Glomerulonephritis, is a term used to refer to several kidney diseases (usually affecting both kidneys). Many of the diseases are characterised by inflammation either of the glomeruli or small blood vessels in the kidneys, hence the name, but not all diseases necessarily have an inflammatory component.
As it is not strictly a single disease, its presentation depends on the specific disease entity: it may present with isolated hematuria and/or proteinuria (blood or protein in the urine); or as a nephrotic syndrome, a nephritic syndrome, acute kidney injury, or chronic kidney disease.
Glomerulonephritis refers to an inflammation of the glomerulus, which is the unit involved in filtration in the kidney. This inflammation typically results in one or both of the nephrotic or nephritic syndromes.
The nephrotic syndrome is characterised by the finding of edema in a person with increased protein in the urine and decreased protein in the blood, with increased fat in the blood. Inflammation that affects the cells surrounding the glomerulus, podocytes, increases the permeability to proteins, resulting in an increase in excreted proteins. When the amount of proteins excreted in the urine exceeds the liver's ability to compensate, fewer proteins are detected in the blood - in particular albumin, which makes up the majority of circulating proteins. With decreased proteins in the blood, there is a decrease in the oncotic pressure of the blood. This results in edema, as the oncotic pressure in tissue remains the same. This is worsened by the secretion of the hormone Aldosterone by the adrenal gland, which is secreted in response to the decrease in circulating blood and causes sodium and water retention. Hyperlipidemia is thought to be a result of the increased activity of the liver
The nephritic syndrome is characterised by blood in the urine and a decrease in the amount of urine in the presence of hypertension. In this syndrome, inflammatory damage to cells lining the glomerulus are thought to result in destruction of the epithelial barrier, leading to blood being found in the urine. At the same time, reactive changes may result in a decrease in kidney blood flow, resulting in a decrease in the production of urine. The renin-angiotensin system may be subsequently activated, because of the decrease in perfusion of juxtaglomerular apparatus, which may result in hypertension.
Glomerulonephritis may be caused by specific problems with the body's immune system, but the precise cause of some cases is unknown. Damage to the glomeruli causes blood and protein to be lost in the urine. The condition may develop after survival of the acute phase of rapidly progressive glomerulonephritis. In about a quarter of people with chronic glomerulonephritis there is no prior history of kidney disease and the disorder first appears as chronic renal failure.
There is no specific prevention for most cases of glomerulonephritis. Some cases may be prevented by avoiding or limiting exposure to organic solvents, mercury, and nonsteroidal anti-inflammatory analgesics.
Some forms of glomerulonephritis are diagnosed clinically, based on findings on history and examination. Other tests may include:
- Urine examination
- Blood tests investigating the cause, including FBC, inflammatory markers and special tests including (ASLO, ANCA, Anti-GBM, Complement levels, Antinuclear antibodies
- Biopsy of the kidney
Glomerulonephritis may be a temporary and reversible condition, or it may get worse. Progressive may result in chronic kidney failure and end stage kidney disease. If nephrotic syndrome is present and can be controlled, other symptoms may be controlled. If it can't be controlled, end-stage kidney disease may result.
Treatment varies depending on the cause of the disorder, and the type and severity of symptoms. High blood pressure may be difficult to control, and it is generally the most important aspect of treatment.
Medicines that may be prescribed include:
- Blood pressure medications