Defining AKD: The Spectrum Of AKI, AKD, And CKD
Mar 30, 2023
Abstract
The Kidney Disease Improving Global Prognosis (KDIGO) guidelines address the definition, classification, and management of acute kidney injury (AKI) and chronic kidney disease (CKD). In practice, some acute kidney diseases and disorders (AKD) have clinical presentations that do not meet the criteria for AKI or CKD. In principle, these symptoms may be caused by the same disease that causes AKI or CKD and can be detected, evaluated, and treated before evolving into AKI or CKD. In 2020, KDIGO convened a consensus meeting to review recent evidence on the epidemiology of AKD and to harmonize the definition and classification of AKD with the KDIGO definition and classification of AKI and CKD Alignment.
Keywords
Acute kidney disease; Acute kidney injury; Chronic kidney disease; Kidney Disease Improving Global Outcomes guidelines; Cistanche benefits
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The Kidney Disease Improving Global Prognosis (KDIGO) guidelines address the definition, classification, and management of acute kidney injury (AKI) and chronic kidney disease (CKD) [1,2]. AKI and CKD are common presentations of heterogeneous diseases. In practice, some acute kidney diseases and disorders (AKD) have clinical manifestations that do not meet the criteria for AKI or CKD. In principle, these manifestations may be caused by the same disease that causes AKI or CKD and can be detected, evaluated, and treated before evolving into AKI or CKD. The lack of accepted definitions and nomenclature for these presentations represents a logical gap in the classification of kidney diseases and disorders (KD), leaving patients and clinicians without management recommendations that might improve care and outcomes.
James et al. [5] conducted a data review of a comprehensive approach to laboratory measurements in the Canadian provincial universal health care system and showed that AKD without AKI (using the KDIGO definition) was present in approximately 3.8% of those who underwent laboratory measurements, equivalent to approximately 1.5% of the provincial population, approximately 1/3 of CKD and 3 times more AKI. AKD without AKI is associated with an increased risk of death and renal failure requiring replacement therapy compared to patients with NKD. In people without pre-existing CKD, AKD patients without AKI had an increased risk of new-onset CKD compared to those without AKD. In people with prior CKD, AKD without AKI was associated with an increased risk of CKD progression compared to people without AKD. In general, patients with AKD without AKI have a lower or similar risk of adverse outcomes than patients with AKI.
A review of data from Sawhney et al [6,7] suggests that many of the available AKI studies include people whose serum creatinine (Scr) changes within 7 days (AKI in the KDIGO guidelines) and people whose Scr changes between 8 - 90 days (AKD without AKI in the KDIGO guidelines). Additional data presented at the meeting (Sawhney, personal communication) compared outcomes for AKI and AKD without AKI (using the KDIGO definition) in the UK, Denmark, and Canada using a similar approach to James et al [5]. Patients with AKD without AKI had similar short- and intermediate-term mortality rates to those with AKI, which is consistent with the results of James et al. In conclusion, the data from James et al.[5] and Sawhney et al.[6,7] provide a substantial evidence base that AKD without AKI as defined by KDIGO is common and harmful and provides a basis for accepting the current definition of AKD by KDIGO.
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Figure 1 provides a conceptual framework for the time course of the KD spectrum, defined as abnormalities in the renal structure or function with health consequences. AKD and CKD are distinguished by the length of disease, which is <3 months or ≥3 months, respectively. By definition, AKD precedes CKD, but AKD may also be superimposed on preexisting CKD, either due to another disease or due to the worsening of the same disease. AKI is a subgroup of AKD defined as an abnormal renal function for more than 6 h-1 week. AKI may occur at the onset of AKD or after the onset of AKD. AKD without AKI is a subgroup of AKD in which structural or functional kidney abnormalities are not as severe or do not progress as quickly as AKI. NKD does not represent a known KD and is defined as an abnormality of kidney structure or function that is not abnormal or does not affect health. People who do not have AKI, AKD, or CKD are classified as having NKD.
Figure 2 details the conceptual overlap and diagnostic criteria for each disorder, based on duration and measures of function and structure. criteria for AKI and CKD are defined by existing KDIGO guidelines. criteria for CKD are intended to address most presentations of chronic disease and disorders, but criteria for AKI are intended to be more restrictive, rather than addressing all presentations of acute disease and disorders. functional criteria for AKI include Scr elevated within 2-7 days or oliguria ≥ 4 hours for 3 months. structural criteria for AKI and criteria for resolution of AKI are not included in the KDIGO guidelines and may be considered by a future KDIGO AKI guideline update workgroup. functional and structural criteria for CKD are GFR <60 mL/min/1.73 m2 or markers of renal impairment for ≥ 3 months. Markers of renal injury include a wide range of biomarkers of renal origin: proteinuria or proteinuria; fluid, electrolyte, and acid-base disturbances; abnormal urinary deposits; imaging abnormalities; pathological abnormalities; and history of renal transplantation (thus renal transplant recipients would be considered to have CKD regardless of functional or structural abnormalities of the transplanted organ).
