The Case

A woman presents with serum creatinine of 2.6 mg/dL, mild left flank pain, and perinephric stranding of the left kidney on CT. Ultrasound shows no hydronephrosis. The left kidney measures 11.6 cm — normal size. Lasix renogram reports a 25%/75% split function with “no real flow” to the left kidney and no nephrogram formation. Urology raises lactate dehydrogenase (LDH) as a screen for renal ischemia and asks whether CT angiography of the renal arteries is warranted.

That is the entire case summary. Five data points. Each one matters.

The question is not whether this is renal infarction. The data already point at that answer. The question is how we confirm it, characterize the cause, intervene if the window is still open, and protect the contralateral kidney.

Why This Diagnosis Hides

Acute renal infarction is rare in the reported literature and under-diagnosed in practice. A 1940 autopsy series of 14,411 patients found an incidence of 1.4% [1]. A four-year emergency-department series of approximately 250,000 patients identified only 17 cases — 0.007% [1]. These numbers are almost certainly a floor, not a ceiling. Renal infarction is missed or diagnosed late because the presentation mimics more common conditions. Korzets and colleagues, reviewing 11 cases at Meir Hospital from 1997 to 2000, found that working diagnoses on admission were renal colic in two, pyelonephritis in three, renal carcinoma in one, digitalis intoxication in one, and suspected endocarditis in one [2]. In no case was renal infarction the initial diagnosis. Time from emergency-department presentation to definitive CT diagnosis ranged from 24 hours to 7 days.

Radhakrishnan summarizes the current state bluntly in UpToDate: time to diagnosis following presentation is often more than two days, with less than 50% of patients diagnosed promptly [1]. That diagnostic delay is clinically consequential. Revascularization — whether catheter-directed thrombolysis or surgical thrombectomy — has a narrow window. By the time the diagnosis is made, the window is often closed.

Reading the Renogram

The patient’s Lasix renogram is the diagnostic hinge — but the data have to be read correctly.

A standard MAG3 or DTPA renogram has three phases:

1. Vascular / perfusion phase (0-30 seconds) — bolus arrival reflecting renal blood flow
2. Cortical / parenchymal phase (30 seconds to 3 minutes) — tracer uptake into functioning tubules, producing the nephrogram
3. Excretion phase (3-30 minutes, with or without furosemide) — collecting-system washout reflecting drainage

Lasix provocation exists to distinguish true obstruction (slow washout, T½ > 20 minutes by the O’Reilly criteria) from a dilated-but-non-obstructed collecting system [3]. It is an obstruction study. It has nothing to say about perfusion or parenchymal function.

When a renogram shows “no nephrogram,” two mechanisms can produce that pattern:

The patient’s 11.6 cm left kidney is normal-sized. A chronically ischemic or end-stage kidney atrophies, typically to below 9 cm. Her perinephric stranding is acute. Her back pain is acute. The pattern is inflow failure, not parenchymal collapse.

The Lasix component of her study is uninterpretable and diagnostically irrelevant. You cannot wash out what never arrived. Whoever ordered the study was thinking obstruction first — reasonable given elevated creatinine and flank pain, even though the ultrasound was clean — and what came back was a phase-1 catastrophe. Read the study for what phase 1 shows: arterial inflow to the left kidney is absent.

The Laboratory Anchor — LDH

The single most useful laboratory marker for acute renal infarction is lactate dehydrogenase. Elevation is sensitive, the pattern is tissue-specific, and the magnitude tends to be dramatic enough to make the signal unambiguous when present.

The Hazanov 2004 Medicine (Baltimore) cohort — 44 patients with renal infarction and atrial fibrillation at Kaplan and Sheba Medical Centers in Israel, 1984-2002 — is the anchor reference [4]. Their findings:

The tissue-specific pattern matters as much as the absolute number. In renal infarction, LDH rises sharply while aspartate aminotransferase (AST) and alanine aminotransferase (ALT) stay preserved. The liver is not injured. The heart is not injured. The kidney is. Radhakrishnan, citing multiple series, states the diagnostic formulation: “In the appropriate clinical setting, an elevated serum LDH (often more than two to four times the upper limit of normal) with little or no rise in serum aminotransferases is strongly suggestive of renal infarction” [1]. Differential considerations for this enzyme pattern are narrow and usually easily distinguishable — late myocardial infarction, hemolysis, and kidney transplant rejection.

