"Different specialists including at least the pediatrician, nephrologist and nutritionist are necessary to achieve optimal treatment".
DR. FRANCISCO JAVIER LAVILLA ROYO
SPECIALIST. NEPHROLOGY DEPARTMENT
The term glomerulonephritis means inflammation of the glomerulus.
The glomerulus is the anatomical unit of the kidney where the blood's clearance or filtration function lies.
If there is an abnormal behavior, it can manifest itself in the form of a decrease in the volume of filtered blood (deterioration of renal function) or in the form of a loss of the selective filtration property.
The loss of selective filtration will lead above all to the elimination through the urine of different elements of the blood (such as red blood cells) and substances that are usually not lost or are lost in minimal quantities (such as blood proteins, albumin, gamma globulins, etc...).
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What are the symptoms of glomerulonephritis?
In the first case there is usually a rapid deterioration of kidney function with a decrease in the amount of urine, which is very pathological with the presence of red blood cells and cellular detritus in the form of cylinders that can be observed under the microscope.
As a consequence of these alterations a significant retention of liquids can appear with the appearance of arterial hypertension and cardiac insufficiency.
The nephrotic syndrome usually evolves with a preserved or slightly deteriorated renal function but with a very important loss of proteins through the urine.
This loss of protein in the urine leads to a decrease in the number of proteins in the blood with the appearance of edema due to the extravasation of water from the vessels, and a compensatory response by the liver that, when trying to counteract this deficit of proteins by manufacturing more, causes an increase in lipid levels.
The most common symptoms are:
- Red urine due to hematuria or dark brown color.
- Decrease in the formation of urine.
- Increase in respiratory effort.
- Headache, Hypertension, Fatigue.
- Pale skin and mucous membranes.
Do you have any of these symptoms?
You may have glomerulonephritis
What causes glomerulonephritis?
The etiology of glomerulonephritis usually lies in a defective behavior of the immune system. A pathological behavior of T-lymphocytes with direct damage to the basement membrane may be the origin of minimal change glomerulonephritis.
On the other hand, the organism can consider some protein of the kidney as strange, acting directly against it or making antibodies that join with that protein causing immune complexes in the own membrane giving rise to proliferative glomerulonephritis as the extracapillary ones. Also strange antigens can appear in the systemic circulation in front of which the corresponding antibodies are produced that bind to those proteins previously deposited in the glomerulus, as it can happen in non-proliferative glomerulonephritis like the membranous glomerulonephritis (in which the strange antigen can be tumoral), or proliferative like the endocapillary (where the antigen is usually bacterial) and a subgroup of extracapillaries.
Finally, the antibodies can be united with those antigens in the circulation giving rise to immunocomplexes that later are deposited in the glomerulus as it happens in the mesangial glomerulonephritis.
Classification of glomerulonephritis
A proliferation of different cells may appear, and these are called proliferative glomerulonephritis.
This proliferation can cause as consequence an alteration of the glomerular architecture with the appearance of cellular accumulations in the form of crescents (proliferative extracapillary glomerulonephritis), of a basal membrane invaded by cellular elements coming from the own mesangio and that extend below the epithelium (mesangiocapillary glomerulonephritis) and even by the occlusion of the capillary loops by cells coming from the own endothelium (proliferative endocapillary glomerulonephritis).
The rest of glomerulonephritis are called non-proliferative, characterized by the predominance of protein deposition over cell proliferation or by lesions that are difficult to characterize.
In those that predominates the protein deposit, this deposit can occur in the own basal membrane with a thickening of this membrane towards the epithelial side arriving to include the extensions of the epithelial cells (membranous glomerulonephritis), or also to produce deposits in the mesangium with an increase of the same one (mesangial glomerulonephritis).
How are glomerulonephritis diagnosed?
The filtration work carried out by the structure of the glomerulus involves not only the elimination of water but also, selectively, of substances present in the blood. Any alteration that arises in this anatomical and physiological structure will give rise to anomalies in the filtration work carried out.
In a first clinical evaluation it will always be necessary to evaluate the existence or not of proteinuria as well as its quantification, the presence of associated hematuria, the development of renal insufficiency and the existence of arterial hypertension.
The importance of the renal biopsy lies in the fact that it allows us not only to know where the histological affectation is or what mechanisms are involved, but also the degree of severity of this affectation, a crucial point when initiating and deciding what type of therapeutic management is required.
Clinical criteria can be used but the diagnosis requires histological confirmation. There is an exception, the disease of minimal changes in the child. This considers a positive response to steroid treatment as a diagnosis.
How are glomerulonephritis treated?
The treatment of glomerulonephritis will depend on the anatomopathological diagnosis (not only in terms of its filiation but also its severity) and the clinical course it presents (existence of a deterioration of renal function, speed of its evolution, presence of nephrotic syndrome, etc...).
Given that most of the glomerulonephritis in its etiopathogenesis presents an anomalous behavior of the immune system or in its development intervenes cells or substances with inflammatory capacity, the use of immunosuppressors is usually quite extended.
The corticosteroids are the most used, mainly of first line when it is a glomerulonephritis of minimum lesions or when clinically the glomerulonephritis is like a nephrotic syndrome.
Other more powerful immunosuppressants such as cyclophosphamide and chlorambucil are used in glomerulonephritis with rapid deterioration of renal function or that have not responded to steroids.
Cyclosporine is used almost exclusively in glomerulonephritis with nephrotic syndrome as long as its use is not associated with further deterioration of kidney function, and there has been no response to steroids.
Other therapeutic procedures such as plasmapheresis emerged with the idea of eliminating from the blood those antigens or immune complexes that favor the development of glomerulonephritis, especially when it behaves as a proliferative one.
The elimination of the source of antigens that are suspected to be in the genesis of a glomerulonephritis is also an aspect to try as it happens mainly with the membranous, mesangial glomerulonephritis or even in a very particular group of membranoproliferative (like those associated to virus C).
Finally, therapeutic abstention is an option to be considered when we are faced with a very advanced glomerulonephritis or on the contrary stabilized and with little repercussion, or that has not responded to drugs of habitual use in these cases (corticoids, cyclophosphamide), knowing that they are not medications free of side effects that can mortgage the future of the patient, to pass later to other options like dialysis or transplantation.
Where do we treat it?
IN NAVARRE AND MADRID
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Specialists of the Nephrology Service
The Nephrology Service of the Clínica Universidad de Navarra has more than five decades of experience, both in the diagnosis and treatment of all kidney pathologies and in the transplant of this organ.
Our specialists have completed their training in centers of national and international reference.
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