Renal infarction

INTRODUCTION — Renal infarction is rare, and it is often missed or diagnosed late because the presentation is similar to that of common conditions such as nephrolithiasis and pyelonephritis. Depending upon the severity, renal infarction can lead to renovascular hypertension, chronic kidney disease, and end-stage kidney disease.

The two major causes of renal infarction are thromboemboli and in situ thrombosis. Thromboemboli usually originate from a thrombus in the heart or aorta, and in situ thrombosis is usually due to an underlying hypercoagulable condition or injury to or dissection of a renal artery. Either thromboemboli or in situ thrombi may cause complete occlusion of the main renal artery or smaller segmental branch arteries [1,2]. Because atheroemboli are small and typically lead to incomplete arterial occlusion of more distal vessels, atheroemboli often lead to secondary ischemic atrophy rather than renal infarction. (See "Clinical presentation, evaluation, and treatment of renal atheroemboli", section on 'Kidney injury'.)

Thromboembolic renal infarction is reviewed here. The major sources of embolism from the heart, thromboembolism from aortic plaque, and the manifestations of atheroembolic disease are discussed separately. (See "Echocardiography in detection of cardiac and aortic sources of systemic embolism" and "Thromboembolism from aortic plaque" and "Embolism from atherosclerotic plaque: Atheroembolism (cholesterol crystal embolism)".)

EPIDEMIOLOGY

●Prevalence – Renal infarction is rare [1-7]. In a study of 14,411 autopsies published in 1940, the incidence of renal infarction was 1.4 percent [7]. In a later series of approximately 250,000 patients seen at an emergency department over four years, only 17 (0.007 percent) were diagnosed with acute renal infarction [2].

The frequency of renal infarction is probably higher than reported in the above studies since clinical diagnosis of renal infarction is frequently missed or delayed because the patients present with abdominal or flank pain that mimic other, more common conditions, such as nephrolithiasis and pyelonephritis. (See 'Clinical features' below.)

●Age and comorbidities – In a series of 438 patients with renal infarction that was diagnosed between 1993 and 2013, the median age at presentation differed depending on the underlying etiology: cardiogenic (65 years), renal artery injury (43 years), hypercoagulable state (62 years), and idiopathic (49.5 years) [8].

Patients in the cardiogenic group more frequently had a history of hypertension, diabetes mellitus, cardiovascular disease, heart valve disease, and atrial fibrillation than their counterparts in the other three groups.

ETIOLOGY AND PATHOGENESIS — The major etiologies of renal infarction include cardioembolic disease, renal artery injury (most commonly due to dissection of the artery), and hypercoagulable states (table 1) [1,4,6,8-10]:

●Cardioembolic disease – In the series of 438 patients with acute renal infarction cited above, 244 (55.7 percent) patients had cardioembolic renal infarction, 211 of whom had atrial fibrillation [8]. Underlying cardiac disease in the cardioembolic group included cardiomyopathy, endocarditis, and artificial valves thrombi. Thrombi from atheroma of the suprarenal aorta were seen in seven patients.

Renal infarction is more common among patients with atrial fibrillation. In a cohort study that included approximately 30,000 patients with atrial fibrillation, compared with the general Danish population, males and females with atrial fibrillation had an increased relative risk of thromboembolic events (4 and 5.7, respectively) [11]. Among 621 individuals with arterial thromboembolism, 2 percent of presentations involved the renal artery. Of note, renal infarction may be the first manifestation of atrial fibrillation, and, in established cases of atrial fibrillation, many patients who developed renal infarction were subtherapeutic on warfarin [9].

●Renal artery injury – In the case series cited above, 33 patients (7.5 percent) had underlying renal artery injury [8]. Underlying diseases included renal artery dissection, trauma, Marfan syndrome, and polyarteritis nodosa.

Other, less common etiologies reported elsewhere associated with renal artery injury include fibromuscular dysplasia, Ehlers-Danlos syndrome [1], segmental arterial mediolysis (SAM) [12], renal artery occlusion following an endovascular aortic or renal intervention [2,13-17], and cocaine use [18].

●Hypercoagulable state – In the case series cited above, 29 patients (6.6 percent) had a hypercoagulable state due to hereditary thrombophilia in six, hyperhomocysteinemia in four, antiphospholipid syndrome in four, and nephrotic syndrome in one [8].

Renal infarction has also been reported in association with coronavirus 2019 (COVID-19), both in native [19-23] and in transplanted kidneys [24]. This may be due to endothelial dysfunction and activation of the coagulation cascade resulting from the inflammatory response in the setting of COVID-19 [21].

Renal infarction may also be seen among females using oral contraceptive pills [25-27]. Other cardiovascular adverse effects of oral contraceptive pills are discussed at length elsewhere. (See "Combined estrogen-progestin contraception: Side effects and health concerns", section on 'Cardiovascular effects'.)

