Kidney Infection - Find a Doctor and Get Information

Medical professionals generally distinguish between primary and secondary glomerulonephritis.

Experts define primary glomerulonephritis as autoimmune-induced inflammation of the glomeruli without an underlying disease.

Secondary glomerulonephritis develops as a result of a pre-existing kidney condition or a disease that occurred prior to the kidney inflammation. One example is post-streptococcal glomerulonephritis. 

An infection with Group A streptococci, which frequently affect the upper respiratory tract, triggers the production of antibodies. These antibodies target the bacteria on the one hand, but also the body’s own structures with a similar surface structure on the other.

The antibodies attach themselves to the glomeruli in the form of immune complexes. The immune system attacks them, leading to 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 in the context of the autoimmune diseases lupus erythematosus and Goodpasture syndrome, or as part of granulomatosis (a rheumatic disease).

Glomerulonephritis is a kidney disease that occurs when the glomeruli become inflamed @ Bungon /AdobeStock

For glomerulonephritis to cause any symptoms at all, more than 50 percent of the kidney tissue must be affected by inflammation. As a result, many inflammatory processes in the glomeruli go undetected. If, however, there is significant damage to the glomeruli, a complex of symptoms may develop, also known as nephrotic syndrome.

Nephrotic syndrome is particularly common in people with chronic glomerulonephritis. Due to impaired filtration, increased amounts of protein are found in the urine. Doctors refer to this as proteinuria. As a result, protein levels in the blood are reduced, leading to hypoproteinemia.

Due to the lack of proteins, the colloid-osmotic pressure in the blood vessels decreases. Fluid from the blood plasma moves out of the blood vessels into the surrounding tissue, where it accumulates (edema). 

The less protein there is in the blood, the more pronounced this edema becomes. The body attempts to compensate for the protein loss as quickly as possible by producing increased amounts of lipoproteins in the liver. This leads to elevated blood lipid levels and an unfavorable ratio of the various blood lipids.

Acute and rapidly progressing glomerulonephritis, on the other hand, more frequently leads to nephrotic syndrome. A characteristic feature here is the so-called Volhard triad.

It consists of:

• Blood in the urine (hematuria)
• Fluid retention in the tissues
• High blood pressure
• Pain in the flank region
• Reduced urine output (anuria)
• Development of pulmonary edema
• Severe shortness of breath

In nephrotic syndrome, the filtration barrier is compromised, allowing valuable substances such as proteins to leak into the urine @ PATTARAWIT /AdobeStock

A urine test provides the first indications of kidney inflammation. Depending on the severity of the disease, blood or proteins may be present in the urine.

Large amounts of blood in the urine are visible to the naked eye, whereas proteins cause the urine to appear cloudy. Another important diagnostic procedure when glomerulonephritis is suspected is a laboratory blood test.

In nephrotic syndrome, blood lipid levels are elevated, while blood protein levels are reduced. An increase in creatinine levels is an indication of kidney dysfunction and, in the worst case, may signal impending kidney failure. 

Blood in the urine @ GladkovPhoto /AdobeStock

Other diagnostic methods include:

• Ultrasound examination (sonography) of the kidneys
• A microscopic examination of kidney tissue (kidney biopsy) Kidney function tests
• Measurement of the glomerular filtration rate or renal plasma flow

It is also important to identify the cause of glomerulonephritis. Therefore, the doctor will specifically look for possible underlying conditions such as vasculitis, autoimmune disorders, or infectious diseases.

Treatment depends on the cause of the disease and the functional status of the kidneys. Some forms of glomerulonephritis respond well to glucocorticoids such as prednisolone. Other forms, however, such as rapidly progressive glomerulonephritis, require additional immunosuppressive medications.

If the kidney inflammation manifests as nephrotic syndrome, patients are given diuretics. These help reduce edema. In most cases, elevated blood lipid levels often normalize on their own as part of the treatment for nephrotic syndrome. Nevertheless, the doctor may prescribe statins to lower these levels.

If glomerulonephritis has progressed to the point where the kidneys are failing, dialysis is necessary. In this procedure, an external machine cleans the blood of waste products.

In cases of chronic kidney failure, a kidney transplant is necessary, in which a donor kidney takes over the functions of the diseased kidney.

The prognosis for glomerulonephritis depends primarily on how quickly doctors diagnose and treat the disease. Undiagnosed inflammation of the glomeruli can progress to a chronic form and lead to kidney failure. In addition, chronic glomerulonephritis increases the likelihood of cardiovascular disease.

The prognosis is particularly poor for rapidly progressive glomerulonephritis (RPGN), a form of acute glomerulonephritis. If left untreated, the kidneys’ filtration function declines by half within a few months. It rarely takes more than a year for complete kidney failure to set in.