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

Classical pathway C3 convertase

Membrane
(C4 + C2) (C4bC2a)
attack complex

Recruitment of
C3 C3b PMNs
C3a Opsonization,
phagocytosis

Alternative pathway C3 convertase

Anaphylaxis,
Microbial surfaces Chemotaxis
(polysaccharides)
 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
 RenalUS-nl to slightly enlarged kidneys
CXR-Central venous congestion
Occasionally enlarged cardiac shadow
Hypocomplementemia
Normal complement
PIGN
Bacteria (GAS, S. viridans,
pneumococcus, S. aureus, S.
epi, atypical mycobacterium, HUS
meningococcus, Brucella,
Leptospirosis,
Propionibacterium) IgA Nephropathy
Viruses (VZV, EBV, CMV, rubeola)
HSP

Parasites (Toxo, Trich,
Riskettsia)
Membranoproliferative GN Alports / TBMD
SLE Nephrotic Syndrome
Cryoglobulinemia
Bacterial Endocarditis
Shunt nephritis
Myoglobin IGAN Hypercalciu Meatal
Hemaglobin Benign ria Stenosis
Bile Familial Nephrolithi Urethritis
Urate Glomerul asis Bladder
Crystals onephritisTrauma tumor
Beets MPGN Sickle Cell Menstrual
Blackberry HSP NSAIDS contamin
SLE Renal V. ation
Food dye
Alport Thrombos Diaper rash
Drugs
Pyelonephri is
Exercise
tis Cystitis
PIGN
 Nephrotic Syndromes Hurler
Acquired Glomerular Gaucher Disease
Disease Wilson Disease
MPGN SC
SLE Leukemia
IGAN Lymphoma
SBE Infectious
DM PSGN
HTN HIV nephropathy
HUS HEP B and C
Genetic Disorders Malaria
Nail-patella syndrome Syphilis
Alport syndrome Pyelonephritis
Fabry Disease Drugs/toxins
Glycogen storage disease
CF
 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