INTRODUCTION — 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 [6]. In a later series of almost 250,000 patients seen at an emergency department over four years, only 17 (0.007 percent) were diagnosed with acute renal infarction [7]. Depending upon the severity, it can lead to renovascular hypertension, chronic kidney disease, and end-stage kidney disease.
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 presentation' below.)
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 [1,7]. Atheroemboli often lead to secondary ischemic atrophy rather than renal infarction due to their nondistensibility, irregular shape, and small size. Atheroemboli often lead to incomplete arterial occlusion of more distal vessels. (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)".)
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) [1,3,5,8-10]:
●Cardioembolic disease – In a series of 438 patients with renal infarction that was diagnosed between 1993 and 2013, 244 (55.7 percent) patients had cardioembolic renal infarction, and 211 patients had atrial fibrillation [9]. 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 almost 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 [8].
●Renal artery injury – In the case series cited above, 33 patients (7.5 percent) had underlying renal artery injury [9]. 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 [7,13-17], 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 [9].
Renal infarction has also been reported in association with 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 [9]. 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 PRESENTATION
Demographic features — In the series of 438 patients with acute renal infarction cited above, the following demographic features were noted [9]:
●The median age differed depending on the underlying etiology: cardiogenic (65 years), renal artery injury (43 years), hypercoagulable state (62 years), and idiopathic (49.5 years).
●Patients in the cardiogenic group more frequently had a history of hypertension, diabetes mellitus, cardiovascular disease (CVD), heart valve disease, and atrial fibrillation than their counterparts in the other three groups.
History and physical examination — Patients with acute renal infarction typically complain of the acute onset of flank or abdominal pain, frequently accompanied by nausea, vomiting, and, occasionally, fever [1-4,7-9,29]. In the series of 438 patients cited above, flank pain was seen in 50 percent, abdominal pain in 53 percent, nausea in 16.9 percent, vomiting in 13 percent, and fever in 10 percent [1]. Bilateral renal involvement was present in 16.9 percent [9].
These findings may be accompanied by an acute elevation in blood pressure that is presumably mediated by increased renin release [1,7,30,31]. Signs of extrarenal embolization (such as focal neurologic deficits and mesenteric and limb ischemia) can 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.
Rarely, angiographic evidence of renal infarction is an incidental finding in patients with no prior history suggestive of such an event [7].
Laboratory manifestations — The following laboratory findings are typically seen in patients with acute renal infarction [1,3,28-32]. The frequency of the major findings and characteristic laboratory data come from the series of 438 patients cited above [9]:
●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 [9], 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 [3,28,30].
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 [1-3,28,30,33]. 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 [33].
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 [3,31,34].
In patients who are at risk for systemic embolization and present with symptoms suggestive of renal infarction, we obtain the following laboratory tests [2]:
●Complete blood count with differential
●Serum creatinine and lactate dehydrogenase (LDH)
●Urinalysis and urine culture
●Electrocardiogram to evaluate for atrial fibrillation
Computed tomography (CT) without contrast is usually the preferred initial test for flank pain since it is the gold standard for the diagnosis of kidney and ureteral stones, which are much more common than renal infarction [3]. (See "Kidney stones in adults: Diagnosis and acute management of suspected nephrolithiasis", section on 'Noncontrast CT'.)
Among patients who have a clinical presentation consistent with renal infarction rather than nephrolithiasis, a contrast-enhanced CT should be performed instead of CT without contrast. The classic finding is a wedge-shaped perfusion defect. Magnetic resonance imaging (MRI) with gadolinium is an alternative to CT [35], 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'.)
A radioisotope scan may show a segmental or generalized decrease in kidney perfusion. 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 [3]. 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 [3].
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 [36]. However, neither nephrolithiasis nor pyelonephritis is associated with an elevation in serum LDH.
Urinalysis may not help distinguish between these conditions due to an overlap in findings. Acute pyelonephritis is characterized by a predominance of pyuria, bacteruria, and, occasionally, by the presence of white cell casts on urine microscopy. Renal infarction often presents with a predominance of hematuria, but may also be associated with pyuria, although usually without bacteruria. Nephrolithiasis may present with any of these findings on urinalysis.
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. A history of atrial fibrillation or recent intra-arterial manipulation increases the likelihood of renal infarction or mesenteric ischemia.
INITIAL EVALUATION
Evaluate the likelihood of benefit from revascularization — 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 whether or not the renal vessel is completely or partially occluded (using information obtained by computed tomography angiography [CTA] in most patients).
