Matthew A. Meissner, MD
Ganesh V. Raj, MD, PhD, FACS
BASICS
DESCRIPTION
• Renal infarction is a rare condition that occurs secondary to any process that interrupts or halts blood flow to the kidney causing necrosis and cessation of function
• Most commonly caused by thromboembolic phenomenon in conditions such as atrial fibrillation (a-fib), bacterial endocarditis, or cardiac mural thrombi
EPIDEMIOLOGY
Autopsy data reveal an estimated prevalence of 0.48–1.4%
RISK FACTORS
• Acute tubular necrosis
• Antiphospholipid antibody syndrome
• Atherosclerosis
• A-fib
• Chagas disease
• Cocaine abuse
• Collagen vascular disease
• Congestive heart failure
• Diabetes mellitus
• Dilated cardiomyopathy
• Endocarditis
• Hypercoagulable states (factor V Leiden)
• Hypertension
• Iatrogenic (surgical manipulation of renal vasculature)
• Intimal dissection
• Long bone fractures (fat emboli)
• Myocardial infarction
• Patent foramen ovale (paradoxical embolism)
• Pyelonephritis
• Renal artery aneurysm and stenosis
• Renal artery or vein thrombosis
• Sickle cell disease causing papillary necrosis
• Trauma: Blunt or iatrogenic
• Valvular heart disease
Genetics
• Patients with inherited hypercoagulable disorders such as factor V Leiden mutation, protein C or S deficiency, lupus, antiphospholipid antibody syndrome, neurofibromatosis, Ehler–Danlos, and other collagen vascular disorders are at increased risk
• Familial history of coronary artery disease, diabetes, or metabolic syndrome portends an increased risk for these diseases, and consequently, renal infarction
PATHOPHYSIOLOGY
• The main mechanism is embolization of the renal vasculature:
– Clot emboli are the most common (a-fib)
– Atherosclerotic emboli
– Vegetative emboli (endocarditis)
– Fat emboli
• Renal arterial occlusion is more common on the left side, due to the more acute angle of the left renal artery with the aorta (1)
• Acute infarction due to trauma may show a hematoma in the vessel wall (intimal flap); infarction due to clot emboli will reveal a clot, blocking the renal artery or its branches (2)[C]
• Renal vasoconstriction from sepsis, α-adrenergics, cocaine, others
ASSOCIATED CONDITIONS
• Aneurysms of the aorta or renal artery
• Angina
• Atrial fibrillation
• Claudication
• Collagen vascular disease (Ehlers–Danlos)
• Congestive heart failure
• Mesenteric ischemia
• Patent foramen ovale
• Prosthetic heart valve
• Sub acute bacterial endocarditis (SBE)
• Polyarteritis nodosa with vasculitis
• Sickle cell disease (papillary necrosis)
GENERAL PREVENTION
• Reduce risk factors for coronary artery disease (CAD), hypertension, and diabetes
• Appropriate anticoagulation for a-fib, deep vein thrombosis, and valvular heart disease
• Treatment of hypercholesterolemia with statins
• Measures to reduce the risk of trauma (seat belts)
DIAGNOSIS
HISTORY
• A high suspicion is mandated in patients with underlying heart disease, hypercholesterolemia, or recent trauma who present with abdominal or flank pain
• Suspect a ventricular thrombus in patients with a recent myocardial infarction
• Acute flank pain: ∼75%
• Nausea/vomiting: ∼50%
• Gross hematuria may be seen
ALERT
The symptoms associated with acute renal infarction closely mimic those of an acute episode of urolithiasis or pyelonephritis resulting in delayed diagnosis. This detrimentally impacts long-term renal function and potential for recovery.
PHYSICAL EXAM
• Diffuse abdominal pain without peritonitis
• CVA tenderness
• Fever
• Acute hypertension
• Flank ecchymosis in trauma patients
• Heart murmur
• Peripheral vascular disease
• Decreased urine output
• Abdominal bruit from an aneurysm
DIAGNOSTIC TESTS & INTERPRETATION
Lab
• Leukocytosis: 70% of patients
• Elevated or normal creatinine
• Microscopic hematuria: 80% of patients
• Proteinuria: 90% of patients
• Elevated LDH: 100% of patients. If LDH is elevated with normal transaminases, this is highly suggestive of renal infarction in the presence of appropriate symptoms.
• Elevated ALT: 83% of patients
• Elevated AST: 66% of patients
Imaging
• The best study is abdominal CT with and without IV contrast
• Classic CT findings of renal infarction:
– Lack of IV contrast uptake in affected kidney
– Areas of low attenuation secondary to local edema
– Sharply demarcated, wedge-shaped area of devascularized infarct
– Cortically based, hypodense areas triangular in shape, widest part at the cortex (base of infarct)
– Cortical rim sign: Perfusion to infarcted aspect of cortex is maintained by collateral branches, showing a thin rim of enhanced cortex (3)[C]
• IVP reveals poorly or nonvisualized kidney on the affected side
• Renal ultrasound with Doppler flow
ALERT
A noncontrast CT, often obtained due to suspicion for renal colic, will fail to show a renal infarct.
