Wednesday, February 3, 2010

Mycophenolate mofetil and intravenous cyclophosphamide are similar as induction therapy for class V lupus nephriti

Original Article

Kidney International (2010) 77, 152–160; doi:10.1038/ki.2009.412; published online 4 November 2009
Mycophenolate mofetil and intravenous cyclophosphamide are similar as induction therapy for class V lupus nephritis

Jai Radhakrishnan1,6, Dimitrios-Anestis Moutzouris2,6, Ellen M Ginzler3, Neil Solomons4, Ilias I Siempos5 and Gerald B Appel1

Class V lupus nephritis (LN) occurs in one-fifth of biopsy-proven cases of systemic lupus erythematosus. To study the effectiveness of treatments in this group of patients, we pooled analysis of two large randomized controlled multicenter trials of patients with diverse ethnic and racial background who had pure class V disease. These patients received mycophenolate mofetil (MMF) or intravenous cyclophosphamide (IVC) as induction therapy for 24 weeks, with percentage change in proteinuria and serum creatinine as end points. Weighted mean differences, pooled odds ratios, and confidence intervals were calculated by using a random-effects model. A total of 84 patients with class V disease were divided into equal groups, each group had comparable entry variables but one received MMF and one received IVC. Within these groups, 33 patients on MMF and 32 patients on IVC completed 24 weeks of treatment. There were no differences between the groups in mean values for the measured end points. Similarly, no difference was found regarding the number of patients who did not complete the study or who died. In patients with nephrotic syndrome, no difference was noted between those treated with MMF and IVC regarding partial remission or change in urine protein. Hence we found that the response to MMF as induction treatment of patients with class V LN appears to be no different from that to IVC.

Sunday, January 31, 2010

Thursday, January 21, 2010

Experts: Sitting too much could be deadly

LONDON – Here's a new warning from health experts: Sitting is deadly.

Scientists are increasingly warning that sitting for prolonged periods — even if you also exercise regularly — could be bad for your health. And it doesn't matter where the sitting takes place — at the office, at school, in the car or before a computer or TV — just the overall number of hours it occurs.

Research is preliminary, but several studies suggest people who spend most of their days sitting are more likely to be fat, have a heart attack or even die.

In an editorial published this week in the British Journal of Sports Medicine, Elin Ekblom-Bak of the Swedish School of Sport and Health Sciences suggested that authorities rethink how they define physical activity to highlight the dangers of sitting.

While health officials have issued guidelines recommending minimum amounts of physical activity, they haven't suggested people try to limit how much time they spend in a seated position.

"After four hours of sitting, the body starts to send harmful signals," Ekblom-Bak said. She explained that genes regulating the amount of glucose and fat in the body start to shut down.

Even for people who exercise, spending long stretches of time sitting at a desk is still harmful. Tim Armstrong, a physical activity expert at the World Health Organization, said people who exercise every day — but still spend a lot of time sitting — might get more benefit if that exercise were spread across the day, rather than in a single bout.

That wasn't welcome news for Aytekin Can, 31, who works at a London financial company, and spends most of his days sitting in front of a computer. Several evenings a week, Can also teaches jiu jitsu, a Japanese martial art involving wrestling, and also does Thai boxing.

"I'm sure there are some detrimental effects of staying still for too long, but I hope that being active when I can helps," he said. "I wouldn't want to think the sitting could be that dangerous."

Still, in a study published last year that tracked more than 17,000 Canadians for about a dozen years, researchers found people who sat more had a higher death risk, independently of whether or not they exercised.

"We don't have enough evidence yet to say how much sitting is bad," said Peter Katzmarzyk of the Pennington Biomedical Research Center in Baton Rouge, who led the Canadian study. "But it seems the more you can get up and interrupt this sedentary behavior, the better."

Figures from a U.S. survey in 2003-2004 found Americans spend more than half their time sitting, from working at their desks to sitting in cars.

Experts said more research is needed to figure out just how much sitting is dangerous, and what might be possible to offset those effects.

"People should keep exercising because that has a lot of benefits," Ekblom-Bak said. "But when they're in the office, they should try to interrupt sitting as often as possible," she said. "Don't just send your colleague an e-mail. Walk over and talk to him. Standing up."

Tuesday, January 12, 2010

Monday, January 11, 2010

Renal and cardio-protective effects of direct renin inhibition: a systematic literature review

Journal of Hypertension
Issue: Volume 27(12), December 2009, p 2321–2331
Copyright: © 2009 Lippincott Williams & Wilkins, Inc.
Publication Type: [Meta-analyses]

aDepartment of Clinical Pharmacology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands
bGeorge Institute for International Health, University of Sydney, Sydney, Australia

Results: Fifty-two articles were included. Blood pressure reductions were generally insufficient using early generation DRIs. However, recent DRIs have greater blood pressure-lowering effects. Preclinical and clinical studies showed profound effects of DRIs on markers of renal function, including clear increases in renal plasma flow and reductions in albuminuria. These effects were observed either alone or in combination with other RAAS inhibitors and suggest potential large renal protective benefit. DRIs improved hemodynamic cardiovascular parameters, such as total peripheral resistance, arterial pressure and left ventricular mass index, to a similar extent as those observed with other RAAS inhibitors. Furthermore, addition of DRIs to optimal heart failure treatment resulted in further reductions in B-type natriuretic peptide.


Conclusions: Evidence from preclinical and clinical studies suggests that DRIs may have renal and cardiovascular effects beyond their ability to lower blood pressure. Results of ongoing hard outcome trials are awaited to definitively assess the renal and cardio-protective effects of these agents.