glomerulonephritis for gpvts
TRANSCRIPT
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Nephritic Sx & Nephrotic Sx
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Case report 1
18 yr old man
Bilateral loin pain
Macroscopic haematuria
Sore throat started one day earlier
BP 140/90; euvolaemic
Creatinine 120 mol/l Proteinuria and haematuria on dipstix
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Case Report 2
20 yr old lady
Completely well
Haematuria on dipstix
No proteinuria
Normotensive
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Case Report 3
12 year old boy
Impetigo two weeks earlier
Headache
Oliguric
Frothy dark coloured urineHypertensive
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Case report 4
15yr old woman
3/12 ankle swelling; face and fingers
swollen in the am BP 130/80; JVP normal; Leg oedema
Creatinine 54 mol/l
Cr Cl 140 ml/min Albumin 18 g/l
24 hr u.protein 10 g
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Case Report 5
30 year old man,diabetic
Known hypertensive
Ankle oedema
Dipstix: ++++ proteinuria
Creatinine 124 mol/l (80120)
Albumin 30 g/l (3645)
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Case Report 6
50 year old obese man
Hypertension 10 years
NIDDM 3 years
No retinopathy
Creatinine 124 mol/l24 hr urine protein 2 g
HbA1 9.6%
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Structure of thefiltration barrier
Podocyte
Foot processes
Fenestratedendothelium
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Minimal change disease
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Glomerular changes in disease
ProliferationSclerosis
Necrosis
Increase in mesangial
matrix
Changes to basementmembrane
Immune deposits
Diffuse vs focal
Global vs segmental
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Common Syndromes
Nephrotic Syndrome
Nephritic Syndrome
Rapidly Progressive GN
Loin Pain Haematuria Syndrome
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Features of Glomerular Disease
Proteinuria
Haematuria
Renal Failure
Salt and Water Retention
Loin Pain
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Salt and Water Retention
Hypertension
Oedema
Oliguria
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Loin Pain
Rare
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Proteinuria
Marker of renal disease
Risk factor for
cardiovascular disease
Dyslipidaemia
Hypertension
Something more?
24 hr protein vs urine
protein:creatinine ratio
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Nephrotic syndrome
Proteinuria > 40 mg/m2*hr
Hypoalbuminaemia (
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Learning Points
Clinical features
Commonest types
Prognosis
Causes
Treatments
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Nephrotic Syndrome
Causes of primary idiopathic NS
Minimal change disease
Mesangial proliferation
Focal segmental glomerulosclerosis
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Minimal Change Disease
Usually children
Nephrotic syndrome withhighly selective
proteinuria andgeneralised oedema
Rarely hypertension orARF
T cell mediatedVPF
Steroid sensitive usually
Spectrum of disease toFSGS
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Focal Segmental
Glomerulosclerosis
Juxtamedullary glomeruli
may be missed due to
sampling error
Older patients
Less sensitive to
immunosuppression
Hypertension,
haematuria, progressive
CRF
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FSGS:
Familial
VUR
Drug abuse
Obesity
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Common types of GN
Primary
Thin membrane disease
IgA disease
Minimal Change / FSGS spectrum
Membanous Nephropathy
Secondary
PSGN & Diabetic Glomerulosclerosis
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Rarer Types
Diffuse endocapillary proliferative GN
(post infectious GN)Crescentic GN
Membanoproliferative / mesangiocapillary
GN
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Nephritic Syndrome
Haematuria
Hypertension
Oliguria
Edema
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Rapidly progressive GN
Nephritic or nephrotic onset
ESRF in six months
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General Treatment of GN
Control BP
Angiotensin blockade
Statin
Lose weight
Stop smoking
(pneumococcal prophylaxis)
(anticoagulation)
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Help!
I need a volunteer!
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Case report 1
18 yr old man
Bilateral loin pain
Macroscopic haematuria
Sore throat started one day earlier
BP 140/90; euvolaemic
Creatinine 120 mol/l Proteinuria and haematuria on dipstix
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Case 1: indicative answers
IgA Disease
Renal failure, proteinuria, haematuria,
oedema, hypertension, oliguria, loin pain
All except oedema and oliguria
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Mesangial IgA disease
Classical BergersDisease
Microscopic haematuria
Proteinuria (rarelynephrotic)
Hypertension
Chronic renal failure
? Failure of hepaticclearance of IgA
Association with GIdisease
No specific treatment
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Ig A Nephropathy
Ig A nephropathy is the most common primary
GN worldwide
Usually present with hematuriaEpisodes of gross hematuria are precipitated by
flu like illness, exercise
Urinary protein excretion usually non-nephrotic
Associated with chronic liver ds, psoriasis, IBD
and HIV disease.
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Ig A Nephropathy
Only 30% of patients with IgA
nephropathy has progressive disease.
In progressive disease, use of fish oil maybe beneficial.
Immunosuppressive therapy in patients
with Ig A nephropathy has not consistentlyshown to be of benefit
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Case Report 2
20 yr old lady
Completely well
Haematuria on dipstix
No proteinuria
Normotensive
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Case 2: indicative answers
Exclude menstruation!
