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Clinical presentation, evaluation, and treatment of renal atheroemboli

Clinical presentation, evaluation, and treatment of renal atheroemboli
Literature review current through: Jan 2024.
This topic last updated: Sep 12, 2023.

INTRODUCTION — Renal and systemic atheroemboli (also called cholesterol crystal emboli) usually affect older patients with diffuse erosive atherosclerosis. Cholesterol crystal embolization occurs when portions of an atherosclerotic plaque break off and embolize distally, resulting in partial or total occlusion of multiple small arteries (or glomerular arterioles), leading to tissue or organ ischemia [1].

Clinical issues related to renal atheroemboli will be reviewed here. Discussions of cholesterol crystal embolization in general and thromboembolic renal infarction are presented separately:

(See "Embolism from atherosclerotic plaque: Atheroembolism (cholesterol crystal embolism)".)

(See "Renal infarction".)

RISK FACTORS — Atheroembolization is a complication of severe atherosclerosis. Thus, risk factors for atheroembolic disease, such as older age, male sex, diabetes, arterial hypertension, hypercholesterolemia, and cigarette smoking, are the same as for the development of atherosclerosis [2-7]. (See "Overview of established risk factors for cardiovascular disease", section on 'Established risk factors for atherosclerotic CVD'.)

Inciting events — Once formed, an atherosclerotic plaque may be disrupted by a variety of inciting events, producing cholesterol crystal emboli. These inciting events can be classified broadly into the following:

Iatrogenic event, usually induced by angiography, cardiovascular surgery, thrombolytic therapy, or anticoagulation

Spontaneous event, induced by hemodynamic stress

Cholesterol crystal embolization is iatrogenic in more than 70 percent of cases [7-9]. It is often seen following manipulation of the aorta or other large arteries during angiography, angioplasty, or cardiovascular surgery. Mechanical aortic trauma, induced by radiological catheters or vessel manipulation/clamping, causing plaque disruption, has a key role [2-10].

Angiography is the most common triggering event, accounting for as many as 80 percent of iatrogenic cases [7-9]. The incidence of clinically apparent atheroemboli after angiography has not been well defined. The best risk estimates are summarized here:

Coronary angiography is the most common angiographic procedure causing embolism, associated with an incidence varying from 0.06 to 1.8 percent [6,11-13]. As an example, the incidence of atheroembolism following diagnostic cardiac catheterization was evaluated in a prospective study that included 1786 consecutive patients; clinical atheroembolism (cutaneous or renal) was diagnosed in 25 (1.4 percent) [6]. Sixteen patients (0.9 percent) developed acute kidney injury that was thought to be due to renal atheroembolism rather than contrast-associated acute kidney injury since it persisted for at least two weeks. However, not all patients with acute kidney injury had other evidence of peripheral embolization. The risk may be lower with a brachial rather than an iliofemoral approach since most atherosclerotic plaques are in the abdominal aorta [14]. (See "Complications of diagnostic cardiac catheterization", section on 'Renal atheroemboli'.)

Patients who undergo renal angiography for suspected atherosclerotic renal artery stenosis often have diffuse atherosclerosis and are at especially high risk. A summary of reported studies of such patients suggests an overall incidence of approximately 2 percent [14].

Additional cardiovascular procedures associated with renal atheroembolism include percutaneous transluminal and transcatheter aortic valve implantation (TAVI) and balloon aortic valvuloplasty (BAV) [15].

It has also been suggested that treatment with warfarin, heparin, or thrombolytic agents may cause atheroemboli, perhaps because anticoagulation may interfere with the healing of ulcerated atheromatous plaques [3,7,16-18]. However, anticoagulant-associated atheroembolism is uncommon, even in patients with severe aortic plaque (0.7 to 1 percent) [19,20]. In addition, most patients with atheroemboli associated with anticoagulation have a second potential trigger, usually recent angiography. Anticoagulation is the sole inciting event in only 7 percent of such patients [10]. There are a few reports of patients with cholesterol crystal embolization following treatment with a direct oral anticoagulant (DOAC) [21-24].

