Analysis of the renal function

It is the non-toxic form of ammonia that is generated in the body from the degradation of proteins from both the diet and physiological turnover.

Due to its small size, it presents a variable reabsorption and secretion in the renal tubule accompanying the water. The values normally observed in blood for an individual in fasting are: 0.1-0.5 g./l.

The retention of urea in the blood reflects renal malfunction globally, although it is affected by a diet rich in protein, by liver function and by catabolic states.

In addition, in the tubule, urea accompanies water, so that if diuresis is elevated, water excretion is greater and therefore urea will be eliminated. On the contrary, if the subject presents a low diuresis (dehydration, hemorrhage, heart failure, renal failure, etc.) the reabsorption will increase, and therefore the concentration of urea in the blood.

They are free ions (such as Sodium (Na), Potassium (K), Chlorine (Cl) and Bicarbonate (HCO3)) that exist in body fluids. All metabolic processes in the body affect the concentration of electrolytes in blood and urine. Their concentration (mmol/l) is decisive for the osmolarity, hydration status and pH of body fluids.

Along the nephron, the electrolytes are reabsorbed or secreted as needed to regulate their blood concentration and to regulate both the osmotic charge and the pH of the urine.

The existence of a renal pathology will be reflected in the imbalance of the concentration of these substances in both blood and 24-hour urine. The interpretation of these determinations is complex since many pathologies, other than renal, alter their concentration.

Together with other tests such as clarification of creatinine, determination of blood and urine urea, determination of Calcium (Ca) and Phosphorus (PO4H3-) in blood and urine, etc., represent a good approximation of renal function.

Protein in the urine or proteinuria does not normally appear in urine except in certain circumstances such as pregnancy, after sport, after a long time on your feet, etc. However, there are pathological causes that manifest themselves with proteinuria.

The laboratory study of proteinuria begins with the determination of the concentration of total protein in urine. If its presence is detected, it must be ruled out that it is due to a non-renal pathology involving increased production, as in myeloma, fever, inflammatory processes, burns, etc. Once these possibilities have been ruled out, the cause will be renal. In this case, proteinuria may be due to an alteration of the glomerulus that allows proteins to filter and/or an alteration of the tubule, which does not reabsorb them.

• Glomerular Proteinuria: To study it, a protein of a limit size for filtration is determined, for example albumin, and another large protein that under normal conditions does not filter, such as immunoglobulins. If these proteins appear in urine, they indicate a glomerular lesion.
• Tubular Proteinuria: to study it, a protein is determined that filters into the glomerulus but is totally reabsorbed in the tubule, so it should not appear in the urine. Small proteins are determined, such as retinol transport protein, a1-microglobulin, b2-microglobulin, etc., if they appear in urine it is because the tubule is not reabsorbing correctly.
• Mixed Proteinuria: all types of proteins appear in urine because they are damaged both in the glomerulus and the tubule of the nephrons. All the parameters described above will indicate that there is kidney damage.