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Internal Diseases
Propaedeutics Department
Professor T.A. Dronova
Lecture
GLOMERULONEPHRITIS
GLOMERULONEPHRITIS
Group of diseases with affection of
GLOMERULONEPHRITIS
Nomenclature
Inflammation with leukocyte infiltration,
antibody deposition, &/or compliment
activation
Primary - when major problem starts in
the glomeruli
Secondary - when involvement is part of
systemic disease (SLE, diabetes
mellitus, amyloidosis)
GLOMERULONEPHRITIS
Nomenclature
Glomerular injury
Acute over days or weeks
Subacute or rapidly progressive - over weeks
or few months
Chronic - over many months or years
Glomeruli involvement
Focal minority (< 50%)
Diffuse majority (> 50%)
Segmental - part
Global almost all
GLOMERULONEPHRITIS
Nomenclature
Proliferative increase in glomerular cell
number (due to infiltration by leukocytes or
resident glomerular cells proliferation)
Proliferation of resident glomerular cells:
Intracapillary / endocapillary endothelial or
mesangial cells
Extracapillary Bowmans space (most
proximal portion of renal tubule)
GLOMERULONEPHRITIS
Nomenclature
Crescent half-moon-shaped collection of
GLOMERULONEPHRITIS
Essentials of diagnosis
Hematuria, dysmorphic red cells, red
GLOMERULONEPHRITIS
Primary
Minimal change glomerular disease
Membranous glomerulonephritis
Membranoproliferative glomerulonephritis
Ig A nephropathy
Crescentic rapidly progressive
GLOMERULONEPHRITIS
Secondary
Common
SLE
Polyarteritis nodosa
Diabetes mellitus
Amyloidosis
Schonlein-Henoch disease
Malarial nephropathy
GLOMERULONEPHRITIS
Secondary
Uncommon
Pre-eclampsia & eclampsia
Malignancy associated paraproteinemia
Cryoglobulinemia
Rheumatoid artritis
Scleroderma
Hemolitic uremic syndrome
Wegeners granulomatosis
Cytomegalovirus nephropathy
AIDS nephropathy
GLOMERULONEPHRITIS
Pathogenesis (2 main processes )
Circulating immune complex deposition
most common
GLOMERULONEPHRITIS
Secondary mechanisms
Circulating immune complex deposition &
GLOMERULONEPHRITIS
Pathogenesis
Antigens
Exogenous:
Bacteria
Viruses
Parasites
Drugs
Endogenous:
Host antigens
Immune complex-mediated
glomerulonephritis - causes
Bacteria:
Beta-hemolitic streptococcus group A
Streptococcus viridans (in endocarditis)
Streptococcus pneumoniae
Staphylococcus
Treponema pallidum (syphilis)
Gonococcus
Salmonella
Meningococcus
Immune complex-mediated
glomerulonephritis - causes
Viruses:
Hepatitis B & C
Epstein-Barr virus
Coxsackie virus
Varicella
HIV
Mumps
Measles
Immune complex-mediated
glomerulonephritis - causes
Parasites:
Plasmodium malariae
Schistosomatosis
Filariasis
Toxoplasmosis
Drugs:
Penicillamine
Host antigens:
DNA in SLE
Malignant tumors
GLOMERULONEPHRITIS
Clinical picture
1 of 5 clinical presentations:
Asymptomatic proteinuria &/or
microscopic hematuria
Acute nephritic syndrome
Nephrotic syndrome
Rapidly progressive glomerulonephritis
Chronic glomerulonephritis
glomerulonephritis
Poststreptococcal glomerulonephritis
leading cause of acute nephritic
syndrome
(most common)
Ig A nephropathy
Schonlein-Henoch purpura
Wegeners granulomatosis
Goodpastures syndrome
Polyarteritis nodosa
Acute interstitial nephritis
Essential mixed cryoglobulinemia
Poststreptococcal glomerulonephritis
After pharyngeal or cutaneous infection with
Poststreptococcal glomerulonephritis
Diagnosis - at least 2 of 3 features:
Group A beta-hemolytic streptococcus (nephritic
dull
Decreased diuresis sometimes anuria
(may be frequent tenesmus)
Bed rest
Salt free diet
Protein restriction in ureamia
Daily record of fluid intake & excretion
Daily weighing (body fluid status change)
Regular measurement of blood pressure
Diuretics (reduce hypertension & edema)
Anti-hypertensive drugs
Antibiotics (in poststreptococcal
glomerulonephritis positive culture)
NEPHROTIC SYNDROME
Features
Heavy proteinuria (> 3g/24 hours)
Hypoalbuminemia (serum albumin
<30g/l)
Edema
Hyperlipidemia (due to increased
hepatic lipoprotein synthesis)
Hypercoagulability
NEPHROTIC SYNDROME
PATHOGENESIS
Proteinuria: capillary wall injury of glomeruli
NEPHROTIC SYNDROME
PATHOGENESIS
Generalized edema:
Salt & water retention
Hypoalbuminemia - decrease colloid
NEPHROTIC SYNDROME
PATHOGENESIS
Hypercoagulability:
Increased urinary antithrombin III loss
Altered levels &/or activity of protein C &
protein S
Hyperfibrinogenemia increased hepatic
synthesis
Impaired fibrinolysis
Increased tendency of platelet
aggregation
NEPHROTIC SYNDROME
1.
