Glomerulonephritis is a kidney disorder characterized by inflammation of the glomeruli

QUESTION

A 19-year-old student complains of headache, swollen legs and dark colored urine. Urinalysis shows 4 for blood, 3 protein, and casts. His serum BUN and creatinine are elevated, and his blood pressure is 162/88. He denies any medical history or medication use but does report that he had a sore throat and fever 2 weeks ago that resolved spontaneously after 1 week of symptoms. You suspect that he has glomerulonephritis. What is the connection between the sore throat and the glomerulonephritis and describe the pathogenesis behind this disorder. Please add references.

ANSWER

Glomerulonephritis is a kidney disorder characterized by inflammation of the glomeruli, the tiny filtering units in the kidneys. It can be caused by various factors, including infections, autoimmune diseases, and certain medications. In the case of the 19-year-old student, his recent history of sore throat and fever provides important clues to the underlying cause of his glomerulonephritis.

The connection between the sore throat and glomerulonephritis lies in the development of a post-streptococcal glomerulonephritis (PSGN). PSGN is a type of glomerulonephritis that occurs as a result of an immune response to an infection, particularly with a group A beta-hemolytic Streptococcus bacteria. This type of bacteria is known to cause strep throat, an infection that commonly affects the throat and tonsils.

The pathogenesis of PSGN involves the immune system’s response to the streptococcal infection. During the infection, the bacteria release antigens that trigger an immune response. In some individuals, the immune system produces antibodies that can cross-react with components of the glomeruli in the kidneys. These antibodies form immune complexes that get deposited within the glomeruli, leading to inflammation and damage.

The immune complexes activate the complement system, a part of the immune response that triggers an inflammatory cascade. This cascade results in the recruitment of immune cells, such as neutrophils, and the release of inflammatory mediators. The influx of immune cells and the release of mediators lead to the destruction of the glomerular filtration barrier, which normally prevents the passage of blood cells and large proteins into the urine. As a result, red blood cells, protein, and casts (cellular debris) appear in the urine.

The increased permeability of the glomerular filtration barrier also impairs its ability to effectively filter waste products from the blood. This dysfunction leads to the retention of substances like blood urea nitrogen (BUN) and creatinine, resulting in elevated serum levels. Additionally, the inflammation and damage to the glomeruli can affect the normal regulation of blood pressure, leading to hypertension.

In summary, the connection between the student’s sore throat and glomerulonephritis is the development of post-streptococcal glomerulonephritis. The pathogenesis involves the formation of immune complexes in response to the streptococcal infection, which then leads to inflammation and damage within the glomeruli. This process disrupts the filtration function of the kidneys, resulting in blood and protein in the urine, elevated BUN and creatinine levels, and hypertension.