Female or black patients, or those with severe kidney disease, may be resistant to initial treatment more often than other patients with ANCA-associated small-vessel vasculitis. Increased risk for relapse appears to be related to the presence of lung or upper airway disease and anti-PR3 antibody seropositivity.

Objective. Predictors of treatment resistance and relapse have been identified in patients with antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis in the Glomerular Disease Collaborative Network (GDCN) in the southeastern US. This study was undertaken to evaluate the applicability of those predictors in an independent cohort followed up by the French Vasculitis Study Group.Methods. Predictors of treatment resistance were evaluated using logistic regression models and reported as odds ratios (ORs) with 95% confidence intervals (95% CIs). Predictors of relapse were evaluated using Cox proportional hazards models and reported as hazard ratios (HRs) with 95% CIs. Models were controlled for age, sex, race, baseline serum creatinine level, and cyclophosphamide therapy. Conclusion. Our findings indicate that older age is a predictor of treatment resistance, and that PR3 ANCA and lung involvement are predictors of relapse in both cohorts. Discrepancies in predictors of treatment tract resistance may reflect differences in access to care, and differences in predictors of relapse may reflect variations in disease expression.

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A within-group risk factor analysis was conducted to predict angiographic change in the Cholesterol Lowering Atherosclerosis Study, a randomized, placebo-controlled trial of colestipol plus niacin therapy in men with previous coronary bypass surgery. Global angiographic change, including both native coronary arteries and bypass grafts after 2 treatment years, was the end point. Risk factors included on-trial clinical measures, plasma lipids, lipoproteins, and apolipoproteins. Univariate analysis indicated that risk factors previously observed by others in epidemiologic investigation of ischemic heart disease-total cholesterol, LDL cholesterol, non-HDL cholesterol, triglycerides, apolipoprotein B, and diastolic blood pressure-had significant effects in the placebo-treated group. Univariate analysis indicated significant effects of apolipoprotein C-III in drug-and placebo-treated groups. Multivariate analysis indicated the predominant risk factor predicting the probability of global coronary progression was non-HDL cholesterol in placebo-treated subjects and the content of apolipoprotein C-IlI in high density lipoproteins of drug-treated subjects. Both drug-and placebo-treated group findings point to an important role for triglyceride-rich lipoproteins in progression and regression of human atherosclerosis. (Circulation 1990;81:470-476) T hree controlled clinical trials (the Lipid Research Clinics Coronary Primary Prevention Trial, the Helsinki Heart Study, and the Coronary Drug Project) have shown that the incidence rate of coronary heart disease can be reduced by drugs that lower total plasma cholesterol. [1][2][3] see p 694 Although reduction of total plasma cholesterol was a common feature of these trials, the drugs tested reduced cholesterol levels through different mechanisms and produced widely different patterns of lipoprotein transport. The mechanism(s) of benefit in these trials is believed due to a primary effect of lowering blood lipids or lipoproteins on coronary atherosclerosis at the level of the arterial wall.

RRT is justifiable for liver transplant candidates with ARF. Though mortality was high, a substantial percentage (31%) of patients survived to liver transplant. Postoperative mortality is increased compared with all other liver transplant recipients, but is acceptable considering the near-universal mortality without transplantation.