Paraquat (PQ) has known negative human health effects, but continues to be commonly used worldwide as a herbicide. Our clinical data shows that the main prognostic factor is the time required to achieve a negative urine dithionite test. Patient survival is a 100% when the area affected by ground glass opacity is <20% of the total lung volume on high-resolution computed tomography imaging 7 days post-PQ ingestion. The incidence of acute kidney injury is approximately 50%. The average serum creatinine level reaches its peak around 5 days post-ingestion, and usually normalizes within 3 weeks. We obtain two connecting lines from the highest PQ level for the survivors and the lowest PQ level among the non-survivors at a given time. Patients with a PQ level between these two lines are considered treatable. The following treatment modalities are recommended to preserve kidney function: 1) extracorporeal elimination, 2) intravenous antioxidant administration, 3) diuresis with a fluid, and 4) cytotoxic drugs. In conclusion, this review provides a general overview on the diagnostic procedure and treatment modality of acute PQ intoxication, while focusing on our clinical experience.

Paraquat intoxication is characterized by multi-organ failure, causing substantial mortality and morbidity. Many paraquat patients experience acute kidney injury (AKI), sometimes requiring hemodialysis. We observed 222 paraquat-intoxicated patients between 2000 and 2012, and divided them into AKI (n = 103) and non-AKI (n = 119) groups. The mortality rate was higher for AKI than non-AKI patients (70.1% vs. 40.0%, P < 0.001). Patients with AKI had a longer time to hospital arrival (P = 0.003), lower PaO 2 (P = 0.006) and higher alveolar-arterial O 2 difference (P < 0.001) 48 h after admission, higher sequential organ failure assessment 48-h score (P < 0.001), higher severity index of paraquat poisoning (SIPP) score (P = 0.016), lower PaCO 2 at admission (P = 0.031), higher PaO 2 at admission (P = 0.015), lower nadir PaCO 2 (P = 0.001) and lower nadir HCO 3 (P = 0.004) than non-AKI patients. Multivariate logistic regression indicated that acute hepatitis (P < 0.001), a longer time to hospital arrival (P < 0.001), higher SIPP score (P = 0.026) and higher PaO 2 at admission (P = 0.014) were predictors of AKI. The area under the receiver operating characteristic curve confirmed that an Acute Kidney Injury Network 48-hour score ≥ 2 predicted AKI necessitating hemodialysis with a sensitivity of 0.6 and specificity of 0.832. AKI is common (46.4%) following paraquat ingestion, and acute hepatitis, the time to hospital arrival, SIPP score and PaO 2 at admission were powerful predictors of AKI. Larger studies with longer follow-up durations are warranted.

Our data showed that plasma paraquat concentration is good predictor of survivors but is not good predictor of non-survivors in the low plasma paraquat level.

Acute kidney injury (AKI) is a systemic disease associated with widespread effects on distant organs, including the heart. Normal cardiac function is dependent on constant ATP generation, and the preferred method of energy production is via oxidative phosphorylation. Following direct ischemic cardiac injury, the cardiac metabolome is characterized by inadequate oxidative phosphorylation, increased oxidative stress, and increased alternate energy utilization. We assessed the impact of ischemic AKI on the metabolomics profile in the heart. Ischemic AKI was induced by 22 minutes of renal pedicle clamping, and 124 metabolites were measured in the heart at 4 hours, 24 hours, and 7 days post-procedure. Forty-one percent of measured metabolites were affected, with the most prominent changes observed 24 hours post-AKI. The post-AKI cardiac metabolome was characterized by amino acid depletion, increased oxidative stress, and evidence of alternative energy production, including a shift to anaerobic forms of energy production. These metabolomic effects were associated with significant cardiac ATP depletion and with echocardiographic evidence of diastolic dysfunction. In the kidney, metabolomics analysis revealed shifts suggestive of energy depletion and oxidative stress, which were reflected systemically in the plasma. This is the first study to examine the cardiac metabolome after AKI, and demonstrates that effects of ischemic AKI on the heart are akin to the effects of direct ischemic cardiac injury.