MR 7/27/09

J. Chen

Background
Pathophysiology
Histologic Findings
Clinical
History
Physical
Lab

Differential Diagnosis
Treatment
Follow Up

Glomerulonephritis-various renal diseases in

which inflammation of the glomerulus,
manifested by proliferation of cellular
elements, is secondary to an immunologic
mechanism
Most associated with postinfectious state
4-12yr with peak 5-6years
Male:Female 1.7-2:1
Prognosis is good

Winter and Spring-respiratory infection

Latency

period 10 days for pharyngitis

Summer and Fall-associated with pyoderma

Latent

period difficult to determine

Not fully understood

Immune Complexes localize on glomerular
capillary wall and activate the complement
system (Zymogen and GAPDH)
Activation of complement cascade generates
C5a and platelet derived inflammatory
mediators
Various cytokines initiate an inflammatory
response manifested by cellular proliferation
and edema of glomerular tuft

Ab-Ag complexes

C3 convertase

Classical pathway
(C4 + C2)

C3

(C4bC2a)

Membrane
attack complex

C3b

Recruitment of
PMNs

C3a

Alternative pathway
Microbial surfaces
(polysaccharides)

C3 convertase

Opsonization,
phagocytosis

Anaphylaxis,
Chemotaxis

Measurable reduction in volume of

glomerular filtrate
Decreased capacity to excrete salt and water
leading to expansion of extracellular fluid
volume
Responsible for edema and in part for
hypertension, anemia, circulatory
congestion, encephalopathy

Light Microscopy-Glomerular tufts enlarged

and swollen

Electron-dense deposits (humps) in the

subepithelial space

History: latent period 7-21 days btw

streptococcal infection and glomerulonephritis
characteristics
Edema most frequent manifesting symptom
85%
Abrupt

onset
Periorbital area, may be generalized

Gross hematuria 30-50%

Smoky, cola,

rust, tea colored

+/- oliguria
Various degree of malaise, lethargy, anorexia,
fever, abdominal pain, headache

Hypertensive encephalopathy-HA, vomitting,

depressed sensorium, confusion, visual
disturbances, aphasia, memory loss,
convulsions, coma
Possible dyspnea, orthopnea, cough
Pallor

Edema
Systolic and Diastolic HTN to varying degree
(Inc ECF, cytokines with pressor effects)
Pallor
Pulmonary rales
Bradycardia/tachycardia
Depressed sensorium

Urine-output reduced, concentrated, acidic

Hematuria
Proteinuria
Glucosuria
RBC Casts-60-85%
Hyaline and/or cellular casts

Renal:
Elevation of BUN/Cr usually modest
Electrolytes usually normal (hyperK and met
acid with significant renal impairment)

Streptococcal infection:
Culture from Pharynx and skin may be
positive
Strep ab titers more meaningful

Measured at 2-3 wk intervals-Rise more significant

Hemolytic Complement
C3

decreased in 90%
C4 normal
C5 decreased
Complement levels return to normal 6-8 weeks
after onset

Mild Anemia-parallels the degree of ECF

expansion
WBC-Nl
Plts-Nl

Renal US-nl to slightly enlarged kidneys

CXR-Central venous congestion
Occasionally

enlarged cardiac shadow

Hypocomplementemia

PIGN

Normal complement

Bacteria (GAS, S. viridans,

pneumococcus, S. aureus, S. epi,
atypical mycobacterium,
meningococcus, Brucella,
Leptospirosis,
Propionibacterium)
Viruses (VZV, EBV, CMV, rubeola)
Parasites (Toxo, Trich,
Riskettsia)

Membranoproliferative GN
SLE
Cryoglobulinemia
Bacterial Endocarditis
Shunt nephritis

HUS
IgA Nephropathy
HSP
Alports / TBMD
Nephrotic Syndrome

Treatment mainly supportive

Hospitalization indicated if:significant HTN,
Oliguria, Generalized Edema, High Cr or K
Antibiotics do not influence course of
disease-however, administered to ensure
eradication of disease

Fluid Restriction
Salt Restriction
Loop Diuretics
Antihypertensives
Limited activity
Dialysis if necessary

Prognosis usually excellent

0.5% mortality due to pulmonary edema or pneumonia

<1% progress to CKD stage 5

Follow-up
Must

ensure that HTN controlled, Edema

resolved, hematuria/ proteinuria resolved, Cr
normalized

Gross hematuria resolves within 2 weeks

Complement low for 6-8 weeks
Proteinuria remains upto 6 months
Hematuria remains upto 2 years