Glomerulonephritis

1. GlomerulonephritiGlomerulonephriti
ss

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3. Glomerular DiseaseGlomerular Disease
(Glomerulopathies)(Glomerulopathies)
Diverse disease processes that
mainly affect the glomerulus
and include, but are not limited to,
glomerulonephritis.
Glomerular Disease may beGlomerular Disease may be
primary or secondary to systemicprimary or secondary to systemic
disease.disease.

4. NephritisNephritis
Nephritis are theNephritis are the
inflammatory renal diseasesinflammatory renal diseases
of different etiology. Inof different etiology. In
dependence of longevitydependence of longevity ofof
inflammatory process and ainflammatory process and a
morphological variant ofmorphological variant of
defeat of we can subdividedefeat of we can subdivide
them on acute and chronicthem on acute and chronic
ones.ones.

5. Acute glomerulonephritisAcute glomerulonephritis
lastslasts no more than 12no more than 12
monthsmonths and an outcomeand an outcome
of disease can be aof disease can be a
complete recovery, orcomplete recovery, or
transition in a chronictransition in a chronic
glomerulonephritis.glomerulonephritis.

6. We can establish the diagnosisWe can establish the diagnosis
of chronic glomerulonephritis,of chronic glomerulonephritis,
whenwhen duration of diseaseduration of disease
exceeds 6 monthsexceeds 6 months after theafter the
beginning of acute process:beginning of acute process:
a primary chronica primary chronic
glomerulonephritisglomerulonephritis

7. We can confirm this diagnosisWe can confirm this diagnosis
on the basis of structuralon the basis of structural
changes (according tochanges (according to
additional methods of research)additional methods of research)
and morphological changes inand morphological changes in
biopsy a of material withoutbiopsy a of material without
acute process in the anamnesisacute process in the anamnesis
((a latent glomerulonephritisa latent glomerulonephritis).).

8. GlomerulonephritisGlomerulonephritis
is a group of inflammatoryis a group of inflammatory
diseases of kidneys withdiseases of kidneys with
inclusion autoimmuneinclusion autoimmune
mechanisms and primary defeatmechanisms and primary defeat
of renal glomeruli and involvingof renal glomeruli and involving
in pathologic process of renalin pathologic process of renal
channels, interstitial tissue andchannels, interstitial tissue and
vessels.vessels.

9. PyelonephritisPyelonephritis
is an inflammatory disease ofis an inflammatory disease of
kidneys of an infectious originkidneys of an infectious origin
with primary localization ofwith primary localization of
process in interstitial tissue andprocess in interstitial tissue and
obligatory defeat of system ofobligatory defeat of system of
renal calyces and pelvises.renal calyces and pelvises.

10. GlomerulonephritisGlomerulonephritis is a groupis a group
ofof b bilaterial, difffuse, geneticallyilaterial, difffuse, genetically
caused immuno-inflammatorycaused immuno-inflammatory
disease of kidneys with primarydisease of kidneys with primary
defeatdefeat renal glomerulirenal glomeruli andand thethe
subsequent involving in processsubsequent involving in process
renal channels, interstitial tissuerenal channels, interstitial tissue
and vesselsand vessels..

11. Infectious agents are the mostInfectious agents are the most
common inciting antigenscommon inciting antigens
associated with immune complexassociated with immune complex
mediated glomerulonephritis. Post-mediated glomerulonephritis. Post-
streptococcal glomerulonephritis isstreptococcal glomerulonephritis is
the most common form ofthe most common form of
glomerulonephritis in children andglomerulonephritis in children and
occurs following a skin oroccurs following a skin or
pharyngeal infection with Group Apharyngeal infection with Group A
beta-hemolytic streptococci.beta-hemolytic streptococci.

12. ETIOLOGYETIOLOGY
The most important agents are:The most important agents are:
 Group A β-hemolytic streptococciGroup A β-hemolytic streptococci
type 12 (associated with pharynges) –type 12 (associated with pharynges) –
5 – 10%.5 – 10%.
 Group A β-hemolytic streptococciGroup A β-hemolytic streptococci
type 49 (associated with impetigo,type 49 (associated with impetigo,
skin infections) about 25%.skin infections) about 25%.

13. Post-infectious glomerulonephritisPost-infectious glomerulonephritis
has also been associated with otherhas also been associated with other
infectionsinfections::
BacterialBacterial
ViralViral
ParasiticParasitic
RickettsialRickettsial
FungalFungal

14. The precise nature of the antigensThe precise nature of the antigens
involved in the formation of theinvolved in the formation of the
nephritogenic immune complexes isnephritogenic immune complexes is
unknown. Streptococcal antigenicunknown. Streptococcal antigenic
substances have beensubstances have been
inconsistently detected in glomeruliinconsistently detected in glomeruli
and circulating immune complexesand circulating immune complexes
have been detected in somehave been detected in some
patients.patients.

