google ads
Kidney: Renal Infarction Imaging Pearls - Educational Tools | CT Scanning | CT Imaging | CT Scan Protocols - CTisus
Imaging Pearls ❯ Kidney ❯ Renal Infarction

-- OR --

  • “Renal infarcts can arise from a number of processes such as thromboembolism, vasculitis, and trauma, but most of them commonly occur secondary to cardiovascular disease. The imaging appearance of an infarct depends on the territories of vascular compromise and extent of associated parenchymal involvement. For example, thrombosis of a small vessel may cause a segmental infarct and resultant focal wedge-shaped areas of apparent infiltration secondary to hypoperfusion. On the other hand, occlusion of the renal artery will cause a global insult. Such an infarct may appear as an enlarged kidney with preserved reniform shape.”
    Infiltrative Renal Malignancies: Imaging Features, Prognostic Implications, and Mimics
    Sweet DE et al.
    RadioGraphics 2021; 41:0000–0000
  • “The renal parenchyma will appear diffusely infiltrated and hypoenhancing, with preserved enhancement in a subcapsular rim owing to perfusion from capsular arteries that arise as early branches from the renal artery (cortical rim sign). When present, this unique feature can be useful in distinguishing infarct from pyelonephritis. At follow-up imaging, the infarcted segments will often demonstrate parenchymal volume loss and persistent hypoenhancement.”
    Infiltrative Renal Malignancies: Imaging Features, Prognostic Implications, and Mimics
    Sweet DE et al.
    RadioGraphics 2021; 41:0000–0000
  • “The ‘‘flip-flop enhancement’’ is a characteristic radiologi- cal finding of renal infarction described on CT images. This appearance is generated by hyperattenuation of the infarcted renal parenchyma in contrast-enhanced CT on delayed phase, showing inverted enhancement compared to the same hypodense region on corticomedullary and nephrographic phases. Flip-flop enhancement can be observed for up to several hours after intravenous injection of contrast agents (24–48 h) in about 70–75% of cases of renal ischemia. Pathologically, this sign could be due to an increased permeability through the damaged capillary that causes extravasation of contrast agent from the ischemic glomerular membrane to the extracellular space.”
    ‘Flip-flop enhancement’ in renal infarction
    Claudio Leto et al.
    Abdominal Radiology (2019) 44:1625–1626
  • Differential diagnosis for the imaging appearance of renal infarction includes pyelonephritis, since in both conditions post-contrast CT images demonstrate a focal wedge-like region of reduced enhancement on early phases, compared with the normal portions of the kidney. However, in kidney infection, neither the ‘‘cortical rim sign’’ nor ‘‘flip-flop enhancement’’ are found in CT imaging.
    ‘Flip-flop enhancement’ in renal infarction
    Claudio Leto et al.
    Abdominal Radiology (2019) 44:1625–1626
  • “Renal cell carcinoma (RCC) is the most common malig- nancy to involve the IVC, with caval extension seen in 4–10%. Any venous tumor thrombus is consid- ered Robson Stage IIIa, while in the Internal Union Against Cancer tumor-node-metastasis (TNM) classification, renal vein only, infradiaphragmatic IVC, and supradiaphragmatic IVC involvements correspond to T3b, T3c, and T4b, respec- tively. CT has been shown to have negative and positive predictive values for venous extension of 97% and 92%, respectively, with the corticomedullary phase of enhancement being most useful.”
    The inferior vena cava: a pictorial review of embryology, anatomy, pathology, and interventions
    David S. Shin et al.
    Abdominal Radiology https://doi.org/10.1007/s00261-019-01988-3
  • Acute Renal Infarction: Causes
    Thromboembolism
    - Thrombus in the left side of the heart or aorta
    - Aneurysm of the aorta or renal artery
    - Atherosclerosis
    - Subacute bacterial endocarditis (septic emboli)
    - Transcatheter embolization and other endovascular procedures
    - Dissection of the aorta or renal artery
  • Acute Renal Infarction: Causes
    - Vasculitis
    -- Polyarteritis nodosa
    -- SLE
    -- Drug-induced vasculitis
    - Trauma
    -- Avulsion of the renal artery
    -- Occlusion of the renal artery
    -- Penetrating vascular injury
    - Paraneoplastic syndrome
    - Hypercoagulable state
    - Acute venous occlusion