Hemodynamic stress leading to spontaneous embolization was the most common form in historical reports [25-28]. However, as noted, most cases are now related to iatrogenic triggers.

CLINICAL PRESENTATION — Cholesterol crystal embolization to the kidney typically produces a subacute kidney injury observed several weeks or more after a possible inciting event [10]. Severe hypertension may also be present. Less commonly, acute kidney injury occurring within one to two weeks after the inciting event may be seen, usually in association with massive embolization. Patients with renal atheroemboli are typically older (mean age was 71 to 72 years in two large series) [7,8], have a bland urine sediment [3,7,29,30], and may have peripheral eosinophilia [7].

However, kidney injury due to atheroemboli is not the most common presentation; rather, it is often found after the patient has presented in some other way. This is likely because, when it occurs, atheroembolism is ubiquitous, affecting varied vascular distributions. Thus, kidney disease from atheroembolism is part of a multisystem disorder. The clinical presentation is more frequently related to atheroembolization of the skin (producing "blue toe syndrome" (picture 1) or livedo reticularis (picture 2)), mesentery (producing intestinal ischemia, gastrointestinal bleeding, or pancreatitis), and/or central nervous system (producing transient ischemic attack, confusion, or visual symptoms). Presenting symptoms may also be subtle and nonspecific, such as fever, myalgias, headache, and weight loss. In addition, patients at risk for atheroembolism are not routinely monitored for worsening kidney function. (See "Embolism from atherosclerotic plaque: Atheroembolism (cholesterol crystal embolism)".)

Kidney injury — Atheroembolism is not uncommon as a cause of acute kidney injury in older adult patients. This was illustrated in a series of 259 patients over the age of 60 years who underwent kidney biopsy for acute kidney injury; 7 percent had atheroembolic disease [31].

The kidney manifestations of atheroembolic disease are usually different from those seen with thromboemboli (clot emboli). Thromboemboli primarily occur in patients with atrial arrhythmias or a prior myocardial infarction. They tend to produce complete arterial occlusion and renal infarction, leading to flank pain, hematuria, and an elevated lactate dehydrogenase with relatively normal transaminases [32]. (See "Renal infarction".)

By comparison, atheroemboli are typically nondistensible and irregularly shaped; as a result, they tend to produce incomplete occlusion with secondary ischemic atrophy rather than renal infarction [3]. With time, a foreign body reaction often ensues, causing intimal proliferation, giant cell formation, and further narrowing of the vascular lumen [2]. This reaction presumably contributes to the progressive decline in kidney function that often occurs for three to eight weeks after the procedure [2].

The net effect of this pathogenic process, when combined with varying amounts of cholesterol embolization, is three somewhat different clinical presentations [2,4,7,33,34]:

Marked kidney function impairment with an acute onset, seen within one to two weeks of a clear inciting event, is most frequently due to massive atheroembolization.

The most common presentation of the disease is subacute kidney injury, in which progressive kidney dysfunction occurs in staggered steps, separated by periods of stable kidney function (often referred to as a "staircase pattern"). In this setting, kidney function impairment is usually observed several weeks or more after a possible insult; others, however, present with uremia and no clear precipitating event. This presentation is probably due to some combination of recurrent plaque embolization and foreign body reaction.

The least common presentation is the patient with chronic stable kidney function impairment and clinical features similar to those with ischemic nephropathy (due to bilateral renal artery stenosis) and nephrosclerosis, which frequently coexist with cholesterol emboli. The role of cholesterol embolization in patients with ischemic nephropathy and nephrosclerosis is somewhat unclear. Many such patients are misdiagnosed because the crystal embolization is clinically silent (ie, extrarenal signs are frequently absent) and kidney or skin biopsy is not performed. If a biopsy is performed, evidence for cholesterol embolization, which can be patchy, may be absent. The presence and clinical consequences of intimal proliferation and vascular-lumen narrowing are probably common features of these disease processes.

