The microvilli greatly increase the luminal surface area of the cells, presumably facilitating their reabsorptive function as well as putative flow sensing within the lumen.

[citation needed][5] In relation to the morphology of the kidney as a whole, the convoluted segments of the proximal tubules are confined entirely to the renal cortex.

Further reading: Drugs secreted in the kidney Most of the ammonium that is excreted in the urine is formed in the proximal tubule via the breakdown of glutamine to alpha-ketoglutarate.

[13] The alpha-ketoglutarate generated in this process is then further broken down to form two bicarbonate anions,[13] which are pumped out of the basolateral portion of the tubule cell by co-transport with sodium ions.

[15] Acute tubular necrosis occurs when PTECs are directly damaged by toxins such as antibiotics (e.g., gentamicin), pigments (e.g., myoglobin) and sepsis (e.g., mediated by lipopolysaccharide from gram-negative bacteria).

Renal tubular acidosis (proximal type) (Fanconi syndrome) occurs when the PTECs are unable to properly reabsorb glomerular filtrate so that there is increased loss of bicarbonate, glucose, amino acids, and phosphate.

In these situations, PTECs may be directly affected by protein (e.g., proteinuria in glomerulonephritis), glucose (in diabetes mellitus), or cytokines (e.g., interferon-γ and tumor necrosis factors).

There are several ways in which PTECs may respond: producing cytokines, chemokines, and collagen; undergoing epithelial mesenchymal trans-differentiation; necrosis or apoptosis.