Year : 2002 | Volume
: 13 | Issue : 1 | Page : 55--59
Acute Renal Failure After Cardiac Catheterization and Coronary Artery Bypass Graft in an Elderly Patient
Muna Al Nimri, Maan Hadidi
Department of Nephrology, King Hussein Medical Center, Amman, Jordan
Muna Al Nimri
Consultant Nephrologist, King Hussein Medical Center, P.O. Box 961538, Amman 11196
We report the occurrence of atheroembolic disease in an elderly patient with coronary artery disease who had cardiac catheterization followed by coronary artery bypass graft. The patient developed acute renal failure and extra-renal manifestations with biochemical and clinical evidence of deep organ involvement which ended in death due to severe cardiac failure despite improvement of renal function.
|How to cite this article:|
Al Nimri M, Hadidi M. Acute Renal Failure After Cardiac Catheterization and Coronary Artery Bypass Graft in an Elderly Patient.Saudi J Kidney Dis Transpl 2002;13:55-59
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Al Nimri M, Hadidi M. Acute Renal Failure After Cardiac Catheterization and Coronary Artery Bypass Graft in an Elderly Patient. Saudi J Kidney Dis Transpl [serial online] 2002 [cited 2020 Feb 24 ];13:55-59
Available from: http://www.sjkdt.org/text.asp?2002/13/1/55/33203
Renal cholesterol embolization syndrome (CES) develops when cholesterol crystals and atheromatous material, typically from atherosclerotic plaques in the aorta, shower the distal arterial tree. It usually occurs after mechanical trauma or use of thrombolytic agents. Although well described for many years, exact incidence of CES is not known. Its manifestations are quite variable ranging from a mild sub-clinical course to a rapidly fatal illness.
A 60-year-old male patient was admitted at the King Hussein Medical Center, Amman, Jordan with anginal chest pain in September 1997. An electrocardiogram showed inferolateral wall injury; the patient was normotensive, cigarette smoker 40 pack-years, and denied any previous history of diabetes mellitus. The baseline serum creatinine was 115.2 µmol/L. Cardiac catheterization showed three vessel coronary artery disease and his serum creatinine in the first two consecutive days post-catheterization were 124 µmol/L and 132.9 µmol/L. Aortocoronary bypass surgery was performed two weeks later and post-operatively there was a decrease in urine output with a transient deterioration of his kidney function, which was managed conservatively. He stayed in the hospital for one week and was discharged with a serum creatinine of 168.3 µmol/L. He was prescribed one tablet each of aspirin (325 mg) and ranitidine (150 mg) daily.
Two weeks later, he was re-admitted with generalized weakness, malaise, vague epigastric pain, aching pain in the back and lower limbs, nausea and vomiting, associated with dark bluish discoloration of both lower limbs. On physical examination, he was found to be somnolent, moderately dehydrated and afebrile with a blood pressure of 185/95 mm Hg, and a pulse of 100 beats/min. Fundoscopy was normal, there was no carotid bruit, lung auscultation revealed harsh vesicular breathing with bilateral expiratory wheeze. Heart examination showed regular rhythm with no murmurs. There was epigastric tenderness with no organomegaly on abdominal examination. Peripheral pulses were felt equally in the upper and lower limbs. Neurological examination showed a globally depressed sensorium, with no focal deficit.
Laboratory investigations revealed an elevated ESR of 60 mm in the first hour, hemoglobin 130 gm/l, white blood cells (WBC) 9200/cu mm, serum urea nitrogen 64.8 mmol/L, creatinine 655.6 µmol/L, potassium 7 mmol/l, normal liver function tests and normal cardiac enzymes.
Urinalysis showed 1+ protein, 8-10 red blood cells and 2-3 white blood cells per high power field. Hepatitis B antigen and C antibody were negative and serum complement levels C3, C4 were normal.
A subclavian catheter was inserted and he was dialyzed once. After 48 hours, his urine output started improving and he was managed with intravenous fluids with furosemide. One week after admission, the patient developed icterus and severe epigastric pain. His laboratory data showed the following: ESR 70 mm in the first hour,
WBC 16400/cu mm with neutrophils 90%, lymphocytes 6% and eosinophils 4%, normal platelet count and partial thromboplastin time, prothrombin time of 20 seconds with control being 12 seconds, serum creatinine 363.3 µmol/L, serum alkaline phosphatase 413 U/L, aspartate aminotransferase 74 IU, alanine aminotransferase 86 IU and bilirubin 108.8 µmol/L. An abdominal ultrasound was normal.
The patient remained somnolent, maintained good urine output, his serum creatinine declined to 212.6 µmol/L and blood urea nitrogen to 28.8 µmol/L and his blood pressure was within normal limits. However, he developed gangrenous changes in the toes of both feet along with skin ulceration over both lower limbs.
Two weeks after admission he had a cardiac arrest and passed away.
The diagnosis of CES was considered in this patient as he had important and recognized pre-disposing conditions for embolization. Harrington et al in 1968 first addressed the association between angiography and CES.  Ramirez et al in 1978 reported the incidence of CES after angiographic procedures to be as high as 30%, and showed an incidence of spontaneous atheroembolism of only 4.3%. 