Urinary findings — The urinalysis in patients with renal atheroemboli is typically benign with few cells or casts, a finding consistent with ischemic atrophy [3,7,29,30]. Proteinuria is usually not a prominent feature, except in patients with underlying diabetic nephropathy [8]; however, nephrotic-range proteinuria (as high as 11 g/day) has been rarely reported [2,30,35]. Some patients have an active urinary sediment, including hematuria and, rarely, red cell casts. In this setting, an acute glomerulonephritis or vasculitis may be suspected, particularly if there are extrarenal manifestations [36]. (See 'Evaluation and diagnosis' below.)

Eosinophiluria also may be seen if the urine sediment is examined with Hansel's stain soon after the renal atheroemboli [37]. One report of 52 patients noted eosinophiluria in only 14 percent [2]. However, many of these patients may have been evaluated after the acute phase, a time at which eosinophil activation would have ceased.

Eosinophilia and hypocomplementemia — Two other abnormalities that commonly occur during the acute phase are eosinophilia and hypocomplementemia; these changes may reflect immunologic activation at the surface of the exposed atheroemboli [33,38,39]:

In a study of 354 patients, 238 (67 percent) had an eosinophil count >500 cells/microL [7].

Hypocomplementemia has been reported in 39 percent of patients in one study [28]. However, this finding has not always been confirmed by other reports [8,9].

EVALUATION AND DIAGNOSIS — The diagnosis of renal atheroemboli requires a high index of suspicion and knowledge of the associated risk factors. A clinical diagnosis can be made when a potential inciting event (usually angiography) is followed by the delayed onset of kidney injury (typically several weeks or longer rather than hours or days), particularly when there are signs of extrarenal atheroemboli. Kidney biopsy is regarded as the definitive method for diagnosis. Alternatively, biopsy of a skin lesion (if present) is a simple, minimally invasive procedure with a high diagnostic yield. Less commonly, histological confirmation may be made in other organs, such as the gastrointestinal tract.

However, tissue biopsy is not necessary in patients with iatrogenic atheroembolic kidney disease presenting with all of the following features of the classical clinical triad:

A precipitating event (such as aortic or coronary angiography)

Subacute or acute kidney injury

Typical skin findings, such as blue toe syndrome (picture 1) and/or livedo reticularis (picture 2)

In addition, a biopsy may be deferred in patients with suspected atheroembolic kidney disease if retinal cholesterol crystal emboli (Hollenhorst plaques) are present (picture 3). Like histology, funduscopy examination may confirm the diagnosis and should never be omitted.

Conversely, kidney biopsy is crucial for diagnosis of cases with a chronic, smoldering presentation of renal atheroembolization. A tissue sample is also required to make a definitive diagnosis in patients presenting with a spontaneous (rather than iatrogenic) form of the disorder [8-10].

History and physical examination — The history should identify potential complications of atheroembolic disease, including skin discoloration of the lower extremities; neurologic deficits, including amaurosis fugax; and abdominal pain and gastrointestinal bleeding [2,3,16]. Since most cases are associated with an iatrogenic event, the history should also identify previous angiographies, cardiovascular surgeries, or recent initiation of anticoagulation.

The physical examination should identify new or worsened arterial hypertension; cyanosis or discrete gangrenous lesions in the toes with intact peripheral pulses (blue toes) (picture 1); livedo reticularis; focal neurologic deficits; confusion; orange plaques in the retinal arterioles, called Hollenhorst plaques (picture 3); and gastrointestinal bleeding [7]. (See "Embolism from atherosclerotic plaque: Atheroembolism (cholesterol crystal embolism)".)

Laboratory studies — Eosinophilia, eosinophiluria, and hypocomplementemia, if present, may suggest atheroemboli. These findings generally resolve within one week [2,37-39] and are therefore signs of recent disease. Persistence or recurrence is suggestive of continued atheroembolization. However, these findings are also associated with other kidney diseases, including some forms of glomerulonephritis. (See "Glomerular disease: Evaluation and differential diagnosis in adults".)

