Microalbumin 

Microalbumin 

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Microalbuminuria is defined as excretion of 30–300 mg of albumin per 24 hours (or 20–200 mcg/min or 30–300 mcg/mg creatinine) on 2 of 3 urine collections. [1]

The detection of low levels of albumin excretion (microalbuminuria) has been linked to the identification of incipient diabetic kidney disease. This phase calls for aggressive management to prevent or retard overt diabetic nephropathy.

The reference ranges for microalbumin are detailed in the table below. [2, 3]

Table 1. American Diabetic Association Classification of Microalbuminuria (Open Table in a new window)

Spot Collection

Timed Collection

24-hr Collection

Category

Less than 30 mcg/mg creatinine

Less than 20 mcg/min

Less than 30 mg

Normal

30-300 mcg/mg creatinine

20-200 mcg/min

30-300 mg

Microalbuminuria

More than 300 mcg/mg creatinine

More than 200 mcg/min

More than 300 mg

Clinical albuminuria

 

The etiologies of microalbuminuria are as follows: [4]

Early proteinuria of any cause

Acute hyperglycemia

Urinary tract infection

Marked hypertension

Congestive heart failure

Menses (false positive)

Causes of overt proteinuria are as follows:

Amyloidosis

Bladder tumor

Congestive heart failure

Glomerulonephritis

Goodpasture syndrome

Heavy metal poisoning

Nephrotoxic drugs

Polycystic kidney disease

Preeclampsia

Systemic lupus erythematosus

Urinary tract infection

Specifics for collection and panels are as follows:

Specimen type: Urine

Container: Plastic urine tube

Collection method: 24-hour collection or random urine specimen

Specimen volume: 5 mL

Other instructions are as follows:

No preservatives in 24-hour collection container

Confirm positive findings with second specimen

Microalbuminuria is defined as excretion of 30–300 mg of albumin per 24 hours (or 20–200 mcg/min or 30–300 mcg/mg creatinine) on 2 of 3 urine collections. [1]

The detection of low levels of albumin excretion (microalbuminuria) has been linked to the identification of incipient diabetic kidney disease. This phase calls for aggressive management, to prevent or retard overt diabetic nephropathy.

Microalbuminuria is a predictor of outcome in patients with renal disease. Additionally, it is a predictor of morbidity and mortality in patients who do not have evidence of significant renal disease. In patients with hypertension, microalbuminuria has been correlated to left ventricular hypertrophy. Both in hypertensive and normotensive patients, microalbuminuria predicts an increased risk of cardiovascular morbidity and mortality.

Although 24-hour excretion has traditionally been preferred, the albumin/creatinine ratio has been shown to be a similarly valid screening tool for diabetic nephropathy. [5, 6]

See the list below:

Annual screening for microalbuminuria is indicated for all individuals with diabetes mellitus.

Screening for microalbuminuria is used in the diagnosis of renal dysfunction. [2]

In diabetic and hypertensive patients, microalbuminuria is a predictor of future development of clinical renal disease. It is also a predictor of cardiovascular morbidity and mortality.

Doing a 24-hour urine collection for proteinuria and creatinine clearance is unnecessary because a spot urine sample to measure urine albumin to creatinine ratio is quite sufficient for diagnosis and therapy. [3] More importantly, exercise, dietary protein, and sustained upright posture tend to increase albumin excretion rates.

Conventional 24-hour urine collection for albumin shows wide variation in excretion of albumin in urine. Additionally, it is very inconvenient to the patient. The albumin-creatinine ratio in early morning spot urine collected on awakening (before breakfast or exercise) is considered as a valid test for albumin excretion in urine. It is simple and inexpensive; it does not require a timed 24-hour collection of urine; and, most importantly, it gives a quantitative result that correlates well with 24-hour urine values over a wide range of protein excretion. A ratio of albumin (mcg/L) to creatinine (mg/L) of less than 30 is normal; a ratio of 30-300 signifies microalbuminuria and values above 300 are considered as macroalbuminuria. [3] On a standard urine dipstick, 10-20 mg/dL is the minimal detection limit of protein. If the dipstick is positive, then the patient likely has microalbuminuria. [3] Microalbuminuria is not detectable by the urine dipstick.

