Biomedical Laboratory Science

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Showing posts with label Urea. Show all posts
Showing posts with label Urea. Show all posts

Saturday, October 29, 2016

Evaluation of Diabetic Marker HbA1c and Anemia in the Context of Kidney Disease

Each year, more than 100,000 people in the United States are diagnosed with kidney failure, the final stage of kidney disease.1 The most common cause is diabetes, accounting for nearly 44 percent of new cases. Often, a consequence of kidney disease is anemia. This occurs when kidneys fail to generate enough erythropoietin hormone to trigger adequate red blood cell production. For decades, clinicians have successfully used the hemoglobin A1c (HbA1c or A1C) assay to monitor long-term blood glucose control for patients with chronic diabetes. More recently, researchers have studied the HbA1c assay’s use as a potential diagnostic marker for diabetes complications such as kidney disease.

The HbA1c test measures average plasma glucose—hemoglobin in a red blood cell that was combined with glucose over the previous eight to 12 weeks. The higher the HbA1c value, the greater the risk that the diabetes patient will develop kidney disease, and perhaps, anemia, a common consequence of renal disease. However, a chemically modified derivative of hemoglobin called carbamylated hemoglobin (CHb) can affect the accuracy of the HbA1c test results. Studies have shown that the formation of CHb due to abnormal urea concentration is linked to both the severity and the duration of renal failure. Research findings have inspired conflicting viewpoints on the efficacy of HbA1c test results in the presence of CHb and on the level of CHb it takes to affect results. This article explores the links between diabetes and renal failure. It discusses what research has discovered about the effect of CHb on HbA1c testing. Finally, it shows how testing technology has improved to ensure HbA1c testing accuracy.



Sunday, July 24, 2016

Current Approaches for the Detection of Acute Kidney Injury

Acute kidney injury (AKI) is a recognized complication in hospitalized patients. A report in 2009 from National Confidential Enquiry into Patient Outcome and Death (NCEPOD) suggested that AKI was frequently undetected in hospital patients thus contributing to patient morbidity and mortality. Clinical guidelines for recognition and treatment for acute kidney injury were published by NICE (the National Institute for Health and Care Excellence) in 2013 and reported an associated mortality with AKI of more than 25–30%. This guideline also recognized the prevalence of AKI in the primary care population in patients with or without acute illness. NICE also recognized the impact of AKI on healthcare resources, with costs (excluding those in the community) of £434–620 million per year, more than that associated with breast, lung and skin cancer combined

AKI is characterized by an acute loss of the kidney’s excretory capacity leading to accumulation of waste products such as urea and creatinine, and decreased urine output. It is associated with rapid decline in glomerular filtration rate and increases in potassium, phosphate and hydrogen ions. It has varied causes and may be secondary to a non-renal event, thus may be common in hospitalized patients and critically ill patients. It may go undetected in primary care as it can occur without any symptoms. There are associations between co-morbidities, current medications, acute illness and AKI resulting in the high morbidity associated with the condition and the impact on healthcare resources.



Source: cli-online
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