Acute Kidney Injury, Critical Illness
Conditions
Keywords
renal resisitive index, surgical ICU, Cystatin C
Brief summary
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.
Detailed description
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.
Interventions
None listed
Sponsors
Aswan University
Study design
Observational model
COHORT
Time perspective
PROSPECTIVE
Eligibility
Sex/Gender
ALL
Age
18 Years to 80 Years
Healthy volunteers
No
Inclusion criteria
* Patients with severe pre-eclampsia and eclampsia. * Polytraumatized patients. * Patients admitted to ICU with sepsis. * Both genders. * Patients above 18 years.
Exclusion criteria
* patients known to have CKD. * patients with congenital renal anomalies. * patients with renal transplantation.
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| Early detection of acute kidney injury. | Day 0,1,2,3,7 | Renal artery resistive index will be measured daily.Cystatin C will be measured on admission, after 24 hours and 72 hours. |
| Diagnosis of acute kidney injury. | Day 0,1,2,3,7 | Renal artery resistive index will be measured daily.Cystatin C will be measured on admission, after 24 hours and 72 hours. |
Secondary
| Measure | Time frame | Description |
|---|---|---|
| To grade the severity of AKI. | day 0,1,2,3,7 | 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. |
| To predict clinical outcome (clinical improvement) | Day 0,1,2,3,7,30 | To predict clinical outcome (clinical improvement) at 30 days |
| To predict clinical outcome (necessity for renal replacement therapy) | Day 0,1,2,3,7,30 | To predict clinical outcome (necessity for renal replacement therapy) at 30 days |
| To predict clinical outcome (death) | Day 0,1,2,3,7,30 | To predict clinical outcome (death) at 30 days. |
Countries
Egypt
Contacts
CONTACTSoudy S Hammad, MD
CONTACTTarek S Hemaida, MD
PRINCIPAL_INVESTIGATORMohamed H Abolwafa, MSc
Aswan University
PRINCIPAL_INVESTIGATORAhmed E Abd Elrahman, MD
Sohag University
Outcome results
None listed