Grona N. V.

Microalbuminuria is an Early Diagnostic and Clinical Marker for Prognosis of Target Organ Damage in Arterial Hypertension

About the author:

Grona N. V.



Type of article:

Scentific article


The prevalence of hypertension, chronic kidney disease and end­stage renal disease attributable to hypertension continues to rise worldwide. Identifying the precise prevalence of chronic kidney disease attributable to hypertension is difficult owing to the absence of uniform criteria to establish a diagnosis of hypertensive nephropathy. Essential hypertension usually clusters with other cardiovascular risk factors such as age, overweight, diabetes, insulin resistance and dyslipidemia. The target organ damage such as left ventricular hypertrophy, hypertensive nephropathy, acute coronary syndrome, stroke and cognitive dysfunction takes place early in course of hypertension. Though the prevalence of hypertension is high, the relationship between microalbuminuria and target organ damage in hypertension is not well studied. Microalbuminuria is a strong and independent indicator of increased cardiovascular risk among individuals with and without diabetes. Therefore, microalbuminuria can be used for stratification of risk for cardiovascular disease. At present, the most likely possibility is that a common pathophysiologic process, such as endothelial dysfunction, chronic low­grade inflammation, or increased transvascular leakage of macromolecules, underlies the association between microalbuminuria and cardiovascular disease, but more and prospective studies of these hypotheses are needed. Albumin is a relatively large, negatively charged protein. The filter through which albumin must pass before entering the urine, the glomerular capillary wall, is size and charge selective. Microalbuminuria is thought to be a consequence of an increased albumin leakage through the glomerular capillary wall as a result of increased permeability of the wall, an increased intraglomerular pressure, or both. For example, hyperglycemia and high blood pressure are generally accepted risk factors for development of microalbuminuria. Both can increase intraglomerular pressure. They can alter the charge selectivity of the glomerular capillary wall, thereby increasing its permeability. In a healthy kidney >99 % of filtered albumin is reabsorbed in the proximal tubules. Some data suggest that microalbuminuria, at least in patients with hypertension and type 2 diabetes, is associated not only with increased glomerular protein passage but also with an absence of a compensatory increase in tubular reabsorption of albumin. A pronounced increase in albumin filtered by the glomerulus will lead to excessive supply of albumin to the renal tubule, eventually exceeding tubular reabsorptive capacity, and thus to increased albumin excretion in the urine. Theoretically, endothelial dysfunction could cause albuminuria by increasing glomerular pressure and glomerular barrier permeability. Endothelial dysfunction can be defined as any change in endothelial properties that is inappropriate with regard to the preservation of organ function. The findings support the concept that impaired endothelial nitric oxide synthesis plays a role in the association of microalbuminuria with cardiovascular disease risk. This is reflected by expressions such as “microalbuminuria is a risk indicator for cardiovascular disease”, and “microalbuminuria is a marker of endothelial dysfunction” and early stage of hypertensive nephropathy. Once microalbuminuria is present, cardiovascular risk factor reduction should be more “aggressive”. Early screening of patients with essential hypertension for microalbuminuria and aggressive management of positive cases might reduce the burden of chronic kidney diseases and cardiovascular diseases in the community.


arterial hypertension, microalbuminuria


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Publication of the article:

«Bulletin of problems biology and medicine» Issue 3 part 2 (111), 2014 year, 11-16 pages, index UDK 612. 12­008. 331+616. 61­008. 64]:612. 466. 22