Nephrotic syndrome

Nephrotic syndrome is defined by the presence of protein in the urine in amounts greater than 3.5 grams per day, decreased levels of protein in the blood, increased levels of lipids in the blood and urine, and edema. It is a clinical picture that appears as a consequence of a lesion of the glomerulus wall, a functional unit of the kidney where the blood is filtered and the blood is purified.

How is it produced?

When an injury occurs in the wall of the capillaries that make up the glomeruli, the permeability of the structure increases, so that plasma proteins that in normal conditions would not pass into the urine do so and are lost. In this way, proteinuria appears and there is a decrease in the levels of proteins in the blood plasma. Consequently, the pressure within the circulatory stream decreases, so there is fluid that seeps out of the vessels and edema occurs.

Likewise, as fluid leaks and plasma pressure decreases, the volume also decreases, thus activating hormonal and nervous compensation mechanisms that promote water and salt retention, thereby increasing edema.

The decrease in proteins at the plasma level also leads to an increase in its hepatic synthesis, a fact that also increases the production of lipids in the blood, which, when filtered through the damaged glomeruli, produce a leakage of lipids into the urine (lipiduria). This increase in blood lipids can lead to thromboembolism.

The main cause of nephrotic syndrome in children is primary minimal change glomerulonephritis, while in adults the first cause is membranous glomerulonephritis. It should be said, however, that if we talk about the most common global cause of nephrotic syndrome, this is glomerulonephritis secondary to diabetes. Other primary glomerulonephritis that can cause nephrotic syndrome are focal sclerosing or mesangiocapillary.

With regard to glomerular lesions secondary to other pathologies, it is worth highlighting, in addition to the already mentioned diabetes, systemic lupus erythematosus, Schönlein-Henoch disease, rheumatoid arthritis, cryoglobulinemia, sarcoidosis and amyloidosis. Other glomerular lesions that can trigger this syndrome are some infections, certain drugs, and tumors of the kidney tissue.

Symptoms

This syndrome is the most common presentation of glomerular disorders. Edema, the main sign of the disease, can appear all over the body. Initially they are mild, in areas such as the eyelids or the sacrum (especially in children) and in the lower extremities, although they can become general, which we know as anasarca. They are soft edemas, which under pressure leave fovea, that is, the mark of the pressure that is made on them remains when it stops being exerted.

Renal failure may appear, although it does not always occur and if it does, it is usually in advanced stages of nephrotic syndrome. It can be caused by cell death of the tubules through which urine is filtered, by their obstruction by proteins in the urine, or by compression by the surrounding edema.

The increase in coagulation capacity and the proportion of lipids in the blood favors the risk of thrombus formation, especially in the territory of the renal vein. If a renal vein thrombosis occurs, low back pain, hematuria, proteinuria and decreased kidney function usually appear.

The decrease in the levels of gamma globulins and lymphocytes in the blood predisposes to the appearance of infections, especially peritonitis, pneumonia and meningitis.

Another alteration that can be observed is the involvement of the tubules of the nephrons, with which the loss of glucose, phosphates, amino acids, potassium and bicarbonate in the urine can occur, which is known as Fanconi syndrome. Likewise, in the analysis, a decrease in sodium levels can be observed.

Diagnosis

An attempt should be made to identify the cause that produces nephrotic syndrome for its best treatment. The edema clinic will be the one that will put you on the track to perform a urine analysis collected over 24 hours, where you can see proteinuria at nephrotic levels (more than 3.5 mg per day), as well as the presence of lipids in urine, mainly in the form of fatty casts.

The blood test will show high levels of lipids in the blood, either cholesterol, triglycerides or both, a decrease in plasma protein levels and a probable alteration in kidney function, which will be assessed with the levels of urea and creatinine. You can also see other values ​​that may indicate the cause of the disorder, such as autoimmune antibodies, rheumatoid factor, or amyloid factor.

Sometimes it may be necessary to perform a kidney biopsy, although this invasive technique should be reserved for specific cases, such as adults whose cause remains unknown after the analytical study, children who do not respond to treatment with corticosteroids, diabetic patients with an evolution atypical of his disease or with the clinical and analytical suspicion of amyloidosis.

Treatment

Treatment should be that of the cause whenever possible. In children, since in 80% of cases the cause is a primary minimal change glomerulonephritis, which responds well to treatment with corticosteroids, they will be treated empirically with them for 8 weeks and their evolution will be monitored.

There are general treatment measures, such as the relative rest of the patients, which reduces the pressure on the sloping edematous areas, a fact that favors the passage of fluid back into the bloodstream and, therefore, the decrease in edema and improvement of diuresis.

Salt intake in the diet should be restricted to avoid increasing fluid retention and ensuring that there is a protein intake of high biological value. Fluid intake should be restricted in case of severe or generalized edema. The diet should also be low in fat and enhance fiber.

For the treatment of edema, the patient can benefit from the use always under medical supervision of diuretics, initially thiazides, and if there is no response, loop diuretics such as furosemide, which can be combined with spironolactone.

cardiovascular risk and improved glomerular filtration will be controlled by regulating blood pressure levels with antihypertensive drugs of the ACEI or ARA-II type and improving blood lipid levels with anti-lipid-lowering drugs, especially statins.

Renal vein thrombosis prophylaxis should be performed in bedridden patients by administering subcutaneous heparin.

Precautionary measures

There are not too many preventive measures for this syndrome, but it is always advisable to ensure an adequate intake of water, 1.5-2 liters per day, to promote proper kidney function, and maintain a healthy and balanced diet, low in salt and fat .