Patients who are treated with chronic hemodialysis (HD) experience premature cardiovascular disease and an increased mortality. N-3 polyunsaturated fatty acids (PUFA) may be effective in the secondary prevention of cardiovascular disease, but the effects of n-3 PUFA has not previously been examined in HD patients. It was hypothesized that secondary prevention with n-3 PUFA would reduce the number of cardiovascular events and death in patients who are treated with chronic HD. A randomized, double-blind, placebo-controlled intervention trial compared the effect of n-3 PUFA and a control treatment as secondary prevention of cardiovascular events in HD patients. The primary outcome was a composite of total cardiovascular events and death. A total of 206 patients were randomly assigned to treatment with n-3 PUFA or control treatment and followed for 2 yr or until reaching a predefined end point. During the trial, 121 (59%) of 206 patients reached a primary end point. N-3 PUFA had no significant effect on the primary composite end point of cardiovascular events and death (62 versus 59; NS). In the n-3 PUFA group, a significant reduction was seen in the number of myocardial infarctions (four versus 13; P ‫؍‬ 0.036). This trial was limited by a relatively small number of patients and a large number of withdrawals. However, it is concluded that treatment with n-3 PUFA did not reduce the total number of cardiovascular events and death in this high-risk population. N-3 PUFA significantly reduced the number of myocardial infarctions as a secondary outcome, a finding that might be of clinical interest.Clin J Am Soc Nephrol 1: 780 -786, 2006. doi: 10.2215/CJN.00630206 P atients who are treated with chronic hemodialysis (HD) have a high incidence of cardiovascular disease (CVD) and an increased premature mortality (1,2). Traditional risk factors of CVD are frequent in patients with kidney disease (3); in addition, the uremic milieu results in inflammation (4), specific alterations in lipid metabolism (5), and accumulation of uremic toxins (6), which may contribute to the high risk for CVD. During recent years, there has been focus on the need for intervention trials to prevent CVD and reduce mortality in this high-risk population (7).Evidence exists from both epidemiologic (8) and interventional studies (9) that n-3 polyunsaturated fatty acids (PUFA) might be effective as secondary prevention of CVD and possibly prevent sudden cardiac death (10). However, a recent Cochrane analysis concluded that there is no clear evidence that n-3 PUFA reduce cardiovascular mortality and that there is a need for additional intervention studies in this area of research (11). The possible mechanisms of n-3 PUFA include a lipidlowering effect, with a reduction in plasma triglycerides (12) and a mild antihypertensive effect (13). Several other possible protective mechanisms of n-3 PUFA also have been reported, such as anti-inflammatory (14), antiatherosclerotic (15), antithrombotic (16), and antiarrhythmic (17). The effect of n-3 PUFA on CVD has ...

The transition from day to night is associated with a pronounced decline in diuresis with reductions in the amount of excreted water, electrolytes, and other end products of our metabolism. Failure to do so leads to a large urine output at night, a condition known as nocturnal polyuria, encountered in a large proportion of children with nocturnal enuresis. The aim of this study was to clarify the mechanisms responsible for the nocturnal polyuria seen in enuretics with inadequate response to desmopressin (dDAVP). Forty-six enuretics (7-14 yr of age) and fifteen age-matched controls were admitted for a 24-h protocol with standardized fluid and sodium intake, comprising urine collections, blood sampling, and blood pressure monitoring. We included patients with severe enuresis (5 +/- 1 wet nights/wk) showing <50% reduction in wet nights on dDAVP. We characterized the patients on the basis of their nocturnal urine production. The children with nocturnal polyuria excreted larger amounts of sodium and urea at night than nonpolyurics and controls. Solute-free water reabsorption as well as urinary arginine vasopressin and aquaporin-2 excretion were normal in polyurics, and no differences were found in atrial natriuretic peptide, angiotensin II, aldosterone, and renin levels. Urinary prostaglandin E2 (PGE2) excretion was significantly higher in polyurics. The nocturnal polyuria in children with dDAVP-resistant nocturnal enuresis seems to be the result of augmented sodium and urea excretion. The high urinary PGE2 levels found in these children point toward a role for increased prostaglandin synthesis in the pathogenesis of enuresis-related polyuria.

Background and objectives: This study aimed to investigate the development of new-onset diabetes mellitus (NODM) in a prospective study of 97 nondiabetic uremic patients.Design, setting, participants, & measurements: Included were 57 kidney recipients (Tx group, age 39 ؎ 13 years) and 40 uremic patients remaining on the waiting list for kidney transplantation (uremic controls, age 47 ؎ 11 years). All were examined at baseline before possible transplantation and after 12 months. The prevalence of diabetes, prediabetes, insulin sensitivity index (ISI), and insulin secretion index (Isecr) were estimated using an oral glucose tolerance test with measurements of plasma glucose and plasma insulin.Results: One year after transplantation NODM was present in 14% (8 of 57) compared with 5% (2 of 40) in the uremic control group (P ‫؍‬ 0.01). ISI in the Tx group deteriorated from 6.8 ؎ 3.9 before transplantation to 4.9 ؎ 2.8 at 12 months after transplantation (P ‫؍‬ 0.005), and a slight increase in Isecr from 37 ؎ 19 to 46 ؎ 22 (P ‫؍‬ 0.02) was seen. No significant changes occurred in the uremic controls (ISI was 7.9 ؎ 5 and 8.5 ؎ 5, and Isecr was 31 ؎ 17 and 28 ؎ 15). Using multivariate ordinal logistic regression, pre-Tx ISI and age predicted NODM (odds ratios: 0.82, P ‫؍‬ 0.01 and 1.06, P ‫؍‬ 0.02, respectively).Conclusions: One year after kidney transplantation, NODM was present in 14% of patients. This was mainly caused by an increase in insulin resistance and was observed despite improvement in insulin secretion.