Recovery of renal function after renal failure due to cholesterol crystal embolism

J. L. Górriz, A. Sancho, R. Garcés, F. Amorós, J. F. Crespo and L. M. Pallardó

Department of Nephrology, Hospital Universitario Dr Peset, Valencia, Spain

Sir,

Cholesterol crystal embolism (CCE) is not a widely recognized cause of kidney failure [1]. Previous reports have emphasized the progressive nature of renal insufficiency from this cause [2], and reports of improvement of renal function after CCE are rare [24]. We present a case of CCE with secondary kidney failure, livedoid lesions and lower limb intermittent claudication, in which complete recovery of renal function occurred after several months.

Case. A 53-year-old male, with a long-standing history of hypertension and ischaemic cardiopathy was admitted for cardiological evaluation. He was a non-smoker, and was chronically treated with 50 mg/day atenolol, 40 mg/day isosorbide mononitrate and 200 mg/day aspirin. On admission, serum creatinine level was 106 µmol/l, proteinuria was absent and the urine sediment was normal. No other relevant data were found. Coronary angiography via the femoral artery was performed, and a critical stenosis of the left anterior descending coronary artery was detected. One month later, he complained of headache, intermittent claudication of the lower limbs at 50–100 m and diffuse abdominal tenderness that did not respond to antiacids and analgesics. Blood pressure was 200/120 mmHg and livedoid lesions were evident in the abdominal wall and the legs. No bruits were detected. Feet pulses were preserved and symmetric. Maleolar oedema without fovea was present. Laboratory evaluation revealed 29.4 mmol/l urea, 256.3 µmol/l serum creatinine, 51 UI/l creatine kinase, 18 UI/l AST, 338 UI/l LDH, 6.45 mmol/l total cholesterol, 2.04 g/l triglycerides and 547.2 µmol/l uric acid. The white blood cell count was 8.500/µl with 11.1% of eosinophils. ESR was 62 mm/h. Tests for ANA, ANCA, antiphospholipid antibodies, syphilis, cryoglobulins, hepatitis B and C virus and HIV antibodies were negative. Urinalysis showed: 192 mmol/24h Na+, 240 mmol/24h Cl-, 51 mmol/24h K+, 82,08 mmol/24h Urea, 848 µmol/24h creatinine, 180 mOsm/l osmolarity and urine sediment containing 25–50 red cells and 10–25 white cells per high-power field. Proteinuria was 1.2 g/day. Urine culture was negative. Funduscopy showed splinter haemorrhages without Hollenhorst plaques. Doppler sonographic study of carotid and femoral arteries was normal. Scintigraphy study with 99Tcm-MAG3 revealed poor perfusion and loss of excretory function in both kidneys.

A livedoid skin lesion was biopsied revealing the presence of cholesterol crystal emboli that occluded the lumen of the dermis media arterioles. Renal function deteriorated later and serum creatinine increased to a peak of 574.2 µmol/l on day 82 after the coronariography. Later, a slow and progressive recovery of the renal function was detected with a urea level of 18.3 mmol/l and serum creatinine level of 203 µmol/l at 6 months. A further improvement was detected and at the 24 month-follow-up, the urea level was 11.3 mmol/l and the serum creatinine was 123 µmol/l. Proteinuria was negative and the urine sediment was normal. Intermittent claudication of the lower limbs improved after the third month. Treatment during this time period included 10 mg/day amlodipine, 50 mg/day atenolol and 4 mg/day doxazosine. The renal function has remained stable after 24 months of follow-up (Figure 1Go).



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Fig. 1. Evolution of renal function.

 
Comment. Although partial improvement of renal function has been described after CCE [24,5], almost complete recovery of renal function has only been reported in five cases in the literature [3,4] (MEDLINE, 1980–1998), but none of them returned completely to the previous renal function. In most of these patients a nephrotoxic component of the contrast media could not be ruled out in the pathogenesis of the kidney failure, particularly when the renal function declined immediately after the surgical or radiological procedure [2]. Renal insufficiency due to CCE usually sets in gradually, reaching a maximum of serum creatinine 3–6 weeks after the procedure, and up to 40–50% of cases require dialysis [5]. Early deterioration of the renal function has been linked with a higher mortality rate of these patients and a worse prognosis for the recovery of renal function. Conversely, improvement of renal function is uncommon, in no more than 11.5% of the cases, and it occurs in those patients having less severe deterioration of renal function and in those without associated renal injuries [24]. This improvement is usually gradual, over several months, and there is no specific treatment that modifies the spontaneous course. The therapeutic measures are directed at withdrawing anticoagulant treatments, controlling hypertension and hyperlipidaemia, as well as avoiding nephrotoxic insults.

In our patient, the progressive increase in blood urea and creatinine levels 1 month after the coronariography makes it very improbable that radiocontrast-agent nephrotoxicity was the cause of the renal failure, and the findings in the skin biopsy were diagnostic of CCE. This case is remarkable because of the near complete recovery of the glomerular filtration rate, despite the severe deterioration of renal function. Previously normal renal function, the patient age, and probably the limited atherosclerotic disease could favour the almost complete recovery of renal function after CEE [2]. Concomittant to the improvement of the renal function, livedoid skin lesions progressively disappeared, and the intermittent claudication of the lower limbs also improved. This evolution could be related to the recanalization of the organized thrombus, weeks or months after cholesterol crystal embolization, as has been shown in animal and human studies [6]. Nevertheless, recovery may be due to other factors including partial, instead of total, occlusion of the vasculature by the cholesterol crystals, as well as resolution of concurrent acute tubular necrosis in border line ischaemic areas, the development of collateral flow, or hypertrophy of surviving nephrons [24]. The evolution of our patient suggests that transitory renal insufficiency due to CCE could be more frequent than it has been recognized, and the 2 year follow-up shows that long-term stable renal function can be maintained, particularly in patients with preserved initial renal function.

References

  1. Zuccala A, Zucchelli P. A renal disease frequently found at postmortem, but rarely diagnosed in vivo. Nephrol Dial Transplant 1997; 12: 1762–1767[Free Full Text]
  2. Thadhani RI, Camargo CA, Xavier RJ, Fang LS, Bazari H. Atheroembolic renal failure after invasive procedures. Natural history based on 52 histologically proven cases. Medicine (Baltimore) 1995; 74: 350–358[ISI][Medline]
  3. Mannesse CK, Blankestijn PJ, Man in't Veld AJ, Schalekamp MA. Renal failure and cholesterol crystal embolization: a report of 4 surviving cases and a review of the literature. Clin Nephrol 1991; 36: 240–245[ISI][Medline]
  4. Smith MC, Ghose MK, Henry AR. The clinical spectrum of renal cholesterol embolization. Am J Med 1981; 71: 174–180[ISI][Medline]
  5. Scolari F, Bracchi M, Valzorio B et al. Cholesterol atheromatous embolism: an increasingly recognized cause of acute renal failure. Nephrol Dial Transplant 1996; 11: 1607–1612[Abstract]
  6. Okten LB Jr. Experimental production of atheromatous embolism in human beings and experimental animals. Surgery 1959; 68: 685–689




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