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 impairment, new or worsened hypertension, or symptoms such as flank pain, hematuria, and fever.
●Patients who have an arterial dissection as the cause of renal infarction.
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.
Evaluation of the likelihood of benefit from revascularization is based upon the following factors:
●Type of vessel – The risk of parenchymal damage is dependent upon the type of the vessel involved (main, segmental artery, or subsegmental artery) [37]. 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, we examine the degree of occlusion (complete or partial) 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.
Evaluate for a hypercoagulable state or other predisposing condition — In the absence of a preexisting diagnosis, all patients with renal infarction should undergo evaluation for atrial fibrillation. In addition, we evaluate all patients for an underlying hypercoagulable state. Details regarding the diagnosis of atrial fibrillation and of a hypercoagulable state are presented elsewhere. (See "Evaluating adult patients with established venous thromboembolism for acquired and inherited risk factors" and "Atrial fibrillation: Overview and management of new-onset atrial fibrillation".)
TREATMENT — The optimal treatment for renal infarction due to thromboemboli, in situ thrombosis, or renal artery dissection is uncertain given the absence of comparative studies. Reported approaches include anticoagulation, percutaneous endovascular therapy (thrombolysis, thrombectomy with or without angioplasty, or stent placement), and open surgery. Surgical intervention is an option for patients with renal infarction resulting from a traumatic renal artery occlusion or aortic dissection extending into the renal artery (algorithm 1) [38-41].
Main and major segmental renal artery involvement — We attempt to restore perfusion in patients with main renal artery occlusion [37]. Intervention may be considered in patients with first order branch occlusion in the setting of a solitary kidney or significantly reduced kidney function (eg, estimated glomerular filtration rate [eGFR] <50 mL/min/1.73 m2). Among those not likely to benefit from intervention, we typically treat with anticoagulation or antiplatelet therapy. (See 'Evaluate the likelihood of benefit from revascularization' above.)
Patients likely to benefit from revascularization — Patients likely to benefit from revascularization should be referred immediately to a vascular interventional radiology or vascular surgery service for percutaneous endovascular therapy (PET) (algorithm 1) [38,42]. PET may include local thrombolysis, thrombectomy, angioplasty, and stent placement [43-45]. The choice of the optimal endovascular procedure is usually left to the interventionalist or surgeon. If significant residual vascular abnormalities are seen after thrombectomy, the vessel is treated with angioplasty with or without placement of a stent. If PET is not available, such patients should undergo systemic thrombolysis [46]. Details regarding the assessment of whether or not a patient is likely to benefit from revascularization are discussed above. (See 'Evaluate the likelihood of benefit from revascularization' above.)
Intraprocedural heparin is usually administered during thrombolysis and stopped shortly after the procedure. Patients who have an underlying vascular abnormality, or who underwent angioplasty or stent placement should be treated with aspirin 81 mg and clopidogrel 75 mg for three to six months after the procedure followed by aspirin alone thereafter. In addition, we treat patients who have an underlying hypercoagulable state or atrial fibrillation who have a stent placed with anticoagulation and low-dose aspirin (eg, 81 mg daily). Anticoagulation in patients with hypercoagulable state or atrial fibrillation is discussed elsewhere:
●(See "Atrial fibrillation in adults: Use of oral anticoagulants", section on 'Choice of anticoagulant'.)
●(See "Atrial fibrillation in adults: Selection of candidates for anticoagulation".)
Where vascular interventional services are not available, systemic fibrinolytic therapy may be used, although the data to support this approach are sparse [47]. 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 [36,42-44,48,49]. Delayed therapy is likely to be effective in patients with a partial occlusion and in patients with thrombotic occlusion [38].
PET leads to successful reperfusion in most patients with renal infarction without significant therapy-associated complications; however, renal outcomes were only improved in some patients [36,43,44,48,50-54]. 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 [36]. 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 [48]. 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 [42]. 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.
Patients unlikely to benefit from revascularization — In patients who have a main renal artery occlusion but who are unlikely to benefit from revascularization (see 'Evaluate the likelihood of benefit from revascularization' above), our approach depends upon our assessment of how much time has elapsed since the infarction (algorithm 1):
●Patients with a remote infarction – Patients who are asymptomatic (ie, no acute symptoms such as flank pain) and who have a small, atrophic kidney or a wedge-shaped parenchymal perfusion defect on the affected side are likely to have a remote infarct. Such patients should undergo an evaluation for atheroembolic risk factors such as atrial fibrillation (see "Atrial fibrillation: Overview and management of new-onset atrial fibrillation"). If such an evaluation is negative, then an evaluation to look for a hypercoagulable state should be completed (see 'Evaluate for a hypercoagulable state or other predisposing condition' above). If, after this evaluation, there is no indication for anticoagulation, we manage these patients with aspirin therapy. (See 'Incidentally detected renal infarct or atrophic kidney' below.)