Thin membrane disease (possibly IgA
disease)
Commonest cause of isolated microscopic
haematuria in this age group.
At this age, urological cause unlikely; nil
to suggest infection / urolithiasis
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Thin membrane disease
Most common GN
Microscopic haematuria
Familial
Benign
No treatment needed
Most young people with
isolated microscopichaematuria have thinmembrane disease
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Case 3: indicative answers
Acute nephritic syndrome
Post-streptococcal glomerulonephritis
Diffuse proliferative endocapillary
glomerulonephritis
Due to salt and water retention, so salt
restriction or loop diuretic
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Acute Post-Infectious GN
Usually occur in children
Post-streptococcal GN is the most common cause of
post infectious GNOccurs after a streptococcal sore throat or impetigo
Caused by Group A, beta-hemolytic streptococci,
particularly nephritogenic strainsType 1,4,12
(throat) and 2,49(skin)
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Acute Post-Infectious GN
Acute onset of gross hematuria (COLA
COLORED) or microscopic hematuria
after latent period of 10-14 days.Edema/hypertension
RBC casts on U/A
Elevated creatinine, increased ASO titer
Decreased complement level
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Acute Post-Infectious GN
LMDiffuse proliferative and exudative
GN
IFIgG and C3 lumpy, bumpy
EMSub epithelial Hump or Flame
like deposits
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Diffuse Endocapillary Proliferative GN
(Post Streptococcal GN)
Diffuse endocapillaryproliferative GN
Post infectious; usually
Gp A Strep Acute nephritic syndrome
Uraemia rare
Self-limited; rarely death
from
BP Abnormal RUA for up to
2 yrs
Circulating immunecomplex mediated
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Acute Post-Infectious GN
Renal biopsy is generally not required.
Treatment is supportive and consist of
sodium restriction, control of BP and
dialysis if this become necessary.
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Complications of the Nephr itic Syndrome
Hypertensive encephalopathy (seizures, coma)
Heart Failure (pulmonary oedema)
Uraemia requiring dialysis
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Prognosis in the Nephr itic Syndrome
More than 95% of children make a complete recovery
Chronic renal impairment in the longer term is uncommon in
children
Bad prognostic features include severe renal impairment at
presentation and continuing heavy proteinuria and
hypertension
Adults more likely to have long term sequellae than children
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Case report 4
15 yr old girl
3/12 ankle swelling; face and fingers
swollen in the am BP 130/80; JVP normal; Leg oedema
Creatinine 54 mol/l
Cr Cl 140 ml/min
Albumin 18 g/l
24 hr u.protein 10 g
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Case 4: indicative answers
Minimal changefocal segmentalglomerulosclerosis spectrum
Very nephroticAge and borderline BP make FSGS more
likely than MCN
Effect of loss of colloid osmotic pressuregradient across glomerulus causinghyperfiltration
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Case Report 5
30year old man,diabetic
Known hypertensive
Ankle oedema
Dipstix: ++++ proteinuria
Creatinine 124 mol/l (80120)
Albumin 30 g/l (3645)
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Case 5: indicative answers
Nephrotic syndrome secondary to diabetes
/ membranous disease
Refer urgently to nephrology
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Diabetic glomerulosclerosis
Retinopathy
Hypertension
MicroalbuminuriaNephrotic syndrome
Renal failure
usually progressivePoor prognosis on
RRT
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What wed like!
Demography including tel no and occupation
Reason for referral: presenting complaint,expectations
Co-morbidities, incl other diagnoses, smoking,alcohol and BMI, social care needs
Examination
Medications (incl recently stopped), allergies etcTreatment and investigations to date
Special requirements (eg interpreter)
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Case Report 6
50 year old obese man
Hypertension 10 years
NIDDM 3 years
No retinopathy
Creatinine 124 mol/l
24 hr urine protein 2 g
HbA1 9.6%
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Case 6: indicative answers
Obesity-related FSGS more likely than diabetic
nephropathy (duration diabetes, absence of
retinopathy)
Worsening nephrotic syndrome and progressive renal
failure; Death from cardiovascular cause before
reaches ESRF
Stop smoking, lose weight, improve glycaemic control,regular exercise, healthy diet, moderate alcohol in that
order
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Case 6: indicative answers contd
Lack of ownership of responsibility for own health
Withdrawal symptoms (smoking)
Denial of calorie intake
Difficulty exercising due to immobility
No!
Problems with MDRD equation
No evidence of benefit of ACE inhibitors in absence proteinuria Dangers of ACE inhibitors in patients with angioneurotic
oedema, hypotension or bilateral renal artery stenosis
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Lessons
Not all abnormal urinalysis is a UTI
Acute pyelonephritis is very rarely bilateral
H t i
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Haematuria
Urologist or Nephrologist?
Age
Other features
proteinuria etcUrine microscopy for
casts
Phase contrast
microscopy
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Non-dysmorphic vs dysmorphic
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RBC Cast
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AntiGBM disease
RPGN + Lunghaemorrhage
Destructive processmedical emergency!
Antibody-mediated
One hit
High doseimmunosuppression
Plasma exchange
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Any Questions?
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Whoopee! Its .........
.Coffee Time