Nephritic-Nephrotic Flashcards
Nephritic Syndrome
GBM disruption HTN Elevated Cr and BUN Oliguria and Hematuria RBC casts in urine Protein in urine is <3g/day
Nephrotic Syndrome
Podocyte disruption + impaired charge barrier
Proteinuria is >3g/day with hypoalbuminemia, hyperlipidemia, edema
Primary or secondary
Hypercoagulable (antithrombin III loss)
Susceptible to infection
Acute poststreptococcal glomerulonephritis
Nephritic Ususally pediatric LM- enlarge hypercellular glomeruli IF- Starry sky, granular with GBM and mesangium deposits of IgG IgM and C3 EM- IC humps Reaction to M-protein Kids 2-4 weeks post strep. Type III hypersensitivity Peripheral/ periorbital edema Cola urine HTN Strep titers +, and low complement due to C3 deposits Can progress to RPGN in adults
Rapidly progressive glomerulonephritis
Nephritic
LC- crescents (fibrin and macrophages, C3b) in glomeruli
Poor prognosis, decreased renal function in dd to ww
3 types
1. Linear- Ab against GBM and Alveolar BM collagen, hematuria and hemoptysis in young men tx: plasmapheresis
2. Granular- PSGN or diffuse proliferative GN
Ab-Ag IC deposition subendothelial, seen in SLE
3. Pauci-immune:
c-ANCA - Granulomatosis with polyangiitis (nasal symptoms)
p-Anca - Microscopic polyangiitis or Churg-Strauss
Diffuse proliferative glomerulonephritis
SLE- presents often as both nephrotic and nephritic
From SLE or MPGN
LM- wire looping of capillaries
EM- subendothelial and intramembranous deposition of IgG ICs and C3
IG- granular
IgA nephropathy (Berger disease)
Nephritic
LM- meansgial proliferation
EM- mesangial IC deposits (IgA and C3)
IF- IgA ICs in mesangium
Renal pathology of Henoch-Schönlein purpura
Episodic gross hematuria with resp./GI infections
Alport syndrome
Nephritic Mutation in alpha chains in collagen, thinning and splitting (lamina densa) of GBM (XLR or AD) Eye, glom. and deafness Gross hematuria with normal complement Basket weave on EM
More benign thin basement membrane disease family history of microscopic hematuria
Membranoproliferative glomerulonephritis
MPGN often presents as both nephritic and nephrotic
IC deposition (granular)
Thick GBM on LM
Type I: MPGN: subendothelial associated with HCV and HBV, SLE, MGUS, cryoglubulinemia with tram-track appearance
Type II: Dense deposit disease- intramembranous, associated with C3 nephritic factor (Ab stabilizes C3 convertase) so over-active complement leads to inflammation and low circulating C
Minmal change disease
Nephrotic LM- normal IF- normal EM- effacement of foot processes Most common pediatric nephrotic syndrome Often 1˚, rarely 2˚ to infection, immunization Rarely 2˚ to cytokine damage from lymphoma 1˚ responds to corticosteroids Selective loss of only albumin
Focal segmental glomerulonephropathy
Nephrotic LM- segmental sclerosis and hyalinosis IF- often negative, but some granular IgM, C1, C3 EM- effacement of foot processes Affects some parts of some glomeruli African and Hispanic populations 1˚ or 2˚ to HIV, Sickle cell, heroin, obesity, IFN treatment, congenital CKD Poor response to corticosteroids May progress to CKD
Membranous glomerulonephropathy
Nephrotic
LM- diffuse capillary and GBM thickening
IF- granular, IC deposition in SLE
EM- Subepithelial deposition is “spike and dome”
Most common 1˚ nephrotic in caucasian adults
1˚ Ab to PLA2R
2˚ to NSAIDs, penicillamine, Au, Hepatitis B/C, syphilis, SLE or tumors.
Poor response to steroids
Can progress to CKD
Hypercoagulable renal vein thrombosis
Amyloidosis
Nephrotic
LM- congo red staining shows apple-green birefringence, in the mesangium
AL and AM amyloid systemic conditions
1˚ AL protein (MM)
2˚ SAA protein (chronic inflammation)
Associated with Fanconi syndrome with hyperKalemia
Diabetic glomerulonephropathy
Nephrotic
LM- mesangial expansion, GBM thickening, eosinophilic nodular glomerulosclerosis (Kimmestein-Wilson lesions)
Glycosylation of GBM leads to permeability and thickeing
Glycosylation of eff. art. leads to hyalinosis decreasing GFR and mesangial expansion
Microalbuminuria from hyperfiltration injury
Slow progress with ACEIs
Retinopathy precedes nephropathy
Pre-eclampsia
Nephrotic
Poor perfusion of placental artery (no dilation)
Changes in prostaglandins, with hypercoag. and vasoconstriction
Young primigravid mothers, glomerular endotheliosis
HTN, bland UA, edema, uremia, hypocalciuria
Tubulointerstitial disorders
Can be caused by glomerular injury, immune mediation, intrarenal dynamics, DM, stones, obstruction
Present: mild to moderate proteinuria, sterile pyuria
