Clinical Significance

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. 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 than10 % 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. 

_{Source: Roche Cobas ALBT2 Method Sheet Version 3.0 2023-10}