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| Year : 2011 | Volume
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| Issue : 2 | Page : 327-330 |
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| Cholesterol crystal embolization (CCE): Improvement of renal function with high-dose corticosteroid treatment |
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Madhav Desai1, R Ram1, Aruna Prayaga2, KV Dakshinamurty1
1 Department of Nephrology, Nizam's Institute of Medical Sciences, Hyderabad, India
2 Department of Pathology, Nizam's Institute of Medical Sciences, Hyderabad, India
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| Date of Web Publication | 18-Mar-2011 |
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 Abstract | | |
Cholesterol crystal embolization (CCE) is an important and often under-diagnosed cause of renal insufficiency in patients with atherosclerosis. So far, only statins are the mainstay of therapy and the role of corticosteroids is controversial. We describe a 57-year-old gentleman who presented with accelerated hypertension and renal failure three months after coronary angiogram. Renal biopsy showed cholesterol clefts in the arteriole. Initially, management with antihypertensives alone (already receiving statins since angiogram) was unsuccessful. A trial of highdose corticosteroids resulted in an improvement of the general condition in the next two days, and the serum creatinine reduced gradually to 1.6 mg/dL over the next one month. In conclusion, highdose corticosteroids are useful in the treatment of CCE associated renal failure, especially in cases with no spontaneous recovery of function.
How to cite this article:
Desai M, Ram R, Prayaga A, Dakshinamurty K V. Cholesterol crystal embolization (CCE): Improvement of renal function with high-dose corticosteroid treatment. Saudi J Kidney Dis Transpl 2011;22:327-30 |
How to cite this URL:
Desai M, Ram R, Prayaga A, Dakshinamurty K V. Cholesterol crystal embolization (CCE): Improvement of renal function with high-dose corticosteroid treatment. Saudi J Kidney Dis Transpl [serial online] 2011 [cited 2022 Aug 14];22:327-30. Available from: https://www.sjkdt.org/text.asp?2011/22/2/327/77621 |
| Introduction | |  |
Cholesterol atheroembolism is characterized by multisystem organ dysfunction resulting from occlusion of small to medium-sized arteries (100-150 μm) by atheromatous plaque. [1],[2],[3],[4],[5] This entity was first described in 1862 by the German pathologist, Panum, and was recognized as a clincopatholgic entity in 1945 by Flory. The proximity of the kidneys to the abdominal aorta and the significant renal blood supply makes the kidney a frequent (50%) [6] target organ for atheroemboli.
| Case Report | | |
A 57-year-old male hypertensive for the past one year was admitted in a local hospital in April 2009 with exertional dyspnea and chest pain. He had a long-standing history of smoking. Coronary angiography showed 40% blockage in the left anterior descending artery, and he was advised antiplatelet agents and statins. The serum creatinine was around 1.2 mg/dL before and one week after the procedure. Three months later, he presented to us with acute onset of shortness of breath. Examination revealed blood pressure of 200/110 mmHg, bibasal crackles in the lungs and gallop heart sounds. Laboratory investigations showed serum creatinine 6.2 mg/dL and erythrocyte sedimentation rate 30 mm in the first hour. He was treated with vasodilators, furosemide and oxygen. After stabilization, renal biopsy was performed, which revealed cholesterol clefts in the arterioles [Figure 1]. Initially, he was managed conservatively with antihypertensive medication and we waited for spontaneous recovery of renal function. Investigations for eosinophilia and eosinophiluria and hypocomplementemia were negative. Serum creatinine increased to 7.4 mg/dL in the next 10 days. He developed repeated episodes of accelerated hypertension, which required six different classes of antihypertensive drugs. Doppler study was negative for renal artery stenosis and showed diffuse atherosclerosis in other arteries. Serum creatinine later decreased to 6.7 mg/dL. One week later, he developed purple-toes and the erythrocyte sedimentation rate increased to 60 mm in the first hour. He also developed anorexia and malaise and the serum creatinine increased to 7.5 mg/dL. Oral prednisolone was administered at a dose of 1 mg/kg/day. Within two days, the patient's general condition improved clinically and the serum creatinine decreased to 1.6 mg/ dL over the next one month. No further cutaneous lesions appeared and steroids were tapered over the next four weeks. His last visit serum creatinine was 1.6 mg/dL [Figure 2]. | Figure 1: Renal biopsy showing cholesterol clefts (arrows) in the arteriole (hematoxylin– eosin stain
× 200).