Tissue biopsy — If the diagnosis remains in doubt, biopsy of a skin lesion (if present) or the kidney may be required. Although percutaneous kidney biopsy produces a relatively small sample, it appears to detect atheroemboli in over 75 percent of cases [30]. The cholesterol crystals within the emboli are dissolved during tissue fixation; what is therefore observed are pathognomonic biconvex, needle-shaped clefts ("ghosts") within the occluded vessel (picture 4A-B) [2,16,35]. The intraluminal lesions are often accompanied by a perivascular inflammatory reaction that may contain eosinophils [38].

Focal segmental glomerulosclerosis may also be seen on kidney biopsy, especially in patients with heavy proteinuria [35]. Why this occurs is not clear, but both ischemic injury and hyperfiltration injury in nonischemic nephrons may contribute [35]. (See "Focal segmental glomerulosclerosis: Pathogenesis", section on 'Pathogenesis of secondary FSGS'.)

In a patient with otherwise unexplained kidney failure, the finding of atheroemboli on kidney biopsy is virtually diagnostic of at least a contributory role for atheroembolic kidney disease.

Differential diagnosis — Renal atheroemboli developing after angiography or vascular surgery has to be differentiated from radiocontrast media-induced or postischemic acute tubular necrosis (ATN). Extrarenal emboli, if present, favor the diagnosis of atheroemboli. In addition, the course of the two disorders is generally different [2]. Patients with ATN characteristically have an acute and progressive rise in the serum creatinine concentration within several days of the procedure that then stabilizes and returns to or near the baseline level after a variable period of 4 to 21 days. (See "Kidney and patient outcomes after acute kidney injury in adults".)

By contrast, atheroembolic disease directly due to a procedure is typically associated with a subacute decline in kidney function that becomes apparent weeks after the procedure. The serum creatinine concentration rises gradually, reaching its peak at three to eight weeks [2]. Scarring of the arterial lesions or new emboli contribute to the late progression.

The diagnosis of renal atheroemboli may be difficult to establish in patients with spontaneous disease, atypical clinical findings, and/or multiorgan involvement. Other diseases associated with eosinophilia and eosinophiluria include acute interstitial nephritis and systemic vasculitis. Renal atheroembolic disease can often be distinguished from a systemic vasculitis or interstitial nephritis by urinalysis (the urine sediment is typically bland with atheroembolic disease) and/or antineutrophil cytoplasmic antibody (ANCA) testing [4]. As previously mentioned, however, there are some patients with atheroemboli who have an active urine sediment [36]. (See "Overview of and approach to the vasculitides in adults".)

TREATMENT AND PROGNOSIS — There is no specific therapy for atheroembolic kidney disease. Therapeutic modalities are mostly preventive and supportive. General issues related to the medical and surgical therapy of atheroembolic disease are discussed in detail separately. In addition, all patients should be aggressively treated for secondary prevention of cardiovascular disease. These modalities include statins, aspirin, blood pressure control, cessation of smoking, and, in patients with diabetes, glycemic control. (See "Embolism from atherosclerotic plaque: Atheroembolism (cholesterol crystal embolism)" and "Prevention of cardiovascular disease events in those with established disease (secondary prevention) or at very high risk".)

In patients with atheroembolic disease, secondary prevention relies upon removal of the causes of atheroembolism and prevention of new showers of atheroemboli. Consideration should be given in affected patients to withdrawal of anticoagulation and avoidance or postponement of new radiologic and/or vascular surgery procedures, if possible. (See "Embolism from atherosclerotic plaque: Atheroembolism (cholesterol crystal embolism)", section on 'Preventing recurrent embolization'.)

There is no proven effective medical therapy in patients with atheroembolic kidney disease. Observational studies suggest that statin use may be associated with better outcomes [7,8]. As an example, a study followed 354 patients with renal atheroembolic disease for a mean of two years; 116 eventually required dialysis, and 102 died [8]. Baseline use of statins was independently associated with a lower risk of developing end-stage or death (relative risk 0.53, 95% CI 0.36-0.77).

A potential benefit of low-dose glucocorticoids has been reported in retrospective series [9,40], but this finding was not confirmed in a prospective study [7].