  • Acute renal infarction is a relatively rare and scarcely reported condition. Contrast enhanced CT scan is essential for diagnosing this condition. The most common etiology of this condition is cardioembolic, however up to 59% of cases could be classified as idiopathic acute renal infarction. Here we present a case of a 41 year-old male who was admitted for acute onset right flank pain with fevers and rigors. A CT abdomen with contrast showed findings concerning for right pyelonephritis or renal infarction. Urinalysis was negative for infection. He did not respond to treatment with intravenous antibiotics and was thus diagnosed with acute renal infarction. Work-up for common etiologies was negative and the renal infarction was presumed to be idiopathic. He was discharged home on Enoxaparin. In conclusion, acute renal infarction is a rare condition which should be suspected in patients presenting with acute flank/abdominal pain in whom the more common etiologies have been ruled out.
    Acute renal infarction: A diagnostic challenge.
    Markabawi D, Singh-Gambhir H
    Am J Emerg Med. 2018 Jul;36(7):1325.e1-1325.e2.
  • “Acute renal infarction is a relatively rare and scarcely reported condition. Contrast enhanced CT scan is essential for diagnosing this condition. The most common etiology of this condition is cardioembolic, however up to 59% of cases could be classified as idiopathic acute renal infarction.”
    Acute renal infarction: A diagnostic challenge.
    Markabawi D, Singh-Gambhir H
    Am J Emerg Med. 2018 Jul;36(7):1325.e1-1325.e2.
  • “Renal infarction occurs in a variety of clinical setting .The most common cause is thromboembolism from cardiovascular disease. The most common clinical manifestation is sudden onset of flank or back pain. Hematuria, proteinuria, fever, and leukocytosis may be present.”
    CT Evaluation of Renovascular Disease
    Akira Kawashima, MD • Carl M. Sandler, MD • Randy D. Ernst, MD Eric P. Tamm, MD • Stanford M. Goldman, MD • Elliot K. Fishman
    RadioGraphics 2000; 20:1321–1340
  • “Acute infarcts typically appear as wedge-shaped areas of decreased attenuation within an otherwise normal-appearing kidney. When large areas of the kidney are involved, an increase in the size of the kidney due to edema can be seen. In global infarction, the entire kidney is enlarged and its reniform configuration remains preserved.”
    CT Evaluation of Renovascular Disease
    Akira Kawashima, MD • Carl M. Sandler, MD • Randy D. Ernst, MD Eric P. Tamm, MD • Stanford M. Goldman, MD • Elliot K. Fishman
    RadioGraphics 2000; 20:1321–1340
  • Acute cortical necrosis, a rare form of acute renal failure, results from ischemic necrosis of the renal cortex with sparing of the renal medulla. The pathophysiology of this condition is complex and has been attributed to ischemia due to vasospasm of small vessels, toxic damage to glomerular cap- illary endothelium, and primary intravascular thrombosis. The process is either multifocal or diffuse; in most cases, it is bilateral.
    CT Evaluation of Renovascular Disease
    Akira Kawashima, MD • Carl M. Sandler, MD • Randy D. Ernst, MD Eric P. Tamm, MD • Stanford M. Goldman, MD • Elliot K. Fishman
    RadioGraphics 2000; 20:1321–1340
  • “This condition is associated with complications of pregnancy, including abruptio placentae and septic abortion. Other causes include sepsis, shock, venomous snake bite, severe dehydration, transfusion reaction, and hemolytic uremic syndrome. Cortical necrosis can result from any condition that produces acute, prolonged shock.”
    CT Evaluation of Renovascular Disease
    Akira Kawashima, MD • Carl M. Sandler, MD • Randy D. Ernst, MD Eric P. Tamm, MD • Stanford M. Goldman, MD • Elliot K. Fishman
    RadioGraphics 2000; 20:1321–1340
  • “Helical CT performed during the arterial phase can show enhancing interlobar and arcuate arteries adjacent to the nonenhancing cortex. Characteristic parenchymal findings include enhancement of the medulla but no en- hancement of the cortex. A rim of subcapsular cortical enhancement is also a characteristic finding because of collateral flow from the capsular vessels.”
    CT Evaluation of Renovascular Disease
    Akira Kawashima, MD • Carl M. Sandler, MD • Randy D. Ernst, MD Eric P. Tamm, MD • Stanford M. Goldman, MD • Elliot K. Fishman
    RadioGraphics 2000; 20:1321–1340
  • Enhancement of the juxtamedullary zone of the cortex may be present. Therefore, the necrotic cortex appears as a hypoattenuating zone circumscribing the kidneys adjacent to the renal capsule. Renal function is usually diminished. The kidneys become progressively smaller over several months. A single thin rim of calcification or “tramline” calcification can form in the renal cortex . The characteristic cortical calcification appears as early as 1–2 months after the event.
    CT Evaluation of Renovascular Disease
    Akira Kawashima, MD • Carl M. Sandler, MD • Randy D. Ernst, MD Eric P. Tamm, MD • Stanford M. Goldman, MD • Elliot K. Fishman
    RadioGraphics 2000; 20:1321–1340
  • “Although renal infarcts are common after FEVAR, the clinical relevance of these events appears to be limited, with less than one-quarter of patients with renal infarcts experiencing a decline in renal function.”