Other lab findings from the Hazanov and related series [1,2,4,5]:

• White blood cell count mean 11,000/µL — elevated, contributing to the pyelonephritis mimic
• C-reactive protein elevated in the Bourgault 2013 French cohort in 77.6% [5]
• Serum creatinine variable — the Oh 2016 Korean cohort reported a median presenting creatinine of 0.95 mg/dL with eGFR 75.9 ± 25.8, reflecting predominantly unilateral disease in a population whose contralateral kidney was already compensating [6]. The Hazanov cohort, weighted toward AFib and larger emboli, had a mean admission creatinine of 1.79 ± 1.66 mg/dL [4]. AKI incidence in Oh 2016 was 20.1% overall and 38% in the renal-artery-injury subgroup, highlighting the variability [6].

Imaging Hierarchy

The Hazanov cohort also provides the cleanest comparison of imaging sensitivity for the diagnosis [4]:

The 11% ultrasound sensitivity is worth sitting with. Every patient with suspected renal infarction who gets only an ultrasound and goes home is at substantial risk of a missed diagnosis. Our patient’s ultrasound did what ultrasound does well (rule out obstruction) and nothing else.

The modern workup has coalesced around contrast-enhanced CT as the primary diagnostic test, with CTA as the cause-definition test. UpToDate’s recommendation is “immediate CTA in most patients” once renal infarction is suspected [1]. The Oh 2016 Korean cohort (438 patients across 9 hospitals, 1993-2013) defined renal infarction radiologically as “single or multiple wedge-shaped parenchymal perfusion defects” on imaging [6] — a definition that presumes contrast-enhanced CT or CTA.

The Cortical Rim Sign

Tell the radiologist to look for the cortical rim sign on her CTA.

The cortical rim sign is a thin band of enhancing subcapsular cortex surrounding an otherwise unenhanced kidney. It represents the subcapsular cortex receiving continued perfusion through capsular collateral arteries even when the main renal artery is occluded. The inner parenchyma — dependent entirely on renal artery flow — is dead. The rim is alive.

Korzets reported it in several of their 11 cases [2]. Wong and colleagues described it systematically in the radiology literature. It is pathognomonic for renal infarction when present, and it distinguishes infarction from pyelonephritis (where the pattern is low-attenuation lesions extending from the capsule inward, often with abscess formation).

Etiology — What Caused It

The Oh 2016 Korean multicenter cohort of 438 patients remains the largest characterization of renal-infarction etiology [6]. Distribution:

Of the 244 cardioembolic cases, 211 (87% of the cardioembolic group) had atrial fibrillation. The remaining cardioembolic etiologies included cardiomyopathy, infective endocarditis, prosthetic valve thrombosis, and suprarenal aortic atheroma thromboemboli (7 cases). Patients in the cardioembolic group were older and had higher rates of hypertension, diabetes, and cardiovascular disease than patients in the other groups.

Diagnostic Workup Algorithm

flowchart TD
    A[Acute flank/abdominal pain<br/>+ Cr elevation OR<br/>risk factors for embolism] --> B{Initial workup}
    B --> C[CBC with diff<br/>BMP + LDH<br/>AST/ALT<br/>UA + urine culture<br/>ECG]
    C --> D{LDH > 2-4× ULN<br/>with preserved<br/>AST/ALT?}
    D -->|Yes| E[High suspicion<br/>for renal infarction]
    D -->|No, but suspicion remains| E
    E --> F[Contrast-enhanced CT<br/>OR CTA with venous phase]
    F --> G{Findings}
    G -->|Wedge-shaped defect<br/>or absent enhancement<br/>+/- cortical rim sign| H[Diagnosis confirmed]
    G -->|Renal artery occlusion/<br/>dissection| I[CTA confirms cause]
    G -->|Renal vein thrombosis<br/>on venous phase| J[RVT pathway]
    G -->|Indeterminate| K[Consider catheter angiography]
    H --> L{Time since onset<br/>< 6 hours?}
    I --> L
    L -->|Yes + main renal artery| M[Interventional radiology<br/>catheter-directed thrombolysis<br/>or mechanical thrombectomy]
    L -->|No, or segmental only| N[Anticoagulation<br/>per UTD algorithm]
    J --> O[Anticoagulation +<br/>evaluate for nephrotic syndrome,<br/>hypercoagulable state, malignancy]
    N --> P[Etiology workup:<br/>ECG rhythm strip + telemetry<br/>TTE, consider TEE<br/>D-dimer, troponin<br/>Hypercoagulable panel if indicated]
    M --> P
    P --> Q[Long-term anticoagulation<br/>decision<br/>HTN management<br/>contralateral kidney<br/>protection]