●Idiopathic – No cause could be identified in 132 patients (30.1 percent) in the series cited above [8]. In another study of 27 consecutive patients with nontraumatic acute renal infarction, 16 (59 percent) had no discernible structural or arrhythmic heart disease and were classified as idiopathic [28].

CLINICAL FEATURES

Clinical manifestations — Although renal infarction is usually unilateral, bilateral kidney involvement has been reported in nearly 20 percent of cases [8,29]. Patients with acute renal infarction typically complain of the acute onset of flank or abdominal pain, frequently accompanied by nausea, vomiting, and, occasionally, fever [1-5,8,9,30]. In the series cited above of 438 patients with renal infarction, the following symptoms and signs were observed:

●Flank pain – 50 percent

●Abdominal pain – 53 percent

●Nausea – 17 percent

●Vomiting – 13 percent

●Fever – 10 percent

These findings may be accompanied by an acute elevation in blood pressure that is presumably mediated by increased renin release [1,2,31,32]. Signs of extrarenal embolization (such as focal neurologic deficits and mesenteric and limb ischemia) also may be seen.

Some patients can be asymptomatic and their renal infarcts are brought to clinical attention by incidental discovery on an imaging study performed for an unrelated condition. (See 'Incidentally detected renal infarct or atrophic kidney' below.)

Laboratory findings — The following laboratory findings are typically seen in patients with acute renal infarction [1,4,28,30-33]. The frequency of the major findings and characteristic laboratory data come from the series of 438 patients cited above [8]:

●Hematuria was present in 32 percent of patients and proteinuria in 12 percent.

●The mean serum creatinine concentration was 1.0 mg/dL (84.0 micromol/L), range 0.4 to 5.6 mg/dL; 31 to 495 mmol/L.

In another study, the reduction in kidney function was most pronounced in patients with bilateral disease or a large, unilateral embolus [1].

●In the series cited above [8], the serum lactate dehydrogenase (LDH) concentration was increased (mean 656 international units/L [range 152 to 7660]). Some smaller studies have had higher mean serum LDH levels of 1100 to 1570 international units/L [4,28,31].

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 [1,3,4,28,31,34]. This pattern of enzyme elevation can also be seen in other conditions that are usually easily distinguishable from renal infarction, including late myocardial infarction, hemolysis, and kidney transplant rejection [34].

Other findings included a mildly elevated white blood cell count (mean 11,000/microL) and an increase in serum C-reactive protein.

DIAGNOSIS — Since the presenting symptoms of renal infarction are not unique, the time to diagnosis following presentation is often more than two days, with <50 percent of patients being diagnosed promptly [4,32,35]. Early diagnosis of renal infarction is critical in those patients who are candidates for revascularization. (See 'Evaluate potential benefit of prompt revascularization' below.)

When to suspect renal infarction — Renal infarction should be suspected in any patient with acute onset flank or abdominal pain who has one or more risk factors for systemic embolization (eg, atrial fibrillation with suboptimal or no anticoagulation), or in any patient with presumed renal colic or pyelonephritis whose initial evaluation suggests an alternative diagnosis. (See 'Differential diagnosis' below.)

Evaluation — In patients with suspected renal infarction, we take a history to determine the duration of symptoms, perform a physical examination, and obtain the following tests [3]:

●Complete blood count with differential

●Serum creatinine and lactate dehydrogenase (LDH)

●Urinalysis and urine culture

●Electrocardiogram to evaluate for atrial fibrillation

●Contrast-enhanced CT (computed tomography; or magnetic resonance imaging [MRI] with gadolinium as an alternative)

Because many patients with renal infarction are presumed to have renal colic, the initial imaging study obtained in the emergency department may be a noncontrast CT or an ultrasound. However, neither of these studies are adequate to evaluate renal infarction. (See 'Making the diagnosis' below.)

Making the diagnosis — Renal infarction is diagnosed by contrast-enhanced imaging, typically contrast-enhanced CT. The classic finding is a wedge-shaped perfusion defect, though the entire kidney may not enhance in cases of complete main renal artery occlusion. MRI with gadolinium is an alternative to CT [36], although the use of gadolinium should be based upon the patient's kidney function as discussed at length elsewhere. (See "Patient evaluation before gadolinium contrast administration for magnetic resonance imaging", section on 'Approach to preventing nephrogenic systemic fibrosis' and "Patient evaluation before gadolinium contrast administration for magnetic resonance imaging", section on 'Patient risk factors for nephrogenic systemic fibrosis'.)

While radioisotope scans were commonly used in the past, their use has been largely supplanted by newer imaging techniques. Ultrasonography is much less sensitive. The sensitivity of these imaging procedures was evaluated in a series of 44 patients with atrial fibrillation and a diagnosis of embolic renal infarction [4]. The sensitivity was 97 percent (36/37) with radioisotope renal scan, 80 percent (12/15) with contrast-enhanced CT, and only 11 percent with kidney ultrasound [4].

