According to a publication from the State University of New York at Buffalo, most symptoms of proximal renal tubular acidosis do not stem from the acidic blood levels that characterize the disease. Instead, University at Buffalo researchers believe other factors are responsible for most of the symptoms associated with the condition.
About Proximal Renal Tubular Acidosis
Proximal renal tubular acidosis (pRTA) is a disease of the kidneys, and more specifically, the proximal tubules.
Proximal tubules are cells that make up a large part of the kidneys’ structure, and play an important role in filtering toxic waste from the bloodstream into urine. In individuals with pRTA, proximal tubules are less effective at removing acidic substances from the bloodstream, leading to low blood pH levels (acidosis).
The malfunction seems to be rooted in missing or malfunctioning sodium bicarbonate transporters (NBCe1), bicarbonate transporters that are largely responsible for maintaining intracellular pH levels at homeostatic levels throughout the body.
Though it is often thought that these low blood pH levels are responsible for other complications related to pRTA such as corneal swelling, weak teeth, and poor physical development, new research from the University at Buffalo is challenging the common presumption.
Normalizing pH in Mice
Again, mice were “asked” to put their health on the line for the sake of medical advancement.
Mark Parker, an assistant professor at the University at Buffalo’s Department of Physiology and Biophysics, lead the research which studied the effects of blood pH levels on the mice over time.
Unlike real patients with pRTA, the mice used in the study were engineered to have NBCe1 transporters in their kidneys. In healthy individuals, NBCe1 transporters are found in cells across the body. In pRTA patients, however, these transporters are often missing. Adding NBCe1 transporters to the mice’s kidneys allows them to filter acids from their blood like a healthy human kidney would.
Combined with early alkali therapy (the only accepted method of treating pRTA – a fancier way of saying a literal baking soda prescription), Parker and his team were able to normalize the blood pH levels of the study mice. However, the team found that other symptoms of pRTA persisted, despite effectively regulating blood pH even in utero.
Despite normal pH levels, mice were still displaying weak teeth, corneal edema, and slow physical maturation. Nearly every symptom experienced by pRTA patients, “except the low blood pH,” were found to persist in the subjects.
The team concluded that these resilient symptoms could not be linked to pH levels, and that the lack of NBCe1 transporters elsewhere in the body could play a role. “Thus, alkali therapy is not a panacea for this disease,” Parker commented.
Instead, the assistant professor believes research into the sodium bicarbonate transport pathway could help the very few people in the world living with pRTA (about 15 cases total). Finding ways to help the cells take up NBCe1 molecules could make the difference in achieving a meaningful recovery for pRTA patients.
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