The risk of embolization after an angiographic procedure is about 43% in elderly high-risk patients, and about 5% following vascular surgery. Moreover, at least 61% of patients with renal CES had a recognized predisposing factor.  Thus, it is very likely that both radiological and surgical manipulation of the aorta and its branches are associated with increased risk of fragments of atheromatous material embolizing.
Most cases of CES followed difficult or prolonged manipulation of catheters within severely diseased aortas, and this mechanical trauma is the most plausible explanation of cholesterol embolization. However, others have reported embolization following easy placement of the catheters as well,  suggesting that forced distention of the aorta during contrast injection may also play a role.
Cholesterol embolization syndrome is relatively rare, because platelet fibrin thrombi normally adhere to the exposed surfaces of ulcerated plaques, stabilize cholesterol crystals and prevent their embolization, and the syndrome usually occurs only in patients with extensive atheroembolic disease. 
The past decade had witnessed an increasing incidence of CES associated with the use of thrombolytic agents (streptokinase) in the management of deep vein thrombosis, which was first reported by Glassock et al.  Other reports have described a variable number of patients who developed acute renal failure as a result of CES after the use of streptokinase for the treatment of acute myocardial infarction.  The first reported case of atheroembolic acute renal failure following use of recombinant tissue plasminogen activator (t-PA), was published by Gupta et al in 1993.  Primary renal allograft non-function caused by cholesterol embolization from the donors' aorta has also been reported. 
The majority of reports suggest that cholesterol embolization is a progressive, irreversible disease with a high mortality of about 81%.  It is interesting to note that our patient had a fatal outcome due to cardiac failure despite improvement noted in his kidney function. This acute improvement in renal function was probably a temporary phenomenon resulting from a cessation of renal embolization. 
Our patient had extra-renal manifestations with evidence of deep organ involvement which was demonstrated by clinically visible jaundice and abnormalities in liver function tests. Involvement of the gastrointestinal system in atheroembolism has varied from 18-48% in various reported series, and commonly involves the liver (17%)  followed by the pancreas.  The intestinal tract may be involved at any site along its length, and lesions ranging from massive gastric infarction to small intestinal obstruction and even perforation of the jejunum as a complication of atheroembolization have been described.  However, deep organ involvement has only infrequently been correctly attributed to embolism during the patient life. 
Skin and skeletal muscle signs and symptoms often dominate the initial clinical presentation. Our patient had livido reticularis, purpura, and areas of necrosis leading to ulceration on cutaneous examination, which were typically distal to the major site of atherosclerosis in the aorta beyond the renal arteries. Normally, the skin lesions commonly appear over the lower back, buttocks, lower abdomen and legs.  Muscle pain is localized to the back, lower abdomen and the legs. Even frank rhabdomyolysis has been reported. 
The spectrum of diseases caused by cholesterol embolization ranges from being asymptomatic to a rapidly progressive multisystem failure.  Specific organ involvement is identified from clinical and laboratory examination and, biopsy specimens and autopsies. Most patients diagnosed as having atheroembolic renal disease have been over the age of 60 years, and none have been younger than 50 years. 
Clinicians first confronted with this syndrome often diagnose sepsis or vasculitis. Furthermore, standard laboratory tests are often abnormal in CES and lead to more confusion. An elevated ESR is found in 97% of cases which, although non-specific, may be viewed as evidence of infection or inflammation (vasculitis), which is further supported by the presence of leukocytosis and eosinophilia seen in 57% and hypo-complementemia seen in 25-70% of the cases.  In fact, cholesterol crystals do evoke an inflammatory response in the embolized vessels.
Except when multiple complications of atheroembolism are present concurrently, a diagnosis of atheroembolic renal disease can be made only by examination of excised tissues. If there is an involved area in the skin, a cutaneous biopsy can enable a quick diagnosis; the same is true of skeletal muscle of the legs in a patient with suspected CES.
Renal biopsy should be considered if there are no cutaneous or muscle signs or symptoms, and clinicians should alert the pathologist receiving these specimens that CES is suspected. This is because, wash out of cholesterol crystals in formalin fixed tissue is frequent and may mislead the pathologist.  Renal biopsy offers a definitive means of establishing the diagnosis, and has been carried out in a limited number of patient's.  Usually, there are no characteristic urinary abnormalities.
Presently, no treatment is available for CES and therefore invasive vascular procedures are best avoided in elderly patients, and when necessary, use of softer, more flexible catheters is recommended. 
Therapy is mainly supportive and dialysis is used when indicated and may permit time for partial return of renal function. Anticoagulants are neither effective nor rational considering the pathogenesis of disseminated cholesterol embolism. Improved operative techniques have reportedly reduced the incidence of surgically induced cholesterol embolization. 
Atheroembolic renal disease is more common than was previously thought, and should be considered in the differential diagnosis of multisystem disease in an elderly patient with multiple risk factors, presenting with deterioration of renal function after a vascular, radiographic or surgical procedure, or after receiving a thrombolytic agent. Certain cutaneous changes, fever, and exacerbated hypertension with unexplained renal failure should heighten suspicion especially when the patient has history of some complications of atherosclerosis. Death is most commonly due to cardiac causes. 
Since the population at risk for CES is growing, and the disease is iatrogenic in origin in most cases, we should expect to encounter CES with greater frequency as a cause of acute renal failure among the elderly population in the future. 
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