Diagnostic Procedures/Surgery
• Renal angiography will diagnose any renal vascular occlusion and allow for intervention
• ECG to diagnose arrhythmias
• Echocardiography for diagnosis of mural thrombi and valvular vegetations
Pathologic Findings
• Acutely, histology demonstrates apoptosis of glomerular and renal tubular epithelial cells
• Chronic changes include necrosis and nuclear loss in glomeruli and tubules
DIFFERENTIAL DIAGNOSIS
• Acute abdominal processes (acute mesenteric ischemia, appendicitis, bowel obstruction)
• Cystic renal disease
• Pyelonephritis
• Renal artery stenosis
• Renal calculi
• Renal tumor
• Renal vein thrombosis
TREATMENT
GENERAL MEASURES
• The optimal therapy for renal infarction is not clear
• Initial therapy includes supportive measures with IV fluids and pain control
• Since thromboembolic disease is the most common cause of renal infarction, primary anticoagulation is considered 1st line
• Other acute treatment options include thrombolysis, endovascular stenting, and thrombectomy
MEDICATION
First Line
• Antihypertensives to control hypertension
• Anticoagulation therapy:
– Heparin: Start with a bolus of 80 U/kg followed by a continuous infusion titrated to a therapeutic PTT
– Begin warfarin therapy concurrently, goal INR of 2–3
– Continue in patients with known causes of thromboembolic disease
Second Line
• Thrombolytic therapy may be used, especially in unstable patients
– Direct intra-arterial infusion to limit systemic side effects
– Many contraindications: Cerebral malignancy or AVM, history of cerebral hemorrhage, GI bleed, active hemorrhage, or aortic dissection
– Relative contraindications: Pregnancy, major surgery within the last 3 wk, uncontrolled hypertension
SURGERY/OTHER PROCEDURES
• Surgical intervention is not considered a primary treatment for thromboembolic renal infarction. Exceptions include:
– Young patients diagnosed within 6 hr of the infarct.
– Bilateral infarcts or infarcts in a solitary kidney.
• For traumatic injuries leading to renal infarction (avulsion of the renal pedicle), open surgical repair may be attempted during exploration for other injuries.
ADDITIONAL TREATMENT
Radiation Therapy
N/A
Additional Therapies
Percutaneous angioplasty of the renal artery or thrombectomy
Complementary & Alternative Therapies
N/A
ONGOING CARE
PROGNOSIS
• The duration of renal ischemia is the critical factor in determining prognosis
• Prognosis also depends on the cause of the infarct and the amount of parenchyma affected
• Patients often die of illness related to the comorbid medical conditions causing the infarct
COMPLICATIONS
• Chronic renal insufficiency
• Renal atrophy
• Hypertension
FOLLOW-UP
Patient Monitoring
• Regular blood pressure monitoring to assess for new-onset hypertension following infarct
• Follow-up imaging to monitor the progression or remission of an infarct
• Medical therapy for underlying condition that led to the infarct
• Monitoring of serum creatinine
Patient Resources
N/A
REFERENCES
1. Fergany A, Novick AC. Renovascular hypertension and ischemic nephropathy Chapter 39. In: Wein AJ, ed. Campbell-Walsh Urology. 10th ed. Philadelphia, PA: Elselvier/Saunders; 2012:1047–1083.
2. Rajeev TP, Köhler TS, Ryndin I, et al. Case report: Renal infarct mimicking renal mass: Further rationale for minimally invasive management. J Endourol. 2007;21:1065–1068.
3. Lang EK, Sullivan J, Frentz G. Renal trauma: Radiologic studies. Comparison of urographic, computerized tomography, angiography, and radionuclide studies. Radiology. 1985;154(1):1–6.
ADDITIONAL READING
Saeed K. Renal Infarction. Int J Nephrol Renovasc Dis. 2012;5:119–123.
See Also (Topic, Algorithm, Media)
• Flank Pain
• Renal Colic
• Renal Infarction Image 
• Renal Trauma, Adult
• Renal Trauma, Pediatric
• Renal Artery Stenosis/Renovascular Hypertension
• Sickle Cell Disease, Urologic Considerations
CODES
ICD9
• 440.1 Atherosclerosis of renal artery
• 584.5 Acute kidney failure with lesion of tubular necrosis
• 593.81 Vascular disorders of kidney
ICD10
• I70.1 Atherosclerosis of renal artery
• N17.0 Acute kidney failure with tubular necrosis
• N28.0 Ischemia and infarction of kidney
CLINICAL/SURGICAL PEARLS
• Renal infarction is most commonly due to thromboembolic disease from underlying medical conditions.
• Prompt diagnosis is paramount for preserving renal parenchyma and function.
• Signs and symptoms may mimic more common GU or intra-abdominal pathology.
• Renal infarction should be in the initial differential diagnosis of nephrolithiasis and pyelonephritis.
• Anticoagulation therapy is the primary form of treatment for renal infarction.