[Late recovery of renal function in a patient with acute on chronic renal failure treated with peritoneal dialysis]. / Tardivo recupero della funzione renale in un paziente con insufficienza renale acuta su cronica trattato con dialisi peritoneale.

Contrast-induced nephropathy has become a significant source of hospital morbidity and mortality particularly in patients with multi-organs defects. No current treatment can reverse or ameliorate contrast induced nephropathy once it occurs, but prophylaxis is possible. We present the case of a 61-year-old male patient with concomitant chronic kidney disease (CKD stage III K/DOQI) and diabetes complicated by severe multi-vascular disease, who developed acute kidney damage probably due to the simultaneously exposure to intravascular contrast media and cholesterol crystal embolism. In addition, owing to rapid deterioration of renal function, this patient started renal replacement therapy. No renal biopsy was performed due to the poor clinical condition of the patient. After a month of hemodialysis, he switched to a peritoneal dialysis procedure to which specific treatment for vascular lesions, including antibiotics, prostanoids, hyperbaric oxygen therapy, antiaggregants/anticoagulants and physiotherapy, was associated. After 7 months, the dialysis treatment was stopped and he began intensive clinical follow-up. At present, the patient is in conservative medical treatment (the Tenckhoff catheter has been removed), he is in good condition and severe vascular lesions are absent. Our conclusion is that contrast-induced nephropathy in vasculopathic diabetic patients requires a multidisciplinary approach. In particular, good cooperation between nephrologists and angiologists is useful to avoid rapid and chronic deterioration of renal failure and to prevent the onset and development of severe vascular damage.

An experimental model of lacunar infarction: embolization of microthrombi.

OBJECTIVES: Microthrombi are undoubtedly the most common embolic material in the cerebral circulation, originating from even minor irregularities of the arterial wall, fibrillating atria, cardiac valves, and patent foramen ovale. Thrombus fragments are globular and likely to completely obstruct terminal vessels. In contrast, previous work with "atheroemboli" of needle-like cholesterol crystals rarely cause occlusions or infarctions instead creating small foci of inflammation. In this work, we asked if microthrombi would occlude terminal vessels and create lacunar type infarctions in the subcortical tissues of the rat brain where, as in human brain, collateral flow is limited relative to the cortex. METHODS: Three treatment groups of adult male Sprague-Dawley rats were studied. All groups underwent general anesthesia with monitoring of temperature and blood pressure during cannulation of the right internal carotid artery. In the group embolized with thrombus fragments (n = 12), animals had injections of 300 fragments of thrombus size 60 to 100 microns, the cholesterol group (n = 6) had injections of 300 cholesterol crystals of similar size, and the control group (n = 4) had injections of saline. Brains were harvested at 4 days with perfusion fixation and were examined by immunohistochemical staining for breaks in the blood brain barrier (BBB) (albumin), microglial activation (CD11b), astrocyte activation (GFAP), and infarction (loss of NeuN staining). Size and location of the areas of injury and infarction were recorded. RESULTS: Clot fragments caused discreet infarcts in 10/12 animals that were 0.1-1.7 mm in diameter and coincided with activation of microglia and astrocytes. In some areas, necrosis was already underway at this early time point. Consistent with our previous work, the infarcts caused by cholesterol crystals were smaller (P = .014). Foci of BBB disruption and microglial activation were distributed throughout the brain whereas areas of infarction were found almost exclusively in subcortical tissues (P = .029). CONCLUSIONS: Injecting microthrombi reproducibly caused areas of necrosis resembling lacunar type infarctions. These were primarily located in the striatum and thalamus presumably because these areas lack the branching, collateral network seen in the cortex. In addition, these data give further evidence that the extent of brain injury from emboli depends upon composition and shape as well as size.

Cognitive dysfunction in cholesterol embolic disease.

A patient who developed neurological and renal complications following coronary angiogram and coronary artery bypass grafting is reported. Neurological involvement was in the form of fluctuating sensorium and a subcortical pattern of dementia. Renal failure was seen in the form of raised urea and creatinine levels. Renal biopsy revealed the cause of the renal failure to be due to cholesterol embolic disease. While the sensorium often improved following renal replacement therapy (dialysis), the dementia was poorly responsive to therapy. The patient succumbed due to progressive renal failure. Awareness of the protean manifestations and a high index of suspicion are essential for appropriate diagnosis in order to enable the clinician to accurately prognosticate in this often fatal disease.

Temporary spinal cord stimulation for peripheral cholesterol embolism.

Cholesterol embolism is often an unrecognized complication of some cardiac and vascular procedures (i.e. coronarography, angioplasty, aortocoronary bypass, abdominal aortic aneurysmectomy) and of therapies affecting coagulation (thrombolysis, anticoagulation). The degree of pain associated with ischaemic and necrotic lesions secondary to cholesterol embolism involving the lower limbs is disproportionate to the extension of tissue involvement. Spinal cord stimulation (SCS) has been recognized as effective in relief of pain of ischaemic and neuropathic nature, although its mechanism of action is still not completely clear. The authors are unaware of previous reports of peripheral cholesterol embolism treated by SCS. Two case reports of inferior limb ischaemia secondary to cholesterol embolism in patients who had undergone cardiac invasive procedures. Temporary surgical implantation of SCS devices, which were removed after 4 to 6 weeks. Pain relief was achieved within 1 to 4 hours of surgical procedure. Any analgesic medications could be immediately discontinued. Pain control was effective and normal daily activities were rapidly regained. Ischaemic lesions healed within 4 to 6 weeks of SCS. Pain control is the most critical aspect of the management of peripheral cholesterol embolism without visceral organ involvement. SCS provided effective pain relief in the reported cases and its established ability to improve peripheral microcirculation allowed rapid resolution of necrotic lesions. Temporary SCS should be considered in the management of painful necrotic skin lesions secondary to iatrogenic cholesterol embolism.