Climate Change is Turning Dehydration into a Deadly Epidemic | JSTOR Daily
Richard J Johnson, a kidney specialist at the University of Colorado, helped organise the World Congress of Nephrology in Canada in 2011. There, he learned about the strange new form of chronic kidney disease spreading through Central America. Researchers from various countries were beginning to get together and discuss the evidence. Like others, Johnson began to think about possible causes.
His own research was focused on the sugar #fructose – identifying its role in obesity, high blood pressure and heart disease. When a person eats fructose, the liver bears most of the brunt, but some of the sugar eventually ends up in the kidney. With each meal, fructose enters the kidney tubules, where it is metabolised into uric acid and causes oxidative stress, both of which can damage the kidney.
At first, Johnson thought people in the sugarcane fields could be eating so much of the plant itself that they were generating high levels of uric acid and oxidative stress in their kidneys. But, he calculated, even sucking on sugarcane all day wouldn’t produce enough fructose to cause disease. Then he discovered that, under certain conditions, the body processes regular carbohydrates to make its own fructose. And one of the triggers of this deadly alchemy is simple dehydration.
Until that point, nephrologists had thought that dehydration could only cause acute kidney injury, but Johnson’s findings put a new spin on the role of insufficient water intake. Could dehydration day in, day out be causing continuous fructose overproduction that, in turn, could be leading to long-term kidney damage?
Johnson took his theory to the lab, where his team put mice in chambers and exposed them to hours of heat at a stretch. One group of mice was allowed to drink unlimited water throughout the experience, while a second group had water only in the evenings. Within five weeks the mice with a restricted water intake developed chronic kidney disease. During the day, loss of salt and water caused the mice to produce high levels of fructose, and crystals of uric acid would sometimes form as water levels dropped in their urine. When the scientists disabled the gene that metabolises fructose and repeated the experiment, neither group developed chronic kidney disease.
Johnson took these results to a meeting of the Program on Health and Work in Central America, or SALTRA, in Costa Rica in 2012, where they caught the attention of García-Trabanino: “I was astonished. His animal models were absolutely in line with our findings.”
The two collaborated to investigate the biochemical effects of dehydration on workers in the fields of El Salvador. Levels of uric acid started high in the morning and increased throughout the day. “Some patients just had sheets of uric acid crystals in their urine,” Johnson says.
From these studies, Johnson believes that heat stress and dehydration drive the production of fructose and vasopressin, which also damages the kidney. However, he believes that another mechanism may also play a part in the epidemic: rehydration with sugary drinks. Frequently, not trusting the quality of local drinking water, workers drink sodas and soft drinks, and experimental evidence suggests that doing so can lead to even more kidney damage.
“At this stage, that heat stress and dehydration might be causing this problem is still a hypothesis,” Johnson admits. “Although it is a strong one.”