Early plasma increase in creatinine following significant kidney hypoperfusion
Background: The limitation of plasma creatinine in AKI diagnosis is mainly due to its delayed increase from time of insult, and hence resulted in delayed diagnosis. Earlier diagnosis is made possible with the discovery of various new AKI biomarker of injury. However, their performance in heterogenou...
| Main Authors: | , , , |
|---|---|
| Format: | Conference or Workshop Item |
| Language: | English |
| Published: |
2012
|
| Subjects: | |
| Online Access: | http://irep.iium.edu.my/37398/ http://irep.iium.edu.my/37398/1/11._Translational_2012_Early_Cr.pdf |
| Summary: | Background: The limitation of plasma creatinine in AKI diagnosis is mainly due to its delayed increase from time of insult, and hence resulted in delayed diagnosis. Earlier diagnosis is made possible with the discovery of various new AKI biomarker of injury. However, their performance in heterogenous ICU population is influenced by the time of measurement from time of insult. We aimed to investigate this by measuring these biomarkers near to the time of insult, in the emergency department (ED), and during the first week of ICU and hospital stay in 3 patient groups identified as high risk for AKI.
Methods: Plasma and urinary cystatin C (CysC) and neutrophil-gelatinase-associated-lipocalin (NGAL), urine gamma-glutamyl transpeptidase (GGT), α- and π- glutamyl S-transferase (GST) were measured in patients following cardiac arrest, sustained or profound hypotension, or probable ruptured abdominal aortic aneurysm. Sampling was done at ED arrival, ICU entry, and at 4, 8, 16 h, and on day 2, 4 and 7. AKI was defined as creatinine increase >0.3mg/dl within 48-h or 50% within 7-days for <48-h (T-AKI) or ≥48-h (Sustained-AKI).
Results: Of the 77 patients, 45 developed AKI (27 T-AKI, 18 Sustained-AKI). In 37 (80%) AKI was diagnosed in the ED, with the mean time of insult of 1.2 ± 0.7 hours. Only a maximum percentage of 27 ± 13 % can be explained by total loss of GFR for the duration from insult to measurement. In 17 of these, AKI was no longer present on ICU entry based on creatinine, and there was no associated increase in injury biomarkers. Plasma and urine NGAL, and cystatin C increased progressively from no AKI, T-AKI and S-AKI [p<0.0001]. Urine NGAL and π-GST measured on ICU admission predicted death and dialysis.
Conclusions: Early increase of plasma creatinine following significant renal hypoperfusion is common and cannot be solely explained by reduced renal perfusion. Sustained-AKI is associated in a more severe renal tubular injury. In the presence of high creatinine in the ED, urine NGAL or π-GST measurement may assist in further clinical decision making.
|
|---|