AKI diagnosis, etiology, and management
Early identification of patients with AKI is one of the most critical unmet needs of physicians in their daily clinical practice. Based on the high potency of biomarkers in the enrichment of clinical information, the expert panel suggests a modification of the KDIGO stages. Stage 1 AKI can be stratified as two substages to improve the diagnostic accuracy of AKI by the application of biomarkers. The substages are categorized by either both, serum creatinine and damage biomarkers are positive or only one of the criteria is positive. Patients with a positive damage biomarker but a negative serum creatinine may be diagnosed with subclinical AKI- shedding light in the creatinine-blind window, providing an aid in the planning of therapy and management of AKI patients (Figure 1) (2).
AKI progression and kidney recovery
Transient AKI has better clinical outcomes than the persistent AKI, which is defined as the AKI period longer than 48 hours. To better understand the AKI patient’s progression, novel biomarkers are suggested to aid in the prediction (2).
Damage and Functional Biomarkers
AKI typically does not occur as an isolated clinical picture, but rather as a symptom of another event (such as shock or hypovolemia). The cause may be pre-renal, intra-renal or post-renal.
About 60% of the cases are pre-renal and caused are by conditions that result in low kidney perfusion such as low fluid intake or a reduced blood volume due to sepsis or heart failure (3). This initially leads to reduced kidney function and but is not necessarily resulting in tubular damage, only if the condition remains for a long period of time. Intra-renal AKI occurs in about 35% of cases. Toxic medications or bacterial infections can cause direct damage to the kidneys, destroying nephrons, the functional unit filtrating the blood. About 5% of AKI cases are caused by post-renal conditions such as obstructions resulting from kidney stones or a tumor (4).
Though about 20 damage biomarkers are in the pipeline of clinical research, biomarkers for the assessment of functional impairment are limited to serum creatinine, Cystatin C and proenkephalin.
Generally, AKI cannot be linked to specific symptoms and standard diagnostics are failing in acute care settings due to slow changes in such as dynamic condition. The recommended inclusion of new biomarkers in the assessment of AKI is a big step ahead to improve patient management and to start rethinking the definition of AKI.
(1) Farrar A. Acute Kidney Injury. Nurs Clin North Am. 2018 Dec;53(4):499-510. doi: 10.1016/j.cnur.2018.07.001. Epub 2018 Oct 11. PMID: 30388976.
(2) Ostermann M, Bellomo R, Burdmann EA, Doi K, Endre ZH et al; Conference Participants. Controversies in acute kidney injury: conclusions from a kidney disease: Improving Global Outcomes (KDIGO) Conference. Kidney Int. 2020 Aug;98(2):294-309. doi: 10.1016/j.kint.2020.04.020. Epub 2020 Apr 26. PMID: 32709292.
(3) Gameiro, J., Lopes, J.A. Complete blood count in acute kidney injury prediction: a narrative review. Ann. Intensive Care 9, 87 (2019). https://doi.org/10.1186/s13613-019-0561-4
(4) Jonathan S Chávez-Iñiguez, Goretty J Navarro-Gallardo, Ramón Medina-González, Luz Alcantar-Vallin, Guillermo García-García, "Acute Kidney Injury Caused by Obstructive Nephropathy", International Journal of Nephrology, vol. 2020, Article ID 8846622, 10 pages, 2020. doi.org/10.1155/2020/8846622
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