2.
3.
4.
5.
6.
NEPHROTIC SYNDROME
CLINICAL FEATURES
Edema:
Peripherial oedema involving upper
& lower limb
Intense edema of scrotum or vulva
may occur
May be bilateral hydrothorax
NEPHROTIC SYNDROME
Clinical Features
Edema of intestine causes anorexia,
NEPHROTIC SYNDROME
Clinical Features
Hypercoagulability: peripheral arterial
NEPHROTIC SYNDROME
INVESTIGATIONS
Urine - proteinuria
24 hours urinary proteins: usually > 3 g/day
Serum albumin: < 3g/day (total serum protein <6
mg/dl)
Low density lipoprotein - elevated,
high density lipoprotein - normal
Raised ESR due to increased serum fibrinogen
Urine red cells & red cell cast
Blood sugar for diabetes & antinuclear factor for
SLE
Hepatitis B serology, serum complements
NEPHROTIC SYNDROME
INVESTIGATIONS
Renal biopsy: confirms diagnosis
Renal biopsy contraindicated:
Children under 10 years
Known diabetes mellitus
Patient on drug (penicillamine)
NEPHROTIC SYNDROME
COMPLICATIONS
Protein malnutrition
Hypercoagulability - due to rise in
NEPHROTIC SYNDROME
MANAGEMENT
Diet: low salt diet, moderate protein restriction
NEPHROTIC SYNDROME
COMPLICATION MANAGEMENT
A. Venous thrombosis due to
hypercoaguloability
Prolonged bed rest should be avoided
In renal vein thrombosis - anticoagulants
B. Sepsis
Aggressive treatment of infection with
antibiotics
C. Oliguric renal failure
Maintain blood pressure & fluid volume
Albumin infusion, mannitol may initiate
diuresis
NEPHROTIC SYNDROME
MANAGEMENT
Specific therapy:
Minimal change disease (most common cause of
nephrotic syndrome in children, 20% in adult) prednisolone
Membraneous gloumerolunephritis (most
common cause of nephrotic syndrome in adult
after 30 age [5th-6th decade], high incidence of
renal vein thrombosis, in 50% - occult neoplasm
of lung, stomach & colon) - prednisolone &
azathioprine, chlorambucil or cyclophosphamide
Other causes - SLE: prednisolone & azathioprine
CHRONIC
GLOMERULONEPHRITIS
Persistent proteinuria &/or hematuria & renal
insufficiency with slow progression over years
Diagnosis:
upon routine urinanalysis
routine blood tests with unexplained anemia
elevated blood urea nitrogen & creatinine
discovery of bilateral small kidneys on abdominal
imaging
5. during evaluation for secondary causes of
hypertension
6. during clinical exacerbation of glomerulonephritis
triggered by pharyngitis or other infections
1.
2.
3.
4.
CHRONIC
GLOMERULONEPHRITIS
Manifestation of virtually all of major
glomerulonephritis
Renal biopsy typically reveals a variable
combination of proliferative, membranous,
sclerotic changes, depending on the causative
glomerulopathy
CHRONIC
GLOMERULONEPHRITIS
Arteriosclerosis, induced by secondary
CHRONIC
GLOMERULONEPHRITIS
2 periods:
I. Renal compensation stage (nitrogen
CHRONIC
GLOMERULONEPHRITIS
I. Renal compensation stage (signs &
CHRONIC
GLOMERULONEPHRITIS
I. Renal compensation stage:
Increased BP
Left ventricular hypertrophy
Urinalysis: proteinuria, cylindruria (waxy casts)
Leached erythrocytes (usually - small qauntity)
Increased serum cholesterol
Hypoproteinemia due to permanent proteinuria
CHRONIC
GLOMERULONEPHRITIS
II. Renal decompensation stage (nitrogen
disease
Osteosclerosis
Renal osteodystrophy
Osteomalacia: kidney failure to convert
Renal osteodystrophy
Hyperparathyroid bone disease: secondary
Amenorrhea in females
Loss of libido in both sexes
5. CVS Disorders
Hypertension
Atherosclerosis
Pericarditis
8. Skin abnormalities
Yellow brown pigmentation due to accumulation
of urinary pigment in skin especially urochromes
9. Neuromuscular disturbances
a. Neuropathy
sensory neuropathy
motor neuropathy
autonomic neuropathy
b. Myopathy
anemia
3. Ultrasound examination describes renal
size & defines or excludes obstructions
4. IVP size, shape & position of kidney &
calculi
replaced by dialysis
The endocrine & metabolic functions renal transplantation
Approximate
frequency
68%
Proteus mirabilis
12 %
Klebsiela
aerogens
4%
Approximate
frequency
Streptococcus
faecalis
6%
Staphylococcus
saprophyticus
or epidermidis
10%
Approximate
frequency
68%
Proteus mirabilis
12 %
Klebsiela
aerogens
4%