Nephritic Syndrome

Nephritic Syndrome
  • an Inflammatory process
  • When it involves glomeruli, it leads to
    • Hematuria and RBC casts in urine.
    • Associated with azotemia, oliguria, hypertension (due to salt retention), and proteinuria (< 3.5 g/day)
Acute poststreptococcal
Rapidly progressive
Diffuse proliferative
IgA nephropathy
(Berger disease)
Alport syndrome
Most frequently seen in children. Occurs ~2 weeks after group A streptococcal infection of the pharynx or skin.
RBC Cast
Resolves spontaneously.

Presents with:
 Peripheral and periorbital edema,
 Dark urine (cola-colored), and

—glomeruli enlarged and hypercellular.
IF—(“starry sky”) granular appearance (“lumpybumpy”) due to IgG, IgM, and C3 deposition along GBM and mesangium.
EM—subepithelial immune complex (IC)

Type III hypersensitivity reaction.

 anti-DNase B titers and  complement levels
LM and IF—crescent-moon shape A. Crescents consist of fibrin and plasma proteins (e.g., C3b) with glomerular parietal cells, monocytes, and macrophages.
Several disease processes may result in this pattern, including:
Goodpasture syndrome:
type II hypersensitivity; antibodies to GBM and alveolar basement membrane Ž linear IF
Granulomatosis with polyangiitis (Wegener):

ƒƒMicroscopic polyangiitis

Poor prognosis.
Rapidly deteriorating renal function (days to weeks).

Due to SLE or MPGN.

LM—“wire looping” of capillaries.
EM—subendothelial and sometimes
intramembranous IgG-based ICs often with C3 deposition.

Most common cause of death in SLE. DPGN and MPGN can present as nephrotic syndrome and nephritic syndrome concurrently
Often presents/flares with a URI or acute gastroenteritis.
Episodic hematuria with RBC casts.

LM—mesangial proliferation.
EM—mesangial IC deposits.
IF—IgA-based IC deposits in mesangium.
Seen with Henoch-Schönlein purpura


Deafness &
less commonly, Eye problems

Mutation in type IV collagen Ž thinning
and splitting of the glomerular basemen membrane.

Most commonly X-linked