Renal ischaemia rarely hurts. It raises blood pressure and reduces filtration. Therefore the renal territory in a course on atherosclerosis is about hypertension, CKD and the morphological end-point, not about "lower back pain".
Two related but not identical concepts.
Renal artery stenosis of atherosclerotic origin — usually the ostium and the proximal third, often against the background of an aorta strewn with plaques. A haemodynamically significant stenosis activates the renin-angiotensin axis: vasoconstriction, sodium retention, renovascular hypertension. Bilateral stenosis or stenosis of the artery of a solitary kidney also causes ischaemic nephropathy with a decline in eGFR, sometimes acute kidney failure after ACE inhibitors/ARBs (a classic teaching red flag).
Atherosclerotic nephrosclerosis is the morphological diagnosis of an ischaemically shrunken kidney against the background of atherosclerotic disease of the renal vessels: finely granular surface, thinning of the cortex, hyalinised glomeruli, sclerosis of the stroma, hyalinosis of the arterioles. It often coexists with hypertensive nephrosclerosis: both mechanisms in one person. At a pathological anatomy exam they are distinguished by predominance: the "atherosclerotic" emphasis is on stenosis of the large renal arteries and ischaemic retractions; the "hypertensive" one on arteriolosclerosis.
Clinical markers that should make you think of renovascular atherosclerosis (a teaching list, not RCT criteria): onset of severe hypertension after 55 years; resistant hypertension; asymmetry of kidney size; pulmonary oedema without an obvious cause ("flash pulmonary edema"); rising creatinine on an ACE inhibitor; a bruit over the projection of the renal arteries; coexisting PAD or CHD.
ESC/EAS 2025: moderate CKD (eGFR 30–59) is high risk; severe CKD (eGFR <30) is very high, with an LDL-C target as for very high risk. That is, even without a "diagnosis of renal artery stenosis", a reduced eGFR already changes the lipid target.
The boundary of the lesson. Large RCTs of revascularisation of atherosclerotic renal artery stenosis (ASTRAL, CORAL) did not show an advantage of routine stenting over medical therapy in the populations studied. Therefore the course does not teach "found a stenosis — stent it". The indications for revascularisation remain narrow and belong to nephrology/interventional radiology, not to this lesson. The student is required to recognise the morphology of nephrosclerosis; the indication for a stent — not.
Another boundary. Not every CKD in a smoker with hypertension is atherosclerotic nephrosclerosis. Diabetic nephropathy, glomerulonephritides and drug-induced injuries must be in the differential. The Kazakhstan Ministry of Health protocol No. 196 requires assessment of eGFR and albuminuria and exclusion of nephrotic syndrome as a cause of secondary dyslipidaemia — this is a different line of thought: not "the kidney was damaged by atherosclerosis" but "the kidney itself disrupts the lipids".