Differential diagnosis — The two conditions that most closely mimic the clinical presentation of acute renal infarction are renal colic (flank pain and hematuria) and acute pyelonephritis (flank pain and fever). In a report of 14 patients, for example, eight had an admission diagnosis of nephrolithiasis [37]. (See "Kidney stones in adults: Diagnosis and acute management of suspected nephrolithiasis" and "Acute complicated urinary tract infection (including pyelonephritis) in adults and adolescents".)

Salient features that may distinguish renal infarction from obstructing urinary stone disease and/or pyelonephritis are as follows:

●A history of atrial fibrillation increases the likelihood of renal infarction [38,39].

●Costovertebral angle tenderness suggests nephrolithiasis or pyelonephritis rather than renal infarction [38,39].

●An elevation in serum LDH suggests renal infarction rather than nephrolithiasis or pyelonephritis.

●Varying degrees of hematuria and/or pyuria may occur in renal infarction, nephrolithiasis, and pyelonephritis. However, the absence of hematuria suggests renal infarction rather than nephrolithiasis, and the absence of pyuria suggests renal infarction rather than pyelonephritis [38,39].

●Kidney imaging with CT or ultrasound reliably detects urinary tract obstruction (hydronephrosis) due to urinary stones.

●Kidney imaging may be similar in renal infarction and pyelonephritis. However, CT findings that support the diagnosis of pyelonephritis include low attenuation lesions extending to the renal capsule on contrast enhancement with or without edema, and complications such as renal abscesses. The "cortical rim sign," which is seen in some cases of renal infarction, but not in pyelonephritis, refers to perfusion of an intact subcapsular renal cortex supplied by collateral circulation [40].

Other conditions that can mimic some of the features of renal infarction include mesenteric ischemia and other causes of abdominal pain, such as cholecystitis and pancreatitis.

INITIAL MANAGEMENT — The initial management of renal infarction is directed at rapidly determining which patients may benefit from revascularization, and then promptly referring such patients to a vascular interventional radiology or vascular surgery service [41-44]. However, the optimal treatment for renal infarction due to thromboemboli, in situ thrombosis, or renal artery dissection is uncertain given the absence of comparative studies.

Immediate computed tomography angiography (CTA) in most patients — Following the demonstration of renal infarction on contrast imaging, evaluation of the aorta and renal arteries should be performed in most patients with a CT angiogram (CTA) or magnetic resonance (MR) angiogram to determine the etiology of the infarction and to guide subsequent management.

However, we do not obtain a CTA when the initial diagnostic CT demonstrates an atrophic kidney or a dense wedge-shaped scar, which suggest a remote event without viable tissue. Such a kidney may also have collateral circulation formed, which will reduce the potential benefit from correcting the renal artery occlusion. Under these circumstances, revascularization may be of negligible benefit; these patients are managed in the same way as patients with an incidentally detected renal infarction. (See 'Incidentally detected renal infarct or atrophic kidney' below.)

Evaluate potential benefit of prompt revascularization — For patients in whom we obtain a CTA (see 'Immediate computed tomography angiography (CTA) in most patients' above), we evaluate the time since onset of ischemia (determined by duration of symptoms and signs), the size of kidney parenchyma threatened by the infarction, the kidney function (ie, estimated glomerular filtration rate [eGFR]), and the CTA-determined degree of renal vessel occlusion (ie, complete or partial).

Based upon these factors, the following patients are, in general, more likely to benefit from revascularization than others:

●Complete main renal artery (or major segmental branch) occlusion of <6 hours duration, or a complete occlusion of the main renal artery (or a major segmental branch) if it is perfusing a solitary kidney, or when there is significant reduction in the kidney function (eg, eGFR <50 mL/min/1.73 m²).

●Partial main or major segmental renal artery occlusion of <24 hours duration.

●Partial main or major segmental renal artery occlusion of 24 hours duration or more in the presence of significant kidney function impairment, new or worsened hypertension, or symptoms such as flank pain, hematuria, and fever.

●Arterial dissection as the cause of the renal infarction.

Patients who are likely to benefit from revascularization, as summarized above, should be referred immediately to the interventional radiology or vascular surgery service. (See 'Urgent revascularization for select patients' below.)

Additional discussion of the factors used to evaluate the potential benefit of revascularization is presented below:

●Type of vessel – The risk of parenchymal damage is dependent upon the type of the vessel involved (main, segmental artery, or subsegmental artery) [45]. Occlusion of the main renal artery threatens loss of function of the entire kidney. Occlusion of the segmental arteries generally leads to hypoperfusion of large portions of the kidney, which may be significant in patients with a single kidney or in patients with marked impairment of kidney function. Occlusion of a subsegmental artery generally leads to a wedge-shaped defect in the parenchyma.

