Renal Infarct & Vascular Disease
- A renal infarct is a piece of kidney that lost its blood supply — on nephrographic-phase CT it is a sharply outlined wedge that simply doesn't light up while the rest of the kidney does.
- The classic shape is a wedge pointing inward toward the hilum, because the renal arteries branch like a fan and each end-artery branch feeds a triangular slice. A thin enhancing rim of cortex along the outer edge (the cortical rim sign) is the late, helpful clue.
- The usual culprit is an embolus (often from the heart) or in-situ trouble like dissection, vasculitis, or trauma. Renal vein thrombosis is the opposite story: a swollen, engorged kidney with a clotted drain.
- For the chronic cousin, renal artery stenosis, Doppler has real cutoffs: a peak systolic velocity of 180 cm/s and a renal–aortic ratio of 3.0, which together gave sensitivity 85% and specificity 76% in the series that derived them.
- The big mimics are pyelonephritis and a hypovascular tumor — margins, texture, and the clinical story break the tie.
Think of the kidney as a city that runs entirely on one set of power lines. The renal artery comes in, splits into branches, and each branch lights up its own neighborhood. Cut one line and that neighborhood goes dark — the lights don't flicker, they just stop. A renal infarct is exactly that: a blackout in a slice of kidney, drawn with surprisingly crisp borders because the plumbing is built like a fan.
That fan shape is the whole reason infarcts look the way they do, so let's start there.
Why infarcts are wedge-shaped
The renal artery doesn't supply the kidney as one big soggy sponge. It branches into segmental arteries, then interlobar, arcuate, and interlobular arteries — and, here's the important part, these are end arteries with essentially no backup connections between them. Each one owns its territory outright, like food courts that refuse to share fries. Block one branch and the slice it feeds dies cleanly, with no neighboring vessel sneaking in to rescue it.
Because that territory is a cone of tissue with its tip at the hilum (where the artery enters) and its base at the outer cortex, the dead zone shows up as a wedge — narrow toward the center, wide toward the surface. Block the main renal artery instead and the whole city goes dark: a global infarct.
Findings by modality
CT
The diagnosis basically requires contrast. On an unenhanced scan an acute infarct can look completely normal — you can't tell which neighborhood lost power until you turn the lights on. The fix is intravenous iodinated contrast, whose brightness depends on how that material soaks into perfused tissue (the physics lives in attenuation and radiographic contrast).
- Nephrographic phase: the infarcted wedge stays dark while everything around it glows. The margins are sharp and geographic — infarcts have clean edges, and smudgy, ill-defined dark areas point you elsewhere. The wedge is uniformly dark, not striped.
- The cortical rim sign: a thin outer ribbon of cortex still enhances even though the wedge behind it is dead, because the capsule gets a side-channel supply from capsular vessels that don't run through the blocked branch. It is a delayed finding — it takes time to develop after the occlusion — so a very fresh infarct won't have it yet, and its presence favors infarct over infection or tumor.
- Arterial phase / CT angiography: the cause. Hunt for a filling defect or abrupt cutoff in a segmental or main renal artery (embolus or thrombus), an intimal flap (dissection, spontaneous or extending from the aorta), beading or microaneurysms (vasculitis), and an aortic thrombus or aneurysm that could be the source.
- Delayed / excretory phase: in a global infarct, the kidney never excretes; in a segmental one, the calyces under the wedge may not opacify. A persistent nephrogram with delayed excretion in a swollen kidney is the venous story instead (see below).
- Chronic infarct: the wedge scars down to a sharp cortical notch with a thinned cortex over a normal calyx — different from the post-pyelonephritic scar, which sits over a blunted calyx.
Ultrasound
Gray-scale ultrasound is often normal in an acute infarct, or shows a subtle wedge of altered echogenicity. Color and power Doppler are the useful bits: an absent-flow wedge in a segmental infarct, no intrarenal arterial flow at all in a global infarct, and — for renal artery stenosis — the spectral tracings that carry the thresholds in "The numbers." Contrast-enhanced ultrasound, where available, shows the non-perfused wedge as crisply as CT does.
MRI
MRI shows the same wedge: reduced enhancement on post-gadolinium T1 sequences, with restricted diffusion in the acute phase, and it can add MR angiography for the renal arteries when iodinated contrast is off the table. Renal vein thrombosis is well seen as absent flow void or a filling defect on contrast-enhanced MR venography.
