Protein differentiation in urine allows the origin of proteinuria to be identified. Depending on the mechanism of origin, the following protein forms are distinguished:
- Prerenal: depletion of the reabsorption capacity of the intact tubules through the proliferation of a tubular filterable (small) protein in the blood.
- Renal (possibly with haematuria): loss of protein due to damage to the glomeruli (glomerular proteinuria) and/or the tubules (tubular proteinuria).
- Postrenal: usually bleeding into the urinary tract.
Urinary protein electrophoresis is used for the orientation differentiation of proteinuria on the basis of the molecular size of the excreted proteins.
In early diabetic nephropathy, only albumin with a molecular size of about 67 kD is initially excreted (selective glomerular proteinuria). With increasing glomerular damage, higher molecular weight proteins also occur (non-selective glomerular proteinuria: IgG+albumin).
With tubular damage, however, low-molecular proteins(alpha1-microglobulin) are excreted more frequently.
Postrenal proteinuria: IgG/ erythrocytes; alpha2-macroglobulin albumin
In the presence of monoclonal gammopathy, proteinuria caused by monoclonal immunoglobulin light chains (Bence-Jones proteins) can also be detected before kidney damage occurs ("overflow proteinuria").
Urine immunofixation electrophoresis is used for the specific detection of monoclonal light chains in urine.