    
Incidence and Clinical Significance of Renal Infarct After Fenestrated Endovascular Aortic Aneurysm Repair 
Burke LMB et al.
AJR 2017; 208:885–890 



  • “Renal ischemia remains a known compli- cation of FEVAR, with clinical studies showing variable rates of renal impairment after FEVAR of juxtarenal abdominal aortic aneurysms. Studies show that 11– 35% of patients experience a transient increase in serum creatinine levels (defined as a > 30% increase in serum creatinine level), and 0–4% of patients require temporary or permanent dialysis.”

    
Incidence and Clinical Significance of Renal Infarct After Fenestrated Endovascular Aortic Aneurysm Repair 
Burke LMB et al.
AJR 2017; 208:885–890

  • “Our data show a gradual mild increase in baseline serum creatinine level in all patients undergoing FEVAR, regardless of whether the patient had a renal infarct. This nding mirrors a recent study from France , which found an increase in serum creatinine level during the first week after FEVAR.”

    
Incidence and Clinical Significance of Renal Infarct After Fenestrated Endovascular Aortic Aneurysm Repair 
Burke LMB et al.
AJR 2017; 208:885–890

  • “Although the presence of renal infarct af- ter FEVAR is relatively common in our pa- tient population, it seems to carry little clini- cal relevance. This information is useful to interpreting radiologists when determining the urgency to report such findings, as well as when explaining the clinical relevance to referring clinicians and to patients undergo- ing FEVAR.” 


    Incidence and Clinical Significance of Renal Infarct After Fenestrated Endovascular Aortic Aneurysm Repair 
Burke LMB et al.
AJR 2017; 208:885–890

  • “Fat retention in the bladder was found in 5 patients (5.4%) after partial nephrectomy, but was not observed in any patients after total nephrectomy. No fat retention was seen immediately after partial nephrectomy (4–8 days), but occurred 2–15 months after the surgery. Subsequently, intravesical fat retention disappeared in 3 patients (8, 24, and 16 months later), and it persisted from 19–22 months after surgery in the remaining 2 patients. Collecting system repair occurred in 25 patients (27%) with partial nephrectomy. There was no statistically significant association between fat retention in the bladder and intraoperative collecting system repair (p = 0.12). The association with intravesical fat retention was not significant for either tumor size, distance to the collecting system, or the R.E.N.A.L. Nephrometry Score.”