Nuclear medicine
Renal scintigraphy shows an infarct as a photopenic defect (segmental) or a non-functioning kidney (global). The captopril-augmented study is a functional test for renovascular hypertension; the MAG3, DTPA, and captopril renography page explains how it works.
Catheter angiography
Angiography confirms the occlusion, dissection, or stenosis and is the road to treatment — thrombolysis or thrombectomy for an acute occlusion, stenting for a dissection or a stenosis in the right patient. It is not where the diagnosis is made.
The company infarcts keep: other renal vascular disease
Infarcts are one chapter of a larger book about renal blood flow. A few neighbors worth knowing:
| Entity | What's happening | Imaging tell |
|---|---|---|
| Embolic infarct | Clot travels from elsewhere (heart, aorta) and plugs a branch | Wedge defect; hunt for a cardiac or aortic source, and for infarcts in the spleen too |
| Renal artery dissection | A tear sends blood into the artery wall | Intimal flap; downstream wedge or global infarct |
| Renal vein thrombosis | The drain clots, not the supply | Swollen kidney, delayed or persistent nephrogram, filling defect in the vein, perinephric stranding |
| Renal artery stenosis | Chronic narrowing, not full blockage | Small kidney with delayed enhancement; Doppler velocity criteria; secondary hypertension |
| Vasculitis (e.g. polyarteritis nodosa) | Inflamed small and medium vessels | Multiple small peripheral infarcts, microaneurysms on angiography |
| Traumatic vascular injury | Intimal tear, thrombosis, or avulsion after blunt force | Segmental or global infarct with a laceration or hematoma for company; see below for how the AAST grades it |
Note that renal vein thrombosis flips the story: it's a backed-up drain, not a cut supply, so the kidney gets engorged and swollen rather than going dark, and contrast lingers instead of failing to arrive. Think of it in nephrotic syndrome, dehydration in infants, and tumor thrombus from a renal cell carcinoma.
For the chronic, blood-pressure-driven flavor of vascular disease, the dedicated page on renal artery stenosis is the place to go — that's a slow squeeze with a whole different clinical story, not an acute blackout. The Doppler numbers below are the part most worth carrying between the two pages.
The numbers
| What | Threshold / value | Why it matters |
|---|---|---|
| Renal artery peak systolic velocity (PSV) for renal artery stenosis | 180 cm/s | The ROC-optimal direct velocity cutoff in the single series that tested it; read together with the ratio below |
| Renal–aortic ratio (RAR) for renal artery stenosis | 3.0 | Renal artery PSV divided by aortic PSV; corrects for the patient's overall flow state |
| Adult kidney length at sonography (median) | 11.2 cm left, 10.9 cm right | The baseline for calling a kidney "small" (chronic ischemia, old global infarct) or "swollen" (venous thrombosis); varies with age, sex, and habitus |
| AAST 2018 kidney grade for a segmental or complete infarct due to vessel thrombosis without active bleeding | Grade IV | A traumatic infarct is a high-grade injury even with no bleeding |
| AAST 2018 kidney grade for main renal artery or vein laceration, hilar avulsion, or a devascularized kidney with active bleeding | Grade V | The pedicle injury; the kidney is usually lost |
| A CT attenuation or size threshold for calling a wedge an infarct | None widely accepted | The diagnosis is the sharp, geographic, non-enhancing wedge in a vascular territory, with or without the rim sign |
| Time for the cortical rim sign to appear | No robust figure | Treat it as a delayed sign; its absence early on does not exclude infarct |
How good is the test
For acute renal infarction itself there is no robust pooled sensitivity or specificity figure for CT, MRI, or ultrasound; contrast-enhanced CT is the accepted reference standard in practice, but that is convention, not a pooled accuracy figure. For renal artery stenosis, Doppler with the combined criteria above — PSV 180 cm/s and RAR 3.0 — gave sensitivity 85% and specificity 76% in the single series that derived them by ROC analysis. That is respectable for a screening test done at the bedside without contrast, and it is why a positive Doppler goes on to CT or MR angiography rather than straight to the catheter lab.