●Time from onset of ischemia – The time since onset of ischemia also impacts the likelihood that parenchymal damage may be amenable to recovery. The kidney parenchyma is less likely to recover if the duration of ischemia is long. Symptoms such as acute flank pain, nausea, vomiting, and acute rise in blood pressure often suggest a recent event (typically less than one week old). On the other hand, a small kidney on the affected side suggests that there has been prolonged ischemia. Often, patients are incidentally found to have wedge-shaped parenchymal perfusion defects on abdominal imaging performed for another unrelated indication. In such situations, the age of the infarct is undetermined and should be treated as remote, unless symptomatic.

●Kidney function impairment – The degree of kidney function impairment may depend upon the extent of parenchymal damage as well as function of the contralateral (uninvolved) kidney. In patients with normal kidney function, even complete unilateral renal artery occlusion may not affect the overall kidney function. However, this is not the case in patients who present with acute kidney injury (AKI) or have preexisting chronic kidney disease. There may also be marked loss of kidney function in situations where there is occlusion of bilateral renal arteries, or occlusion of the renal artery perfusing a single functioning kidney.

●Partial or complete occlusion – By CTA, the degree of occlusion (complete or partial) is determined by visualizing contrast uptake in the parenchyma perfused by the involved vessel and in the ipsilateral collecting system. In general, a partial occlusion with preserved perfusion of the parenchyma may suggest reversibility of the ischemia. Complete occlusions within six hours of onset may also be reversible.

Urgent revascularization for select patients — Patients likely to benefit from revascularization (see 'Evaluate potential benefit of prompt revascularization' above) should be referred immediately to a vascular interventional radiology or vascular surgery service for percutaneous endovascular therapy (PET), though surgical intervention may be preferred for patients with renal infarction resulting from a traumatic renal artery occlusion or aortic dissection extending into the renal artery [41,46]. PET may include local thrombolysis, thrombectomy, angioplasty, and stent placement [47-49]. If significant residual vascular abnormalities are seen after thrombectomy, the vessel may be treated with angioplasty with or without placement of a stent.

Systemic fibrinolytic therapy may be used in settings where PET is unavailable [50], provided that vascular injury (eg, dissection or trauma) is not the cause of renal infarction. However, the data to support this approach are sparse [51]. The risks of significant bleeding are higher with systemic thrombolytic therapy than with local thrombolysis in the setting of PET. Contraindications to fibrinolytic therapy are discussed elsewhere. (See "Acute ST-elevation myocardial infarction: The use of fibrinolytic therapy", section on 'Contraindications'.)

The maximum duration of complete renal artery occlusion beyond which thrombolysis would no longer be beneficial is unknown. One study reported little benefit after 90 minutes, while other studies have found some benefit up to several days later [37,46-48,52,53]. Delayed therapy is likely to be effective in patients with a partial occlusion and in patients with thrombotic occlusion [41].

PET leads to successful reperfusion in most patients with renal infarction without significant therapy-associated complications; however, kidney outcomes were only improved in some patients [37,47,48,52,54-58]. Observational studies of intra-arterial thrombolytic therapy illustrate the range of findings:

●One study included 14 patients with acute embolic renal artery occlusion who were treated with intra-arterial thrombolysis using urokinase, streptokinase, or recombinant tissue plasminogen activator [37]. The diagnosis of renal infarction was made within 36 hours in only eight patients; the delay in diagnosis in the remaining patients was as long as eight days after onset of symptoms. Complete renal artery occlusion was noted in five patients, and partial occlusion was noted in eight patients (main renal artery in four and segmental arteries in four); one patient had bilateral renal artery occlusion. Revascularization was successful in 13 patients. Patients with complete main renal artery occlusion failed to have an improvement in kidney function after revascularization. By contrast, stabilization or slight improvement of kidney function was observed in patients with partial occlusion or with complete occlusion of segmental branches. Gross hematuria and postprocedural hematoma were noted in one patient each, neither requiring intervention.

●In a series of 10 patients with occlusion of the main renal artery or a segmental branch (three thrombotic, two embolic, one associated with aortic occlusion, and the remainder as a complication of renal artery angioplasty), all received intra-arterial thrombolysis with urokinase or streptokinase; percutaneous transluminal angioplasty was performed in five patients [52]. Therapy was initiated within 24 hours in only three patients, with the remainder being treated up to five weeks after onset of symptoms. Successful revascularization confirmed by arteriography was achieved in 7 of 10 patients. Of these seven patients, recovery of kidney function occurred in three patients who had been treated at one, two, and six days after onset of symptoms. As a complication of thrombolytic therapy, one patient with an aortic occlusion developed an embolic infarction of the superior mesenteric artery necessitating a colonic resection.

