The use of reliable biomarkers is becoming increasingly important for the improved management of patients with acute and chronic kidney diseases.
Acute kidney injury (AKI) is sudden damage to the kidneys that causes them to stop working properly. If the injury is not diagnosed in time, the kidneys become overwhelmed and start to shut down. This then causes abnormal levels of salts and chemicals to build up in the body, eventually stopping the other organs in the body from working properly.
Therefore it is essential that AKI is detected early and treated promptly.
Normally the diagnosis of AKI is done by examining for substances that are normally eliminated by the kidney, such as urea and creatinine
The National Kidney Foundation (NKF) and the National Kidney Disease Education Program (NKEDP) recommend that people who are at high risk be screened for kidney disease to detect it in its earliest stages. Risk factors can include diabetes, heart disease or people with a family history of having kidney disease They recommend that people between the age of 12 and 70 that suffer from diabetes be screened for kidney disease at least once a year.
There are two main tests to screen for kidney disease.
1. Urine Protein
When functioning normally the kidney is able to actively dispose of various proteins such as Albumin and Creatinine.
This test may be done on a 24-hour urine sample, both urine albumin and creatinine can be measured in a random urine sample and the albumin/creatinine ratio (ACR) can be calculated.
2. Estimated glomerular filtration rate (eGFR)
The glomerular filtration rate is a test that estimates how much blood passes through the glomeruli (tiny filters in the kidney that filter waste from the blood) every minute. The filtration rate decreases as waste products begin to accumulate in the blood when there is evidence of kidney failure.
A blood creatinine test or a Cystatin C test is usually performed in order to calculate the eGFR.
Research is being done to develop potential novel biomarkers that are able to detect kidney damage much earlier. One of these biomarkers is Neutrophil gelatinase-associated lipocalin (NGAL)
In human studies, the expression of the NGAL messenger ribonucleic acid (mRNA) and protein has been shown to be significantly increased in the kidney tubules when kidney damage has occurred. Increased levels are seen in as little as 2 hours after injury and are proportional to the severity of the injury.
Are you developing an assay to detect kidney disease?
BBI can help.
We offer a diverse range of markers that are ideal for numerous applications including life science research, immunodiagnostic platform assays, ELISA’s, lateral flow, and quality assurance control manufacture.
See the table below for details on our flagship products of renal markers.
|NGAL||NGAL (neutrophil gelatinase associated lipocalin) is a marker for acute kidney injury. NGAL levels rise rapidly after renal injury. This marker responds earlier than other renal status markers like serum creatinin.|
|Human Albumin||Human Albumin is a protein that binds many blood components, from metal ions, fatty acids and bilirubin to drugs and hormones, to enable their transport. It has a mol wt of 66kDa and pI 4.7.|
|Alpha-1 Microglobulin||Alpha 1 microglobulin (A1M) is a highly glycosylated protein of 27KDa with a heterogeneous charge which forms complexes with IgA and albumin. Raised levels of A1M in urine are a good indicator of renal tubular dysfunction.|
|Retinol Binding Protein||Retinol Binding Protein (RBP) is a protein of 21 kDa and pI of 4.7. In conjunction with Prealbumin it is useful for assessing nutritional status. RBP is readily filtered by the glomerulus and absorbed by the proximal renal tubules; as such it is valuable for the assessment of renal tubular function.|
|Cystatin C||Cystatin C is a small cysteine proteinase inhibitor of molecular weight 13 kDa present in all human body fluids. It is a marker for allograph function in adult transplant patients. Cystatin C regulates extracellular cysteine protease activity, which results from microbial invasion or release of lysosomal proteinases from dying or diseased cells. It is freely filtered by the glomerular basement membrane (GBM) and serum concentration has been shown to correlate well with glomerular filtration rate (GFR).|