Albumin Random Urine Quantitative
| Abbrev Code: | UMALBR | ||
| Order Code: | LAB3838 | Order Name: | Albumin Random Urine Quantitative |
| Methodology: | Roche: Immunoturbidimetric Tina Quant
Vista: Nephelometric |
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| CPT Codes: | 82043 x1, 82043 x1, 82570 x1, 82570 x1 | ||
| Test Includes: | Creatinine Urine mg/dL; Albumin Urine mg/L; Albumin Urine mg/g Cr | ||
| Turnaround Time: | Performed and reported 24 hours/day. | ||
| Special Instructions: | NKDEP/IFCC consensus guidelines (2009) state: Use of the term "Urine Albumin" is recommended; "Microalbumin" is discouraged | ||
| Associated Links: | |||
Collection Instructions
| Specimen: | Urine, random collection |
| Optimal Volume: | Submit entire collection, analysis requires 0.6 mL |
| Container: | Plastic leakproof container, sterile |
| Collection Instructions: | Acceptable urine samples: Second morning urine, first morning urine with simultaneous albumin and creatinine. Frozen urine is not recommended. |
Processing and Shipping
| Specimen Processing: | Mix collection well before aliquot is taken. Aliquot 1 mL, 0.6 mL minimum. Store in refrigerator. |
| Shipping Instructions: | Ship at refrigerated temperature. |
| Stability: | Roche: 7 days at room temperature; 1 month refrigerated; 6 months frozen.
Vista: To be determined by M Health Fairview Labs. |
| Test Performed at or Referral Lab | Chemistry (CSC Maple Grove, Roche-Grand Itasca, Roche-Lakes, Roche-Northland, Roche-Range, Roche-UMMC East) |
Interpretive
| Reference Range: | Urine Chemistry Reference Ranges |
| Use: | Early predictor of clinical diabetic nephropathy. Kidney changes include a rise in urinary albumin secretion detectable only by sensitive assays. At this stage, Albustix is negative and renal function is normal by standard assays.
Albumin is a non-glycosylated protein with a molecular weight of 66000 daltons. It is synthesized in liver parenchymal cells at a rate of 14 g/day. Quantitatively, albumin is normally the most important protein component (> 50 %) in plasma, CSF and urine. A small, but abnormal albumin excretion in urine is known as microalbuminuria. Causes of microalbuminuria can be glomerular (e.g. due to diabetic microangiopathy, hypertension, minor glomerular lesion), tubular (inhibition of reabsorption) or postrenal. Microalbuminuria is defined as an albumin:creatinine ratio of 17 to 299 for males and 25 to 299 for females. A ratio of albumin:creatinine of 300 or higher is indicative of overt proteinuria. Due to biologic variability, positive results should be confirmed by a second, first-morning random or 24-hour timed urine specimen. If there is discrepancy, a third specimen is recommended. When 2 out of 3 results are in the microalbuminuria range, this is evidence for incipient nephropathy and warrants increased efforts at glucose control, blood pressure control, and institution of therapy with an angiotensin-converting-enzyme (ACE) inhibitor (if the patient can tolerate it). Albumin is also a marker protein for various forms of proteinuria. In selective glomerular proteinuria, 100-3000 mg albumin/g creatinine are excreted in the urine. Non-selective glomerular proteinuria is characterized by elevated excretion of high-molecular weight proteins (IgG more than 10 % of the albumin value). Prerenal proteinuria is recognized by a discrepancy between albumin and total protein (albumin accounting for less than 30 %, with concurrent elevation of total protein). Simultaneous elevation of albumin and microproteins is found in glomerulotubular proteinuria occurring due to overloading of tubular reabsorption in glomerulopathy (e.g. nephrotic syndrome), combined glomerular tubulointerstitial nephropathy or in renal failure following diabetic nephropathy or other causes (overflow proteinuria). Albumin has two main functions in plasma: maintaining the oncotic pressure (80 % due to albumin in plasma) and transport. It is the most important transport protein for substances having low water solubility (such as free fatty acids, bilirubin, metal ions, hormones and pharmaceuticals). Depressed albumin levels are caused by hyperhydration, hepatocellular synthesis insufficiency, secretion disorders in the intravascular space, abnormal distribution between the intravascular and extravascular space, catabolism and loss of albumin, acute phase reactions and congenital analbuminemia. |
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