●In a retrospective study of 42 patients, 13 patients were treated with PET and the remaining with conservative care [46]. Main renal artery involvement was noted in 85 percent of patients treated with PET as compared with 20 percent treated with conservative care. Partial or complete restoration of flow was confirmed in all patients treated with PET. At a median follow-up of 30 months, mean creatinine clearance (CrCl) in the PET group had declined from 74 to 55 mL/min. Two patients required permanent dialysis despite PET, both with complete renal artery occlusion of their transplanted kidney. In the conservative care group, median follow-up was 13 months and mean CrCl declined from 66 to 60 mL/min. There were no procedural complications reported in this study.

SUBSEQUENT MANAGEMENT — After referring select patients for urgent revascularization (see 'Initial management' above), the subsequent management of renal infarction includes an evaluation for thromboembolic risk factors and treatment with appropriate antithrombotic therapy.

Identify thromboembolic risk factors — In the absence of a preexisting diagnosis or vascular abnormality (eg, dissection), all patients with renal infarction should undergo an evaluation for thromboembolic risk factors, such as atrial fibrillation or a hypercoagulable state. This evaluation includes the following elements:

●Echocardiography – We perform echocardiography to detect cardiac and aortic sources of systemic embolism. Since it affects management, an echocardiogram is indicated even in patients with a new diagnosis of atrial fibrillation (see "Role of echocardiography in atrial fibrillation"). The choice between transthoracic echocardiography and transesophageal echocardiography is discussed elsewhere. (See "Echocardiography in detection of cardiac and aortic sources of systemic embolism".)

●Cardiac monitoring for atrial fibrillation – Unless atrial fibrillation was diagnosed on the initial electrocardiogram (see 'Evaluation' above), cardiac monitoring is warranted to detect paroxysmal atrial fibrillation. To increase the detection of subclinical atrial fibrillation, prolonged cardiac monitoring (eg, 30-day ambulatory monitoring) is warranted in most patients. (See "Overview of the evaluation of stroke", section on 'Monitoring for subclinical atrial fibrillation'.)

●Laboratory assessment of a hypercoagulable state – For patients without atrial fibrillation or an identified source of systemic embolism on echocardiogram, we evaluate for an underlying hypercoagulable state. (See "Evaluating adult patients with established venous thromboembolism for acquired and inherited risk factors".)

Antithrombotic therapy — Barring contraindications, we initiate one or more antithrombotic agents in patients with renal infarction (algorithm 1).

Initiate anticoagulation in select patients — We generally treat patients with an identified thromboembolic risk factor (see 'Identify thromboembolic risk factors' above) with systemic anticoagulation; the exception is for patients with thromboembolism from aortic plaque, in whom antiplatelet therapy may be preferred. The choice of anticoagulant, its dose, titration, and duration depend upon the underlying condition. These details are discussed elsewhere:

●(See "Atrial fibrillation in adults: Use of oral anticoagulants", section on 'Choice of anticoagulant'.)

●(See "Direct oral anticoagulants (DOACs) and parenteral direct-acting anticoagulants: Dosing and adverse effects", section on 'Direct factor Xa inhibitors'.)

●(See "Selecting adult patients with lower extremity deep venous thrombosis and pulmonary embolism for indefinite anticoagulation".)

●(See "Atrial fibrillation in adults: Selection of candidates for anticoagulation".)

●(See "Thromboembolism from aortic plaque".)

Determine need for antiplatelet therapy — For a patient with renal infarction, antithrombotic regimens include antiplatelet therapy alone, antiplatelet therapy plus anticoagulation, or anticoagulation alone (algorithm 1). The selection of the antithrombotic regimen depends on whether the patient was a candidate for revascularization (see 'Evaluate potential benefit of prompt revascularization' above):

●Patients referred for revascularization – In patients referred for revascularization, the antithrombotic regimen depends on whether an identified thromboembolic risk factor (eg, atrial fibrillation) prompts treatment with an anticoagulant (see 'Initiate anticoagulation in select patients' above):

•Patients treated with anticoagulation – In patients treated with anticoagulation who undergo angioplasty or stent placement, or who have an underlying vascular abnormality, we add low-dose aspirin 81 mg daily for three to six months after the procedure. In patients who do not undergo angioplasty or stent placement and who do not have an underlying vascular abnormality, we treat with anticoagulation alone.

•Patients not treated with anticoagulation – In patients not treated with anticoagulation who undergo angioplasty or stent placement, or who have an underlying vascular abnormality, we treat with aspirin 81 mg and clopidogrel 75 mg daily for three to six months after the procedure followed by aspirin alone thereafter. In patients who do not undergo angioplasty or stent placement and who do not have an underlying vascular abnormality, we treat with lifelong aspirin 81 mg daily.

●Patients not referred for vascularization – In patients not referred for revascularization, the antithrombotic regimen depends on the age of the infarct and on the presence or absence of thromboembolic risk factors.

