum creatinine and urine output daily to assess renal function in patients with AKI, and to adjust drug doses (not rated);

6. Renal biopsy is recommended if laboratory data make it difficult to distinguish subphenotypes of drug-related AKI (not rated);

7. For patients with eGFR<30mL/min/1.73㎡, follow-up of renal disease is required (not graded);

8. More frequent follow-up and assessment of renal function are recommended for patients with changes in key parameters, such as those with CKD and those with congestive heart failure, cirrhosis, or malignancy before AKI (not rated);

9. It is recommended that patients with drug-related AKI should avoid nephrotoxic drugs or combination drugs; if necessary, avoid simultaneous use and reduce nephrotoxicity (not rated);

10. If the patient has risk factors for kidney damage, such as hypotension, hyperglycemia, anemia, etc., they should try to avoid exposure to nephrotoxic substances or drugs (not rated);

11. If the patient develops a high concentration of the related drug during the acute phase of AKI, then the related drug should be tested even if the nephrotoxic drug is discontinued (not rated);

12. RRT therapy can reduce drug toxicity, and patients with life-threatening fluid, electrolyte, or acid-base imbalances should start RRT immediately (not rated);

13. Determine the timing of RRT cessation based on serum creatinine, urine output, fluid, and acid-base balance before dialysis; for drug dose adjustment during recovery, in addition to expected diafiltration, renal clearance should also be estimated (not rated);

14. After the occurrence of drug-related AKI, it should be recorded in detail, and the patient and other medical staff should be informed to avoid similar situations (not rated);

15. The use of biomarkers and real-time testing is recommended to accurately assess renal function in patients undergoing RRT (not rated);

16. It is recommended to follow up in the same medical institution, and to repeatedly evaluate renal function (not rated);

17. In the case of drug-related AKI incidents, it is recommended to report to an official organization (not rated);

18. It is recommended to develop a risk model for RRT-dependent events within 90 days of recovery in patients with drug-related AKI (not rated);

19. Patients with drug-related AKI should be followed up for 90 days after recovery (not rated);

20. Ultrafiltration intensity, fluid balance, cardiovascular stability, and optimal antibiotic dosing should be prioritized, predicting the likelihood of recovery of renal function (not rated).

Medication management after recovery from AKI

1. CKD patients who frequently use angiotensin-converting enzyme inhibitor (ACEI) or angiotensin receptor blocker (ARB) before AKI, should re-accept ACEI or ARB treatment after AKI recovery (2D);

2. Serum creatinine and potassium ion concentrations should be monitored 1 to 2 weeks after re-accepting ACEI or ARB therapy (2D);

3. There is no need to stop ACEI or ARB therapy before surgery or cardiac catheterization (2D);

4. ACEI or ARB treatment after AKI reduces the risk of death (2D).

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