By Liji Thomas, MD
Glomerulonephritis (GN) is a condition in which the kidneys are inflamed. The glomeruli are the filtering mechanism of the kidneys. They consist of a tuft of highly coiled capillaries cupped in a double fold of membrane. Waste or toxic material is rapidly filtered out of the blood flowing through the capillaries, through the basal membrane of the glomerulus, and is removed into urine. All the necessary constituents of the blood are reabsorbed.
Glomerulonephritis has a variety of causes. In this condition, protein and blood cells seep out of the blood through the inflamed glomerular capillaries and are lost in urine. Other associated findings are high blood pressure and anemia.
Common symptoms include:
- Abdominal pain
- General malaise and fatigue
- Loss of appetite
- Joint pains or body aches
- Swelling of ankles and feet, the face, or whole body, due to lack of sufficient protein in the blood
- Bleeding through the feces or the nose
- Dark or bloody urine
- Foamy urine, due to the presence of protein in the urine
- Cough or breathlessness due to the escape of fluid from the bloodstream into the lungs – due to the loss of protein in urine, causing reduced blood protein levels, which results in failure to keep fluid in the blood
Complications of glomerulonephritis include:
- Kidney failure
- Chronic kidney disease
- Chronic or repeated kidney infections
- Fluid overload
- High blood pressure
- Malignant hypertension
- Frequent infections
- Acute nephritis
- Nephrotic syndrome with massive protein loss
- Salt and water imbalance, leading to other symptoms like weakness or arrhythmic heart beat
There are two classifications of glomerulonephritis:
- Acute GN – this type is brought on by an abnormal immune reaction, following a mild streptococcal infection elsewhere in the body. The antibodies to streptococci bind to glomerular cells, which are then destroyed by the immune system.
- Chronic – this type is usually the sequel of acute GN, but a quarter of these patients do not have any history of GN in the past.
Risk factors for glomerulonephritis include:
- Streptococcal infections
- Viral infections
- Abscesses or heart infections
- Exposure to hydrocarbon solvents
- Hematologic conditions, including blood or lymphatic cancers
Causes of Glomerulonephritis
Glomerulonephritis can be caused by a variety of diseases, either primarily affecting the glomeruli, or involving them as part of a widespread disease process. Some of the common causes include:
- Amyloidosis, a condition in which glassy-appearing protein material accumulates in various organs like the kidney, disrupting their function.
- Inflammation and blockage of kidney blood vessels, either alone or as part of a generalized auto-immune disorder, as is seen in systemic lupus erythematosus.
- Glomerular destruction by toxicity of drugs like NSAIDs.
- Diseases which affect the blood vessel wall, such as Henoch-Schönlein purpura.
- Damage to the kidney caused by the deposition of heavy protein molecules in the kidney tubules, as in IgA nephropathy.
- Antibodies formed against a component of glomerular cells, leading to their destruction, which is called anti-glomerular basement membrane antibody disease.
- Focal segmental glomerulosclerosis.
- Goodpasture syndrome, in which there is autoimmune disease of the small blood vessels in the kidney, causing them to be inflamed.
Glomerulonephritis is a clinical diagnosis, but may be confirmed by kidney biopsy. Imaging tests include CT, ultrasound scans, and intravenous pyelography. Blood and urine tests are needed to find the cause of the disease where possible. Treatment of this condition involves symptomatic measures, as well as the prevention of complications. This includes:
- Control of high blood pressure
- Steroids to control inflammation
- Immunosuppressants to relieve autoimmune damage
- Relieve the filtering load on the kidney, by restricting fluids, salt, and protein intake
- Dialysis, if kidney function is failing
- Kidney transplant if the kidney failure is permanent and leads to terminal kidney disease
Last Updated: Oct 12, 2015