Dear Editor:
Cholesterol Embolism (CE) is a serious complication of invasive intravascular processes and anti-coagulation treatments in patients with arteriosclerosis and ulcerated aortic plaques. In addition to affecting the kidney, cholesterol crystals may also affect small-diameter arteries in other areas, such as the central nervous system, the coronary arteries, the mesentery, and the pancreas, damage to which is one of the principal causes of mortality in these patients.1
A male patient aged 78 years had a personal history of chronic kidney disease that was probably secondary to arterial hypertension and diabetes mellitus (baseline serum creatinine 1.5mg/dl), was a former smoker and had hypercholesterolaemia. In February 2007 he was diagnosed with ischaemic cardiopathy with a severely diseased vessel, and an angioplasty was performed and a stent implanted.Amonth after this procedure, the patient came to the Emergency Room due to frank haematuria related with an excess of oral anticoagulants. The patient was admitted due to finding high levels of serum creatinine at 4.5mg/dl. A physical examination was performed and an arrhythmia was detected by cardiac auscultation, and cyanosis was detected in the first, third and fifth toes on the right foot. The systematic urine analysis showed blood +++ and the 24-hour protein count was 1.2g/day. Other analytical alterations that we detected were as follows: haemoglobin 10.6g/dl, eosinophilia 7.6%, and a decrease in complement C3, 69mg/dl (NV: 79-152) and complement C4, 11mg/dl (NV:16-32). In the kidney ultrasound, the kidneys appeared with cortical cysts, but with no other morphological changes and no sign of enlargement. The echocardiogram showed a decreased EF (29%). Due to lack of improvement of renal function, it was necessary to begin haemodialysis as replacement therapy. During the seventh haemodialysis session, 15 minutes after having begun, the patient went into cardiac arrest and could not be revived.
Given that sudden death had arisen from an unclear cause, a necropsy was carried out (thoracic-abdominal study), which revealed a severe aortic atheromatosis and a digestive haemorrhage in the ileum as the most relevant macroscopic findings. The microscopic study revealed the presence of cholesterol crystals in small-diameter arteries in the kidneys, stomach, spleen, pancreas and prostate.
Although CE may occur spontaneously in patients with atheromatosis who suffer a breakage in the plaque,2 in most cases it is derived from inadequate treatment in invasive procedures (angioplasty or vascular surgery) and, over the long term, from anti-coagulation treatment.3 Depending on the location of the plaque, migration of cholesterol crystals to multiple organs has been described; these include the central nervous system, the retina, coronary arteries, the pancreas and the adrenal glands. In the case of the kidney, such damage can manifest itself as acute (during the first week following the procedure), sub-acute (weeks or months later), or it can be chronic.1
In our case, although there was a high probability that the acute renal failure (ARF) was due to a CE, the autopsy was what confirmed that the kidneys were affected by cholesterol crystals, and that crystals were also present in other organs. There is no cure for CE, so the treatment options are based on symptomatic and preventative measures;1,4 its mortality rate is high.5 As with other forms of ARF, the mortality of the patients with CE is not due to ARF (in our case, the patient had begun replacement therapy and was on dialysis when he went into cardiac arrest). Rather, it results from the concomitant visceral ischaemia.1 In this case, the ultimate cause of the patient’s death may have been the haemorrhage in the ileum shown in the macroscopic study, which we cannot confirm as the pathological examination of the brain has not been carried out.
