Kidneys in systemic disease Flashcards
What is the number one cause of ESRF in the UK?
Diabetes mellitus nephropathy
What is the first manifestation of diabetic nephropathy? How can this be discovered?
Microalbuminuria- 30-300mg of albumin excreted per day.
24h collection of urine OR early morning urine albumin:creatinine ratio >3
Why does GFR initially increase in pre-diabetic nephropathy?
Dilatation of the afferent arteriole due to release of vasoactive mediators (inflammation)
What structural changes are seen in diabetic nephropathy, in order of disease progression?
Renal hypertrophy
Mesangial expansion and nodule formation
GBM thickening
Tubulo-interstitial fibrosis
How is diabetic nephropathy generally managed?
Tight control of HbA1c
Tight BP control (ACE inhibitors/ARBs)
Statins
Why are ACE inhibitors used in diabetic nephropathy?
Allows the efferent arteriole to dilate; this lowers the pressure in the glomerulus and hence protects against proteinuria
Why is it important to try and protect the renal function of diabetic patients?
Diabetic patients have poor survival on dialysis
What are the ANCA-associated small vessel vasculitides associated with kidney involvement?
Wegener’s granulomatosis
Churg-Strauss syndrome
Microscopic polyangiitis
How does renal involvement in systemic vasculitis usually manifest?
Acute kidney injury- e.g. proteinuria, haematuria, red cell casts
Other than the ANCA-positive vasculitides, what other forms of small vessel vasculitis may affect the kidney?
Associated with immune complexes- Henoch-Schonlein purpura, Goodpasture’s syndrome, lupus vasculitis, rheumatoid vasculitis
What is Churg-Strauss characterised by?
Prominent blood eosinophilia, chronic rhinosinusitis, asthma, purpura
What is the “saddle-nose” deformity a sign of?
Wegener’s granulomatosis
How are the small vessel vasculitides treated?
Immunosuppressive therapy- e.g. cyclophosphamide, AZT
Plasma exchange
May eventually require RRT
What proportion of SLE patients have renal manifestations? How do these typically present?
About 50%- proteinuria, increased blood pressure, nephrotic syndrome, microhaematuria, casts
How is proliferative change in SLE managed?
Tight BP control with ACEi/ARB
Immunosuppressive therapy- e.g. cyclophosphamide, AZT, prednisolone
Describe the “typical” patient with renovascular disease.
Patients with existing athersclerotic disease e.g. have IHD, PVD, history of stroke
How does renal artery stenosis present?
Increasing blood pressure resistant to treatment; “flash” pulmonary oedema; AKI after treatment of hypertension with ACEi’s
How is renovascular disease detected?
Utrasound- renal size asymmetry
Doppler US- disturbance in blood flow to the kidney
CT/MR angiography
How is renal artery stenosis treated?
Medical treatment (avoid ACEis in bilateral stenosis) Angioplasty +/- stenting
What might be seen in skull X-ray in myeloma?
Pepper-pot skull (lytic lesions)
What is myeloma characterised by?
Excess production of monoclonal antibody
What is seen on a blood film for myeloma?
Normocytic anaemia; Rouleaux formation (stacks of RBC)
What other investigations may be carried out in myeloma?
X-ray- lytic lesions
ESR and PV- raised
Serum/urine electrophoresis- monoclonal band (of Ig)
Urine- Bence-Jones protein (Ig light chains)
How does renal involvement in myeloma manifest?
AKI
Chronic kidney disease
