Glomerulonephritis Flashcards
etiology of GN
- Primary- idiopathic
2.Secondary
DM, SLE, CTdisease, Amyloidosis,
Infection(Hep B,Malaria),
Drugs(Penicillin,Gold,penicillamine)
Sx of injury to glomeruli
Proteinuria
hematuria
uremia
oliguria
edema
increased BP
Cause of proteinuria
increased capillary permeability
cause of hematuria
rupture of capillary walls
cause of uremia
reduced Glomerular filtration
cause of oliguria
reduced urine production
cause of edema
increased Na+ and water retention
cause of increased BP
disturbance of RAAS
clinical presentation of GN
Urinary abnormalities – proteinuria,
haematuria
Acute nephritic syndrome
Nephrotic syndrome
Rapidly progressing /ARF
CRF
Mixed picture of above
Nephrotic syndrome proteinuria levels
> 3.5g/d
can proteinuria get associated with hematuria in GN
Yupsiee
hematuria with albuminuria is highly suggestive of
GN
what should be ruled out if hematuria presents alone
urological causes
signs of hematuria which suggests glomerular bleeding
presence of RBC casts
dysmorphic figures
Nephrotic syndrome is characterized by
Proteinuria (heavy) 3.5 g/1.73 m2 S.A
Hypoalbuminaemia (<2.5 g/dl)
Oedema
Hyperlipidaemia(increased LDL, VLDL,
IDL)
causes of GN
Primary - idiopathic
Secondary- autoimmund disorders (SLE), diabetic nephropathy, drugs ( gold, penicillamine), infections, malignancy
common malignancies associated with GN
colorectal CA
Bronchial CA
HIstological types of GN
Minimal change disease (25-50%)
Membranous glomerulonephritis (1-
25%)
Focal and segmental glomerulosclerosis
(25%)
Proliferative glomerulonephritis (25%)
characteristics of edema seen in GN
initially dependant pitting
oedema (puffy eyes, swollen legs), later
becomes generalised (ascites, pleural
effusion, scortal edema)
elevated BP is common in nephrotic syndrome (T/F)
false. uncommon. reflex HTN is possible
Dx of Nephrotic syndrome
o Urine analysis
+3 or +4 proteinuria
microscopic haematuria
hyaline, granular casts.
o Serum albumin (< 2.5 g/dl)
o Serum cholesterol, triglycerides & total
lipids
o Blood urea & Serum creatinine
o 24 hr urine protein excretion > 3g/day
o Urine & serum electrophoresis
o Investigations for underlying cause –
ANF, dsDNA, other Ab (ANCA, antiGBM), DM, Multiple myeloma, for
infection (ASOT, Malarial parasite)
o Serum C3 levels
o Biopsy (Indications - Steroid resistant
nephrotic syndrome, Persistent
hypertension and/or haematuria
Mx of nephrotic Syndrome
Diet
o low salt
o normal protein diet
o low fat
Symptomatic treatment of oedema
o diuretics - K+ sparing diuretics, Loop
diuretics, sometimes with thiazides
o plasma (vol. depleted, no response to
diuretics)
Other measures to reduce proteinuria -
ACEI ,NSAIDs
Lipids - statins(Cardiovascular dx –
increased risk due to hyperlipidaemia)
Treat specific glomerular disease
Treat complications - infections
(peritonitis, cellulitis, UTI,LRTI)
Minimal change GN appearance on Microscope
look nearly normal
Colour and appearance of kidneys
Yellowish (lipid nephrosis)
cells of PCT and appearance of foot processes
laden with lipid- PCT
foot processes- fused
etiology of MCGN
T- cell disorders
associated with atopy and viral infections
Secondary to drugs (NSAID, Li, ABx)
associated with HCV, HIV, TB
Complications of Minimal change GN
- Infection
↑ Susceptibility during a relapse
↓ Immunoglobulins
↓ Factor B
Oedema fluid good culture medium
Peritonitis – most frequent
Strep. pneumoniae – most common
organism
Other infections – UTI, pneumonia,
cellulitis - Thrombosis- increased venous
thrombosis
↓ Anti thrombin III
↑ Fibrinogen
Risk greatest when serum albumin is very low
Relapse of MCGN
> 3 days of >3+ urine protein,
associated with oedema
Spontaneous remission towards the end of
second decade in MCGN (T/F)
True
what might influence the course of the disease in MCGN
the duration of treatment
Mx of MCGN
Oral prednisolone
FSGN affects
certain segments of some not all glomeruli
Sx of FSGN
Massive proteinuria/haematuria/HT/renal
impairment
etiology of FSGN
o Primary idiopathic disease
o In association with HIV( collapsing
FSGS) and heroin addiction
o As a secondary event in other forms of
GN- e.g. IGA nephropathy
o As a component of glomerular ablation
nephropathy
o HT, sickle nephropathy, obesity
FSGN responds to steroids (T/F)
False. resistant to steroids
Membranous GN EM findings
Diffuse thickening of the GCBM
Silver stains show spike and dome appearance
Etiology of Membranous GN
o Idiopathic
o Infections- chronic hepatitis B, syphilis,
schistosomiasis, malaria
o Malignant epithelial tumours- colon,
lung, lymphoma, leukaemia
o SLE(class V disease),
o Exposure to organic salts- gold, mercury
o Drugs- penicillamine, captopril
o Metabolic disorders- diabetes,
thyroiditis
Mx of Membranous GN
combination of
corticosteroid+ another agent
BP control- ACEI reduce proteinuria
Consider anticoagulation
prognosis of Membranous GN
One – third – spontaneous remission
One third – remain proteinuric
One third- develop ESRF
clinical features of acute nephritic syndrome
o oedema- periorbital, generalized (mild -
moderate), less marked than in
Nephrotic synd.
