scholarly journals Estimated Glomerular Filtration Rate Correlates Poorly with Four-Hour Creatinine Clearance in Critically Ill Patients with Acute Kidney Injury

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Christopher J. Kirwan ◽  
Barbara J. Philips ◽  
Iain A. M. MacPhee
Keyword(s):  
Acute Kidney Injury ◽  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Critically Ill ◽  
Cystatin C ◽  
Critically Ill Patients ◽  
Filtration Rate ◽  
Kidney Injury ◽  
Serum Cystatin C ◽  
Serum Cystatin

Introduction.RIFLE and AKIN provide a standardised classification of acute kidney injury (AKI), but their categorical rather than continuous nature restricts their use to a research tool. A more accurate real-time description of renal function in AKI is needed, and some published data suggest that equations based on serum creatinine that estimate glomerular filtration rate (eGFR) can provide this. In addition, incorporating serum cystatin C concentration into estimates of GFR may improve their accuracy, but no eGFR equations are validated in critically ill patients with AKI.Aim.This study tests whether creatinine or cystatin-C-based eGFR equations, used in patients with CKD, offer an accurate representation of 4-hour creatinine clearance (4CrCl) in critically ill patients with AKI.Methods.Fifty-one critically ill patients with AKI were recruited. Thirty-seven met inclusion criteria, and the performance of eGFR equations was compared to 4CrCl.Results.eGFR equations were better than creatinine alone at predicting 4CrCl. Adding cystatin C to estimates did not improve the bias or add accuracy. The MDRD 7 eGFR had the best combination of correlation, bias, percentage error and accuracy. None were near acceptable standards quoted in patients with chronic kidney disease (CKD).Conclusions.eGFR equations are not sufficiently accurate for use in critically ill patients with AKI. Incorporating serum cystatin C does not improve estimates. eGFR should not be used to describe renal function in patients with AKI. Standards of accuracy for validating eGFR need to be set.

scholarly journals Acute Kidney Injuries in Children with Severe Malaria

2020 ◽  
Vol 20 (4) ◽  
pp. e312-317
Author(s):  
Folake M. Afolayan ◽  
Olanrewaju T. Adedoyin ◽  
Mohammed B. Abdulkadir ◽  
Olayinka R. Ibrahim ◽  
Sikiru A. Biliaminu ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Severe Malaria ◽  
Diagnostic Criteria ◽  
Cystatin C ◽  
Filtration Rate ◽  
Kidney Injury ◽  
Serum Cystatin C ◽  
Serum Cystatin

Objectives: Serum creatinine levels are often used to diagnose acute kidney injury (AKI), but may not necessarily accurately reflect changes in glomerular filtration rate (GFR). This study aimed to compare the prevalence of AKI in children with severe malaria using diagnostic criteria based on creatinine values in contrast to cystatin C. Methods: This prospective cross-sectional study was performed between June 2016 and May 2017 at the University of Ilorin Teaching Hospital, Ilorin, Nigeria. A total of 170 children aged 0.5–14 years old with severe malaria were included. Serum cystatin C levels were determined using a particle-enhanced immunoturbidmetric assay method, while creatinine levels were measured using the Jaffe reaction. Renal function assessed using cystatin C-derived estimated GFR (eGFR) was compared to that measured using three sets of criteria based on creatinine values including the Kidney Disease: Improved Global Outcomes (KDIGO) and World Health Organization (WHO) criteria as well as an absolute creatinine cut-off value of >1.5 mg/dL. Results: Mean serum cystatin C and creatinine levels were 1.77 ± 1.37 mg/L and 1.23 ± 1.80 mg/dL, respectively (P = 0.002). According to the KDIGO, WHO and absolute creatinine criteria, the frequency of AKI was 32.4%, 7.6% and 16.5%, respectively. In contrast, the incidence of AKI based on cystatin C-derived eGFR was 51.8%. Overall, the rate of detection of AKI was significantly higher using cystatin C compared to the KDIGO, WHO and absolute creatinine criteria (P = 0.003, <0.001 and <0.001, respectively). Conclusion: Diagnostic criteria for AKI based on creatinine values may not indicate the actual burden of disease in children with severe malaria. Keywords: Biomarkers; Acute Kidney Injury; Renal Failure; Glomerular Filtration Rate; Cystatin C; Creatinine; Malaria; Nigeria.

scholarly journals Plasma Cystatin C and Estimates of Glomerular Filtration Rate Using Cystatin C Independently Diagnose Acute Kidney Injury in Critically Ill Patients with Sepsis

2017 ◽  
Vol 16 (1) ◽  
Author(s):  
Azrina Md Ralib ◽  
Iqbalmunawwir Ab Rashid ◽  
Nur Aisyah Ishak ◽  
Suhaila Nanyan ◽  
Nur Fariza Ramly ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Critically Ill ◽  
Cystatin C ◽  
Clinical Setting ◽  
Critically Ill Patients ◽  
Filtration Rate ◽  
Kidney Injury ◽  
The Ideal