15. Since streptococcal antigens do notSince streptococcal antigens do not
always cause disease, otheralways cause disease, other
mechanisms may be involved,mechanisms may be involved,
including alterations in IgG orincluding alterations in IgG or
glomerular components makingglomerular components making
them immunogenic. Antigensthem immunogenic. Antigens
derived from infectious agents mayderived from infectious agents may
bind to glomeruli structures andbind to glomeruli structures and
induce development of in situinduce development of in situ
immune complexes.immune complexes.

16. Pathology and pathogenesisPathology and pathogenesis
Immunofluorescence microscopyImmunofluorescence microscopy
ussually shows immune complexussually shows immune complex
deposition with IgG and C in adeposition with IgG and C in a
granular pattern.granular pattern.

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18. In 2-3 weeks after theIn 2-3 weeks after the
transferred streptococcaltransferred streptococcal
infection immune-inflammatoryinfection immune-inflammatory
reaction is started. Theyreaction is started. They
consider, that immuneconsider, that immune
complexes are the cause notcomplexes are the cause not
only of the occurrence, butonly of the occurrence, but
also of progressing ofalso of progressing of
glomerulonephritis and it’s,glomerulonephritis and it’s,
transition to chronic form.transition to chronic form.

19. Autoimmune genesis ofAutoimmune genesis of
glomerulonephritis can beglomerulonephritis can be
proved by presence in blood ofproved by presence in blood of
the given patients anti-renalthe given patients anti-renal
autoantibodies, which titer isautoantibodies, which titer is
higher at chronic, than at acutehigher at chronic, than at acute
course of disease, and alsocourse of disease, and also
efficiency CS and cytostaticefficiency CS and cytostatic
therapy.therapy.

20. Two variants are ofTwo variants are of
development ofdevelopment of GNGN andand
FormationFormation ICIC are possible.are possible.

21. 1.1. In a blood circulation thereIn a blood circulation there
is a formation of circulatingis a formation of circulating
immune complexes (an antigenimmune complexes (an antigen
+ an antibody + fiber+ an antibody + fiber
complement) whichcomplement) which
subsequently are besieged onsubsequently are besieged on
basal membranes glomerulibasal membranes glomeruli
capillaries or in mesangium andcapillaries or in mesangium and
damage them.damage them.

22. Immune complexes areImmune complexes are
appeared as a result ofappeared as a result of
formation of autoantibodiesformation of autoantibodies
against antigens, which are theagainst antigens, which are the
protein particles of the damagedprotein particles of the damaged
basal membrane and renalbasal membrane and renal
tissue. Linear deposits aretissue. Linear deposits are
formed on basal membrane.formed on basal membrane.

23. Immune complexes, damageImmune complexes, damage
basal membrane and causebasal membrane and cause
migration of leukocytes,migration of leukocytes,
thrombocytes to a place ofthrombocytes to a place of
damage therefore plenty BАS,damage therefore plenty BАS,
which raise the permeability ofwhich raise the permeability of
the capillaries.the capillaries.

24. InIn pathogenesispathogenesis of GN theof GN the
disorders of renal microcirculationdisorders of renal microcirculation
are of the great significant. Increaseare of the great significant. Increase
of intravascular coagulability inof intravascular coagulability in
glomeruli capillaries, aggregation inglomeruli capillaries, aggregation in
them thrombocytes and formationthem thrombocytes and formation
of fibrin are the reasons ofof fibrin are the reasons of
thrombosis of obturation athrombosis of obturation a gleamgleam
of capillaries.of capillaries.

25. Morphologically theMorphologically the
outcome of anyone GN isoutcome of anyone GN is
glomerulosclerosisglomerulosclerosis

26. Normal glomerular structureNormal glomerular structure

27. The immune deposits in membranousThe immune deposits in membranous
glomerulonephritis are located on the subepithelial,glomerulonephritis are located on the subepithelial,
or outer aspect of the glomerular basementor outer aspect of the glomerular basement
membrane as illustratedmembrane as illustrated..

28. Mesangial deposits are illustrated. TheMesangial deposits are illustrated. The
presence of mesangial deposits is generallypresence of mesangial deposits is generally
associated with an increase in mesangialassociated with an increase in mesangial
cellularity.cellularity.

29. Subendothelial deposits characteristic ofSubendothelial deposits characteristic of
membranoproliferative glomerulonephritismembranoproliferative glomerulonephritis
Type I are illustrated.Type I are illustrated.

30. The glomeruli in membranoproliferative glomerulonephritisThe glomeruli in membranoproliferative glomerulonephritis
type I demonstrate mesangial proliferation and mesangialtype I demonstrate mesangial proliferation and mesangial
interposition beneath the capillary loop endothelial cells withinterposition beneath the capillary loop endothelial cells with
formation of "double contours”.formation of "double contours”.

