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Poststreptococcal glomerulonephritis (PSGN) results from a bacterial infection that causes rapid deterioration of the kidney function due to an inflammatory response following streptococcal infection.
The plasmin-binding capacity of streptococcal antigens favors immune complex deposition and inflammation. The typical pathological changes are endocapillary proliferation with varying degrees of leukocyte infiltration, and C3, IgG, and IgM immune deposits.
PSGN is usually an immunologically-mediated, nonsuppurative, delayed sequela of pharyngitis or skin infections caused by nephritogenic strains of S. pyogenes. Reported outbreaks of PSGN caused by group C streptococci are rare.
Symptoms of PSGN can include: Dark, reddish-brown urine. Edema (swelling), especially in the face, around the eyes, and in the hands and feet. Decreased need to pee or decreased amount of urine.
Acute post streptococcal glomerulonephritis are caused by group A beta haemolytic streptococci and follow upper airway infections such as pharyngitis or tonsillitis, by 14 to 21 days and 3-6 weeks after skin infection especially in warmer climates .
Mild to moderate hypertension occurs in more than 75% of patients with acute forms of GN, such as poststreptococcal GN1). Patients with acute GN have hypertension primarily due to sodium retention leading to fluid overload, as evidenced by suppression of the renin-angiotensin-aldosterone (RAAS) system.
Most forms of acute poststreptococcal glomerulonephritis (APSGN) are mediated by an immunologic process. Cellular and humoral immunity is important in the pathogenesis of this disease, and humoral immunity particularly in APSGN. Nonetheless, the exact mechanism by which APSGN occurs remains to be determined.
The streptococcal antibodies measured include the following: Antistreptolysin (ASO) Antihyaluronidase (AHase)
The most consistent and classic diagnostic finding is the presence of glomerular subepithelial electron-dense immune-type deposits, often referred to as humps (see the image below). The deposits are discrete and are commonly found on the part of the glomerular basement membrane overlying the mesangium.
Inflammation of the kidney is called nephritis. In Greek terms, nephro means "of the kidney" and itis means "inflammation." The causes for nephritis include infections, autoimmune disorders and toxins in the body.
Glomerulonephritis can be caused by various of factors including: Toxins or medicines. Viral infections, such as HIV, hepatitis B and C viruses. IgA nephropathy.
The most consistent and classic diagnostic finding is the presence of glomerular subepithelial electron-dense immune-type deposits, often referred to as humps (see the image below). The deposits are discrete and are commonly found on the part of the glomerular basement membrane overlying the mesangium.
The streptococcal antibodies measured include the following: Antistreptolysin (ASO) Antihyaluronidase (AHase)
PIGN can be caused by different kinds of germs, including bacteria and viruses. The most common type of PIGN is caused by a type of bacteria called streptococcus (strep). Post-streptococcal glomerulonephritis most often affects children 1-2 weeks after a streptococcal throat infection (“strep throat").
When the glomerular filtration rate (GFR) declines to 25% of normal, there is impaired synthesis of 1,25-vitamin D3, which impairs the effectiveness of calcium and phosphate resorption from bone by parathyroid hormone (PTH).
b. When the glomerular filtration rate (GFR) declines to 25% of normal, the parathyroid gland is no longer able to secrete sufficient parathyroid hormone (PTH). Correct
The reduced perfusion of the affected kidney activates the renin-angiotensin-aldosterone system , which causes constriction of peripheral arterioles .
a. Hypercalciuria is usually attributable to hyperthyroidism. TRUE
a. They are more common in women than men.
Poststreptococcal glomerulonephritis (PSGN) is characterized by rapid deterioration of kidney functions due to an inflammatory response (type III hypersensitivity reaction) following streptococcal infection. This condition results from specific strains of group A beta-hemolytic streptococci called nephrogenic streptococci. The disease affects the glomeruli and the small blood vessels of the kidneys. PSGN most frequently presents in children 1 to 2 weeks after a sore throat, or 6 weeks after a skin infection (impetigo). [1]
Last Update: March 29, 2021. Continuing Education Activity. Poststreptococcal glomerulonephritis ( PSGN) results from a bacterial infection that causes rapid deterioration of the kidney function due to an inflammatory response following streptococcal infection. PSGN most commonly presents in children 1 to 2 weeks after a streptococcal throat ...
Higher incidence of PSGN in developing countries- due to increased skin infections (pyoderma). Though the incidence in developed countries has gone down, it is still the most common cause of glomerulonephritis (GN) in children in the united states.
Poor hygiene, overcrowding, and low socioeconomic status are important risk factors for streptococci outbreaks, and this explains the higher incidence of PSGN in impoverished countries. Genetic factors are expected to predispose to the condition since almost 40% of patients with PSGN gave a positive family history. There is no specific gene found to cause PSGN. [5]
Other causes of post-infectious glomerulonephritis include bacterial infections including endocarditis, enterocolitis, pneumonia, and intraventricular shunt infections, viral (hepatitis B and C infections, human immunodeficiency virus, cytomegalovirus, Epstein Barr virus, parvovirus B19), fungal (coccidioidomycosis, histoplasmosis), and parasitic infections (malaria, leishmania, toxoplasmosis, and schistosomiasis). [5]
PSGN most frequently presents in children 1 to 2 weeks after a sore throat, or 6 weeks after a skin infection (impetigo). [1] Though the incidence of PSGN has declined in developed countries, the incidence of non-streptococcal organisms is emerging.
Epidemiology. Over the past three decades, PSGN incidence has significantly dropped in developed countries; such as the United States, UK, Central Europe, and Japan. The reason for this progress is the use of antibiotic prophylaxis and the improvement of hygienic states.