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 | Figure 2: The temporal course of serum creatinine in a patient with cholesterol embolism, responded to high dose steroids.
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| Discussion | | |
The risk factors for cholesterol crystal embolization (CCE) are male sex, age >60 years, diabetes mellitus, hypertension, atherosclerotic vascular disease and ischemic nephropathy.
The precipitating factors are vascular procedure-related (angiography, angioplasty, vascular surgery), drug related (anticoagulants, thrombolytic) and spontaneous embolization of the atherosclerotic plaques. In the present case, the risk factor was diffuse atherosclerosis due to smoking, and hypertension and coronary angiogram precipitated the event. He did not respond to conservative therapy and renal failure progressed further.
The inflammatory effects of CCE are mediated by neutrophils and eosinophils in the early phase and by macrophages and multinucleated giant cells in the later stages. In cases of cholesterol emboli, severe renal insufficiency requiring dialysis occurs in approximately 40% of the patients; only half of them recover sufficient renal function to come off dialysis. [7] Frock et al [8] showed that the mortality is significantly higher in patients who progress to endstage renal disease (75%) than those who recover renal function (17%). In our patient, worsening of renal function and development of cutaneous and other symptoms led us to initiate treatment with steroids.
Few studies have indeed shown that low-dose steroids, i.e. 0.3 mg/kg/day, have beneficial effects in the treatment of CCE. [2],[9],[10] Takahashi et al [11] showed that low-dose steroid therapy failed to recover the renal function; however, steroid pulse therapy successfully attenuated CCEinduced renal failure. High-dose steroids have a proven benefit in the treatment of CCE associated renal failure. [5],[12],[13],[14] Hasegawa et al [15] suggested combination therapy with an intermediate dose of steroid (0.6 mg/kg), and plasma exchange in the acute phase may be effective in treating renal cholesterol embolism. Daimon et al showed LDL apheresis followed by corticosteroid therapy as a possible treatment of CCE. Only few other studies showed no improvement of CCE-induced renal failure with steroids. [6],[16] Nakayama et al [17] recommended that early initiation of steroid therapy in CCE improves the outcome. Meta-analysis of the above studies could not be possible because of different patient characteristics, severity of renal failure, absence of renal histology in all cases and lack of uniformity in dose and duration of steroid treatment. Steroids showed an improvement of renal failure even in elderly persons with severe renal failure. [5],[11],[12],[13],[14],[17]
Beneficial effects of steroids are stabilization of renal failure, [2],[5],[9],[14],[17] improvement in nutrition, decrease of lower limb pain and gastrointestinal pain, [1] resolution of cutaneous lesions, [18] improvement in peripheral symptoms [3] and reversal of pulmonary lesions. [14] During treatment, the side-effects of the corticosteroids should be monitored. How long to wait for spontaneous recovery was not clearly described in the literature.
In conclusion, high-dose steroids are useful in the treatment of CCE-associated renal failure without spontaneous recovery of function.
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Correspondence Address:
Madhav Desai
Assistant Professor, Department of Nephrology, Nizam's Institute of Medical Sciences, Panjagutta, Hyderabad - 500 082, Andhra Pradesh
India
 Source of Support: None, Conflict of Interest: None  | Check |
PMID: 21422636 
[Figure 1], [Figure 2] |
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| This article has been cited by | | 1 |
Favorable outcome in atheroembolic renal disease with pulse steroid therapy |
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| Sharma, A. and Hada, R. and Agrawal, R.K. and Baral, A. | | Indian Journal of Nephrology. 2012; 22(6): 473-476 | | [Pubmed] | | | 2 |
Cholesterol embolism syndrome: A rare, but severe complication in patients with atherosclerosis [Cholesterinembolie-Syndrom: eine seltene, aber schwerwiegende Komplikation bei Atherosklerose] |
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| Frank, R.D. | | Deutsche Medizinische Wochenschrift. 2012; 137(21): 1130-1134 | | [Pubmed] | |
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