Renovascular Disease Flashcards
Examples of renovascular disease
-Renal artery stenosis
-Thrombosis
-Cholesterol embolization
-Haemolytic uraemic syndrome
Describe renal artery stenosis
-Renal artery stenosis is the most common cause of secondary hypertension
-Most cases of renal artery stenosis are caused by atherosclerosis but fibromuscular dysplasia involving the vessel wall may be responsible in younger patients
-Rare causes include vasculitis (large vessel), thromboembolism and aneurysms of the renal artery.
Pathophysiology of renal artery stenosis
-Reduction in renal perfusion pressure
=Actives RAAS
=Vasoconstriction and aldosterone production
=Hypertension
-Significant reduction of renal blood flow occurs when there is more than 70% narrowing of the artery, and this is commonly associated with distal, post-stenotic dilatation.
-As the stenosis becomes more severe, global renal ischaemia leads to shrinkage of the affected kidney and may cause renal failure if bilateral or if unilateral in the presence of a single kidney (ischaemic nephropathy).
Clinical features of renal artery stenosis
-Hypertension
-Acute pulmonary oedema (bilateral renovascular disease)
-Progressive renal failure (with bilateral disease)
-Deterioration in renal function when ACE inhibitors or ARBs are administered
-Clinical evidence of generalised vascular disease may be observed, particularly in the legs and in older patients with atherosclerotic renal artery stenosis.
-Asymmetrical kidneys
Investigation of renal artery stenosis
-CT angiography or MR angiography
-Biochemical testing may reveal impaired renal function and an elevated plasma renin activity, sometimes with hypokalaemia due to hyperaldosteronism.
-Ultrasound may also reveal a discrepancy in size between the two kidneys, although this is insufficiently sensitive or specific to be of value in diagnosis of renovascular disease in hypertensive patients.
Management of renal artery stenosis
-Antihypertensive drugs
-Statins
-Low dose aspirin in atherosclerotic disease
-Correct vessel narrowing if young, uncontrollable BP, flash pulmonary oedema, malignant hypertension, deteriorating renal function (angioplasty, stenting)
Overview of acute renal infraction
-Sudden occlusion of renal artery: thrombosis/ thromboemboli causing multiple infracts within renal parenchyma
-P: loin pain of acute onset, non-visible haematuria, sometimes pain absent, severe hypertension. If bilateral, AKI and anuria, evidence of widespread vascular disease, absent femoral pulses and reduced lower limb perfusion
-I: lactate dehydrogenase and CRP raised, CT scan
-M: anticoagulation, stent acutely blocked artery
Describe thrombotic microangiopathies
-Associated with acute damage and occlusion of small blood vessels.
-I: microangiopathic haemolytic anaemia (MAHA), in which haemolysis and red cell fragmentation arise as a consequence of damage incurred to red blood cells during passage through the abnormal vessels. The red blood cell fragments (schistocytes) may be observed on blood films, together with laboratory features of intravascular haemolysis (p. 955), including an elevated unconjugated bilirubin level, raised serum LDH concentration and decreased circulating levels of haptoglobin. A reticulocytosis is often seen. Endothelial injury is pronounced, leading to increased platelet adherence and a marked reduction in the platelet count.
=Haemolytic uraemic syndrome
=Shiga toxin HUS
=Drug induced (VEGF-A)
=Thrombotic thrombocytopenic purpura
=DIC
=Malignancy
=Systemic sclerosis
=Pre-eclampsia
=Malignant hypertension
Features of microangiopathic haemolytic anaemia
-Hypertension
-Low platelets
-Haemolysis: schistocytes (RBC fragments) on blood film
=LDH
=Increased unconjugated bilirubin
=Decreased haptoglobin
Causes of microangiopathic haemolytic anaemia
-Haemolytic uraemic syndrome – infectious – E-Coli O157- typical – complement mutations
-Thrombotic thrombocytopenic purpura – ADAMTS-13 antibodies (fever, fluctuating neurological signs, thrombocytopenia, renal failure)
-Systemic sclerosis
-Malignant hypertension
Describe cholesterol emboli
-P: renal impairment, haematuria, proteinuria and sometimes eosinophilia with inflammatory features that can mimic a small-vessel vasculitis. The symptoms are provoked by showers of cholesterol-containing microemboli, arising in atheromatous plaques in major arteries.
-I: The diagnosis should be suspected when these clinical features occur in patients with widespread atheromatous disease, who have undergone interventions such as surgery or arteriography. They may also be precipitated by anticoagulants and thrombolytic agents. On clinical examination, signs of large-vessel disease and microvascular occlusion in the lower limbs (ischaemic toes, livedo reticularis) are common but not invariable
-M: There is no specific treatment.
Overview of haemolytic uraemic syndrome
-Characterised by thrombotic microangiopathy that predominantly affects the renal microcirculation, with involvement of other organs (including the brain) observed in more severe cases.
-Most common cause of HUS is infection with organisms that produce enterotoxins called Shiga-like toxin or verotoxins (E.coli 0157, Shigella dysenteriae)
-P: haemorrhagic diarrhoea, fever, thrombocytopenia, anaemia, renal failure
Describe large vessel occlusion
-Main renal artery thrombosis/embolus
-Large vessel occlusion must be bilateral to cause AKI(or unilateral in single functioning kidney)
-Oliguria/anuria
-Mild if any loin pain
-Doppler USS or CT angiogram (patchy contrast/ none)
-Revascularisation rarely able to save kidney function
Describe small vessel occlusion
-Cholesterol emboli
-Common after arterial procedures (e.g. coronary angiogram)* Often associated with eosinophilia
-Trash feet
