Vitamin D reduces mortality rate in kidney patients

[Naveed Yaseen]

Activated vitamin D administered to patients with moderate to severe chronic kidney disease (CKD) reduces mortality by a fourth, according to the latest findings.

The findings are based on a study of 1,418 patients with moderate to severely impaired kidney function. They also had high parathyroid hormone levels (hyperparathyroidism), which can contribute to weakening of the bones in CKD patients.

Researchers identified a group that was being treated with calcitriol to lower parathyroid hormone levels, and another group that was not receiving calcitriol.

Patients with advanced CKD take calcitriol, an oral form of activated vitamin D, to treat elevated levels of parathyroid hormone, explained Bryan Kestenbaum of the University of Washington, one of the co-authors of the study.

During a two-year follow-up period, mortality rates were compared for patients who were and were not taking calcitriol. “We then adjusted for differences in age, kidney function, parathyroid hormone levels, other illnesses, and other medications,” says Kestenbaum.

In the adjusted analysis, the overall risk of death was about 26 percent lower for patients taking calcitriol. Patients on calcitriol were also less likely to develop end-stage renal disease, requiring dialysis to replace lost kidney function.

“Recently, there has been an increased focus on the effects of vitamin D beyond those on bone health,” Kestenbaum comments. “Vitamin D deficiency has been associated with risk factors for cardiovascular disease, such as high blood pressure, diabetes, and inflammation.”

These findings will appear in the August issue of the Journal of the American Society of Nephrology.

Block brain enzyme to reduce waistline: Just by blocking a brain enzyme, medical scientists reduced appetite and prompted weight loss, even as the blockage improved the body’s ability to handle blood sugar levels.

“We believe we have identified an important drug development target (enzyme CaMKK2) that could potentially turn into a metabolic triple play: appetite control, weight loss and blood sugar management,” said Tony Means of Duke University, who led the research.

For many years, scientists have been testing every step of appetite stimulation and suppression pathways, to help people control weight and minimise risk of diabetes, heart disease and other conditions.

An empty stomach releases the hormone ghrelin, which launches a cascade of signals. Then CaMKK2 in the ghrelin pathway activates AMPK, an enzyme that stimulates animals to eat and gain weight.

When scientists blocked CaMKK2 in mice with a specialised molecule inhibitor, they found the rodents ate significantly less than untreated mice during a six-day trial, and also lost body weight, which looked encouraging for scientists.

“The fact that blocking CaMKK2 worked in normal mice to make them eat less and lose weight, but not in mice missing the enzyme, provides compelling evidence that CaMKK2 signalling is a requirement for appetite control,” Means said.

They also studied both normal mice and mice missing CaMKK2 to learn how these types responded to low-fat and high-fat diets. After nearly 30 weeks on the specific diets, the normal mice on the high-fat diet became diabetic - they were unable to respond to insulin and weren’t able to manage blood sugar levels well. Normal mice on a low-fat diet stayed healthy.

“Remarkably, we find that blocking CaMKK2 prevents deposits of fat in liver and skeletal muscle that are characteristic of obese, diabetic patients,” Means said. These results were published in the May issue of Cell Metabolism.

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