The mimics that will get you
Two impostors love to dress up as infarcts, and a couple more turn up at the party.
| Mimic | Looks similar because | Tell them apart by |
|---|---|---|
| Acute pyelonephritis | Also produces wedge-shaped areas of reduced enhancement pointing at the hilum | Infected zones are striated (streaky bands radiating outward) with fuzzy margins, perinephric stranding, and a febrile patient with pyuria; an infarct is uniformly dark, sharply marginated, and afebrile — start with the renal infection spectrum if there are stripes and a fever |
| Hypovascular tumor (papillary RCC, lymphoma, metastasis) | A poorly enhancing dark patch | Masses are rounded, bulge or distort the contour, and persist or grow; an infarct respects the kidney's shape, follows a vascular-territory wedge, and scars down over time — when it looks mass-like, detour through RCC subtypes and staging |
| Post-pyelonephritic scar (vs chronic infarct) | Both leave a cortical notch | The infection scar overlies a blunted, clubbed calyx; the infarct scar overlies a normal calyx |
| Renal vein thrombosis | Reduced, patchy enhancement and perinephric stranding | The kidney is swollen, not dark; the nephrogram is delayed and persistent; the vein contains thrombus |
| Acute tubular necrosis or contrast nephropathy | Delayed, persistent nephrogram | Bilateral and global, no wedge, no vascular occlusion, and the story is a recent insult (hypotension, contrast, myoglobin) |
| Radiation or surgical change | A sharply marginated band of non-enhancement | The margin follows a radiation port or a resection plane, not a vascular territory, and the history tells you |
Don't let a normal unenhanced CT reassure you in a patient with sudden flank pain and no stone. The infarct is invisible until the contrast goes in. If the stone hunt is negative and the story is vascular (atrial fibrillation, a recent catheterization, a known aneurysm), ask for the contrast.
Found a clean renal infarct with no trauma? Your next question is "where did the clot come from?" An unexplained infarct is often the kidney quietly reporting a heart problem — atrial fibrillation is a classic source — so the workup frequently points back at the chest, not the abdomen. Check the spleen on the same scan; a second infarct there nearly closes the case for an embolic shower.
Reporting
- Segmental or global, which kidney, which pole, and roughly what fraction of the parenchyma has lost enhancement.
- The vascular finding that explains it: embolus or thrombus (and where it sits), intimal flap, vasculitic beading, an aortic source, or a traumatic injury — and if the arteries look normal, say the cause is not identified.
- The cortical rim sign, present or absent, because it supports the diagnosis and hints at timing.
- The opposite kidney, the spleen, and the aorta: other infarcts, an aneurysm, or a mural thrombus that turns one infarct into a systemic problem.
- Renal vein patency — if the picture is a swollen kidney rather than a dark wedge, say "renal vein thrombosis" and look for tumor thrombus.
- In trauma, the AAST 2018 grade the infarct implies (grade IV for a segmental or complete infarct without bleeding, grade V for hilar avulsion or a devascularized, bleeding kidney), with a link back to the trauma page's full table.
- For stenosis on Doppler: the PSV, the RAR, the waveform downstream, and the kidney length — the referrer will want the numbers, not adjectives.
If you remember nothing else: a renal infarct is a sharply defined, wedge-shaped slice of kidney that won't take up contrast, pointing toward the hilum, sometimes with a rescued rim of cortex on its outer edge. Find that shape, then go looking for the embolus, the dissection, or — in the right setting — the trauma that turned off the lights.
References
- House MK, Dowling RJ, King P, Gibson RN. Using Doppler sonography to reveal renal artery stenosis: an evaluation of optimal imaging parameters. AJR Am J Roentgenol 1999;173(3):761–765. Used for: the renal artery peak systolic velocity threshold of 180 cm/s, the renal–aortic ratio of 3.0 (optimal by ROC analysis), and the combined sensitivity 85% and specificity 76%, in the Key Points, "The numbers," and "How good is the test."
- Emamian SA, Nielsen MB, Pedersen JF, Ytte L. Kidney dimensions at sonography: correlation with age, sex, and habitus in 665 adult volunteers. AJR Am J Roentgenol 1993;160(1):83–86. Used for: the median adult kidney lengths (11.2 cm left, 10.9 cm right) in "The numbers" and the Measurement chip.
- Kozar RA, Crandall M, Shanmuganathan K, et al.; AAST Patient Assessment Committee. Organ injury scaling 2018 update: Spleen, liver, and kidney. J Trauma Acute Care Surg 2018;85(6):1119–1122. Used for: the AAST 2018 grade IV assignment for segmental or complete kidney infarction due to vessel thrombosis without active bleeding, and the grade V assignment for main renal artery or vein laceration, hilar avulsion, or a devascularized kidney with active bleeding, in "The numbers" and "Reporting."
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