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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2011  |  Volume : 22  |  Issue : 2  |  Page : 327-330
Cholesterol crystal embolization (CCE): Improvement of renal function with high-dose corticosteroid treatment

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 Publication18-Mar-2011


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 Top

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 Top

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 Top

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.

   References Top

1.Belenfant X, Meyrier A, Jacquot C. Supportive treatment improves survival in multivisceral cholesterol crystal embolism. Am J Kidney Dis 1999;33:840-50.  Back to cited text no. 1
2.Boero R, Pignataro A, Rollino C, Quarello F. Do corticosteroids improve survival in acute renal failure due to cholesterol atheroembo­lism? Nephrol Dial Transpl 2000;15(3):441.  Back to cited text no. 2
3.Dahlberg PJ, Frecentese DF, Cogbill TH. Cholesterol embolization: Experience with 22 histologically proven cases. Surgery 1989;105: 737-6.  Back to cited text no. 3
4.Daimon S, Motita R, Ohtsuki N, Chikaki H, Jigen K, Koni I. LDL apheresis followed by corticosteroid therapy as a possible treatment of cholesterol crystal embolism. Clin Exp Nephrol 2000;4:353-5  Back to cited text no. 4
5.Fabbian F, Catalano C, Lambertini D, Bordin V, DiLandro D. A possible role of corticosteroids in cholesterol crystal embolization. Nephron 1999;83:189-90.  Back to cited text no. 5
6.Fine M, Kapoor W, Falanga V. Cholesterol crystal embolization: A review of 221 cases in the English literature. Angiology 1987;38:769­-84.  Back to cited text no. 6
7.Lye WC, Cheah JS, Sinniah R. Renal choles­terol embolic disease. Am J Nephrol 1993;13: 489-93.  Back to cited text no. 7
8.Frock J, Bierman M, Hammeke M, et al. Athe­roembolic renal disease: Experience with 22 patients. Nebroska Med J 1994;79:317-21.  Back to cited text no. 8
9.Nakahama H, Sakaguchi K. Small dose oral corticosteroid treatment rapidly improved renal function in a patient with an acute aggravation of chronic renal failure due to cholesterol embolism. Nephrol Dial Transplant 2001;16: 872-3.  Back to cited text no. 9
10.Stabellini N, Cerretani D, Russo G, et al. Renal atheroembolic disease: Evaluation of the effi­cacy of corticosteroid therapy. G Ital Nefrol 2002;19:18-21.  Back to cited text no. 10
11.Takahashi T, Konta T, Nishida W, et al. Renal cholesterol embolic disease effectively treated with steroid pulse therapy. Intern Med 2003; 42:1206-9.  Back to cited text no. 11
12.Graziani G, Santostasi S, Angelini C, Badala­menti S. Corticosteroids in cholesterol embolic syndrome. Nephron 2001;87:371-3.  Back to cited text no. 12
13.Mann SJ, Sos TA. Treatment of atheroembo­lization with corticosteroids. Am J Hypertens 2001;14:831-4.  Back to cited text no. 13
14.Vacher CH, Pache X, Dussol B, et al. Pulmo­nary renal syndrome responding to cortico­steroids: Consider cholesterol embolization. Nephrol Dial Transplant 1997;12:1977.  Back to cited text no. 14
15.Hasegawa M, Kawashima S, Shikano M, et al. The evaluation of corticosteroid therapy in conjunction with plasma exchange in the treatment of renal cholesterol embolic disease.  Back to cited text no. 15
16.Hara S, Asada Y, Fujimoto S, et al. Athero­embolic renal disease: Clinical findings of 11 cases. J Atheroscler Thromb 2002;9:288-91.  Back to cited text no. 16
17.Nakayama M, Nagata M, Hirano T, et al. Low­dose prednisolone ameliorates acute renal fai­lure caused by cholesterol crystal embolism. Clin Nephrol 2006;66:232-9.  Back to cited text no. 17
18.Venzon RP, Bromet DS, Schaer GL. Use of Corticosteroids in the Treatment of Cholesterol Crystal Embolization, Percutaneous Translu­minal Coronary ngioplasty. J Invas Cardiol 2004;16:222-3.  Back to cited text no. 18

Correspondence Address:
Madhav Desai
Assistant Professor, Department of Nephrology, Nizam's Institute of Medical Sciences, Panjagutta, Hyderabad - 500 082, Andhra Pradesh
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Source of Support: None, Conflict of Interest: None

PMID: 21422636

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