The Hallmark of glomerulonephritis is glomerular hematuria (acanthocytes and RBC casts or cellular casts), decline in renal function

and if it occurs rapidly even oliguria, hypertension and edema may be present. On light microscopy, glomerulonephritis may be
notable for “proliferative” changes (an influx of PMN’s). If the damage to the glomerulus is severe, there can be regions of necrosis
(call this necrotizing GN). If the glomerular damage leads to fibrin in the urinary space, a crescent may develop. These terms,
crescentic GN, necrotizing GN, proliferative GN, are descriptive and they don't indicate the cause of the nephritis. The terms acute
nephritis or rapidly progressive GN describe the acuity but also do not indicate the cause. Instead, we typically use clinical
information and the biopsy to characterize the disorder.
For glomerulonephritis cases for H2, we will characterize by the immune mechanism:
Mechanism and
Presentation Light Microscopy EM Immunofluorescence Treatment
Pathologic name
LINEAR Ribbon-like deposits of
STAINING of IgG If there is also IgG Immunosuppressive
pulmonary therapy
Anti-GBM disease involvement, Crescentic GN Diffuse
An autoimmune disease called and/or necrotizing subendothelial Plasmapheresis to
vs. α5 chain of type IV Goodpasture’s GN deposits remove the antibody
collagen, in situ
immune complex
formation

PAUCI-IMMUNE Depends on Immunosuppressive

In most cases, we whether it is part therapy
believe ANCA of systemic Since IF is
activates PMN which illness or renal negative, no
Crescentic GN
damage glomerular limited. May be deposits on EM
and/or necrotizing Negative
endothelium (and cANCA (assoc (IF tells us WHAT
GN
potentially other small with it is, EM tells us
vessels) sinus/respiratory where)
sx) or pANCA
(assoc with GI sx)
GRANULAR STAINING of Presentation Light Microscopy EM and IF Treatment
Immune complexes
(Examples explored in H2)
Post infectious (or post strep) Subepithelial humps AND Typically, benign
1. Antigen from infection subendothelial deposits course and
deposits subendothelial space and 10 days to 2 supportive care
form immune complex in situ or weeks AFTER IF with granular and
circulating immune complexes infection irregular IgG (more earlier
deposit in subendothelial space.
(infection has in course, less-perhaps
These immune complexes are
cleaned up by influx of PMN
resolved, this is a just in those occasional
2. Small amount of antigen is
renal limited humps-once the PMN
Proliferative changes
filtered and lands in subepithelial disorder) have done their work
(influx of PMN’s and
space, small amount of antibody is closed loops)
filtered and binds antigen in situ and
forms a hump. Not a lot of these, but
they persist
Varied Usually “mesangial Electron dense deposits If severe rapid
IgA nephropathy presentations and pattern” (IgA are primarily in the course,
Evolving understanding! IgA is the severity. Ex: - glycosylated and mesangium (which is immunosuppression.
antibody of mucosal immunity, Visible hematuria prominent on PAS contiguous with the If indolent course
patients with this disorder may have within 1-2 days of
stain) subendothelial space and characterized by
abnormal IgA response or type of URI
can invite) an influx of proteinuria, RAAS
IgA with “underglycosylation” -systemic illness
Henoch-Schönlein inflammatory cells blockade
which may make it sticky and
Purpura
SLE nephritis
Autoimmune disorder with circulating immune complexes (mainly IgG but can be all) that deposit in the glomerulus, activate complement
damage the glomeruli. We used this as an example to explain nephritis and nephrosis but students not responsible for more specifics