The clinical status and survival in elderly dialysis: example of the oldest region of France.

BACKGROUND: The number of elderly (≥75 years) patients with end-stage renal disease (ESRD) has increased markedly, including in the Limousin region, which has the oldest population in France. We retrospectively compared outcomes in elderly and non-elderly ESRD patients who started dialysis during two time periods. METHODS: Baseline clinical characteristics, care, and survival rates were assessed in 557 ESRD patients aged ≥75 and <75 years who started dialysis in 2002-2004 and 2005-2007. Survival curves and Cox proportional hazards model were used to assess survival and factors associated with survival. RESULTS: Of the 557 patients, 343 and 214 were <75 years and ≥75 years, respectively. Dialysis was started in 2002-2004 and 2005-2007 by 197 and 146 patients <75 years, respectively, and by 96 and 118 patients ≥75 years, respectively. Median age (73.4 years [interquartile range [IQR] 61.7-79.5 years] vs 69.5 years [IQR 57.4-77.4 years] p = 0.001) and the proportion aged ≥75 years (44.7% vs 32.8%, p = 0.004) were significantly higher in 2005-2007 than in 2002-2004. Improved initial status during 2005-2007 was observed only in patients ≥75 years, with a decrease in some co-morbidities, improved walking and better preparation for dialysis. Mortality rates were significantly lower in 2005-2007 than in 2002-2004 (hazard ratio 0.81, 95% confidence interval 0.69-0.95; p = 0.008), with the difference due to factors associated with clinical status and care. CONCLUSIONS: Improved initial clinical status and better preparation for dialysis, accompanied by increased survival, were observed for patients ≥75 years who started dialysis more recently, perhaps because of early referral to a nephrologist.

Is there a BP benefit of changing the time of aspirin administration in treated hypertensive patients?

BACKGROUND AND DESIGN: The effects of aspirin on blood pressure (BP) are controversial and a chronopharmacological effect of aspirin on 24-hour BP was reported recently in otherwise untreated hypertensive patients. The study was designed to test the timing effect of aspirin dosing on 24-hour BP in treated hypertensive patients routinely taking aspirin for cardiovascular prevention. METHOD AND RESULTS: Seventy-five patients were randomized into two groups. One group was to receive aspirin in the evening then in the morning for 1 month and the other group in the morning then in the evening, following a cross-over design. The principal assessment criterion was 24-hour systolic BP (SBP) measured by 24-hour ambulatory BP monitoring (ABPM). Patients were aged 65 ± 9 years and had been hypertensive for 12 ± 10 years. They were all taking a mean of 2.8 antihypertensive drugs and did not modify their treatment throughout the study. Of the included subjects, 70% were men and 33% were diabetics. Mean 24-hour SBP values were clinically equivalent and were not statistically different, depending on whether the aspirin was taking in the morning or evening (128.3 ± 1.4 vs. 128.3 ± 1.4 mmHg, respectively). Neither was there any significant difference in diurnal and nocturnal SBP or in 24-hour, diurnal, and nocturnal diastolic BP (DBP). CONCLUSION: It does not appear useful to advise patients with long-standing hypertension to modify timing of aspirin intake in order to reduce BP values.

Fenofibrate increases creatininemia by increasing metabolic production of creatinine.

Fenofibrate is a potent hypolipemic agent, widely used in patients with renal insufficiency in whom dyslipidemia is frequent. A moderate reversible increase in creatinine plasma levels is an established side effect of fenofibrate therapy, which mechanism remains unknown. We have previously reported that in 13 patients with normal renal function or moderate renal insufficiency, two weeks of fenofibrate therapy increased creatininemia without any changes in renal plasma flow and glomerular filtration rate [1]. In 13 additional patients, muscular enzymes (AST, GPT, CPK, LDH) and myoglobin were measured before and after 2 weeks on fenofibrate, and the values of creatininemia obtained by the Jaffé technique and HPLC were compared. CPK and AST activity and plasma myoglobin increased in 2 patients with fenofibrate, but muscular enzymes remained unchanged in the population as a whole, and were not correlated to the changes in creatininemia. The changes in creatininemia induced by fenofibrate measured by the Jaffé technique were strongly correlated to those measured by HPLC (r(2) = 0.675, p = 0.0006). Analysis of the pooled data of the two arms of the study showed in 26 patients that two weeks of fenofibrate therapy efficiently reduced total cholesterol and triglycerides plasma levels, and raised creatininemia from 139 +/- 8 to 160 +/- 10 micromol/l (p < 0.0001), but confirmed that creatininuria also increased to the extent that creatinine clearance remained unchanged (68 +/- 6 vs. 67 +/- 6 ml/min, n.s.). It is concluded that the increase in creatininemia induced by fenofibrate in renal patients does not reflect an impairment of renal function, nor an alteration of tubular creatinine secretion, and is not falsely increased by a dosage interference. Fenofibrate-induced increase of daily creatinine production is neither readily explained by accelerated muscular cell lysis. It is proposed that fenofibrate increases the metabolic production rate of creatinine.