Doctors generally differentiate between primary and secondary glomerulonephritis.
Experts define primary glomerulonephritis as autoimmune inflammation of the renal corpuscles without a previous underlying disease.
Secondary glomerulonephritis is caused by a previous kidney disease or a disease that occurred before the kidney inflammation. One example is post-streptococcal glomerulonephritis.
An infection with group A streptococci, which often infect the upper respiratory tract, produces antibodies. These are directed against the bacteria on the one hand, but also against the body's own structures with a similar surface structure on the other.
The antibodies attach themselves to the renal corpuscles in the form of immune complexes. The immune system attacks them, resulting in an inflammatory reaction. Other pathogens can also trigger this type of post-infectious glomerulonephritis.
These include
- staphylococci
- Gram-negative pathogens
- fungi
- various viruses
- parasites
Glomerulonephritis can also occur as part of the autoimmune diseases lupus erythematosus and Good-Pasture syndrome or granulomatosis (rheumatic disease).
For glomerulonephritis to cause any symptoms at all, more than 50 percent of the kidney tissue must be affected by the inflammation. This means that many inflammatory processes in the renal corpuscles remain undetected. However, if there is significant damage to the glomeruli, a symptom complex can develop which is also known as nephrotic syndrome.
Nephrotic syndrome is particularly common in people with chronic glomerulonephritis. Due to the impaired filtration, there is an increased amount of protein in the urine. Doctors refer to this as proteinuria. As a result, the proteins in the blood are lowered, so there is also hypoproteinemia.
Due to the lack of proteins, the colloid osmotic pressure in the blood vessels drops. The fluid from the blood plasma migrates from the blood vessels into the surrounding tissue and accumulates there (edema).
The less protein in the blood, the more pronounced the edema. The body tries to compensate for the loss of protein as quickly as possible and produces more lipoproteins in the liver. This leads to an increase in blood lipid levels and an unfavorable ratio of blood lipids to each other.
Acute and rapidly progressing glomerulonephritis, on the other hand, often leads to nephrotic syndrome. This is characterized by the so-called Volhard triad .
It consists of
- Blood in the urine (haematuria)
- Water retention in the tissue
- high blood pressure
- Pain in the flank area
- Reduced urine production (anuria)
- Development of pulmonary edema
- Severe shortness of breath
The first indication of kidney inflammation is provided by an examination of the urine. Depending on the severity of the disease, blood or proteins may be found.
Large amounts of blood in the urine are visible to the naked eye, while proteins make the urine cloudy. Another important diagnostic procedure for suspected glomerulonephritis is a laboratory blood test.
In nephrotic syndrome, blood lipid levels are elevated, while blood protein levels are low. An increase in creatinine levels is an indication of kidney weakness and, in the worst case, indicates impending kidney failure.
Other diagnostic methods are
- Ultrasound examination(sonography) of the kidneys
- A histological examination of kidney tissue (kidney biopsy) Kidney function tests
- Determination of the glomerular filtration rate or renal plasma flow
It is also important to find the cause of the glomerulonephritis. The doctor therefore looks specifically for possible underlying diseases such as vascular inflammation, autoimmune disorders or infectious diseases.
The treatment depends on the cause of the disease and the functional condition of the kidneys. Some glomerulonephritis can be treated well with glucocorticoids such as prednisolone. Other forms, however, such as rapidly progressing glomerulonephritis, require additional administration of immunosuppressive medication.
If the kidney inflammation manifests itself in the form of nephrotic syndrome, patients are given dehydrating medication (diuretics). These flush out the edema. In most cases, the elevated blood lipid levels normalize on their own as part of the treatment of nephrotic syndrome. Nevertheless, the doctor may use statins to lower them.
If the glomerulonephritis is so advanced that the kidneys fail, dialysis is necessary. Here, an external device cleans the blood of the urinary substances.
In the case of chronic kidney failure, a kidney transplant is necessary, in which a donor kidney takes over the functions of the defective kidney.
The prognosis of glomerulonephritis depends above all on how quickly doctors recognize and treat the disease. An unrecognized inflammation of the renal corpuscles can develop into a chronic form and lead to kidney failure. Chronic glomerulonephritis also increases the likelihood of cardiovascular disease.
The prognosis for rapid progressive glomerulonephritis (RPGN), a form of acute glomerulonephritis, is particularly poor. If left untreated, the filter function of the kidneys is reduced by half within a few months. It rarely takes more than a year for absolute kidney failure to develop.