    CT detection of fat retention in the bladder after partial nephrectomy
 Kazaoka, J., Kusakabe, M., Ottomo, T. et al. 
Abdom Radiol (2017). doi:10.1007/s00261-017-1117-4
  • Renal Infarction: Causes
    - Trauma
    - Embolism from heart
    - Embolism from catheters
    - Sickle cell disease
    - Vasculitis
    - Acute renal vein thrombosis (rare)
  • Renal Infarction: CT Findings
    - May be focal or global, may be single or multiple
    - Wedge shaped areas of decreased attenuation
    - Edematous kidney
    - Cortical rim enhancement
    - Kidney enlarged early and may become atrophic
  • Renal Infarction: Facts
    - Can be segmental or global in extent
    - Can be an isolated process or part of multisystem disease involvement
    - Acute and chronic renal infarction due occur
    - Symptoms may range from acute flank pain, to FUO to hematuria
  • Renal Infarction: CT Findings
    - Focal vs global involvement
    - Usually due to arterial occlusion sudden in onset
    - May be unilateral or bilateral depending on the etiology
    - Cortical rim sign may be seen with global infarction
    - Chronic renal infarction may be seen as a small kidney
  • Renal Infarction: CT Findings
    - Focal vs global involvement
    - Usually due to arterial occlusion sudden in onset
    - May be unilateral or bilateral depending on the etiology
    - Cortical rim sign may be seen with global infarction
    - Chronic renal infarction may be seen as a small kidney
  • “The diagnosis of renal infarction is suggested by an elevated LDH. The diagnosis itself is typically made with computed tomography. The image above is typical. A wedge shaped lesion that does not enhance with contrast is seen. The extent of the infarction depends on which renal artery was occluded and at what level.”
    Renal Infarction
    Weinberg I
    Vascular Medicine Sept 2011
  • “A renal infarction results from disruption of blood flow to the kidney. The disruption can result from an embolus arising in a distant location or from thrombosis of the renal artery. Local renal arterythrombosis can be spontaneous or secondary to trauma. Once the diagnosis is made the reason for the infarction needs to be found. Treatment starts with anticoagulation. Duration of therapy and other treatments such as endovascular intervention depend on the cause, amount of renal damage and hypertension that may result.”
    Renal Infarction
    Weinberg I
    Vascular Medicine Sept 2011
  • “Although most of our cases were straightforward for the diagnosis of renal infarction, cases with tumefactive lesions and global infarctions without the well-known cortical rim sign were particularly challenging. We describe a new sign, flip-flop enhancement pattern, which we believe solidified the diagnosis of renal infarction in five of our cases. The authors recommend further investigations for association of flip-flop enhancement and renal infarction.”
    CT Features of Renal Infarction
    Suzer O et al.
    Eur J Radiol 2002 Oct;44(1):59-64
  • “Acute renal infarction is not as rare as previously assumed. The entity is often misdiagnosed. Unilateral flank pain in a patient with an increased risk for thromboembolism should raise the suspicion of renal infarction. In such a setting, hematuria, leucocytosis and an elevated LDH level are strongly supportive of the diagnosis.”
    The Clinical Spectrum of Acute Renal Infarction
    Korzets Z et al.
    Isr Med Assoc J 2002 Oct;4(10):781-4
  • Renal Infarction: Facts
    - Can be segmental or global in extent
    - Can be an isolated process or part of multisystem disease involvement
    - Acute and chronic renal infarction due occur
    - Symptoms may range from acute flank pain, to FUO to hematuria
  • Renal Infarction: Causes
    - Trauma
    - Embolism
    - Arterial thrombosis
    - Vasculitis
    - Acute renal vein thrombosis
  • "Underlying embolic and hemorrhagic complications are common in patients with acute nontraumatic abdominal pain in the setting of atrial fibrillation and can be accurately seen on CT."

    Spectrum of CT Findings in Patients with Atrial Fibrillation and Nontraumatic Acute Abdomen
    Barajas RF et al.
    AJR 2009;193:485-492

Privacy Policy

Copyright © 2024 The Johns Hopkins University, The Johns Hopkins Hospital, and The Johns Hopkins Health System Corporation. All rights reserved.