•Patients with a remote infarction – Patients without symptoms or with radiographic findings suggestive of remote infarct (ie, an atrophic kidney and/or a wedge-shaped scar) are managed in the same way as patients with an incidentally detected renal infarction. (See 'Incidentally detected renal infarct or atrophic kidney' below.)

•Patients with a more recent infarction – In patients who are symptomatic (or recently symptomatic) and whose imaging suggests a more recent infarct, the antithrombotic regimen depends on the presence or absence of thromboembolic risk factors (eg, atrial fibrillation). (See 'Identify thromboembolic risk factors' above.)

-Patients with thromboembolic risk factors – In patients with an identified thromboembolic risk factor, we generally treat with anticoagulation alone. (See 'Initiate anticoagulation in select patients' above.)

-Patients without thromboembolic risk factors – In patients without an identified underlying thromboembolic risk factor, we anticoagulate for six months, although data supporting this approach are generally lacking. We use direct oral anticoagulants, preferably apixaban due to its lowest renal clearance. Use of warfarin as an alternative anticoagulant is reasonable. For patients treated with warfarin, we target a goal international normalized ratio of 2 to 3, except if the renal infarction occurred in a patient already therapeutic on warfarin, in which case we increase the goal to 2.5 to 3.5. Details regarding choice and dosing of these agents is discussed elsewhere. (See "Direct oral anticoagulants (DOACs) and parenteral direct-acting anticoagulants: Dosing and adverse effects", section on 'Direct factor Xa inhibitors'.)

Following completion of six months of anticoagulation, we initiate lifelong low-dose aspirin (eg, 81 mg daily). The kidney prognosis with anticoagulation has generally been favorable, but there are no reports comparing outcomes with untreated patients [8,31,32,59].

Additional imaging for renal artery dissection — For patients with renal infarction due to nontraumatic renal artery dissection, we obtain brain-to-pelvis imaging with CT or MR angiography to assess for lesions in nonrenal arteries. Extrarenal CT angiography may detect additional arterial dissections and/or aneurysms associated with systemic vascular diseases, such as fibromuscular dysplasia (FMD) or inherited vasculopathies (eg, vascular Ehlers-Danlos syndrome). Extrarenal CT angiography also may be useful to diagnose FMD, since subtle renovascular abnormalities of FMD may be difficult to identify in the setting of acute renal infarct due to local inflammation. (See "Clinical manifestations and diagnosis of fibromuscular dysplasia" and "Clinical manifestations and diagnosis of Ehlers-Danlos syndromes".)

In a study of 61 patients with renal infarction due to nontraumatic renal artery dissection, brain-to-pelvis CT angiography identified FMD in a nonrenal arterial site in 16 patients (26 percent) and dissection or aneurysm in a nonrenal arterial site in 21 patients (34 percent); only 24 patients (39 percent) had an isolated renal artery dissection [60].

Hypertension management — Many patients with acute renal infarction also develop an elevation in blood pressure during the first week after infarction, which may subside over time, unless the patient has underlying hypertension [2]. Antihypertensive therapy is often required.

The increase in blood pressure in the setting of renal artery occlusion is primarily due to release of renin. Thus, in the absence of acute kidney injury (AKI) or hyperkalemia, we prefer angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) for the treatment of hypertension in patients with renal infarction. In those who do have AKI or hyperkalemia, the treatment of hypertension is no different from patients without renal infarction and is discussed at length elsewhere. (See "Management of severe asymptomatic hypertension (hypertensive urgencies) in adults".)

MONITORING AND FOLLOW-UP — Patients with renal infarction should be monitored for recurrent thromboembolic events, complications from therapy (eg, bleeding events), stabilization or deterioration of their kidney function, and for the development of new onset or worsening hypertension. The time interval for follow-up is variable depending upon the severity of the original event, risk of recurrence, and the degree of impairment in kidney function.

●Repeat imaging – There are limited data to inform radiographic monitoring for renal infarcts [8]. For follow-up of patients with acute or subacute renal infarction, we obtain serial abdominal vascular imaging (preferably with magnetic resonance angiography) at 6 and 12 months after the original incident to identify recurrent infarcts or the evolution of local vascular lesions (eg, fibromuscular dysplasia [FMD]) [61]. Patients who develop recurrent or worsening vascular lesions may benefit from a vascular interventional radiology or a vascular surgery consultation. The monitoring of patients with FMD is discussed in detail elsewhere. (See "Treatment of fibromuscular dysplasia of the renal arteries".)

In patients with renal infarct due to nontraumatic renal artery dissection, radiographic monitoring depends on the results of brain-to-pelvis CT or MR angiography (see 'Additional imaging for renal artery dissection' above). For patients with isolated renal artery dissection, radiographic monitoring is similar to that for patients with renal infarction from other causes. By contrast, patients with dissections or aneurysms in nonrenal arteries are at high risk of recurrent renal artery dissection; in such patients, it is reasonable to obtain ongoing, annual assessment with abdominal vascular imaging [60].

