Glomerulonephritis Flashcards Preview

Nephrology > Glomerulonephritis > Flashcards

Flashcards in Glomerulonephritis Deck (15)
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Nephrotic Syn

Urine protein >3500mg/d
Hyercoagulability due to loss of protein C and AT3
Increased risk of infection likely due to immunoglobulin


Minimal change glomerulopathy

Acute onset of edema and weight gain. Urine protein very elevated, complement normal, serology negative

Biopsy: normal glomeruli on light and immunofluorescence. Tubules may have lipid accumulation. Electron shows effacement of epithelial foot processes
Tx with steroids

Secondary causes: NSAIDs, lithium, pamidronate, interferon, hodgkin lymphoma


Membranous glomerulopathy

Edema, nephrotic proteinuria, hypertension, microhematuria, thromboembolic events common (renal vein thrombosis).

Biopsy: glomerular capillary loops that appear thickened w/o proliferative lesions, subepithelial immune dense deposits on electron/immunofluorescence.

1/3 remit spontaneously, generally if no remission after 6-12 months/worsening renal function/thromboembolic events: tx with steroids, cyclophosphamide/calcineurin.

Primary is antibody to phospholipase A2 receptor.
Secondary is malignancy, AI disease, infections.

If cause is secondary, tx precipitating infection or malignancy.

HepB/C, malaria, syphilis, SLE,


Focal Segmental Glomerulosclerosis

Asymptomatic nephrotic proteinuria or edema. Often accompanied by HTN, microscopic hematuria, varying kidney failure.

Serology and complement normal

Biopsy: segmental scars in glomeruli, electron microscopy shows visceral epithelial foot process effacement but no immune deposits

Idiopathic or secondary (HTN, DM, Obesity, sickle cell, HIV, drugs)

HIV is related to collapsing form

Most common form in blacks

Minority of patients have spontaneous remission, otherwise tx with steroids or calcineurin inhibitors


Diabetic Nephropathy

Starts with microalbuminuria, then 10-15 years after DM dx, progresses to overt proteinuria.

Test for proteinuria at dx of DM2 and 5 years after DX of DM1.

Biopsy not indicated unless concerned for alternative pathology.

Tx with ACE or ARB



Progression to overt renal failure within weeks.

May be associated with any etiology or idopathic

typically presents with nephritic syn, variable renal failure, systemic signs either vasculitic (arthritis, epistaxis, hemoptysis) or lung hemorrhage (goodpasture).

Serology may reveal cause. CXR may confirm pulmonary hemorrhage.

Tx with steroids then maybe cyclophosphamide or rituximab. Plasmapheresis if pulmonary hemorrhage or severe renal failure.

particularly common with anti-GBM and pauci-immune small vessel vasculitis



Antibodies against type IV collagen

Generally presents with neprhitic proteinuria

Complement normal, elevated anti-GBM

Goodpastures is pulmonary + renal involvement

Biopsy: proliferative GN, many crescents, linear IgG deposition

Tx Cylcophosphamide/steroids


Nephritic Syn

hematuria with dysmorphic RBCs with or w/o casts

variable protein


Pauci-immune GN

Microscopic vessel vasculitis.


Can be kidney limited or widespread (palpable purpura, pulm disease).


IgA Nephropathy

Asymptomatic microscopic hematuria with or w/o proteinuria. Episodic gross hematuria following URI (synpharyngitic nephritis - occurs shortly after or concomitant with URI).

Serology and complement normal.

Bx: mesangial proliferation on light micro, IgA deposit on immuno.

20 year survival is 75%, can tx with steroids.

Most frequent cause of GN, particularly Asia/Northern europe. Rare in blacks.


IgA Vascultis

AKA Henoch-Schonlein Purpura

Kidney involvement similar to IgA, also have abdominal findings and palpable purpura.


SLE nephritis

May be presenting finding of SLE.

Likely will have SLE serologies (ANA/DNA, low C3/4).

Biopsy: immune complex deposition in all areas of glomerulus.

Tx: depends on class, if 3-4 use aggressive immunosuppresion.


Post-infectious GN

Immune Complex mediated, typically present with acute nephritic syn.

Low C3, Normal C4, ASO titer positve, Anti-DNAse B

Associated with strep/staph infections. Ecoli is risk factor too. Typically present with 7-10 day latent period after infection.

DM is risk factor.

Tx underlying infection.



Very commonly associated with Hep C

Patients with cryoglobulinemia may manifest a spectrum of kidney abnormalities, including mild proteinuria and hematuria, the nephrotic syndrome, and rapidly progressive glomerulonephritis with rapid deterioration of kidney function. C4 (and sometimes C3) complement levels are typically low, and rheumatoid factor is positive.



Histologic findings of mesangial and endocapillary proliferation combined with the thickening of the GBM.

Caused by immune complex deposistion or activation of alternative complement pathway.

Immunoglobulin mediated: SLE, HepC, monoclonal gammopathy

Complement mediated: Dense deposit disease (DDD) or C3 glomerulopathy