Abstract
BackgroundAcute kidney injury (AKI) is common after severe paraquat poisoning and usually heralds a fatal outcome. The rapid large increases in serum creatinine (Cr) exceed that which can be explained by creatinine kinetics based on loss of glomerular filtration rate (GFR).Methods and FindingsThis prospective multi-centre study compared the kinetics of two surrogate markers of GFR, serum creatinine and serum cystatin C (CysC), following paraquat poisoning to understand and assess renal functional loss after paraquat poisoning. Sixty-six acute paraquat poisoning patients admitted to medical units of five hospitals were included. Relative changes in creatinine and CysC were monitored in serial blood and urine samples, and influences of non-renal factors were also studied.ResultsForty-eight of 66 patients developed AKI (AKIN criteria), with 37 (56%) developing moderate to severe AKI (AKIN stage 2 or 3). The 37 patients showed rapid increases in creatinine of >100% within 24 hours, >200% within 48 hours and >300% by 72 hours and 17 of the 37 died. CysC concentration increased by 50% at 24 hours in the same 37 patients and then remained constant. The creatinine/CysC ratio increased 8 fold over 72 hours. There was a modest fall in urinary creatinine and serum/urine creatinine ratios and a moderate increase in urinary paraquat during first three days.ConclusionLoss of renal function contributes modestly to the large increases in creatinine following paraquat poisoning. The rapid rise in serum creatinine most probably represents increased production of creatine and creatinine to meet the energy demand following severe oxidative stress. Minor contributions include increased cyclisation of creatine to creatinine because of acidosis and competitive or non-competitive inhibition of creatinine secretion. Creatinine is not a good marker of renal functional loss after paraquat poisoning and renal injury should be evaluated using more specific biomarkers of renal injury.
Highlights
Deliberate self-poisoning with paraquat, a non-selective contact herbicide, is a major public health problem in many countries in South East Asia [1,2]
The rapid large increases in serum creatinine (Cr) exceed that which can be explained by creatinine kinetics based on loss of glomerular filtration rate (GFR)
All non-survivors had an increase in absolute creatinine greater than 2 mg/dl within 24 hours. This is much greater than the maximum possible predicted by creatinine kinetic studies, which suggests an absolute increase of greater than 1.5 mg/dl could only be seen after approximately 48 hours of an acute decrease in GFR assuming a normal baseline [26,27]
Summary
Deliberate self-poisoning with paraquat, a non-selective contact herbicide, is a major public health problem in many countries in South East Asia [1,2]. Case fatality is between 40–60% [3,4] and death usually occurs within 24–72 hours of ingestion in severe poisoning [4]. AKI is currently defined by either change in creatinine or urine output [11,12] despite inherent limitations of creatinine in sensitivity and specificity to AKI. Changes in these traditional biomarkers may involve a substantial delay and both may be altered by various non-renal factors [13]. Acute kidney injury (AKI) is common after severe paraquat poisoning and usually heralds a fatal outcome. The rapid large increases in serum creatinine (Cr) exceed that which can be explained by creatinine kinetics based on loss of glomerular filtration rate (GFR).
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