Differential Diagnosis

Five conditions span most of the alternatives considered when a patient presents with acute flank or abdominal pain and elevated creatinine.

Korzets’ 11-patient series illustrates how badly this gets missed in practice. Of their cases, “the working diagnoses were renal colic in two, pyelonephritis in three, acute renal carcinoma, digitalis intoxication, and suspected endocarditis in one each” [2]. The initial emergency department diagnosis was renal infarction in zero of eleven patients.

Management

Prognosis

The outcome data from Hazanov 2004 are both more reassuring and more sobering than the “your kidney just died” framing suggests [4]:

The 61% rate of normal renal function at follow-up is almost entirely attributable to contralateral kidney compensation. The infarcted kidney typically does not recover meaningful function after complete main artery occlusion. What recovers is the single remaining functional kidney’s ability to compensate. For a patient with the right kidney doing 75% of baseline function before the event, post-infarction total GFR typically stabilizes around 50-60% of baseline — enough to live a normal life, far from needing dialysis.

The 30-day mortality is not a kidney-failure statistic. It reflects the underlying cardiac disease that caused the embolic event in most cases. Patients die of the stroke that follows the next atrial clot, the myocardial infarction from the shared embolic substrate, or the cardiac decompensation that preceded the event. The kidney tells you about the clot. The clot tells you about the patient.

When the AKI Is Bigger Than Single-Kidney Physiology Predicts

Andy’s instinct here is correct and worth unpacking: her previous creatinines were normal, so why is she in clinical AKI at 2.6? The answer is that the acute creatinine in unilateral renal infarction is not a single-variable problem. It reflects the timing of presentation, the reserve of the contralateral kidney, and any second insult layered on top.

Start with the cohort data. The Hazanov 44-patient cohort had a mean admission creatinine of 1.79 ± 1.66 mg/dL, which rose to 2.43 ± 3.37 during hospitalization [4]. At follow-up, 13% had a creatinine of 1.5-2.0 and 18% had a creatinine greater than 2.0. The Oh 2016 Korean cohort of 438 patients reported that 20.1% developed AKI, with the renal-artery-injury subgroup carrying the highest AKI rate at 38% [6]. A presenting creatinine of 2.6 is therefore within the expected distribution for this disease, not an outlier. The “normal” baseline creatinine of 1.0 and the adult mental model of “one kidney, one-and-a-half creatinine” both come from steady-state physiology after weeks of adaptation — not from the acute phase before hyperfiltration compensation has completed.

The physiologic steady-state math: one kidney producing half the GFR takes days to weeks to compensate via single-nephron hyperfiltration. Acute loss of 50% of functional renal mass, without compensation, roughly doubles serum creatinine from baseline. A pre-event creatinine of 1.0 with acute loss of one kidney predicts a transient peak of 2.0 or higher over the first 48-72 hours, settling to 1.4-1.6 once contralateral hyperfiltration is established. Her 2.6 fits the acute phase of this trajectory — but it is toward the upper end, and that upper end carries clinical meaning.

What pushes the number from “expected for unilateral loss” toward “something else on top”:

In her specific case, a creatinine of 2.6 signals that she likely presented several days into the event. The history of “mild” flank pain is congruent with that timeline — severe acute pain attenuates as the infarct stabilizes. The Hazanov data are instructive here: diagnosis was made on hospital day 1 in only 52% of patients, and the remaining cases were identified over subsequent days without worse outcomes [4]. Late presentation with volume depletion plus possible analgesic exposure is the most likely proximate driver of her number, but bilateral embolic disease is the differential to exclude before comfort sets in.

