Cr(Creatinine) Assay Kit(Colorimetric)

Name: Cr(Creatinine) Assay Kit(Colorimetric)
SKU: DEIABL-M4
Rating: 5 (1 reviews)

Regulatory status: For research use only, not for use in diagnostic procedures.

COA

SDS

Datasheet

Summary

Sample

Serum, plasma and urine

Species Reactivity

Universal

Detection Method

Colorimetric Assay

Intended Use

For quantitative detection of creatinine in serum, plasma and urine.

Contents of Kit

1. ELISA Microplate, 8×12
2. Lyophilized Standard(1000nmol/vial), 2vial, 2-8°C/-20°C
3. Enzyme Solution A, 25ml, 2-8°C (Avoid Direct Light)
4. Enzyme Solution B, 8ml, 2-8°C (Avoid Direct Light)
5. Plate Sealer, 2pieces
6. Product Description

Storage

The kit is stored at 2-8°C (Avoid Direct Light), and not be frozen or thawed. The product is valid for 12 months. After opening, store at 2-8°C, it can be stable for 30 days, avoid contamination.

Precision

Intra-Assay: CV≤6% ,Inter-Assay: CV≤4%

Detection Range

25-800μmol/L

Sensitivity

10μmol/L

General Description

Creatinine is a metabolite of phosphocreatine (p-creatine), a molecule used as a store for highenergy phosphate that can be utilized by tissues for the production of ATP. Creatine either comes fromthediet orissynthesized from the amino acids arginine, glycine, and methionine. This occurs in the kidneys andliver, although other organ systems may be involved and species-specific differences may exist. Creatine andp- creatine are converted non-enzymatically to the metabolite creatinine, which diffuses into the bloodandisexcreted by the kidneys. In vivo, this conversion appears to be irreversible and in vitro it is favoredbyhighertemperatures and lower pH. Creatinine forms spontaneously from pcreatine, and under normal conditions, its formation occurs at a relatively constant rate. Intra-individual variation of creatinine levels is <15% fromday to day, making it a useful marker for normalizing levels of other molecules found in urine. Alteredcreatinine levels may be associated with conditions that result in decreased renal blood flow, such as diabetes and cardiovascular disease.

Standard Curve

Results of a typical standard operation of a creatinine are listed below. This standard curve was generatedat our lab for demonstration purpose only. Users shall obtain standard curve as per experiment by themselves. (OD546)

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Hypertension/prehypertension and its determinants in pediatric IgA nephropathy

MEDICINE

Authors: Fu, Qing-Ying; Ma, Lu; Li, Chang-Chun; He, Zhi-Jun; Wang, Wei-Hua; Luo, Kai-Fa; Liu, Yang; Zhang, Zhi-Hao; Yang, Zai-Bo; Tang, Hai-Lian; Yan, Jun-Hui

Abstract

Immunoglobulin A nephropathy (IgAN) is a major cause of secondary hypertension (HT) of renal origin - a significant prognostic factor of IgAN. In children, similar to HT, prehypertension (pre-HT) is becoming a significant health issue. However, the role of secondary HT and pre-HT (HT/pre-HT) in the progression of pediatric IgAN remains unclear. We investigated the effects of HT/pre-HT on prognosis and its determinants as well as their correlation with clinicopathological parameters to identify more effective therapeutic targets. This single-center retrospective study compared clinicopathological features and treatment outcomes between patients with and without HT/pre-HT in 108 children with IgAN. Independent risk factors for HT/pre-HT were evaluated; segmental glomerulosclerosis was a significant variable, whose relationship with clinicopathological parameters was analyzed. Clinical outcomes of patients with and without HT/pre-HT differed considerably (P = .006) on >= 6 months follow-up. Patients with HT/pre-HT reached complete remission less frequently than those without HT/pre-HT (P = .014). Age, serum creatinine, prothrombin time, and segmental glomerulosclerosis or adhesion were independent risk factors for HT/pre-HT in pediatric IgAN (P = .012,P = .017,P = .002, andP = .016, respectively). Segmental glomerulosclerosis or adhesion was most closely associated with glomerular crescents (r = 0.456,P < .01), followed by Lees grades (r = 0.454,P < .01), renal arteriolar wall thickening (r = 0.337,P < .01), and endocapillary hypercellularity (r = 0.306,P = .001). The intensity of IgA deposits, an important marker of pathogenetic activity in IgAN, was significantly associated with the intensity and location of fibrinogen deposits (intensity:r = 0.291,P = .002; location:r = 0.275,P = .004). HT/pre-HT in pediatric IgAN patients is an important modifiable factor. A relationship is observed between HT/pre-HT and its determinants, especially segmental glomerulosclerosis. Potential therapeutic approaches for IgAN with HT/pre-HT might be directed toward the management of coagulation status, active lesions, and hemodynamics for slowing disease progression.

The CELIOtomy Risk Score: An effort to minimize futile surgery with analysis of early postoperative mortality after emergency laparotomy

SURGERY

Authors: Kao, Angela M.; Maloney, Sean R.; Prasad, Tanushree; Reinke, Caroline E.; May, Addison K.; Heniford, B. Todd; Ross, Samuel W.

Abstract

Background: Emergency surgical services often encounter patients with generalized peritonitis. Difficult perioperative decisions impact morbidity, mortality, cost, and utilization of hospital resources. The ability to preoperatively predict patient nonsurvival despite surgical intervention using clinical physiologic indicators was the aim of this study and would be helpful in counseling patients/families. Methods: A retrospective cohort from an institutional database was queried for nontrauma patients with peritonitis undergoing emergency laparotomy from 2012 to 2016. Time to mortality after surgery was compared: early (<= 72 hours) versus late (>72 hours) and no death. Results: After 534 emergency laparotomies, there were 74 (13.9%) mortalities. Of these, death occurred early (<= 72 hours) after surgery in 28 (37.8%) patients and late (>72 hours) in 46 (62.2%). Early death patients had a significantly more deranged physiology, as evidenced by higher Acute Physiology and Chronic Health Evaluation II scores (mean 28.1 +/- 8.4 vs 22.9 +/- 8.7, P = .01), worse acute kidney injury (preoperative creatinine 3.7 +/- 3.2 vs 1.9 +/- 1.4, P = .001), and greater level of acidosis (pH 7.19 +/- 0.12 vs 7.27 +/- 0.13, P = .017). Additionally, preoperative lactate was significantly increased in patients with early mortality (6.8 +/- 4.1 vs 5.1 +/- 4.0, P = .045). Using logarithmic regression, a nomogram was constructed using age, Glasgow Coma Scale, lactate, creatinine, and pH. This nomogram had an area under the curve of 0.908 on receiver operator curve analysis. A score of 13 equates to greater than 50% risk of early mortality after surgery. Conclusion: Early mortality (<72 hours after emergency laparotomy) is associated with decreased pH, elevated creatinine, and elevated lactate. These factors combined into the nomogram constructed may assist surgical teams with patient and family discussions to prevent futile surgical interventions. (c) 2020 Elsevier Inc. All rights reserved.