Transient Acute Kidney Injury (AKI) is common following significant kidney hypoperfusion

• Main Authors: Md Ralib, Azrina, Pickering, John W., Shaw, Geoffrey M., Thann, Martin, Endre, Zoltan H.
• Format: Article
• Language: English
• Published: Wiley-Blackwell Publishing 2012
• Subjects: R Medicine (General)
• Online Access: http://irep.iium.edu.my/37396/1/9._Nephrology_ANZSN_2012_T-AKI.pdf; http://irep.iium.edu.my/37396/; http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1440-1797

Aim: To investigate transient early acute kidney injury (AKI) that occur in high risk patients. Background: Cardiac arrest resulted in interruption of renal blood flow to end organ including the kidney. AKI was reported to occur in up to 49% of patients following cardiac arrest. Several studies demonstrated a transient early elevation of serum creatinine after the first few hours following cardiac arrest. Serum creatinine level then dropped over the next few days until ICU discharged in those with a better outcome. Whether this changes resulted from altered glomerular filtration rate following cardiac arrest, or due to other factors is unclear. We aimed to investigate this, by correlating it with alternative marker of function, plasma cystatin C and marker of injury by measurement of plasma and urinary biomarker of injury. We hyposthesize that following cardiac arrest, there is a rapid decline in glomerular filtration rate, and injury to epithelial cells secondary to reduced perfusion. Methods: A sub-cohort of patients with transient AKI on ED admission from the Early Detection of Acute Kidney Injury (EDAKI) Study was analyzed. The EDAKI Study was a prospective observational trial of plasma and urine biomarkers of AKI in high-risk patients, which include survivor of cardiac arrest, sustained or profound hypotension, and ruptured abdominal aortic aneurysm. Plasma creatinine, cystatin C (CysC), neutrophil-gelatinase associated lipocalin (NGAL), and urinary alkaline phosphatase (AP), gamma glutamyl transpeptidase (GGT), CysC, and NGAL were measured on admission to the emergency department (ED), on admission to the ICU, and 4, 8, 16 hours, day 2, 4, and 7 were measured. Results: 45 patients were included in this analysis, of which 54% developed AKI. Serum creatinine increased rapidly from baseline on ED admission and gradually decreased within 24 hours. Serum creatinine on ED correlated with arrest time, dose of adrenaline, and amount of defibrillation. There was no correlation with creatinine kinase. Similar pattern of increase level on ED admission were shown in plasma cystatin C, and other plasma and urinary biomarkers of injury. Conclusions: Early elevation of serum creatinine following cardiac arrest is associated with reduced perfusion which contributes to reduced kidney filtration, and kidney tubular dysfunction.