●Patients with more recent infarction – In patients who are symptomatic (or recently symptomatic) and whose imaging suggests a more recent infarct, we initiate anticoagulation. The duration of anticoagulation depends upon the evaluation for a hypercoagulable state and other risk factors for arterial embolization. (See 'Evaluate for a hypercoagulable state or other predisposing condition' above and "Atrial fibrillation: Overview and management of new-onset atrial fibrillation".)
In patients with an identified hypercoagulable state or risk factor for embolization (such as atrial fibrillation), the choice of the anticoagulant, its dose, titration, and duration depends upon the underlying condition. These details for patients with an underlying hypercoagulable state or atrial fibrillation are discussed elsewhere:
●(See "Atrial fibrillation in adults: Use of oral anticoagulants", section on 'Choice of anticoagulant'.)
●(See "Atrial fibrillation in adults: Selection of candidates for anticoagulation".)
In patients without a predisposing underlying condition (eg, hypercoagulable state or atrial fibrillation), we anticoagulate for six months. 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 (INR) 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'.)
The renal prognosis with anticoagulation has generally been favorable, but there are no reports comparing outcomes with untreated patients [9,30,31,55]. Following completion of six months of anticoagulation, we initiate lifelong low-dose aspirin (eg, 81 mg daily).
Minor segmental vessel involvement — Patients with minor segmental vessel involvement resulting from dissection or fibromuscular dysplasia (FMD) that is recent should be referred to vascular interventional radiology or vascular surgery for consideration of PET (algorithm 1) [45].
Minor segmental renal artery occlusion not resulting from FMD or dissection, or one that is remote, should be treated with anticoagulation for a minimum of six months to prevent recurrent thromboembolic events, if indications are identified on hypercoagulable work-up. Choice of an anticoagulant and its titration is identical to patients with main renal artery occlusion who are unlikely to benefit from revascularization. Patients not receiving anticoagulation should be initiated on aspirin 81 mg for life, although there are limited data to support this practice. (See 'Patients unlikely to benefit from revascularization' above and "Atrial fibrillation in adults: Use of oral anticoagulants".)
Patients with underlying hypercoagulable state or atrial fibrillation may require lifelong anticoagulation. Anticoagulation in patients with hypercoagulable state or atrial fibrillation is discussed elsewhere:
●(See "Atrial fibrillation in adults: Use of oral anticoagulants", section on 'Choice of anticoagulant'.)
●(See "Atrial fibrillation in adults: Selection of candidates for anticoagulation".)
Incidentally detected renal infarct or atrophic kidney — Asymptomatic renal infarcts or atrophic kidneys incidentally detected on abdominal imaging performed for an unrelated indication are unlikely to benefit from revascularization due to the duration of ischemia (algorithm 1).
We initiate anticoagulation in patients who have underlying atrial fibrillation or hypercoagulable state. Details regarding the rationale, choice, and dosing of anticoagulants is discussed elsewhere:
●(See "Atrial fibrillation in adults: Use of oral anticoagulants", section on 'Choice of anticoagulant'.)
●(See "Atrial fibrillation in adults: Selection of candidates for anticoagulation".)
In all other patients, we treat indefinitely with aspirin (typically 81 mg/day), although there are limited data to support this approach.
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 [7]. 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), and for stabilization or deterioration of their kidney function. 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.
All patients should receive secondary preventative 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".)
There are limited data to inform monitoring for recurrent renal infarcts [9,56]. However, our practice, which is limited to patients with thrombotic renal infarction, is to perform serial abdominal imaging (preferably with magnetic resonance angiography) at 6 and 12 months after the original incident to look for recurrence of local vascular lesions (eg, fibromuscular dysplasia [FMD]) [57]. Patients who develop recurrent vascular lesions may benefit from a vascular interventional radiology or a vascular surgery consultation.
In patients who have no new infarcts on imaging, no additional imaging is required for surveillance.
Patients not already on anticoagulation who have recurrent emboli should generally initiate anticoagulation unless such therapy is contraindicated.