Introduction: Plasma Cystatin C (CysC) is as an early functional marker for acute kidney injury. Estimates of glomerular filtration rate using CysC (eGFRCysC) has been used in some clinical setting. We evaluated the utility of CysC and eGFRCysC in diagnosing acute kidney injury (AKI) and predicting death in critically ill patients with sepsis.  Materials and method: This is an interim analysis of single centre, prospective observational study of critically ill patients. Inclusion criteria were patients older than 18 years old with sepsis and procalcitonin > 0.5ng/ml. Plasma creatinine and CysC were measured on admission, and eGFRCysC. AKI was defined based on the plasma creatinine criteria of the KDIGO guideline.  Results: Thirty one patients were recruited so far, of which 13 (41.9%) had AKI and six died. CysC were higher in patients with AKI versus No AKI (p<0.001), and corresponding eGFRCysC were lower (p=0.006). CysC and eGFRCysC on ICU admission diagnosed AKI with an AUC of 0.88(0.72 to 1.00), and 0.79 (0.62 to 0.96), respectively. Both did not predict death (AUC 0.59 (0.31 to 0.87) and 0.59 (0.31 to 0.86), respectively). After adjusting for age and SOFA score, both CysC and eGFRCysC independently diagnosed AKI (OR 13 (1.5 to 115) and 1.03 (1.01 to 1.06), respectively). The ideal cut-off point for diagnosing AKI for CysC is 1.5 mg/dl (84% sensitivity and 89% specificity) and for eGFRCysC as 77 ml/min (72% sensitivity and 84% specificity).  Conclusion: Plasma CysC and its estimated GFR independently diagnosed AKI in critically ill patients with sepsis. We suggest the ideal cut-off points of 1.5 mg/dl and 77 ml/min which can be used in the clinical setting in this cohort of patients.

scholarly journals P06 Improving renal function monitoring during chemotherapy- a role for cystatin C?

2020 ◽  
Vol 105 (9) ◽  
pp. e8.2-e9
Author(s):  
Rachel Boys
Keyword(s):  
Acute Kidney Injury ◽  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Cystatin C ◽  
Filtration Rate ◽  
Kidney Injury ◽  
Estimating Equations ◽  
Transformation Factor ◽  
Over Time

AimRenal toxicity causes major morbidity following chemotherapy- abnormal iGFRs may be detected in up to 73.7% of patients.1 Creatinine is universally used as a biomarker to track fluctuating function and to calculate surrogate glomerular filtration rate (GFR) in the form of estimating equations.2 There is concern regarding the suitability of creatinine as a biomarker in this population, and it is proposed that cystatin C as a biomarker alone and also included in estimating equations may offer improved clinical suitability and accuracy.3MethodsIn this prospective, longitudinal study over a period of 18 months, 132 combined isotope GFR (iGFR), creatinine and cystatin C measurements were taken from 48 paediatric oncology patients at a Northern Children’s Hospital. Correlation and agreement analysis was performed for both individual biomarkers and estimating equations. Sensitivity data, along with ROC curve analysis was performed for all biomarkers and estimating equations. Data from three identified patients was isolated to examine individual patient variation over time.ResultsCreatinine identified only 1/32 patients with an abnormal iGFR (<90 ml/min/1.73 m2) compared to cystatin C which identified 12/32. Creatinine values and both estimating equations failed to change significantly over a period of declining iGFR though cystatin C did show a significant inverse increase (p<0.05). Bland Altman analysis for both the creatinine and combined equation showed poor agreement (mean difference -64 ml/min/1.3 m2 and -20 ml/min/1.73 m2 respectively). All biomarkers and equations showed poor sensitivity to detect an abnormal iGFR either below 70 ml/min/1.73 m2 or 90 ml/min/1.73 m2. A transformation factor applied to the equations significantly improved the sensitivity and clinical applicability of all equations. The data from three individual patients failed to reveal any significant intra-patient relationships.ConclusionData from this study cannot support the use of creatinine or cystatin C as a single biomarker to monitor renal function in children undergoing chemotherapy. Newer cystatin C and creatinine combined equations, whilst offering statistical superiority, do not offer the clinical superiority to replace iGFR or provide a tool for accurate dose calculations. A transformation factor can be applied to the results gained from the estimating equations to significantly improve the detection of abnormal iGFR, though work in other patient cohorts is needed to support this. Previous work also supported the use of a transformation factor, though application of their transformation factor to this current cohort failed to replicate the 100% sensitivity findings previously demonstrated4. Three patients were identified from the cohort and their paired iGFR and estimated GFR were monitored prospectively, over a period of approximately a year. Significant variation was observed between iGFR and eGFR at each time point for all three patients and therefore personalisation of GFR estimation from baseline iGFR and demographic data could not be proposed. This requires exploration in a larger cohort with the possible inclusion of additional baseline variables.ReferencesCRUK Survival trends over time in Children’s Cancers. 1.2015. https://www.cancerresearchuk.org/health-professional/cancer-statistics/childrens-cancers/survival#heading-Two Accessed 28th March 2019.NICE ( 2013) CG169 Acute kidney injury: Prevention, detection and management of acute kidney injury up to the point of renal replacement therapy.Barnfield, MC, Burniston, MT, Reid, U, et al. Cystatin C in assessment of glomerular filtration rate in children and young adults suffering from cancer. Nuclear Medicine Communications 2013;34:609–614.Dodgshun, AJ, Quinlan, C, Sullivan, MJ. Cystatin C based equation accurately estimates glomerular filtration rate in children with solid and central nervous system tumours: enough evidence to change practice? Pediatric Blood and Cancer 2016;63:1535–1538.

