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Inflammatory condition of the kidney.
Typically presents with AKI, hypertension, proteinuria and hematuria.
Nephritic range proteinuria is generally considered less than nephrotic range (UPC >2 mg/mg, or protein excretion >40 mg/m²/h), but it can vary
GNs are considered auto-immune in nature, either by reacting directly to antigens in the kidney or systemically (secondary GN) or experiencing some dysregulation of normal immunologic response.
They are graded by the rate of progression when it comes to defining urgency
Acute GN (GN that has injured the kidneys) along with systemic symptoms
Rapidly progressive GN - basically any acute GN that causes your kidneys to fail quickly (days to weeks). Higher priority for intervention like steroids or possibly a biopsy
Recurrent, episodic GN - Typically presents like a GN but recovers in between (specifically looking at resolution/normalization of proteinuria, AKI and any hypertension). Sometimes with enough episodes, some or all of these features may not recover. Think IgA nephropathy, recurrent SLE nephritis flares, etc.
Chronic GN - GN that may not show kidney dysfunction except in proteinuria, hematuria and HTN. Cr may stay normal for years before it starts to decline.
Brown urine, edema/fluid retention/low urine output, HTN
Seizure, headache (due to HTN)
Sore throat or skin infection 1-4 weeks prior (skin > throat)
Immunological response to nephritogenic streptococcus (group A) strains, forming immune complexes of strep Ag+human Ab, that cause inflammation in the kidney (circulating vs “in situ”- glomerular components cross-react with streptococcus Ag) and activate complement, mainly alternate pathway
KFP with signs of AKI: high Cr, K; sAlb rarely low
UA: RBCs, RBC casts, proteinuria (mainly non-nephrotic)
Abs to Strep Antigens: ASO (throat), anti-DNAaseB (skin), Streptozyme (measures 5 types of Abs, includes ASO and ant-DNAaseB)
Serum complements: C3 low, C4 normal or low
Negative: ANA, ANCA
in case of rapid rise in sCr; may cause crescentic GN
if diagnosis unclear
typical finding: large subepithelial immune complexes i.e. “humps” on EM; IgG + C3 on IF
Supportive
If severe course, may need immunosuppression
Manage HTN: low salt intake, diuretics, antihypertensives
C3 and C4 normalize in 6-8 weeks, need to be checked then
Post-infectious GN: if Strep not found, but course is similar, could assume other infection caused GN
Microhematuria can persist ~6-12 months
If C3/C4 not normalized needs further testing: i.e. SLE, MPGN/C3GN, genetic disorders of the complement system
PSGN usually does not recur
PSGN can be subclinical and patients may present years later as CKD of unclear etiology
Abx for Strep (likely not beneficial for existing GN):
Early Abx to treat throat/skin may decrease risk or severity of GN;
To eradicate:
during GN if Strep still detected
in communities with high PSGN incidence
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