Renovascular disease

Renal artery stenosis

• Causes 5% of hypertension
• Usually atheromatous plaque at origin of renal artery
• Bilateral involvement in 50% of affected cases
• Results in stimulation of renin release due to impaired glomerular blood flow + increased sympathetic activity with resultant flushing, loss of nocturnal BP decrease, autonomic instability and rapid BP swings
• GFR is usually <60, with 85% having CKD stage 3-4
• Initial Doppler USS has 70% sensitivity
• Absence of compensatory hypertrophy of contralateral kidney suggests bilateral disease
• MRA has >90% sensitivity and 95% specificity
• Rx – Medical conservative treatment
  • Revascularisation therapy should only be considered if fails or >30% rise in creatinine with medical management

Atheroembolic renovascular disease

• Cholesterol emboli from large arteries e.g. aorta
• Presents 1-14 days after inciting event (i.e. spontaneous embolism, vascular surgery, arteriography, angioplasty, anticoagulation or thrombolytic therapy) with other embolic phenomena (e.g. retinal, CNS, peripheral vascular embolism), accelerated or labile HTN, subacute renal insufficiency over weeks
• Renal infarction is rare
• There is no effective therapy other than supportive care

Thromboembolic renovascular disease

• Large thrombosis of renal vessels (post-traumatic, atherosclerotic or inflammatory) or embolism of thrombotic material (most commonly fat emboli, mural thrombi from heart, bacterial endocarditis or aseptic vegetations OR paradoxical emboli via PFO)
• Acute thrombosis may cause infarction with sudden onset flank pain, tenderness, fever, haematuria, leukocytosis, nausea, vomiting
• May cause rise in AST, LDH and ALP from kidney
• Renal function deteriorates acutely with acute renal failure if bilateral
• Rx
  • Surgical intervention, anticoagulant therapy, intra-renal thrombolysis, percutaneous thrombectomy or conservative approach
  • If acute unilateral, anticoagulant and supportive therapy usually utilised
  • If acute bilateral, medical and surgical approaches have similar outcomes

Renal vein thrombosis

• Associated with trauma, extrinsic compression (tumor, node, AAA), invasion by renal cell carcinoma, dehydration (infants), nephrotic syndrome, pregnancy and COCP use
• Acute cases occur usually in children with sudden loss of renal fuction, fever, chills, flank tenderness (with kidney enlargement), leukocytosis and haematuria
• Haemorrhagic infarction and renal rupture can cause haemorrhagic shock

Malignant hypertension

• Acute progressive renal dysfunction
• Usually in previously hypertensive individuals
• Usually show rapid rise in creatinine, haematuria (macroscopic at times), proteinuria and red/white cell casts in sediment

Last Updated on October 7, 2020 by Andrew Crofton