Discussion: also outperforms currently used clinical thresholds for early

Discussion:  Renal angina index was developed by Goldstein to identify critically
ill patients at greatest risk of AKI.10  In the current study, we operationalize renal
angina index in a tertiary care hospital of a developing country and show that
renal angina index improves prediction of subsequent severe AKI and also
outperforms currently used clinical thresholds for early signs of kidney
injury, or severity of illness scores.

RAI was derived as a composite of risk factors and clinical
signs of AKI. The logic behind the equation dictates that as a patient achieves
higher risk they require less “clinical sign of AKI” early on to fulfill renal
angina. Similarly, if a patient has less risk but shows more overt signs of clinical
AKI signs, renal angina would also be fulfilled.15 RAI derivation was based on available AKI epidemiology
reported in select pediatric populations: children admitted to the ICU carry
increased risk over the general population (4.5–10%),16,17 children receiving bone marrow
transplantation have ~3× risk (11–21%)18, and those who are intubated and on vasopressor support
carry nearly 5× risk versus the general ICU population (51%). 3 The ‘signs of injury’ (i.e.,
kidney pain) in the RAI include GFR and fluid overload.

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Troponin measured in patients
who exhibit cardiac angina, a combination of clinical signs and known coronary
disease risk factors, allows practitioners to rule in myocardial infarction. In
this select, risk-stratified population, troponin has great specificity and
PPV. When measured in patients without cardiac angina, troponin loses
performance. Unfortunately, unlike a heart attack, AKI does not carry an easily
identifiable physical prodrome such as cardiac angina. Simply put, a kidney
attack does not ‘hurt’. So clinicians tried to find a novel renal equivalent of
“cardiac angina” so that a suitable biomarker can be applied to select patients
having high risk of AKI.

Renal angina fulfillment identifies children at the highest
risk of suffering subsequent severe AKI. For a clinician, the ability to
predict the presence of severe AKI 3 days in advance carries obvious benefit.

Fluids are the second most
common intervention in acutely ill patients (after oxygen). The benefits of
early fluid resuscitation in patients with shock and acute kidney injury (AKI)
are already accepted. There is evidence that fluid administration beyond the
correction of hypovolaemia is associated with increased morbidity, a longer
hospital stay and mortality. In a recent article in Critical Care, Wang et al.
analysed the data of 2526 patients admitted to 30 intensive care units (ICUs)
in China and showed that even relatively small degrees of fluid overload were
independently associated with an increased risk of AKI and mortality 19.

In the Rajit
Basu etal study,
based on the most optimal Youden’s index (0.49) and highest negative predictive
value (to safely rule out development of subsequent AKI), an RAI > 8 was
taken as cutoff to label Renal Angina positivity.15 Only day 3 AKI was chosen to define outcome as most PICU
patients develop AKI within this time frame and it surpasses the time frame of
functional AKI (prerenal AKI). Also, time frame of 8 h was kept to assess fluid
overload as it was beyond the generally accepted window of ‘early goal-directed
therapy’ (EGDT) of resuscitation. 20

    In our study a
total of 413 patients were included. Day 0 Renal Angina positive was seen in
16.7% patients. Of  renal angina positive
patients 36.2 %  developed subsequent
severe AKI compared to 2.3 % of the other group, which was highly significant