Kidneys in systemic disease

Question 1

What is the number one cause of ESRF in the UK?

Answer 1

Diabetes mellitus nephropathy

Question 2

What is the first manifestation of diabetic nephropathy? How can this be discovered?

Answer 2

Microalbuminuria- 30-300mg of albumin excreted per day.

24h collection of urine OR early morning urine albumin:creatinine ratio >3

Question 3

Why does GFR initially increase in pre-diabetic nephropathy?

Answer 3

Dilatation of the afferent arteriole due to release of vasoactive mediators (inflammation)

Question 4

What structural changes are seen in diabetic nephropathy, in order of disease progression?

Answer 4

Renal hypertrophy
Mesangial expansion and nodule formation
GBM thickening
Tubulo-interstitial fibrosis

Question 5

How is diabetic nephropathy generally managed?

Answer 5

Tight control of HbA1c
Tight BP control (ACE inhibitors/ARBs)
Statins

Question 6

Why are ACE inhibitors used in diabetic nephropathy?

Answer 6

Allows the efferent arteriole to dilate; this lowers the pressure in the glomerulus and hence protects against proteinuria

Question 7

Why is it important to try and protect the renal function of diabetic patients?

Answer 7

Diabetic patients have poor survival on dialysis

Question 8

What are the ANCA-associated small vessel vasculitides associated with kidney involvement?

Answer 8

Wegener’s granulomatosis
Churg-Strauss syndrome
Microscopic polyangiitis

Question 9

How does renal involvement in systemic vasculitis usually manifest?

Answer 9

Acute kidney injury- e.g. proteinuria, haematuria, red cell casts

Question 10

Other than the ANCA-positive vasculitides, what other forms of small vessel vasculitis may affect the kidney?

Answer 10

Associated with immune complexes- Henoch-Schonlein purpura, Goodpasture’s syndrome, lupus vasculitis, rheumatoid vasculitis

Question 11

What is Churg-Strauss characterised by?

Answer 11

Prominent blood eosinophilia, chronic rhinosinusitis, asthma, purpura

Question 12

What is the “saddle-nose” deformity a sign of?

Answer 12

Wegener’s granulomatosis

Question 13

How are the small vessel vasculitides treated?

Answer 13

Immunosuppressive therapy- e.g. cyclophosphamide, AZT
Plasma exchange
May eventually require RRT

Question 14

What proportion of SLE patients have renal manifestations? How do these typically present?

Answer 14

About 50%- proteinuria, increased blood pressure, nephrotic syndrome, microhaematuria, casts

Question 15

How is proliferative change in SLE managed?

Answer 15

Tight BP control with ACEi/ARB

Immunosuppressive therapy- e.g. cyclophosphamide, AZT, prednisolone

Question 16

Describe the “typical” patient with renovascular disease.

Answer 16

Patients with existing athersclerotic disease e.g. have IHD, PVD, history of stroke

Question 17

How does renal artery stenosis present?

Answer 17

Increasing blood pressure resistant to treatment; “flash” pulmonary oedema; AKI after treatment of hypertension with ACEi’s

Question 18

How is renovascular disease detected?

Answer 18

Utrasound- renal size asymmetry
Doppler US- disturbance in blood flow to the kidney
CT/MR angiography

Question 19

How is renal artery stenosis treated?

Answer 19

Medical treatment (avoid ACEis in bilateral stenosis)
Angioplasty +/- stenting

Question 20

What might be seen in skull X-ray in myeloma?

Answer 20

Pepper-pot skull (lytic lesions)

Question 21

What is myeloma characterised by?

Answer 21

Excess production of monoclonal antibody

Question 22

What is seen on a blood film for myeloma?

Answer 22

Normocytic anaemia; Rouleaux formation (stacks of RBC)

Question 23

What other investigations may be carried out in myeloma?

Answer 23

X-ray- lytic lesions
ESR and PV- raised
Serum/urine electrophoresis- monoclonal band (of Ig)
Urine- Bence-Jones protein (Ig light chains)

Question 24

How does renal involvement in myeloma manifest?

Answer 24

AKI

Chronic kidney disease