Microalbuminuria
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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Overview
Microalbuminuria occurs when the kidney leaks small amounts of albumin into the urine, in other words, when there is an abnormally high permeability[disambiguation needed] for albumin in the renal glomerulus.
Diagnosis
The level of albumin protein produced by microalbuminuria cannot be detected by urine dipstick methods. A microalbumin urine test determines the presence of the albumin in urine. In a properly functioning body, albumin is not normally present in urine because it is retained in the bloodstream by the kidneys.
Microalbuminuria is diagnosed either from a 24-hour urine collection (between 30-300 mg/24 hours) or, more commonly, from elevated concentrations in a spot sample (30 to 300 mg/L). Both must be measured on at least two of three measurements over a two- to three-month period.[1]. An albumin level above these values is called "macroalbuminuria", or sometimes just albuminuria.
To compensate for variations in urine concentration in spot-check samples, it is more typical in the United Kingdom to compare the amount of albumin in the sample against its concentration of creatinine. This is termed the albumin/creatinine ratio (ACR)[2] and microalbuminuria is defined as ACR ≥3.5 mg/mmol (female) or ≥2.5 mg/mmol(male),[3] or, with both substances measured by mass, as an ACR between 30 and 300 µg albumin/mg creatinine[4].
Significance
- an indicator of subclinical cardiovascular disease
- marker of vascular endothelial dysfunction
- an important prognostic marker for kidney disease
- increasing microalbuminuria during the first 48 hours after admission to an intensive care unit predicts elevated risk for acute respiratory failure, multiple organ failure, and overall mortality
- a risk factor for venous thromboembolism [5]
See also
References
- Abid O, Sun Q, Sugimoto K, Mercan D, Vincent JL (2001). "Predictive value of microalbuminuria in medical ICU patients: results of a pilot study". Chest. 120 (6): 1984–8. doi:10.1378/chest.120.6.1984. PMID 11742932.
- Andersen S, Blouch K, Bialek J, Deckert M, Parving HH, Myers BD (2000). "Glomerular permselectivity in early stages of overt diabetic nephropathy". Kidney Int. 58 (5): 2129–37. doi:10.1111/j.1523-1755.2000.00386.x. PMID 11044234.
- Heart Outcomes Prevention Evaluation Study Investigators (2000). "Effects of ramipril on cardiovascular and microvascular outcomes in people with diabetes mellitus: results of the HOPE study and MICRO-HOPE substudy". Lancet. 355 (9200): 253–9. doi:10.1016/S0140-6736(99)12323-7. PMID 10675071.
- Lemley KV, Abdullah I, Myers BD; et al. (2000). "Evolution of incipient nephropathy in type 2 diabetes mellitus". Kidney Int. 58 (3): 1228–37. doi:10.1046/j.1523-1755.2000.00223.x. PMID 10972685.
- Lièvre M, Marre M, Chatellier G; et al. (2000). "The non-insulin-dependent diabetes, hypertension, microalbuminuria or proteinuria, cardiovascular events, and ramipril (DIABHYCAR) study: design, organization, and patient recruitment. DIABHYCAR Study Group". Controlled clinical trials. 21 (4): 383–96. doi:10.1016/S0197-2456(00)00060-X. PMID 10913814.
- Parving HH, Lehnert H, Bröchner-Mortensen J, Gomis R, Andersen S, Arner P (2001). "The effect of irbesartan on the development of diabetic nephropathy in patients with type 2 diabetes". N. Engl. J. Med. 345 (12): 870–8. doi:10.1056/NEJMoa011489. PMID 11565519.
Footnotes
- ↑ "Person—microalbumin level (measured), total micrograms per minute N[NNN].N". Retrieved 2007-07-05.
- ↑ PMID 10333950
- ↑ "Proteinuria". UK Renal Association. December 15, 2005.
- ↑ clinlabnavigator.com > Test Interpretations Last Updated on Saturday, 19 June 2010
- ↑ http://www.ncbi.nlm.nih.gov/pubmed/19417196