The recommended criteria for AKD include functional criteria for AKI or CKD or structural criteria for CKD over a 3-month period. There were no criteria related to the rate of increase in urinary flow rate or Scr between 8 days and 3 months, except for the criteria for AKI. Includes ≥50% rise in Scr from baseline or ≥35% fall in GFR from baseline. (Using the CKD-EPI 2009 creatinine equation to estimate GFR, a 50% increase in steady-state Scr from baseline of ≥0.9 mg/dL for men or ≥0.7 mg/dL for women corresponds to an approximately 35% decrease in eGFR. Notably, using the CKD-EPI 2012 cystatin inhibitor C equation, a 50% increase in steady-state serum cystatin inhibitor C from a baseline value of ≥0.8 mg/L corresponded to a similar decrease in eGFR.) No other biomarkers of function or structure associated with AKI were considered at the meeting. The history of renal transplantation did not meet the criteria for AKD.
The lack of criteria for AKI, AKD, and CKD implies NKD. notably, the assignment of NKD requires the identification of markers of renal damage and GFR. The degree of determination depends on the clinical situation, research question, or public health purpose.
AKD is classified as AKI and CKD, including etiology, to guide etiology-specific treatment. AKD usually has the same cause as AKI, but the GFR has not fallen or has fallen previously enough to meet the criteria for AKI (GFR falls too little or too slowly), or the same as CKD, but has not lasted long enough to meet the criteria for CKD (<3 months). Examples include decreased renal perfusion (volume failure, heart failure, cirrhosis, segmental arterial or venous infarction), parenchymal disease (acute glomerulonephritis, neoplastic nephrotic syndrome, pyelonephritis, interstitial nephritis, papillary necrosis, thrombotic microangiopathy, mild acute tubular necrosis, and mild transplant rejection), and urinary tract obstruction (stones or tumors, especially unilateral). Regardless of the cause, further classification of AKD is based on severity (staging), which guides the treatment of a particular stage. AKD with AKI will be classified according to AKI staging (stages 1, 2, and 3, defined by the severity of oliguria or increased Scr), while AKD without AKI will be classified according to GFR and proteinuria levels (corresponding to CKD categories G and A.) The persistence of AKD after AKI remission represents post-AKI AKD. classification of post-AKI AKD can be difficult because when Scr or extracellular fluid volume is not in a steady state, estimating GFR is challenging. It is reasonable to classify AKD by AKI staging after AKI in the steady state, and by G and A classes in the steady state. Alternatively, the "kinetic eGFR" equation can be used in the non-steady state [8,9].
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In summary, the KDIGO meeting report presents a definition and classification of AKD that allows for a comprehensive approach to interpreting renal functional and structural abnormalities in the AKD and CKD spectrum, including an operational definition of NKD. Links to recommendations for AKD assessment and management could improve clinical practice and patient outcomes, and recommendations for the research agenda should strengthen the evidence base for future recommendations.
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REFERENCES
1. Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. Kdigo clinical practice guideline for acute kidney injury. Kidney Int Suppl. 2012;2:1– 138.
2. Kidney Disease: Improving Global Outcomes (KDIGO). Kdigo 2012 clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney Int Suppl. 2013;3:1–150.
3. Chawla LS, Bellomo R, Bihorac A, Goldstein SL, Siew ED, Bagshaw SM, et al. Acute kidney disease and renal recovery: consensus report of the acute disease quality initiative (adqi) 16 workgroup. Nat Rev Nephrol. 2017;13:241– 57.
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5. James MT, Levey AS, Tonelli M, Tan Z, Barry R, Pannu N, et al. Incidence and prognosis of acute kidney diseases and disorders using an integrated approach to laboratory measurements in a universal health care system. JAMA Netw Open. 2019;2:e191795.
6. Sawhney S, Fluck N, Fraser SD, Marks A, Prescott GJ, Roderick PJ, et al. Kdigo-based acute kidney injury criteria operate differently in hospitals and the community findings from a large population cohort. Nephrol Dial Transplant. 2016;31:922–9.
7. Sawhney S, Fraser SD. Epidemiology of AKI: utilizing large databases to determine the burden of AKI. Adv Chronic Kidney Dis. 2017;24: 194–204.
8. Chen S. Retooling the creatinine clearance equation to estimate kinetic gfr when the plasma creatinine is changing acutely. J Am Soc Nephrol. 2013;24:877–88.
9. Pianta TJ, Endre ZH, Pickering JW, Buckley NA, Peake PW. Kinetic estimation of gfr improves prediction of dialysis and recovery after kidney transplantation. PLoS One. 2015; 10:e0125669.
Andrew S. Levey: Division of Nephrology, Tufts Medical Center, Boston, MA, USA
