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SUMMARY: Accelerated atherosclerosis was reported to be associated with chronic analgesic consumption, but most studies were retrospective, and individual findings have almost never been controlled with regard to other atherosclerotic risk factors. Ten haemodialysis patients with analgesic nephropathy (group I) and 19 haemodialysis patients where renal failure was not caused by analgesic nephropathy (group II) were included in the study. All patients were female without diabetes. Using B‐mode ultrasonography, we compared intima‐media thickness (IMT) in the carotid arteries and plaque occurrence, and their thickness in group I with that in group II. the possible differences in atherosclerotic risk factors in both groups were also investigated. In group I, the average age was 60.2 years, and the average dialysis treatment was 55.7 months. In group II, the average age was 54.6 years, and the average duration of dialysis treatment was 50.4 months. We found no statistically significant difference in the age and duration of dialysis treatment between groups I and II. the IMT values of the carotid arteries (0.97 vs 0.78 mm; P= 0.027) were significantly higher in group I. More patients had plaques in group I (90 vs 57.9%), and the number of plaques (P= 0.037) and their thickness (P= 0.043) were significantly higher in this group. There was no statistically significant difference in the atherosclerotic risk factors between groups I and II. the results indicate that patients with analgesic nephropathy treated with haemodialysis showed advanced atherosclerosis compared with other haemodialysis patients, despite no difference being found in the atherosclerotic risk factors between these patients.
SUMMARY: Accelerated atherosclerosis was reported to be associated with chronic analgesic consumption, but most studies were retrospective, and individual findings have almost never been controlled with regard to other atherosclerotic risk factors. Ten haemodialysis patients with analgesic nephropathy (group I) and 19 haemodialysis patients where renal failure was not caused by analgesic nephropathy (group II) were included in the study. All patients were female without diabetes. Using B‐mode ultrasonography, we compared intima‐media thickness (IMT) in the carotid arteries and plaque occurrence, and their thickness in group I with that in group II. the possible differences in atherosclerotic risk factors in both groups were also investigated. In group I, the average age was 60.2 years, and the average dialysis treatment was 55.7 months. In group II, the average age was 54.6 years, and the average duration of dialysis treatment was 50.4 months. We found no statistically significant difference in the age and duration of dialysis treatment between groups I and II. the IMT values of the carotid arteries (0.97 vs 0.78 mm; P= 0.027) were significantly higher in group I. More patients had plaques in group I (90 vs 57.9%), and the number of plaques (P= 0.037) and their thickness (P= 0.043) were significantly higher in this group. There was no statistically significant difference in the atherosclerotic risk factors between groups I and II. the results indicate that patients with analgesic nephropathy treated with haemodialysis showed advanced atherosclerosis compared with other haemodialysis patients, despite no difference being found in the atherosclerotic risk factors between these patients.
In patients with CRF due to AAN ongoing analgesic use, male gender and increasing proteinuria predict a more rapid decline in renal function. Patients who continue analgesics, those with pre-existing vascular disease and those with more advanced renal impairment at presentation, are at a significantly increased risk of reaching the combined end-point of death or end-stage renal failure requiring dialysis. The design of this study, however, leaves it open to the criticism that selection bias may account for some of its effects, and as with all work on AAN the possible confounding issue of reverse causality is difficult to dismiss.
Analgesic nephropathy is a slowly progressive renal disease, characterised by renal papillary necrosis. Recently, diagnostic criteria for this disease have been defined based on renal computed tomography scanning performed without contrast. The observation of a decreased renal mass of both kidneys, combined with either bumpy contours or papillary calcifications, has been found to have high diagnostic specificity and sensitivity. However, the question remains as to what kind of analgesics can cause analgesic nephropathy. In the majority of early reports about this condition, phenacetin was singled out as the nephrotoxic culprit. However, during the last decade the nephrotoxic potential of nonphenacetin-containing preparations has become apparent. It is clear that people who abuse analgesics prefer combination analgesics containing 2 analgesics combined with caffeine and/or codeine. In contrast, abuse of products containing only aspirin (acetylsalicylic acid) or paracetamol (acetaminophen) is seldom described and associated renal disease is only occasionally reported. Experimental evidence of the nephrotoxicity of analgesic preparations is not well established. The results of studies involving analgesic administration in animals remain contradictory. Clinical evidence linking high consumption of analgesic preparations with analgesic nephropathy is overwhelming. Most patients who admit to over-consuming analgesics have taken preparation containing more than one compound. In recent years, it has become more apparent that preparations not containing phenacetin also have the potential to cause nephrotoxicity manifesting as identical renal lesions. Further epidemiological evidence of the nephrotoxic potential of analgesic combinations has come from case-control studies published during the last decade and from 2 prospective cohort studies. Effective prevention of analgesic nephropathy consists of the prohibition of over-the-counter sales of preparation containing at least 2 analgesics associated with caffeine and/or codeine.
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