A biological index to predict patient outcome in paraquat poisoning

Ragoucy-Sengler, C.; Pileire, B.

doi:10.1177/096032719601500315

Cited by 26 publications

(16 citation statements)

References 8 publications

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“…This small study confirms a previous report (Ragoucy-Sengler and Pileire, 1996) suggesting that the rate of change in creatinine concentration may be useful for predicting death after paraquat poisoning. Further, we demonstrated that the rise in cystatin C (but not NGAL) is also useful in predicting patients who may die.…”

Section: Discussionsupporting

confidence: 91%

“…Further, our study noted that dCr/d t predicts death where the best determinant was a rise >4.3 μmol/L/h (Fig. 2a), which is slightly higher than a rise >3 μmol/L/h in the previous study (Ragoucy-Sengler and Pileire, 1996). These rates of change in creatinine are likely to represent a loss of at least 70–80% of GFR (Waikar and Bonventre, 2009).…”

Section: Discussionmentioning

confidence: 43%

“…For example, acute kidney injury is a prominent manifestation of acute paraquat poisoning which has prompted research into renal biomarkers (Gil et al, 2009; Ragoucy-Sengler and Pileire, 1996). One small study ( n = 18) suggested that an increase in creatinine of >3 μmol/L/h (dCr/d t ) predicts death (Ragoucy-Sengler and Pileire, 1996). The rise in creatinine is probably due to progressive renal impairment and a direct reflection of organ toxicity (Pond et al, 1993).…”

Section: Introductionmentioning

confidence: 99%

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Changes in the concentrations of creatinine, cystatin C and NGAL in patients with acute paraquat self-poisoning

et al. 2011

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An increase in creatinine >3 μmol/L/h has been suggested to predict death in patients with paraquat self-poisoning and the value of other plasma biomarkers of acute kidney injury has not been assessed. The aim of this study was to validate the predictive value of serial creatinine concentrations and to study the utility of cystatin C and neutrophil gelatinase-associated lipocalin (NGAL) as predictors of outcome in patients with acute paraquat poisoning. The rate of change of creatinine (dCr/dt) and cystatin C (dCyC/dt) concentrations were compared between survivors and deaths. Receiver-operating characteristic (ROC) curves were constructed to determine the best threshold for predicting death. Paraquat was detected in 20 patients and 7 of these died between 18 h and 20 days post-ingestion. The dCr/dt ROC curve had an area of 0.93 and the cut-off was >4.3 μmol/L/h (sensitivity 100%, specificity 85%, likelihood ratio 7). The dCyC/dt ROC curve had an area of 0.97 and the cutoff was >0.009 mg/L/h (sensitivity 100%, specificity 91%, likelihood ratio 11). NGAL did not separate survivors from deaths. Death due to acute paraquat poisoning is associated with changes in creatinine and cystatin concentrations. Further validation of these measurements is needed before they can be adopted in guiding intensive treatments.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 43%

Section: Introductionmentioning

confidence: 99%

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Changes in the concentrations of creatinine, cystatin C and NGAL in patients with acute paraquat self-poisoning

et al. 2011

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“…However, some evidence against the conclusion was ignored. Although these works have not been prospectively validated by authors, several studies (4,18,19) confirmed the results of Proudfoot et al (11) and Hart et al (12). In addition, generalizability and consistency exist among the studies using plasma paraquat levels as the prognostic predictor because their results are similar among different study groups (8 -12, 17).…”

Section: Discussionsupporting

confidence: 72%

Repeated pulse of methylprednisolone and cyclophosphamide with continuous dexamethasone therapy for patients with severe paraquat poisoning

Lin¹,

Lin-Tan²,

Chen³

et al. 2006

Critical Care Medicine

116

105

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“…Creatine, creatol and methylguanidine act as a homeostatic antioxidant to reduce circulating free radicals [49]. Generation of free radicals leads to extra production of sCr [50,51] to meet the higher energy demand under oxidative stress as noted following several paraquat poisoning [3]. Therefore we propose that the observed rapid and large rise of sCr is contributed by increased production and conversion of creatine to creatinine.…”

Section: Discussionmentioning

confidence: 98%

Serum creatinine and cystatin C provide conflicting evidence of acute kidney injury following acute ingestion of potassium permanganate and oxalic acid

Wijerathna

Gawarammana

Dissanayaka

et al. 2017

Clinical Toxicology

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Acute Kidney Injury (AKI) is common following deliberate self-poisoning with a combination washing powder containing oxalic acid (H2C2O4) and Potassium permanganate (KMnO4). Early and rapid increases in serum creatinine (sCr) follow severe poisoning.We investigated the relationship of these increases with direct nephrotoxicity in an ongoing multicenter prospective cohort study in Sri Lanka exploring AKI following poisoning. Multiple measures of change in kidney function were evaluated in 48 consenting patients who had serial sCr and serum cystatinC (sCysC) data available.Thirty eight (38/48, 79%) patients developed AKI (AKIN criteria). Twenty eight (58%) had AKIN stage 2 or 3. Initial increases in urine creatinine (uCr) excretion were followed by a substantial loss of renal function. The AKIN stage 2 and 3 (AKIN2/3) group had very rapid rises in sCr (a median of 118% at 24 hours and by 400% at 72 hours post ingestion). We excluded the possibility that the rapid rise resulted from the assay used or muscle damage. In contrast, the average sCysC increase was 65% by 72 hours.In most AKI, sCysC increases to the same extent but more rapidly than sCr, as sCysC has a shorter half-life. This suggests either a reduction in Cystatin C production or, conversely, that the rapid early rise of sCr results from increased production of creatine and creatinine to meet energy demands following severe oxidative stress mediated by oxalic acid and KMnO4. Increased early creatinine excretion supports the latter explanation, since creatinine excretion usually decreases transiently in AKIN2/3 from other causes.

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A biological index to predict patient outcome in paraquat poisoning

Cited by 26 publications

References 8 publications

Changes in the concentrations of creatinine, cystatin C and NGAL in patients with acute paraquat self-poisoning

Changes in the concentrations of creatinine, cystatin C and NGAL in patients with acute paraquat self-poisoning

Repeated pulse of methylprednisolone and cyclophosphamide with continuous dexamethasone therapy for patients with severe paraquat poisoning

Serum creatinine and cystatin C provide conflicting evidence of acute kidney injury following acute ingestion of potassium permanganate and oxalic acid

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