Utility of Serum Cystatin C as a Clinical Measure of Renal Function in Dogs

2008 ◽  
Vol 44 (3) ◽  
pp. 131-138 ◽  
Author(s):  
Astrid Wehner ◽  
Katrin Hartmann ◽  
Johannes Hirschberger
Keyword(s):  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Cystatin C ◽  
Filtration Rate ◽  
Plasma Clearance ◽  
Reference Range ◽  
Serum Cystatin C ◽  
Serum Cystatin ◽  
Test Sensitivity ◽  
Concentration Test

A human kit for cystatin C determination was evaluated for use with canine sera. A reference range was also established. The association between cystatin C and glomerular filtration rate (GFR) was evaluated in 60 dogs with various diseases, by using exogenous creatinine plasma clearance (ECPC) as a measure of GFR. The correlation between cystatin C and ECPC (correlation coefficient [r] = −0.630; P&lt;0.001) was stronger than the correlation between serum creatinine and ECPC (r = −0.572; P&lt;0.001). Nonrenal diseases (e.g., neoplasia, infection) did not influence serum cystatin C concentration. Test sensitivity was significantly better (P&lt;0.001) for cystatin C (76%) than for creatinine (65%). Specificities for the two tests were 87% and 91%, respectively.

scholarly journals Serum cystatin C is a poor biomarker for diagnosing acute kidney injury in critically-ill children

2013 ◽  
Vol 17 (2) ◽  
pp. 92-98 ◽  
Author(s):  
Hanan M. Hamed ◽  
Seham Awad El-Sherbini ◽  
Nahla A. Barakat ◽  
Tarek M. Farid ◽  
Enas Abdel Rasheed
Keyword(s):  
Acute Kidney Injury ◽  
Critically Ill ◽  
Cystatin C ◽  
Kidney Injury ◽  
Critically Ill Children ◽  
Serum Cystatin C ◽  
Serum Cystatin

scholarly journals PAC-mediated AKI protection is critically mediated but does not exclusively depend on cell-derived microvesicles

2019 ◽  
Author(s):  
Hassan Dihazi ◽  
Katrin Schwarze ◽  
Susann Patschan ◽  
Gerhard Anton Müller ◽  
Oliver Ritter ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Renal Function ◽  
Bone Morphogenetic Protein ◽  
Extracellular Vesicles ◽  
Cystatin C ◽  
Kidney Injury ◽  
Serum Cystatin C ◽  
Serum Cystatin ◽  
Morphogenetic Protein ◽  
Angiopoietin 1

Abstract Background: Acute Kidney Injury (AKI) significantly worsens the prognosis of hospitalized patients. In recent years, cell-based strategies have been established as reliable option for improving AKI outcomes in experimental AKI. Own studies focused on so-called Proangiogenic Cells (PACs). Mechanisms that contribute to PAC-mediated AKI protection include production / secretion of extracellular vesicles (MV - microvesicles). In addition, the cells most likely act by paracrinic processes (secretome). The current study evaluated whether AKI may be preventable by the administration of either PAC-derived MV and / or the secretome alone.Methods: AKI was induced in male C57/Bl6N mice (8-12 weeks) by bilateral renal ischemia (IRI - 40 minutes). Syngeneic murine PACs were stimulated with either melatonine, Angiopoietin-1 or -2, or with Bone Morphogenetic Protein-5 (BMP-5) for one hour, respectively. PAC-derived MV and the vesicle-depleted supernatant were subsequently collected and i.v. injected post-ischemia. Mice were analyzed 48 hours later.Results: IRI induced significant kidney excretory dysfunction as reflected by higher serum cystatin C levels. The only measure that improved AKI was the injection of MV, collected from native PACs. The following conditions worsened post-ischemic renal function even further: MV+Ang-1, MV+BMP-5, MV+melatonin, and MV+secretome+Ang-1.Conclusion: Together, our data show that PAC-mediated AKI protection substantially depends on the availability of cell-derived MV. However, since previous data showed improved AKI-protection by PACs after cell preconditioning with certain mediators (Ang-1 and -2, melatonine, BMP-5), other than exclusively vesicle-dependent mechanisms must be involved in PAC-mediated AKI protection.

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