Nephrology Flashcards
Investigations when assessing glomerulonephritis
Blood- FBC, U&Es, LFT, CRP, immunoglobulins, electrophoresis, complement- C3 and C4, autoantibodies- ANA, ANCA, anti-dsDNA, anti-GBM, blood culture, hepatitis serology, ASOT (for strep)
Urine- MC&S, Bence Jones proteins, RBC casts, A:CR, P:CR
Imaging- CXR, renal ultrasound
Renal biopsy- required for diagnosis
Nephritic causes of glomerulonephritis
IgA nephropathy Henoch-Schonlein purpura Post- streptococcal Anti-GBM disease Rapidly progressive GN
What is Berger’s disease?
IgA nephropathy
Clinical picture of IgA nephropathy
Mesangial deposition of IgA complexes Occurs around 12-72 hours after infection- usually URTI Young men classically Macroscopic haematuria Associated with HSP and coeliac
Features of Henoch-Schonlein purpura
Small vessel vasculitis Palpable pruritic rash IgA nephropathy and deposition in skin, joints and gut Abdominal pain Polyarthritis
Treatment of IgA nephropathy
Supportive- fluids and analgesia
ACE-i/ ARB to reduce the proteinuria and protect the renal function
Corticosteroids if persistent
Diagnosis of IgA nephropathy
Renal biopsy showing IgA deposition in the mesangium
Clinical features of post- streptococcal glomerulonephritis
1-2 weeks after streptococcal infection
Evidence of streptococcal infection- low C3 complement levels, raised ASOT and anti-DNAase B
Immune complex formation and inflammation in the glomerulus
Treatment for post-streptococcal GN
Supportive
Abx to clear the streptococcus
Auto-antibodies in anti-GBM disease
Type IV collagen
Presentation of anti-GBM disease
Renal disease- oliguria/ anuria, haematuria, AKI, renal failure
Lung disease- pulmonary haemorrhage, SOB, haemoptysis
Treatment for anti-GBM disease
Plasma exchange
Corticosteroids
Cyclophosphamide
Causes of rapidly progressive GN
Small vessel/ ANCA vasculitis
Lupus nephritis
Anti-GBM antibodies
Primary aetiology of nephrotic syndrome
Minimal change disease, membranous nephropathy, focal segmental glomerulosclerosis, membranoproliferative GN
Secondary aetiology of nephrotic syndrome
DM Lupus nephritis Myeloma Amyloid Pre-eclampsia
Proteinuria results from
Podocyte pathology
Management of nephrotic syndrome
Reduce oedema- fluid and salt restriction, diuresis with loop diuretics
Renal biopsy and then treatment of underlying cause
Biopsy avoided in children unless no response to steroids (not minimal change disease in this case)
Reduce proteinuria- ACE-i/ARB
Heparin/ warfarin
Treatment for minimal change disease
Prednisolone 1mg/kg
Drugs associated with minimal change disease
Lithium
NSAIDs
Commonest glomerulonephritis seen on renal biopsy
Focal segmental glomerulosclerosis FSGS
Secondary causes of FSGS
HIV Heroin Lithium Lymphoma Any cause of decreased kidney mass or number of nephrons- other glomerulonephitides
Treatment of FSGS
ACE-i/ARB and blood pressure control in all
Corticosteroids in primary disease
Presentation of lupus nephritis
Rash Photosensitivity Ulcers Arthritis Serositis CNS effects Cytopenias Renal disease- nephropathy is common
Triad in haemolytic uraemic syndrome
Haemolytic anaemia
Low platelets
AKI with haematuria/proteinuria
Classical secondary cause of haemolytic uraemic syndrome
Shiga toxin producing Escherichia coli 0157:H7
