[citation needed] With severe proteinuria, general hypoproteinemia can develop which results in diminished oncotic pressure.

[14] Thereafter, kidneys retain or reabsorb the filtered proteins and return them to the circulating blood while removing wastes by excreting them in the urine.

[15][14] This is why the concentration of albumin in the urine is one of the single sensitive indicators of kidney disease, particularly for those with diabetes or hypertension, compared to routine proteinuria examination.

More recently developed technology detects human serum albumin (HSA) through the use of liquid crystals (LCs).

The presence of HSA molecules disrupts the LCs supported on the AHSA-decorated slides thereby producing bright optical signals which are easily distinguishable.

The 2005 UK Chronic Kidney Disease guidelines state that protein/creatinine ratio is a better test than 24-hour urinary protein measurement.

[25] It is possible to analyze urine samples in determining albumin, hemoglobin and myoglobin with an optimized MEKC method.

The most common cause is diabetic nephropathy; in this case, proper glycemic control may slow the progression.

Medical management consists of angiotensin converting enzyme (ACE) inhibitors, which are typically first-line therapy for proteinuria.

In patients whose proteinuria is not controlled with ACE inhibitors, the addition of an aldosterone antagonist (i.e., spironolactone)[27] or angiotensin receptor blocker (ARB)[28] may further reduce protein loss.