Proteinuria is aggravated by losing protein in the urine, mainly albumin.
This is a protein present in the blood plasma, produced by the liver, resulting from the metabolism of foods rich in proteins, such as meat, eggs, milk, and derivatives thereof. The average rate of this protein in the blood is between 3.5 and 4.5 g / dl.
It is essential to maintain the normal movement of fluids within the vessels, as well as in the preservation of nutritional status. The loss of protein in the urine is a common finding in many kidney diseases, which may be discrete when the loss is only a few milligrams of protein per day or more intense when there is a loss of several grams of protein per day. When the loss of protein in the urine exceeds 3.5 grams per day, it is called nephrotic proteinuria.
Proteinuria can have four different etiologies or causes. They are:
Glomerular origin: are the normal molecular weight proteins, such as albumin, transferrin, immunoglobulins (IgG and IgA), and other microglobulins that cross the glomerulus filter membrane. When there is a change to the membrane, protein removal in the urine occurs.
Tubular origin: secreted proteins are especially the lysozymes and microglobulins of the proximal renal tubule. The proteins secreted by the wall of the urinary tract: renal pelvis, ureter, bladder, and urethra. The overproduction of low molecular weight proteins accumulates in the blood plasma, but they are small and pass through the filter. As these are produced in large quantities, they exceed the capacity of renal uptake and are eliminated with urine. A typical example is the Bence-Jones protein (immunoprotein), but also amylases and myoglobin.
Proteinuria causes no symptoms and is the first sign of kidney disease in diabetic patients. Its presence is an early sign of kidney damage and indicates a greater likelihood of developing chronic renal failure.
When proteinuria is suspected, the doctor should investigate whether it is persistent or functional. Persistent proteinuria is considered when observed in at least two urine samples within 30 days and is usually associated with underlying renal pathology. Functional proteinuria can be transient or orthostatic, sometimes detected in urine samples or when the patient is standing. The clinical significance is doubtful.
The type of proteinuria can be identified by electrophoresis or immunoelectrophoresis of urinary proteinuria. Although these methods are necessary for some instances, they are expensive and unavailable in many laboratories. A simple and affordable way to identify the type of proteinuria is by comparing the protein detected by the tape immersion with the experimental turbidimetric method, where the use of sulfosalicylic acid is found, which can determine any protein in the urine.
Proteinuria can be persistent and permanent:
- Ligera (hasta 1,0 g/24 h)
- Moderate (1,0-3,5 g/24 h)
- Massive (greater than 3.5 g / 24h / 1.73 body surface area)
- The main consequence of massive proteinuria is edema. The loss of plasma protein also results in malnutrition and all its complications.
The treatment for proteinuria
The treatment consists of substituting the value of the protein and investigating the cause of the loss of the same. Because proteinuria is dependent on the etiology, the treatments are varied.
The primary treatment for proteinuria will be to control blood pressure and blood glucose levels, which can be achieved through lifestyle changes and could include taking additional medications.
If the fluid accumulates in the ankles or around the lungs, you may be given water tablets, a diuretic medication that helps eliminate water from the body.