●Recurrent embolic infarcts – Patients not already on anticoagulation who have recurrent embolic renal infarcts should generally initiate anticoagulation unless such therapy is contraindicated.

Patients who develop recurrent embolic infarcts while on anticoagulation should be assessed for medication adherence and efficacy. Those who are on warfarin may benefit from dietary and medication review to ensure absence of interacting medications or food. Additional cardiac evaluation may be needed. (See "Venous thromboembolism: Anticoagulation after initial management", section on 'Recurrent venous thromboembolism on anticoagulation' and "Atrial fibrillation in adults: Use of oral anticoagulants", section on 'Drug interactions' and "Atrial fibrillation in adults: Use of oral anticoagulants", section on 'Anticoagulant failure'.)

If a complete assessment of medication adherence and efficacy fails to reveal a cause for recurrence, a transition to a different anticoagulant may be necessary. (See "Atrial fibrillation in adults: Use of oral anticoagulants", section on 'Other reasons for switching agents' and "Atrial fibrillation in adults: Use of oral anticoagulants" and "Atrial fibrillation in adults: Selection of candidates for anticoagulation".)

●Preventive care – All patients should receive secondary preventive therapy for vascular disease, and management of chronic kidney disease (when applicable) as discussed elsewhere. (See "Prevention of cardiovascular disease events in those with established disease (secondary prevention) or at very high risk" and 'Hypertension management' above and "Overview of the management of chronic kidney disease in adults".)

INCIDENTALLY DETECTED RENAL INFARCT OR ATROPHIC KIDNEY — Patients with renal infarction who are asymptomatic, whose infarct is in a small, atrophic kidney, and/or whose infarct resembles a wedge-shaped scar are likely to have a remote infarct. Such patients are unlikely to benefit from revascularization due to the duration of ischemia.

Patients with remote infarct should undergo evaluation for underlying thromboembolic risk factors such as atrial fibrillation or a hypercoagulable state (see 'Identify thromboembolic risk factors' above); identified risk factors should be treated with anticoagulation (see 'Initiate anticoagulation in select patients' above). In all other patients, we treat indefinitely with aspirin (typically 81 mg/day), although there are limited data to support this approach.

Patients with a remote infarction who have a concomitant renal artery dissection or aneurysm should undergo additional imaging to assess for extrarenal vascular disease. (See 'Additional imaging for renal artery dissection' above.)

PROGNOSIS — The prognosis following a renal infarction (treated or untreated) is not well defined. Renal infarction primarily occurs in patients who have other conditions associated with morbidity and mortality (eg, atrial fibrillation, diffuse atherosclerotic disease), and patients with renal emboli may have embolization to other organs, such as the brain and intestine [3,4,32]. In a review of 44 cases of renal infarction in patients with atrial fibrillation, the mortality rate was 11.4 percent in the first month after diagnosis [4].

In most studies, serum creatinine was stable or only slightly increased at follow-up [1-4,31,32]. This is not surprising, since only one kidney is usually affected and since, in the absence of further insults, compensatory hypertrophy in the other kidney (or unaffected portions of the ipsilateral kidney) may limit the long-term reduction in estimated glomerular filtration rate (eGFR). New-onset hypertension may resolve spontaneously, but some patients have persistent renin-mediated hypertension [2].

Long-term outcomes were perhaps best described in the series of 44 patients with atrial fibrillation: 38 were treated with heparin and warfarin (seven also received intra-arterial thrombolysis and one also underwent angioplasty), and six did not receive anticoagulation [4]. At a mean follow-up of three years, the following outcomes were reported:

●Sixty-one percent of patients had normal kidney function; 13 percent had mild kidney function impairment (serum creatinine 1.5 to 2 mg/dL [133 to 177 micromol/L]); 18 percent had a serum creatinine >2 mg/dL (177 micromol/L); and 8 percent were being treated with maintenance dialysis.

●Five patients died during the first month after diagnosis (including patients on dialysis).

●Repeat thromboembolic events occurred in 11 patients (13 percent).

The time to diagnosis may be a determinant of kidney outcomes. In a study of 22 patients with documented segmental renal infarction, patients who were diagnosed early (mean time to diagnosis 76 hours) had a nonsignificant trend toward better kidney outcomes compared with those who were diagnosed late (mean time to diagnosis 126 hours) [5]. Preexisting low eGFR and lack of preinfarct anticoagulation were also predictive of persistent kidney dysfunction.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Acute kidney injury in adults".)

SUMMARY AND RECOMMENDATIONS

●Overview – Renal infarction is often missed or diagnosed late because its presentation mimics other common conditions, such as nephrolithiasis and pyelonephritis. It can lead to renovascular hypertension, chronic kidney disease, and end-stage kidney disease. The two major causes of renal infarction are thromboemboli (such as from cardioembolic disease) and in situ thrombosis (such as from renal artery injury or hypercoagulable state). (See 'Introduction' above and 'Etiology and pathogenesis' above.)

