What is the primary clinical consequence of elevated serum ammonia levels?

The primary clinical consequence of elevated serum ammonia levels is neurological deficits. This condition, known as hyperammonemia, can disrupt normal brain function, leading to a range of neurological symptoms. The high levels of ammonia have a neurotoxic effect, which can cause changes in mental status, confusion, lethargy, and eventually progress to more severe manifestations such as seizures, coma, or even death if not addressed promptly.

Ammonia is primarily produced in the body through protein metabolism and is typically converted to urea in the liver for excretion. When the liver is unable to adequately process ammonia due to conditions like liver failure or certain metabolic disorders, ammonia builds up in the bloodstream. The brain is particularly sensitive to elevated ammonia, and the resulting neurotoxicity can lead to what's termed hepatic encephalopathy.

The other options do not serve as primary consequences of elevated serum ammonia levels. For instance, while kidney failure and fatty liver may arise due to various metabolic derangements, they are not direct results of hyperammonemia. Similarly, while hyperglycemia can occur in specific metabolic states, it is not a direct consequence of increased serum ammonia levels.