Clinical Trial Details
— Status: Not yet recruiting
Administrative data
| NCT number |
NCT06202326 |
| Other study ID # |
AKI in critically ill children |
| Secondary ID |
|
| Status |
Not yet recruiting |
| Phase |
|
| First received |
|
| Last updated |
|
| Start date |
April 2024 |
| Est. completion date |
June 2025 |
Study information
| Verified date |
January 2024 |
| Source |
Assiut University |
| Contact |
Nardeen Elway, assistant lecturer |
| Phone |
01212810204 |
| Email |
nardeenchristdd[@]gmail.com |
| Is FDA regulated |
No |
| Health authority |
|
| Study type |
Observational
|
Clinical Trial Summary
To detect frequency of acute kidney injury in critically ill children in Assuit university
hospital.
To detect associated AKI risk factors, severity and outcomes . To assess the value of use of
renal Doppler ultrasound in AKI.
Description:
Critically ill child is defined as a child whose baseline state of health has significantly
changed and whose life is at risk as a result of an illness or injury and they in big need
for intensive care whether medicallyor surgically.
Acute kidney injury (AKI) is characterized by a sudden and generally revertible renal
function impairment , involving inability to maintain the homeostasis, and may or not be
accompanied by reduced diuresis. (1) Acute kidney injury (AKI) is highly prevalent among
hospitalized children, with incidence rates ranging from 5% in non-critically ill children to
50% in those admitted to pediatric emergency units (2). This disease is strongly associated
with worse outcomes, including increased mortality, increased use of mechanical ventilation,
and prolonged hospital stay (3). AKI prevalence due to sepsis ranges from 9% to 40%, involves
poor prognosis, and is associated with a 70% mortality rate (4). Among critically ill renal
impaired patients, about 6% the septic shock, is one of the main causes of AKI. may need
renal replacement therapy (RRT), with a mortality rate increased by 50 to 80%, particularly
associated with sepsis, septic shock, and multiple organ and systems dysfunction MODS (5).
During the childhood, the main AKI causes are sepsis, nephrotoxic drugs, and renal ischemia
in critically ill patients (1) .These patients, particularly those staying in intensive care
units , are exposed to a number of conditions which may result in renal impairment ,thus
significantly increasing the morbidity and mortality rate. (6).
Among the main causes that should be mentioned : hypovolemia leading to hypoperfusion and
consequent hypoxia; inflammatory and thrombotic events caused by bacteremia ; systemic
inflammation from trauma, major surgeries, extracorporeal circulation ;use of vasodilator
drugs such as phosphodiesterase inhibitors, sedatives, epidural blockade; vasopressors; and
use of nephrotoxic drugs as aminoglycosides, amphotericin B, radiological contrasts, and
drugs interfering with the renal hemodynamics such as angiotensin converting enzyme
inhibitors and angiotensin II receptor blockers (3).
In 2004, a consensus definition for AKI was proposed by the Acute Dialysis Quality Initiative
(ADQI) : the RIFLE criteria (risk, injury ,failure, loss, end-stage renal disease) (7) .The
adult-derived RIFLE definition was modified, and then applied and validated in pediatric
patients and renamed as the pediatric RIFLE criteria. pRIFLE stratifies AKI from mild (RIFLE
R, risk) to severe (RIFLE F, failure) based on changes in SCR or estimated creatinine
clearance and urine output .Similar to adult studies AKI defined by these criteria was an
independent risk factor for both increased hospital length of stay and mortality.
Currently, the most widely used criteria for diagnosing and staging AKI is the Kidney Disease
Improving Global Outcomes (KDIGO) criteria, which is based on acute changes in serum
creatinine (sCr) and/or reduced urine output (UO) (8). These criteria have limitations,
especially in children. Significant sCr elevations can be delayed 24 to 48 hours after a
renal insult and are commonly seen only after at least 50% of renal function loss. In
addition, children may have very low sCr levels at baseline, which can make it difficult to
identify relative increases when values remain within normal ranges. To overcome these
limitatio, point-of-care ultrasonography has been proposed as a reliable and safe method to
both diagnose and predict the occurrence of AKI in ICU patients (8).
The AKI diagnosis methods include: clinical evaluation of the urine output and laboratory
tests as urine analysis, blood urea nitrogen, and creatinine, however with low sensitivity
and specificity.(9). Biomarkers for early AKI detection are currently under investigation,
among them neutrophil gelatinase associated lipocalin (NGAL), cystatin C, interleukin 18, and
kidney injury molecule-1(KIM1). Although these markers have good sensitivity and specificity,
they are not routinely used due to their low availability and high costs(10). So there is a
need for a method valid ,early, simple for early detection of AKI.
Renal arterial Doppler-based parameters, such as renal resistive index (RRI) or renal
pulsatility index (RPI), are rapid, noninvasive, and repeatable variables that may be
promising for early AKI detection. Because it reflects resistance to blood flow, lower RRI
values are associated with better renal perfusion, while increased values are associated with
progression to ATN (11). However, there is a lack of evidence supporting the use of this
technique in PICU. Therefore, this study aims to assess the accuracy of renal arterial
Doppler ultrasound (RDU) to predict AKI in mechanically ventilated children.
The complement system, which is a part of the innate immune system, is involved in mechanism
of AKI , and thus could present a unifying therapeutic target in the pathophysiology of AKI
development in children who are critically ill. The complement cascade is made up of three
activation pathways: classic, alternative, and lectin. These three pathways feed into the
"terminal complement cascade." These pathways generate protein fragments that can be
quantified to determine the level of complement activation in each pathway in a given
disease: C4a (classic and lectin pathways), Factors Ba and Bb (alternative pathway), C3a (all
three pathways), and sC5b-9 (terminal pathway). The kidney is particularly susceptible to
complement activation because complement proteins are concentrated in the kidney via
glomerular filtration and activation is promoted via the kidney's acidic environment and
ammonia synthesis (12). Complement factors have been shown to be instrumental in the
pathogenesis of AKI in basic science models of sepsis and ischemia reperfusion injury
(13,14). All three pathways have been implicated in the pathogenesis of a wide variety of
kidney diseases (11,15,16).