●Clinical features – Clinical manifestations of acute renal arterial occlusion include flank pain accompanied by nausea, vomiting, fever, or acute elevation in blood pressure. Hematuria and proteinuria may be present. In the appropriate clinical setting, an elevated serum lactate dehydrogenase is strongly suggestive of renal infarction. (See 'Clinical features' above.)

●Diagnosis – Renal infarction should be suspected in any patient with acute onset flank or abdominal pain who has one or more risk factors for systemic embolization (eg, atrial fibrillation with suboptimal or no anticoagulation), or in any patient with presumed renal colic or pyelonephritis whose initial evaluation suggests an alternative diagnosis. Renal infarction is diagnosed by contrast-enhanced imaging, typically contrast-enhanced CT. (See 'Diagnosis' above.)

●Initial management – The initial management of renal infarction is directed at rapidly determining which patients may benefit from revascularization, and then promptly referring such patients to a vascular interventional radiology or vascular surgery service.

•Immediate computed tomography angiography (CTA) in most patients – Following the diagnosis of renal infarction, evaluation of the aorta and renal arteries should be performed in most patients with a CT angiogram or magnetic resonance (MR) angiogram to determine the etiology of the infarction and to guide subsequent management. However, we do not obtain a CTA when the initial diagnostic CT demonstrates an atrophic kidney or a dense wedge-shaped scar, which suggest a remote infarct without viable tissue. (See 'Immediate computed tomography angiography (CTA) in most patients' above.)

•Urgent revascularization for select patients – Factors that determine the benefit of revascularization include the time since ischemia onset (determined by duration of symptoms and signs), the size of kidney parenchyma threatened by the infarction, the kidney function (ie, estimated glomerular filtration rate), and the CTA-determined degree of renal vessel occlusion (ie, complete or partial). (See 'Evaluate potential benefit of prompt revascularization' above.)

Among patients with renal infarction who may benefit from revascularization, we suggest urgent percutaneous endovascular therapy (PET) rather than medical management alone (Grade 2C). PET may include local thrombolysis, thrombectomy, angioplasty, and stent placement. (See 'Urgent revascularization for select patients' above.)

●Subsequent management – The subsequent management of renal infarction includes an evaluation for thromboembolic risk factors (eg, atrial fibrillation or a hypercoagulable state) and treatment with an appropriate antithrombotic regimen (algorithm 1).

•Antithrombotic therapy – In patients with renal infarction who do not have an identified thromboembolic risk factor, we suggest antiplatelet therapy, either alone or following treatment with an anticoagulant, rather than no therapy (Grade 2C). In such patients, the antithrombotic regimen depends on whether the patient was referred for PET and the time elapsed since the infarction. Patients who have an identified thromboembolic risk factor should, in general, be treated with systemic anticoagulation; concomitant antiplatelet therapy is typically administered to those who undergo angioplasty or stent placement, or who have an underlying vascular abnormality. (See 'Identify thromboembolic risk factors' above and 'Antithrombotic therapy' above.)

•Additional imaging for renal artery dissection – For patients with renal infarction due to nontraumatic renal artery dissection, we obtain brain-to-pelvis imaging with CT or MR angiography. Extrarenal CT angiography may detect additional arterial dissections and/or aneurysms associated with systemic vascular diseases, such as fibromuscular dysplasia. (See 'Additional imaging for renal artery dissection' above.)

•Hypertension management – In patients with renal infarction who develop new onset hypertension, we suggest treatment with angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) rather than other antihypertensive agents (Grade 2C). However, we do not administer ACE inhibitors or ARBs to patients with acute kidney injury or hyperkalemia. In patients with preexisting hypertension whose blood pressure control worsens after renal infarction, we adjust the antihypertensive regimen to include an ACE inhibitor or ARB. (See 'Hypertension management' above.)

●Monitoring and follow-up – Patients with renal infarction should be monitored for recurrent thromboembolic events, complications from therapy (eg, bleeding events), and for stabilization or deterioration of their kidney function. The time interval for follow-up may be variable depending upon the severity of the original event, risk of recurrence, and the degree of impairment in kidney function. (See 'Monitoring and follow-up' above.)

●Incidentally detected renal infarct or atrophic kidney – Patients with renal infarction who are asymptomatic, whose infarct is in a small, atrophic kidney, and/or whose infarct resembles a wedge-shaped scar are likely to have a remote infarct. Such patients are unlikely to benefit from revascularization due to the duration of ischemia. Patients with remote infarct should undergo evaluation for and treatment of underlying thromboembolic risk factors (see 'Identify thromboembolic risk factors' above and 'Antithrombotic therapy' above). In all other patients, we treat indefinitely with low-dose aspirin. (See 'Incidentally detected renal infarct or atrophic kidney' above.)