Reduction in glomerular filtration rate is usually preceded by microalbuminuria. Microalbuminuria signals the renal and cardiovascular complications from diabetes and, therefore, all diabetic patients should have their urine tested for microalbumin on an annual basis. It is unnecessary to test microalbuminuria in patients with established proteinuria. Antihypertensive therapy decreases albuminuria and diminishes its progression even in normotensive diabetic patients. [7]

Therapy with angiotensin-converting enzyme inhibitors (ACEI) reduces the risk of overt nephropathy associated with microalbuminuria in type 1 and 2 diabetes, and similar effect is also seen in patients with type 2 diabetes treated with angiotensin receptor blockers (ARB). [8, 9] Insufficient data exist to validate the use of combination ACEI and ARB therapy in patients with microalbuminuria. The Heart Outcome Prevention Evaluation (HOPE) study demonstrated that diabetic patients with microalbuminuria treated with ACEI have a significantly lower risk of cardiovascular morbidity and mortality. [9]

Albuminuria is a risk factor for progressive renal function loss. Albuminuria can be reduced effectively by inhibitors of renin-angiotensin system (RAS). Maximum reduction of albuminuria to the lowest possible level should be the goal of renoprotective therapy. [10] Up-titration of benazepril or losartan against proteinuria showed further benefit on renal outcome in patients without diabetes but with proteinuria and renal insufficiency. [11]

Guidelines LMP. Microalbuminuria. [September 2, 2012]; Available from: http://santana0612.files.wordpress.com/2009/09/microalb.pdf.

Williamson MA, Snyder LM, Wallach JB. Wallach’s interpretation of diagnostic tests. 9th. Wolters Kluwer/Lippincott Williams & Wilkins Health: Philadelphia; 2011.

MS. G. Pancreatic Hormones and Diabetes Mellitus. Gardner DG SD, editor. Greenspan’s Basic & Clinical Endocrinology. 9th ed. New York: McGraw-Hill; 2011.

http://www.accessmedicine.com/diag.aspx.: McGraw-Hill’s Diagnosaurus; 2012. 2.0:

EV. L. Proteinuria. Medscape Reference. 2012.

BV. Diabetic Nephropathy. Medscape Reference. 2011. [Full Text].

Bargman JM SK. Chronic Kidney Disease. Longo DL FA, Kasper DL, Hauser SL, Jameson JL, Loscalzo J. Harrison’s Principles of Internal Medicine. New York: McGraw-Hill; 2012.

Viberti G, Wheeldon NM. Microalbuminuria reduction with valsartan in patients with type 2 diabetes mellitus: a blood pressure-independent effect. Circulation. 2002 Aug 6. 106(6):672-8. [Medline].

MW. T. Slowing the Progression of Chronic Kidney Disease. Lerma EV BJ, Nissenson AR, editor. CURRENT Diagnosis & Treatment: Nephrology & Hypertension. New York: McGraw-Hill; 2009.

de Zeeuw D, Remuzzi G, Parving HH, Keane WF, Zhang Z, Shahinfar S. Proteinuria, a target for renoprotection in patients with type 2 diabetic nephropathy: lessons from RENAAL. Kidney Int. 2004 Jun. 65(6):2309-20. [Medline].

Hou FF, Xie D, Zhang X, Chen PY, Zhang WR, Liang M. Renoprotection of Optimal Antiproteinuric Doses (ROAD) Study: a randomized controlled study of benazepril and losartan in chronic renal insufficiency. J Am Soc Nephrol. 2007 Jun. 18(6):1889-98. [Medline].

Spot Collection

Timed Collection

24-hr Collection

Category

Less than 30 mcg/mg creatinine

Less than 20 mcg/min

Less than 30 mg

Normal

30-300 mcg/mg creatinine

20-200 mcg/min

30-300 mg

Microalbuminuria

More than 300 mcg/mg creatinine

More than 200 mcg/min

More than 300 mg

Clinical albuminuria

Bishnu Prasad Devkota, MD, MHI, FRCS(Edin), FRCS(Glasg), FACP Professor of Medicine, St Louis University School of Medicine

Bishnu Prasad Devkota, MD, MHI, FRCS(Edin), FRCS(Glasg), FACP is a member of the following medical societies: American College of Physicians, American Medical Informatics Association, Royal College of Physicians and Surgeons of Glasgow, Healthcare Information and Management Systems Society, Royal College of Surgeons of Edinburgh

Disclosure: Nothing to disclose.

Eric B Staros, MD Associate Professor of Pathology, St Louis University School of Medicine; Director of Clinical Laboratories, Director of Cytopathology, Department of Pathology, St Louis University Hospital

Eric B Staros, MD is a member of the following medical societies: American Medical Association, American Society for Clinical Pathology, College of American Pathologists, Association for Molecular Pathology

Disclosure: Nothing to disclose.

Judy Lin, MD

Disclosure: Nothing to disclose.

Microalbumin 

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