Modified Renal Angina Index for Prediction of Severe Acute Kidney Injury

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Prediction of severe AKI is important for timely action. Novel biomarkers have been proposed for the early detection of AKI, but a lack of data on sensitivity and specificity, availability, and high cost also makes it difficult.^1,2 There are only a few studies on the early prediction of severe AKI [Stage 2 and 3 AKI network (AKIN)] based on risk factor stratification in the ICU.³ The Renal Angina Index (RAI), determined based on changes in renal function, was proposed to risk-stratify critically ill children at high risk of AKI. The concept of renal angina was introduced to highlight the characteristics of renal injury as an analogy to the concept of angina pectoris.⁴ The RAI is assumed to serve as a marker for detecting early signs of persistent AKI. The RAI in adults involved a consistent, albeit more complicated, definition compared with that used in pediatric ICU patients [Supplementary Material]. We used AKIN criteria for calculation of AKI (definition of increase in serum creatinine>0.3 mg/dL or urine output<0.5 mL/kg/h for>6 hours). The proposed definition for adult RAI included serum creatinine and urine output. RAI in our study was used with a minor modification, i.e., the addition of diabetes mellitus as a co-morbid condition. This was adapted from an Asian study cohort in countries from Japan and Thailand.⁵ The score was defined as the worst condition score multiplied by the creatinine score and consisted of 1, 2, 3, 4, 6, 8, 10, 12, 24, and 408 [Figure 1]. We used RAI>8 as a cut-off for the prediction of severe AKI, based on a study by Basu et al.⁴ The study comprised 372 adults (age>18) of either sex, admitted to the ICU with stage 1 AKIN. [Supplementary Table 1] Those with stage 3 AKIN at presentation, acute on CKD, previous renal transplantation, and pediatric patients were excluded. RAI was assessed; details of kidney replacement therapy (KRT) and mortality were also reported.

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Figure 1:

Renal angina index (RAI) calculated by the product of the elevated creatinine score in 24 hours and patient condition score which includes diabetes mellitus, ICU admission and vasopressor/ventilator use.

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The mean RAI was 33.7+27.8, with a score>8 in 255 (68.55%). Among individuals with early creatinine elevation, the majority (93.22%) had an RAI>8 [Supplementary Table 2].

The association between RAI and severe AKI was statistically significant. The mean interval between the RAI calculation and the requirement of KRT was 5 (range 1-10) days. KRT was required in 97.9% of patients with RAI>8 and one patient with RAI<8 [Supplementary Table 2]. We also analyzed the sensitivity, specificity, and positive and negative predictive values of early creatinine elevation and RAI with an outcome of KRT. Diagnostic accuracy was higher for the RAI (59.68%) compared to early creatinine elevation (49.46%), indicating that RAI had superior overall performance in predicting the requirement for KRT [Supplementary Table 3]. RAI>8 was present in 89.80% of those who expired whereas only 10.20% had RAI <8 [Supplementary Table 3]. As compared to other studies, our RAI cut-off scores were higher. This is probably because our center being a tertiary referral care hospital, patients are brought sick with inotropes from the beginning and have multiple comorbidities. In the adult population, the RAI score was >24 for the prediction of severe AKI and requirement of KRT; whereas RAI was >16 for mortality prediction. [Figure 2 and Supplementary Figure 1] This score, if validated across a huge sample size and used across multiple tertiary care centers, can be a simple, useful tool in resource-poor settings to predict severe AKI in ICU.

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Figure 2:

Sensitivity, specificity, positive predictive value, and negative predictive value of renal angina index and Early creatinine elevation for predicting requirement of renal replacement therapy.

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