What specific feature of kidney phosphate handling is observed in Fanconi syndrome?

In Fanconi syndrome, a characteristic feature is increased phosphaturia, which refers to the excessive excretion of phosphate in the urine. This occurs due to a malfunction in the renal tubules, specifically in the proximal tubule, where phosphate reabsorption is impaired. In a healthy kidney, a significant amount of the filtered phosphate is reabsorbed; however, in Fanconi syndrome, this reabsorption process is disrupted, leading to elevated levels of phosphate being eliminated from the body through urine.

This condition can result from various underlying causes, including genetic disorders, certain medications, and metabolic conditions, all of which contribute to the dysfunctional phosphate handling and can lead to a clinical presentation of renal tubular acidosis and other electrolyte imbalances.

The other options do not accurately reflect the hallmark of phosphate handling in this syndrome. For instance, increased reabsorption of bicarbonate does not occur; rather, bicarbonate reabsorption is also impaired, contributing to metabolic acidosis. Additionally, while the glomerular filtration rate may be affected in underlying causes, Fanconi syndrome primarily focuses on tubular dysfunction rather than a decrease in GFR. Lastly, decreased urine output is not a feature of this condition; in fact, patients may have normal or increased