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PH-RN13

Vascular diseases of the kidney

How narrowed renal arteries, damaged arterioles, microthrombi and blocked renal arteries or veins injure the kidney: renovascular hypertension, nephrosclerosis, HUS and TTP, infarcts and renal vein thrombosis.

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  • 5 steps · 10 questions
  • 3D normal anatomy

By the end, you can

  • Explain how renal artery stenosis causes renovascular hypertension through renin, and contrast atherosclerotic stenosis with fibromuscular dysplasia.
  • Explain why glomerular filtration behind a tight stenosis depends on angiotensin II, and why ACE inhibitors and angiotensin receptor blockers can lower GFR.
  • Compare benign and malignant nephrosclerosis in their vessels, gross appearance and course.
  • Explain how thrombotic microangiopathy causes kidney injury, haemolysis and low platelets, and distinguish STEC-HUS, complement-mediated HUS and TTP.
  • Relate end arteries to wedge-shaped infarcts, and recognise the causes and effects of renal vein thrombosis, with the key tests and how the main treatments act.

What it is

Vascular diseases of the kidney damage it through its blood supply: narrowing of the renal arteries (renal artery stenosis), disease of the small arteries and arterioles (nephrosclerosis), microthrombi in arterioles and glomeruli (thrombotic microangiopathy), and sudden blockage of an artery (infarct) or of the renal vein (renal vein thrombosis).

4 types to tell apart
Renal artery stenosis
Atherosclerotic (most) or fibromuscular dysplasia; causes renin-driven hypertension and ischaemic loss of kidney function.
Nephrosclerosis
Benign: slow arteriolar narrowing from years of hypertension. Malignant: acute arteriolar necrosis in malignant hypertension.
Thrombotic microangiopathy
Endothelial injury with platelet microthrombi: haemolytic uraemic syndrome (Shiga toxin or complement) and thrombotic thrombocytopenic purpura (ADAMTS13 deficiency).
Renal infarct and renal vein thrombosis
Sudden arterial blockage, usually embolic, or venous thrombosis, often from the hypercoagulable state of nephrotic syndrome.

Normal function

A high-flow circulation built on end arteries

The kidneys receive about a fifth of the cardiac output, far more than they need for oxygen, because the blood is there to be filtered. Each renal artery divides into segmental, interlobar and , then that give off the . These branches are end arteries: they do not join their neighbours, so blocking one leaves its territory with no other supply.

Each afferent arteriole feeds a , and the leaving it feeds a second capillary bed round the tubules or, deep in the medulla, the . Two capillary beds in series mean the tubules suffer whenever glomerular flow fails, and the glomerular capillaries, under high pressure, are exposed to any injury of their endothelium.

Flow and filtration stay nearly constant over a wide range of blood pressure (autoregulation): the afferent arteriole constricts when stretched, and tubuloglomerular feedback tunes it to salt delivery. When perfusion pressure falls, the juxtaglomerular cells release renin. The angiotensin II it generates constricts the efferent arteriole more than the afferent, holding glomerular pressure up, and raises systemic pressure through vasoconstriction and aldosterone.

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