Poststreptococcal Glomerulonephritis Flashcards
What is the aetiology of post streptococcal glomerulonephritis?
Prior infection with group A beta haemolytic streptococci
What is the site of infection?
In children - infection of the mouth and pharynx (tonsillitis, pharyngitis). Typically arises in 1-2 weeks following infection
Soft tissue infections. Typically arises 4-6 weeks following infection
Osteomyelitis (infection of the bone)
In adults - usually not the respiratory tract
What is the pathophysiology behind this disease?
Infection with nephritogenic strains of group A beta-hemolytic streptococci → immune complexes containing the streptococcal antigen deposit within the glomerular basement membrane (likely involves molecular mimicry) → complement activation (↑ consumption of complement factors) → destruction of the glomeruli → immune complex-mediated glomerulonephritis and nephritic syndrome
What are the clinical features?
50% of patients are asymptomatic
Symptoms usually occur 1-6 weeks following an acute infection
Nephritic syndrome signs - Hematuria: tea- or cola-colored urine
Hypertension: can lead to headaches
Edema (prominent facial edema)
Oliguria
Influenza-like symptoms
Flank pain
What is the diagnosis for initial evaluation?
Initial evaluation - urinalysis with microscopy - findings are nephritic sediment. Hematuria with RBC cast, proteinuria, pyuria
Quantification of proteinuria - typically shows non nephrotic range proteinuria
BMP - reveals - increased BUN and creatinine, electrolyte abnormalities
CBC - may show - normocytic normochromic anemia
C3 complement, C4 complement levels - classically shows decreased C3 complement with normal C4 complement
What is the evidence of a preceding group A streptococcal infection?
Antistreptococcal antibody titres - increased ASO (antistreptolysin O antibody),
Increased anti-DNase B antibodies (marker for recent skin and or throat infection by group A beta haemolytic streptococci)
Increased antihyaluronidase antibodies
Isolation of group A beta haemolytic streptococci - pharyngitis: rapid strep test,throat culture. Skin lesion: wound cultures
What are some additional studies, including the indications and findings?
Renal ultrasound - indications - obtained during a diagnostic work up of Hematuria. Findings - typically normal, may show nonspecific increased echogenecity of renal cortex
Renal biopsy - indications - not routinely performed, unless signs of rapidly progressive GN. Findings - proliferative GN with immune complex deposits. Light microscopy - enlarged and hyper cellular glomeruli. Immunofluorescent microscopy - granular deposits in the glomerular mesangium and capillaries. Lumpy bumpy appearance, consisting of IgM, IgG, and C3 complement. Electron microscopy - immune complexes between epithelial cell layer and the glomerular basement membrane (called subepithelial lumps)
What is the treatment for PSGN?
Most cases are self limiting and complications of volume overload are managed with supportive treatment
Supportive therapy -
Management of oedema and volume overload - low sodium diet <2g/day. Fluid restriction <2L/day. Loop diuretics
Antihypertensives - indicated for hypertension refractory to management of oedema and volume overload. Preferred agents include - Ca channel blockers, ACE inhibitors or ARB’s
Antibiotic therapy -
Only administered for those with an active group A strep infection to prevent complications such as abscess, rheumatic fever etc. indications - evidence of active infection to prevent.
What are the complications of PSGN?
Acute renal failure
Rapidly progressive GN
Nephrotic syndrome later in the course of the disease
what is the prognosis of PSGN?
Recovery usually within 6-8 weeks. In children - restitution of kidney function in >90% of cases. In some cases urinalysis may be abnormal for extended periods
In adults - about 50% of cases suffer from persistently reduced renal function
