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Nephrotic syndrome (Clinical presentation (Swollen ankles, Swollen…
Nephrotic syndrome
Clinical
presentation
Swollen ankles
Swollen genitals
Ascites
Periorbital oedema
Swollen hands/arms
SOB
Frequent infections
Aetiology
Idiopathic
Commonest
Neoplastic
lung, colon, breast, lymphoma
Infection
HBV, HCV, HIV, malaria,
schistosomiasis
Drugs
NSAIDs
Penicillamine
anti-TNF
GOLD
Heroin
Autoimmune
SLE, HSP
Sarcoidosis
Vasculitis
IgA nephropathy
Haematological
Sickle cell disease
Types
Focal segmental
glomerulosclerosis
(FSGS)
Aetiology
Idiopathic
Infection: HIV
Autoimmune: IgA nephropathy, vasculitis
Drugs: heroin
Congenital: Alports
Haematological: sickle cell disease
Epidemiology
Black adults
Diagnosis
Histology: focal sclerosis, IgM, C3
Management
Address cause
Steroids (acute), cyclophosphamide (relapses)
Mesangio-
capillary GN
Aetiology
Idiopathic
Infection: HIV, HCV, IE
Autoimmune: SLE
Diagnosis
Biopsy: BM thickening, Ig, complement
Pathophysiology
Immune complex deposition
Complement acitivation and inflammation
Management
Address cause
Steroids (acute), cyclophosphamide (relapses)
Minimal
change
disease
Epidemiology
Common in children (M<5y)
1/4 adult cases
Pathophysiology
?immune related
Aetiology
Idiopathic: commonest in children
Neoplastic: HL
Drugs: NSAIDs
Diagnosis
Biopsy: nil by microscope
EM: fused food processes of podocytes
Management
Address cause
Steroids (acute), cyclophosphamide (freq relapses)
Membraneous
nephropathy
Aetiology
Idiopathic: commonest
Infection: HBV, HCV, schistosomiasis, malaria
Autoimmune: SLE
Neoplastic: lung, colon, breast, lymphoma
Drugs: NSAIDs, penicillamine, TNF-a, GOLD
Haematological: sickle cell
Diagnosis
Histology: thick GBM, IgG, C3
Epidemiology
Commonest cause in adults
Management
Address cause
Pathophysiology
Inflammation and destruction of
GBM by autoimmune process
Complications
Hyperlipidemia
Low oncotic pressure increases lipid synthesis
VTE
Loss of clotting factors and deranged synthesis
DVT, PE, CVST
Infection
Lose immune proteins e.g. Ig, complement
cellulitis, SBP, sepsis
Shock
Hypovolemia
Prognosis
Meaangiocapillary
Insidious decline in renal function
Membraneous
Can resolve spontaneously
FSGS
30% ESRF in 5y
Poor tx response
Recurs after transplant
Minimal change
Steroid responsive
1/3 resolve, 1/3 infreg relapse, 1/3 freq relapse
(steroid dependent)
Diagnosis
Examination
Cardio exam
High JVP, peripheral oedema, pulmonary oedema
Abdo exam
Ascites (shifting dullness), hepatomegaly,
palpable kidneys, peripheral oedema
History
DH
Meds (NSAIDs, anti-TNF, etc), allergies
FH
Renal disease
Autoimmune disease, BBV, malignancy
PMH
Growth and development
Known medical conditions
Autoimmune disease, BBV, malignancy
SH
Living arrangements,
occupation/school, smoking, alcohol, drugs (IVDU)
PC/HPC
Oedema (site, onset, spread, associated symptoms)
Frothy urine, reduced/increased urination
Red flags: weight loss, night sweats, fever, rash
Investigations
Bloods
FBC (infection), CRP (infection), U+E, GFR, Cr (renal function),
LFTs (low albumin), glucose, lipids (hyperlipidemia)
Immune screen (ANA, ANCA, C3/C4, GBM)
BBV screen (HIV, HCV, HBV)
Anti-streptolysin O (post strep)
Blood film (malaria)
Urine
Dipstick (+++ protein)
MCS (RBC, WBC, casts)
ACR (high)
Bedside
Obs (may have HTN)
Weight (fluid overload)
Imaging
CXR: pulmonary oedema
USS: KUB
Biopsy
AVOID IN CHILDREN
Em change only: minimal change
Thick GBM: membranous, mesangiocapillary
Sclerosis: FSGS
Ig, complement (membraneous, mesangiocapillary)
Management
Conservative
Information, advice, support
Monitoring (fluid restruction, U+Es, weights - 0.5-1kg/d)
Referral (nephrology for investigation)
Treat underlying cause
Vaccinations (pneumococcal, influenza)
Medical
Anticoagulation
Indication: nephrotic range proteinuria
Anti-lipid
Indication: hyperlipidemia
E.g. atorvastatin
Diuretics
Indication: oedema
E.g. furosemide
Ant-HTN
Indication: ALL patients
E.g. ACEi ramipril
Immunosuppession
Indication: idiopathic disease
E.g. steroids (acute), cyclophosphamide (relapses),
rituximab (refractory)
Epidemiology
Commonest cause in adults is
membranous nephropathy
Commonest cause in children
is minimal change disease
Pathophysiology
Defect
Podocyte injury in glomerulus,
allowing protein through into urine
Mechanism
Protein loss into urine, including albumin
Reduced serum oncotic pressure from albumin
Reduced albumin disrupts lipid synthesis
Results in oedema and hyperlipidemia
Differentials
Vascular
HF
Metabolic
Liver failure
Definition
Triad of proteinuria (>3.5g/24h or ACR >250mg/mmol),
hypoalbuminuria (<25g/L) and *oedema* often with hyperlipidemia (TC>10mmol/L)