An observational study in Acute Kidney Injury and Critical Illness, sponsored by Aswan University. Recruiting at 1 site in Egypt. Open to participants aged 18 Years to 80 Years. Per ClinicalTrials.gov, last updated 2026-03-10.
Sponsored by Aswan University · Observational
To study the ability of RRI, measured by bedside Doppler ultrasound, in detecting acute kidney injury in high-risk patients admitted to surgical intensive care unit, Aswan university hospital, compared with renal biomarkers and conventional assessment using urine output and serum creatinine levels.
Acute kidney injury (AKI) is a common clinical problem encountered in critically ill patients, frequently in the setting of multiple organ failure, and is an independent risk factor for increase hospital stay and mortality risk.
Early-stage acute kidney injury was first assessed based on the risk, injury, failure, loss and end-stage (RIFLE) criteria in 2004, and then by the Acute Kidney Injury Network (AKIN) criteria in 2007. The Kidney Disease: Improving Global Outcomes (KDIGO) classification, based on both the AKIN and RIFLE criteria, was introduced in 2012, offering an assessment based on baseline creatinine and urine output.
The best strategy in clinical practice is to identify AKI as early as possible, reverse its cause, and even improve the sequelae. In the past decades, several serum creatinine (SCr)-based classification systems have been proposed to define AKI.
The limitations of SCr is that the determinants of SCr (rate of production, apparent volume of distribution, and rate of elimination) are variable. Therefore, there is an unmet need for other objective measures to help detect AKI in a timely manner. The role of several biomarkers in the early prediction or risk assessment of AKI has been proposed, including kidney tubular damage markers (e.g., neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM- 1), liver-type fatty acid-binding protein (L-FABP) and cystatin C).
Cystatin C is a protein from the family of cysteine proteinase inhibitors and is of interest as an early marker of decreased renal function. It is a protein that is synthesized at a constant rate by all cells containing nuclei, secreted into biological fluids: plasma, pleural, ascitic, cerebrospinal fluid, freely filtered through the glomerular membrane (due to its low molecular weight), fully metabolized in the kidneys, not secreted by the proximal renal tubules.
Renal resistive index (RRI) is a noninvasive instrument to evaluate kidney hemodynamics, and it is obtained by analysis of intrarenal arterial waves using Doppler ultrasound.
1,691 studies on the registry are indexed under Acute Kidney Injury; 395 are open to participants now.
This study's planned enrollment of 100 is below the median of 160 across 814 observational studies indexed under Acute Kidney Injury.
Browse Acute Kidney Injury studies →Aswan University is the lead sponsor of 47 studies on the registry; 21 are open to participants now.
Counted across the registry records on this site, refreshed daily.
patients who are admitted to SICU, Aswan university hospital, after polytrauma, pre-eclampsia, eclampsia and sepsis
Go through the criteria one by one — yes, no or not sure — and take the list to your doctor or the study team. Kept in this browser only.
Exclusion Criteria:
Early detection of acute kidney injury.
Renal artery resistive index will be measured daily.Cystatin C will be measured on admission, after 24 hours and 72 hours.
Time frame: Day 0,1,2,3,7
Diagnosis of acute kidney injury.
Renal artery resistive index will be measured daily.Cystatin C will be measured on admission, after 24 hours and 72 hours.
Time frame: Day 0,1,2,3,7
To grade the severity of AKI.
Using the KDIGO criteria, AKI is staged as follows: Stage 1: Increase in serum creatinine to 1.5 to 1.9 times baseline, or increase in serum creatinine by ≥0.3 mg/dL, or reduction in urine output to \<0.5 mL/kg/h for 6 to 12 h. Stage 2: Increase in serum creatinine to 2.0 to 2.9 times baseline, or reduction in urine output to \<0.5 mL/kg/h for ≥12 h. Stage 3: Increase in serum creatinine to 3.0 times baseline, or increase in serum creatinine to ≥4.0 mg/dL, or reduction in urine output to \<0.3 mL/kg/h for ≥24 h, or anuria for ≥12 h, or the initiation of renal replacement therapy, or, in patients \<18 years, decrease in estimated glomerular filtration rate (eGFR) to \<35 mL/min/1.73 m2.
Time frame: day 0,1,2,3,7
To predict clinical outcome (clinical improvement)
To predict clinical outcome (clinical improvement) at 30 days
Time frame: Day 0,1,2,3,7,30
To predict clinical outcome (necessity for renal replacement therapy)
To predict clinical outcome (necessity for renal replacement therapy) at 30 days
Time frame: Day 0,1,2,3,7,30
To predict clinical outcome (death)
To predict clinical outcome (death) at 30 days.
Time frame: Day 0,1,2,3,7,30
Plan to share: No
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Aswan University