Patients with renal atheroemboli have a poor overall prognosis, which in part reflects the severity of the underlying vascular disease [2,7,8]. In the study of 354 patients mentioned above, 33 percent of patients developed end-stage kidney disease, and 28 percent of patients died after a mean follow-up of two years [7].

Kidney injury may be followed by partial recovery of kidney function. In one study, for example, 24 percent of patients with renal atheroemboli but no other complications, such as sepsis or hypotension, had recovery of kidney function [2]. Recovery may be due to a number of factors, including resolution of concurrent acute tubular necrosis (ATN) in borderline ischemic areas, the development of collateral flow, or hypertrophy in surviving nephrons [2,3,29,33].

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 – Cholesterol crystal embolization, or atheroembolization, occurs when portions of an atherosclerotic plaque break off and embolize distally, resulting in partial or total occlusion of multiple small arteries leading to tissue or organ ischemia. Cholesterol crystal embolization usually affects older patients with diffuse erosive atherosclerosis. (See 'Introduction' above.)

Risk factors – Cholesterol crystal embolization is often seen after manipulation of the aorta or other large arteries during arteriography, angioplasty, transcatheter aortic valve implantation (TAVI), balloon aortic valvuloplasty (BAV), or surgery, but may also occur spontaneously. Treatment with warfarin, direct oral anticoagulants (DOAC), heparin, or thrombolytic agents may increase the risk, but anticoagulant-associated atheroembolism is uncommon. (See 'Risk factors' above.)

Clinical presentation – Cholesterol crystal embolization to the kidney typically produces a subacute kidney injury observed several weeks or more after a possible inciting event. However, the presentation is more frequently related to atheroembolization of the skin (producing "blue toe syndrome" (picture 1) or livedo reticularis (picture 2)), mesentery (producing intestinal ischemia, gastrointestinal bleeding, or pancreatitis), and central nervous system (producing transient ischemic attack, confusion, or visual symptoms). (See 'Clinical presentation' above.)

The urinalysis is typically benign with few cells or casts, and proteinuria is usually not a prominent feature; however, nephrotic-range proteinuria has been reported. Some patients have an active urine sediment, including hematuria, and, rarely, red cell casts. Severe hypertension may also be present. Other laboratory findings include eosinophilia and hypocomplementemia, possibly reflecting immunologic activation at the surface of the exposed atheroemboli. (See 'Urinary findings' above and 'Eosinophilia and hypocomplementemia' above.)

Evaluation and diagnosis – A clinical diagnosis of renal atheroemboli can be made when a potential inciting event (usually angiography) is followed by the delayed onset of kidney injury (typically weeks or longer rather than hours or days), particularly when there are signs of extrarenal atheroemboli. Kidney or skin biopsy is regarded as the definitive method for diagnosis. However, a tissue biopsy is not necessary in patients with iatrogenic atheroembolic kidney disease presenting with all of the following features of the classical clinical triad (see 'Evaluation and diagnosis' above):

A precipitating event (such as aortic or coronary angiography)

Subacute or acute kidney injury

Typical skin findings, such as blue toe syndrome (picture 1) and/or livedo reticularis (picture 2)

Differential diagnosis – The differential diagnosis of renal atheroemboli developing after angiography or vascular surgery primarily includes radiocontrast media-induced or postischemic acute tubular necrosis (ATN). These conditions can often be distinguished by the absence or presence of extrarenal emboli and by the clinical course. In addition, the differential diagnosis includes acute interstitial nephritis and systemic vasculitis, particularly in patients with eosinophilia and/or hypocomplementemia. (See 'Differential diagnosis' above.)

Treatment – There is no specific therapy for renal atheroembolic disease. All patients should be aggressively treated for secondary prevention of cardiovascular disease. In addition to statins, this approach includes aspirin, blood pressure control, cessation of smoking, and, in patients with diabetes, glycemic control. (See 'Treatment and prognosis' above.)

Prognosis – Patients with renal atheroemboli have a poor overall prognosis, which in part reflects the severity of the underlying vascular disease. (See 'Treatment and prognosis' above.)

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