31. The major pathogenicThe major pathogenic
categories are inflammatorycategories are inflammatory
(nephritic syndrome) and(nephritic syndrome) and
hemodynamic (nephrotichemodynamic (nephrotic
syndrome).syndrome).
Acute nephritic syndrome isAcute nephritic syndrome is
used synonymously with acuteused synonymously with acute
glomerulonephritis (GN).glomerulonephritis (GN).

32. ClassificationClassification
• 1.1. Acute glomerulonephritisAcute glomerulonephritis
• 2.Subacute malignant2.Subacute malignant
glomerulonephritisglomerulonephritis
• 3.Chronic glomerulonephritis3.Chronic glomerulonephritis

33. Acute glomerulonephritis:Acute glomerulonephritis:
1. Etiology and1. Etiology and
Pathogenesis:Pathogenesis:
 Infectious – immuneInfectious – immune
 Noninfectious – immuneNoninfectious – immune

34. Morphological forms:Morphological forms:
•• Proliferative endocapillaryProliferative endocapillary
•• Proliferative extracapillaryProliferative extracapillary
•• Mesangio-Mesangio- proliferativeproliferative
•• Mesangio-Mesangio- capillarycapillary
•• Sclerotic (fibroplastic)Sclerotic (fibroplastic)

35. Clinical forms:Clinical forms:
•• Monosyndromic variantMonosyndromic variant
•• Polysyndromic variantPolysyndromic variant
•• Nephrotic syndromeNephrotic syndrome

36. Complications:Complications:
•• Acute Renal FailureAcute Renal Failure
•• AAcute Renal hypertensivecute Renal hypertensive
encephalopathyencephalopathy
•• Acute Cardiac FailureAcute Cardiac Failure

37. Character of an outcomeCharacter of an outcome ::
•• RecoveryRecovery
•• Recovery with "defect" - a minorRecovery with "defect" - a minor
uric syndromeuric syndrome
•• Fatal outcomeFatal outcome
••TTransition to corresponding formransition to corresponding form
of CGNof CGN

38. Acute GN is not typical forAcute GN is not typical for
adults.adults.
The chain is characteristic:The chain is characteristic:
quinsy (an aggravation of aquinsy (an aggravation of a
tonsillitis, a pharyngitis or othertonsillitis, a pharyngitis or other
streptococcal infection), in 2-3streptococcal infection), in 2-3
weeks - formation of immuneweeks - formation of immune
complexes, their fixation incomplexes, their fixation in
kidneys. After that the clinicalkidneys. After that the clinical
picture of GN appears.picture of GN appears.

39. Acute GNAcute GN
Monosyndrome/Monosyndrome/
Polysyndrome variantPolysyndrome variant
URINARY syndrom:URINARY syndrom:
proteinuria,hematuria (microproteinuria,hematuria (micro
or macroscopic), castsor macroscopic), casts
HypertensionHypertension
Edema, OliguriaEdema, Oliguria

40. NEPHROTICNEPHROTIC
SYNDROMSYNDROM
1.1. Proteinuria > 3.5 g/24hProteinuria > 3.5 g/24h
2.2. Hypoproteinemia < 65g/lHypoproteinemia < 65g/l
3.3. Edema, OliguriaEdema, Oliguria
4.4. Cholesterol > 5.2 mmol/lCholesterol > 5.2 mmol/l

41. PLAN of investigationPLAN of investigation
Blood test, Urine test,Blood test, Urine test,
Nechiporenko test,ESG.Nechiporenko test,ESG.
Diuresis/ 24 hDiuresis/ 24 h
Urea, creatinine,Urea, creatinine, proteinogram,proteinogram,
coagulogram, CRP, Na, K.coagulogram, CRP, Na, K.
Reberg testReberg test
Eye floor, US of kydniesEye floor, US of kydnies

42. TreatmentTreatment
1.Hospitalisation, bed regimen, diet N71.Hospitalisation, bed regimen, diet N7
2.Antibiotics: Penicillin 4 000000 U /24h2.Antibiotics: Penicillin 4 000000 U /24h
3. Heparin 5 000 x 4 times/ 24 h3. Heparin 5 000 x 4 times/ 24 h
4. Dipiridamol 300 – 350 mg / 24 h4. Dipiridamol 300 – 350 mg / 24 h
5. Prednisolon 1 mg/ kg/ 24 h5. Prednisolon 1 mg/ kg/ 24 h
6. Cytostatics6. Cytostatics
7. Diuretics, hypotensive drugs7. Diuretics, hypotensive drugs
8. Plasmapheresis, haemosorbtion8. Plasmapheresis, haemosorbtion