Pneumoproteins as markers of paraquat lung injury: A clinical case

Hantson, Philippe; Weynand, Birgit; Doyle, Ian; Bernand, Alfred; Hermans, Cédric

doi:10.1016/j.jcfm.2006.09.003

Cited by 10 publications

(10 citation statements)

References 26 publications

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“…A significant increase in serum cystatin C concentration was observed 8 h following acute paraquat poisoning in rats; at 24 h an increase was also detected in bronchoalveolar fluid, however, it was suggested that this was due to leakage from the serum (Hantson et al, 2008a). A previous case report of acute paraquat poisoning also noted an increase in cystatin C and creatinine, similar to our findings (Hantson et al, 2008b). Our study is the first case series to evaluate the rate of change in cystatin C from acute paraquat poisoning.…”

Section: Discussionsupporting

confidence: 92%

“…This is likely to relate to a shorter half-life of cystatin C and therefore time to steady state compared to creatinine. In their patient (who died 92 h after admission) Hantson et al reported a progressive increase in cystatin C concentrations until 70 h post-admission (Hantson et al, 2008b). However, this patient's treatment regimen included haemodialysis, which removes cystatin C from plasma (Mayeur et al, 2010), thereby complicating interpretation of this data.…”

Section: Discussionmentioning

confidence: 98%

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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: 92%

Section: Discussionmentioning

confidence: 98%

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

et al. 2011

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“…While this study had insufficient power to assess formally the diagnostic and prognostic utility of these two biomarkers, it raised questions about the assumptions discussed above favouring damage biomarkers over functional markers in the early diagnosis of AKI. Similarly in other studies, the functional biomarkers serum cystatin C and creatinine concentrations predicted death in severe paraquat poisoning while the injury biomarker serum NGAL did not .…”

Section: Introductionsupporting

confidence: 76%

“…Most studies examining new renal biomarkers in ToxAKI have focused on aminoglycosides, iodinated contrast agents and cisplatin‐induced nephrotoxicity (Table ). The few studies assessing the utility of biomarkers after LDC‐relevant chemical/toxin ingestion have only measured serum creatinine, plasma cystatin C, urinary NGAL and KIM‐1 in small cohorts of patients and with few samples to allow assessment of biomarker profiles after potential renal injury .…”

Section: Introductionmentioning

confidence: 99%

Role of biomarkers of nephrotoxic acute kidney injury in deliberate poisoning and envenomation in less developed countries

Mohamed

Endre

Buckley

2015

Brit J Clinical Pharma

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Acute kidney injury (AKI) has diverse causes and is associated with increased mortality and morbidity. In less developed countries (LDC), nephrotoxic AKI (ToxAKI) is common and mainly due to deliberate ingestion of nephrotoxic pesticides, toxic plants or to snake envenomation. ToxAKI shares some pathophysiological pathways with the much more intensively studied ischaemic AKI, but in contrast to ischaemic AKI, most victims are young, previously healthy adults. Diagnosis of AKI is currently based on a rise in serum creatinine. However this may delay diagnosis because of the kinetics of creatinine. Baseline creatinine values are also rarely available in LDC. Novel renal injury biomarkers offer a way forward because they usually increase more rapidly in AKI and are normally regarded as absent or very low in concentration, thereby reducing the need for a baseline estimate. This should increase sensitivity and speed of diagnosis. Specificity should also be increased for urine biomarkers since many originate from the renal tubular epithelium. Earlier diagnosis of ToxAKI should allow earlier initiation of appropriate therapy. However, translation of novel biomarkers of ToxAKI into clinical practice requires better understanding of non-renal factors in poisoning that alter biomarkers and the influence of dose of nephrotoxin on biomarker performance. Further issues are establishing LDC population-based normal ranges and assessing sampling and analytical parameters for low resource settings. The potential role of renal biomarkers in exploring ToxAKI aetiologies for chronic kidney disease of unknown origin (CKDu) is a high research priority in LDC. Therefore, developing more sensitive biomarkers for early diagnosis of nephrotoxicity is a critical step to making progress against AKI and CKDu in the developing world.

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“…and/or loss of integrity of the BA/BB were induced by ANTU and IPO whereas cytotoxic lesions were mainly associated with PQ. We have shown in previous papers also that the diminution of the number of CC16-immunoreactive cells was mainly apparent following IPO treatment and occurred with less severity following ANTU and PQ treatments (43,44). The three lung toxicants induced a significant reduction of CC16 in BALF.…”

Section: Nsmentioning

confidence: 57%

Kinetics and determinants of the changes of CC16, a lung secretory protein in a rat model of toxic lung injury

Hantson

Bernard

Hermans

2008

Clinical Toxicology

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Bronchiolar insult due to IPO or ANTU resulted in an initial transient increase of serum CC16, parallel to that of albumin in BALF, and a subsequent reduction in both BALF and serum. A slight reduction of CC16 in BALF was already apparent one hour following treatment with PQ. In the serum, CC16 increased to 400% of basal value. With PQ and Na(2)CrO(4), the elevation of CC16 was mainly determined by the degree of renal impairment.

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Pneumoproteins as markers of paraquat lung injury: A clinical case

Cited by 10 publications

References 26 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

Role of biomarkers of nephrotoxic acute kidney injury in deliberate poisoning and envenomation in less developed countries

Kinetics and determinants of the changes of CC16, a lung secretory protein in a rat model of toxic lung injury

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