ACE inhibitors for proteinuria in chronic kidney disease
ACE inhibitors (angiotensin-converting enzyme inhibitors) reduce proteinuria, protein leaking into the urine, by lowering the pressure inside the glomerulus, and so slow chronic kidney disease.
Remember
To cut protein loss and slow chronic kidney disease, lower the pressure inside the glomerulus: an ACE inhibitor does this by dilating the efferent arteriole, and an angiotensin receptor blocker is the alternative.
Memory aid
the efferent arteriole as the exit door
Picture the efferent arteriole as the exit door of the glomerulus: holding that exit open stops pressure building up behind it.
Proteinuria means protein in the urine. It is both a sign of kidney damage and a driver of further damage, so reducing it slows the loss of kidney function.
The glomerulus (the tiny knot of capillaries that filters the blood) is fed by the afferent arteriole, the vessel bringing blood in, and drained by the efferent arteriole, the vessel carrying blood away. Angiotensin II, a hormone that narrows blood vessels, normally tightens the efferent arteriole, which keeps the pressure inside the glomerulus high.
An ACE inhibitor is a drug that blocks the enzyme that makes angiotensin II. The efferent arteriole then dilates, the pressure inside the glomerulus falls, and less protein is forced through the filter into the urine. An ACE inhibitor gives a double benefit: it lowers blood pressure and it reduces proteinuria. The protective effect goes beyond the fall in blood pressure, so an ACE inhibitor is still favoured when blood pressure is already controlled.
An angiotensin receptor blocker blocks angiotensin II at its receptor and acts on the same system. It is the alternative if ACE inhibitor cough is troublesome. Serum potassium should be monitored on either drug, because it can rise.
Diuretics, beta-blockers (drugs that slow the heart and lower blood pressure) and statins (drugs that lower cholesterol) are useful parts of care in chronic kidney disease, but they do not act directly on the pressure inside the glomerulus.
Key facts
- Main medicines
- for proteinuria in chronic kidney disease, these are ACE inhibitors and angiotensin receptor blockers.
- Mechanism
- relaxing the efferent arteriole, the exit vessel of the glomerulus, lets the pressure inside the glomerulus fall, so less protein leaks into the urine.
- Double benefit
- an ACE inhibitor lowers blood pressure and also reduces proteinuria.
- Beyond blood pressure
- in persistent proteinuria, the protective effect goes beyond lowering blood pressure, so an ACE inhibitor is favoured even when blood pressure is already controlled.
- Alternative
- an angiotensin receptor blocker can replace an ACE inhibitor if cough is troublesome.
- Monitoring
- check serum potassium, because ACE inhibitors and angiotensin receptor blockers can raise it.
Exam traps
- A dihydropyridine calcium channel blocker (a drug that relaxes the muscle in artery walls) lowers blood pressure, but it tends to dilate the afferent arteriole, the vessel feeding blood into the glomerulus, so it does not lower the pressure inside the glomerulus the way an ACE inhibitor does.
- A loop diuretic, a drug that makes the kidney pass more salt and water, is used to manage swelling, but it does not dilate the efferent arteriole, so it is less likely to reverse high pressure inside the glomerulus.
- A statin lowers cholesterol and is a sensible part of care in chronic kidney disease because it reduces cardiovascular risk, but it does not act on pressure in the glomerulus or on proteinuria, so it is not the strategy that slows the kidney disease itself.
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