Patients who develop recurrent 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".)
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 [2,3,31]. 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 [3].
In most studies, serum creatinine was stable or only slightly increased at follow-up [1-3,7,30,31]. 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 [7].
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 [3]. 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 renal 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 renal outcomes compared with those who were diagnosed late (mean time to diagnosis 126 hours) [4]. 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
●Renal infarction is an under-recognized condition. It 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. (See 'Introduction' above.)
●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). Often, no underlying cause is found. (See 'Etiology and pathogenesis' above.)
●Clinical manifestations of acute renal arterial occlusion include flank pain accompanied by nausea, vomiting, fever, or acute elevation in blood pressure. However, patients may be asymptomatic. (See 'Clinical presentation' above.)
●In patients suspected of having renal infarction, we obtain a white blood cell count, serum creatinine, lactate dehydrogenase (LDH), aminotransferases, urinalysis, urine culture, and electrocardiogram. We then obtain a computed tomography (CT) of the abdomen without contrast to exclude nephrolithiasis and, if negative, a contrast-enhanced CT to evaluate for infarction. Magnetic resonance imaging (MRI) with gadolinium may also be used when appropriate. (See 'Diagnosis' above.)
●We initially evaluate the likelihood of benefit from revascularization by assessing 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 whether or not the vessel is completely or partially occluded (using information obtained by CT angiography [CTA] in most patients). 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. Those likely to benefit include (see 'Evaluate the likelihood of benefit from revascularization' above):
•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 impairment, new or worsened hypertension, or symptoms.
•Patients who have an arterial dissection as the cause of renal infarction.
●In the absence of a preexisting diagnosis, we evaluate all patients with renal infarction for atrial fibrillation or underlying hypercoagulable state. (See 'Evaluate for a hypercoagulable state or other predisposing condition' above.)
●The optimal treatment of renal infarction is uncertain. However, limited reported experience suggests that the following approach is reasonable:
•Among patients deemed likely to benefit from revascularization (see 'Evaluate the likelihood of benefit from revascularization' above), we suggest referral for immediate percutaneous endovascular therapy (PET) (Grade 2C). PET may include local thrombolysis, thrombectomy, angioplasty, and stent placement. If PET is not available, such patients should undergo systemic thrombolysis. (See 'Main and major segmental renal artery involvement' above and 'Patients likely to benefit from revascularization' above.)
•In patients who have a major renal artery occlusion but who are unlikely to benefit from revascularization (see 'Evaluate the likelihood of benefit from revascularization' above), we suggest antiplatelet therapy, anticoagulation, or both, rather than no therapy, to prevent recurrent infarction (Grade 2C). The choice among these therapies depends upon the time elapsed since the infarction. Long-term anticoagulation may be appropriate in patients with atrial fibrillation or a hypercoagulable state. (See 'Main and major segmental renal artery involvement' above and 'Patients unlikely to benefit from revascularization' above and "Atrial fibrillation in adults: Use of oral anticoagulants".)
•For patients with minor segmental involvement who do not have dissection as the cause of infarction, we suggest antiplatelet therapy, anticoagulation, or both, rather than no therapy, to prevent recurrent infarction (Grade 2C). The choice among these therapies depends upon the time elapsed since the infarction. Long-term anticoagulation may be appropriate in patients with atrial fibrillation or a hypercoagulable state. (See 'Minor segmental vessel involvement' above and "Atrial fibrillation in adults: Use of oral anticoagulants".)
•In patients with asymptomatic renal infarcts or atrophic kidneys that are incidentally detected on abdominal imaging performed for an unrelated indication, we suggest lifelong antiplatelet therapy, rather than no treatment, to prevent recurrent infarction (Grade 2C). Long-term anticoagulation may be appropriate in patients with atrial fibrillation or a hypercoagulable state. (See 'Incidentally detected renal infarct or atrophic kidney' above and "Atrial fibrillation in adults: Use of oral anticoagulants".)
•In the absence of acute kidney injury (AKI) or hyperkalemia, we treat acute elevations in blood pressure with angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs). In those who do have AKI or hyperkalemia, the treatment of hypertension is no different from patients without renal infarction. (See 'Hypertension management' above.)
●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.)
●The prognosis following a renal infarction (treated or untreated) is not well defined. In most studies, serum creatinine was stable or only slightly increased at follow-up. However, recurrent thromboembolism, advanced chronic kidney disease, end-stage kidney disease, and death have been reported. (See 'Prognosis' above.)