o oliguria - UOP <700ml/day
o haematuria (microscopic-macroscopic)
o hypertension
o Circulatory overload (increased JVP,
orthopnoea, 3rd HS, bilateral basal
crepitations)
o Renal impairment
o Elevated blood urea & serum creatinine
causes of acute nephritic syndrome
o Idiopathic - Less common
o Secondary - Post streptococcal
Glomerulonephritis is the commonest
cause
Pathophysio of acute nephritic syndrome
inflammatory damage
to filtration surface, shunting the blood
(glomerular haematuria) → reduced GFR
(Uraemia) → reduced filtrate volume →
reduced distal delivery, constant or
increased Na+ absorption, critical sodium
intake → positive sodium balance →
intravascular volume increase (oedema,
increased CO, hypertension, CCF)
acute nephritic syndrome findings
Skin/ throat sepsis +
Edema Mild/ moderate
Hematuria Macroscopic(often), microscopic
Oliguria +
HTN +
Renal impairment +/-
Circulatory overload +
Nephrotic syndrome
Skin/ throat sepsis -
Edema severe
Hematuria +/-
Oliguria -
HTN +/-
Renal impairment +/-
Circulatory overload -
Ix and findings of acute nephritic syndrome
o Urine microscopy- RBC, RBC casts, WBC,
protein (1 - 2 + on heat test)
o Blood urea, Serum creatinine - elevated
o Creatinine clearance (GFR) - reduced
o CXR
o For the underlying cause – eg ASOT
course and prognosis of acute nephritic syndrome
acute nephritic syndrome can lead to 1. acute renal failure, HT encephalopathy, pulmonary edema
2.Asx, hematuria +/- proteinuria
3. well
1.acute renal failure, HT encephalopathy, pulmonary edema
2.Asx, hematuria +/- proteinuria can lead to either CRF, death
Mx of acute nephritic syndrome
o Monitor - UOP, Weight, BP ,
Macroscopic Haematuria, BU, SE (esp if
ARF)
o Treatment of Strep. Infection -Penicillin
o Fluids - if oliguria - 500 cc + previous
days UOP
o Diet - salt restriction, K+ restriction,
+/- protein reduction to 20g/d if BU is
high
o Diuretics
o Anti- hypertensives
o Treatment of complications (Sometimes
dialysis needed)
LVF
ARF
Hypertensive encephalopathy
Acute proliferative GN aka
Post streptococcal GN
When does PSGN occur
Occurs 1-3 weeks after a group A beta
haemolytic streptococcal infection.(throat
infection/ cellulitis/ otitis media)
PSGN happens only with certain nephritogenic strains (T/F)
True
Most cases of the intial infections of PSGN
pharyngitis or a skin infection
PSGN EM findings
- Glomerulus is enlarged and cellular. 2.Proliferation and swelling of mesangial and
endothelial cells
types of cells that are involved in PSGN
Infiltration by neutrophils and monocytes
UOP for a person who comes with renal failure
Last day UOP + 400cc ( to cover insensible fluid loss)
but the patient will not know how much is the last UOP is, so monitor the patient’s UOP for 1 hour and 30cc
characterstic finding of membranoproliferative GN
double contour or tram track appearance with silver or PAS
etiology of membrano proliferative GN
o Idiopathic
o Type 1 picture may be seen in SLE,
hepatitis B & C, infected AV shunts,
secondary infections, malignancies
The emergency GN condition
Crescentic (Rapidly Progressing) GN
what happens in Crescentic (Rapidly Progressing) GN
rapid and progressive loss
of renal function associated with severe
oliguria
how are crescents formed in RPGN
proliferation of
parietal epithelial cells and infiltration by
monocytes and macrophages
classification of RPGN
Type 1 - anti GBM disease, linear deposits of IgG
eg- 1.Goodpasture’s syndrome
2. Idiopathic anti GBM mediated
Type 2- - Immune complex
mediated disease
Granular deposits of IgG
Post streptococcal, SLE, IgA
nephropathy, HSP
Type 3 - pauci immune type
Systemic vasculitis like polyarteritis
nodosa or Wegener’s granulomatosis
IgA Nephropathy occurs after….
within 1-2 days of a
non-specific URTI
Sx of IgA nephropathy
Recurrent macroscopic or microscopic
haematuria
Serum IgA levels in IgA nephropathy
raised by 50%
EM findings of IgA nephropathy
- Mesangial deposits of IgA.
- Glomerular injury due to activation of
alternate complement pathway. - Mesangial proliferation, focal proliferative
GN or rarely crescentic GN.
diseases associated with IgA nephropathy
HSP, CLCD, coeliac dx, CA
bronchus, sero negative spondyloarthritis
difference between IgA nephropathy and PSGN
IgA - 1-2 days after infection, relapses
PSGN- 10 days after, no relapses
Spot test done on nephrotic syndrome
UPCR ( urine protein creatinine ratio)
GN classification
Divided mainly into 2
1. minimal change Disease
100% clincal picture is nephrotic syndrome
good response to steroids
onset in children
- non minimal change disease
This is divided into two again.
A. Non- proliferative GN ( mostly nephrotic picture )
Eg- membranous GN
FSGN
glomerulosclerosis
B. Proliferative GN ( mostly nephritic)
Acute diffuse proliferative GN
Membranoproliferative GN
Mesangioproliferative GN
RPGN
Abdominal pain in nephrotic syndrome patient
Spontaneous bacterial peritonitis
Renal vein thrombosis
Hypovolemia causing gut ischemia
Gastritis ( steroids given )
