Atheroembolic renal disease is most commonly part of generalized atheroembolic disease, and the 5 most commonly affected organs are skin, lower extremity skeletal muscles, gastrointestinal tract, kidneys, and brain. Clinical manifestations include livedo reticularis, blue toe/purple toe syndrome, abdominal pain and neurological deficits. AERD presents with acute/subacute/chronic renal failure, mild to moderate degree of proteinuria, hematuria, accelerated hypertension or new onset of hypertension. Eosinophilia, eosinophiluria, and hypocomplementemia are known to occur in this disease.[1][8]

There are 3 forms of atheroembolic renal disease:

1. An acute form that develops a few days after the inciting event and is due to a massive embolization
2. The second type of AERD develops subacutely or in a stepwise fashion, probably due to recurrent embolization or endothelial inflammation that follows initial ischemic insult and which results in further vessel occlusion. This is the most frequently observed form of atheroembolic renal disease.
3. A third variety presents as chronic and slowly progressive impairment of renal function and is often mistaken for nephrosclerosis and/or ischemic nephropathy.

The combination of risk factors, inciting or triggering event, acute/subacute renal failure, and signs of peripheral emboli strongly suggest the diagnosis. In the presence of these, the diagnosis of atheroembolic renal disease can be made without doing a kidney biopsy. Renal biopsy, however, may be required in some cases to exclude vasculitis, ATN, allergic interstitial nephritis, etc. and may provide a definite diagnosis.

A skin biopsy may be a simple and minimally invasive way of making the diagnosis if there are skin lesions (digital infarcts, livedo reticularis). In the presence of muscle damage and if a specific muscle can be identified, muscle biopsy may be another minimally invasive way to establish the diagnosis.

There is no specific therapy for atheroembolic renal disease and treatment is mostly symptomatic and supportive. Dialysis may be appropriate if there is no evidence of continued embolic events. Anticoagulation should be discontinued, and performance of more invasive diagnostic/therapeutic vascular procedures or surgery should be avoided or delayed, if possible. Treatment with aspirin and statins, smoking cessation, blood pressure control, and glycemic control should be provided for management of atherosclerosis. Distal protection vascular devices are being used in interventional procedures to prevent embolic material from lodging in distal sites.[1] 

In contrast nephropathy, an increase in serum creatinine starts a day or two after exposure to contrast, serum creatinine peaks in approximately one week and returns to baseline within 10 to 14 days. On the other hand, AERD frequently has a delayed onset, usually days to weeks, and a protracted course. The outcome is often poor, resulting in progressive renal failure requiring dialysis.[8]

Systemic vasculitis is another consideration since there is multisystem involvement and decrease in complement levels in both atheroembolic renal disease and systemic vasculitis. Serological testing, biopsy of affected organ or angiography may be needed to rule this disease out since management and outcome of vasculitis is very different. Subacute bacterial endocarditis may also enter into differential diagnosis due to multisystem manifestations and low complement levels. Rising serum creatinine, mild to moderate degree of proteinuria, hematuria, and eosinophilia may also raise the possibility of acute interstitial nephritis. [2][7]

Chronic forms of atheroembolic renal disease may be mistaken for hypertensive nephrosclerosis or ischemic nephropathy if peripheral manifestations are not obvious or missed. Renal biopsy may be crucial in these cases to make the diagnosis.

Atheroembolic renal disease is associated with poor renal and patient survival. The cause of death is usually multi-organ failure, visceral ischemic disease or cardiovascular disease rather than end-stage kidney failure. Thirty percent of patients require dialysis, and some of them may end up on long-term dialysis. Renal function may improve in approximately one-third of these patients after variable time if there are no more embolic events and tubular recovery ensues.[1][2]

Atheroembolic renal disease is frequently an iatrogenic disease and may follow surgical procedures, angiography, angioplasty or endovascular grafting, may be related to anticoagulation or thrombolytic therapy and presents with acute/subacute/chronic renal failure, mild to moderate degree of proteinuria, hematuria, accelerated hypertension or new onset of hypertension. Differential diagnosis includes contrast nephropathy, allergic interstitial nephritis, acute tubular necrosis. Renal and patient survival are poor and related to a coexistent significant cardiovascular disease.

Restricting the use of angiography and interventional or surgical vascular procedures in those with high risk of atheroembolic events may of important for primary prevention of this disease. Use of alternate diagnstoic procedures like MR angiography or computer-assisted topographic angiography should be considered in high risk patients if the alternate procedure can provide adequate inforamation. Minimizing direct trauma of the tip of the catheter to the atheromatous wall of the vessel may reduce the risk of atheroembolization. Use of embolic protection devices during vascular procedures may catch the athermatous debris and prevent their migration to distal sites and reduce the risk of embolization. [1][9][Level 5]