Back to the Case

Our patient’s data:

• Normal-sized left kidney (11.6 cm) — not chronic end-stage
• Acute perinephric stranding on CT — acute event
• Ultrasound no hydro — not obstructive
• No nephrogram on renogram, no meaningful perfusion — arterial inflow failure
• Cr 2.6 — consistent with single-functional-kidney physiology
• Mild left flank pain — acute, but less severe than the colic of a stone

This is acute left renal infarction from arterial inflow failure. The LDH will almost certainly be elevated 2 to 4 times the upper limit of normal with preserved AST and ALT. The ECG should be obtained immediately to screen for atrial fibrillation. The CTA with venous phase is the right next step to characterize the cause — thrombotic occlusion, dissection, FMD pattern, or renal vein involvement. The echocardiogram should follow within 24-48 hours to identify cardiac embolic source.

Her creatinine of 2.6 deserves a specific thought process, per the section above. It fits the Hazanov cohort distribution (admission mean 1.79, hospital course mean 2.43; 18% above 2.0) and is consistent with acute unilateral loss before full contralateral compensation — but sits in the upper band. The most likely proximate contributors are late presentation with volume depletion, possible NSAID or contrast exposure, and unmasking of pre-existing subclinical CKD. The differential we cannot miss is subclinical injury to the right kidney from the same embolic process. The CTA must image both kidneys with equal care. If the right kidney shows any segmental defect, the embolic source is active and bilateral and the anticoagulation decision gets more urgent.

If symptom onset is within hours and the CTA confirms main renal artery occlusion, interventional radiology consultation for catheter-directed thrombolysis is urgent. If symptom onset is days ago — which her creatinine of 2.6 suggests — management shifts to anticoagulation and etiologic workup.

Either way, the right kidney becomes the clinical focus. It is now doing the work of two, and it is the kidney whose future determines whether she ends up on dialysis or continues a normal life.

Summary Pearls

• Renal infarction hides in the colic / pyelonephritis differential. A 2-3 day diagnostic delay is typical. Less than 50% of patients are diagnosed promptly [1].
• LDH is the single most useful screening lab. 93% of Hazanov’s AFib cohort had LDH > 400, mean 1,100 [4]. The tissue-specific pattern (LDH up, AST/ALT preserved) is diagnostic in the right clinical setting.
• Absent nephrogram on radioisotope scintigraphy in a normal-sized kidney with acute perinephric stranding is renal infarction until proven otherwise. Scintigraphy sensitivity approaches 97% [4]. Lasix provocation adds no information when phase 1 has already failed.
• Ultrasound misses 89% of renal infarctions [4]. Never settle for an ultrasound when the differential includes infarction.
• Contrast-enhanced CT or CTA is the anatomic gold standard. Ask the radiologist to look specifically for the cortical rim sign — pathognomonic when present.
• Atrial fibrillation is the most common single cause. In anticoagulated AFib patients with renal infarction, the majority are subtherapeutic at presentation — it is a compliance / dose-adjustment / drug-interaction problem, not just bad luck [4].
• The revascularization window is narrow. Catheter-directed thrombolysis is feasible within approximately 3-6 hours for main artery occlusion. Beyond that, therapy is anticoagulation and protection of the contralateral kidney.
• Prognosis is better than it feels. 61% of Hazanov’s patients had normal renal function at follow-up — contralateral compensation carries the workload. But 30-day mortality is 11%, reflecting the systemic cardiac embolic substrate, not the kidney itself.
• When AKI magnitude exceeds what single-kidney physiology predicts, the answer is never just the infarcted kidney. A creatinine 2-3 times above the unilateral-infarction expected value signals volume depletion, NSAID / contrast effects, unmasked pre-existing CKD, or — the one you cannot miss — subclinical contralateral injury from the same embolic process. Image both kidneys.
• Protect the single remaining kidney. Avoid nephrotoxins, treat the cardiac or vascular source, monitor for hypertension, and do not overlook the implications of single-kidney-equivalent physiology.

References

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Andrew Bland, MD, FACP, FAAP Medical Associates Department of Nephrology, Dubuque, IA | University of Illinois College of Medicine at Peoria | University of Dubuque PA Program | Butler College of Osteopathic Medicine

Draft for review — pending reference verification via /reference-check.