The passive reabsorption of water by osmosis in the proximal tubule is driven by the transtubular osmotic gradient, which is established through the reabsorption of NaHCO3 and Na+–organic solutes. The osmolality of the interstitial fluid on the basolateral side of the cells is slightly higher than the osmolality of tubule fluid. In the first half of the proximal tubule, more water than Cl− is reabsorbed, leading to an increase in [Cl−] along the length of the tubule. In the second half of the proximal tubule, Na+ reabsorption occurs along with Cl− reabsorption through both transcellular and paracellular pathways. Unlike the first half, the second half of the proximal tubule has different Na+ transport mechanisms and contains very little glucose or amino acids in the tubular fluid. The reabsorption of Na+ with Cl−, rather than organic solutes or HCO3−, is the preferred mechanism in the second half of the proximal tubule due to these differences. The second half of the proximal tubule is also responsible for facilitating the reabsorption of Cl− with Na+. Fanconi syndrome, a renal disease that can be hereditary or acquired, occurs when the proximal tubule is unable to effectively reabsorb HCO3, Pi, amino acids, glucose, and low-molecular-weight proteins. This impaired reabsorption leads to increased urinary excretion of HCO3−, amino acids, glucose, Pi, and low-molecular-weight proteins. Other nephron segments cannot compensate for this inefficient reabsorption, resulting in Fanconi syndrome. The mechanism of transcellular Na+ reabsorption in the second half of the proximal tubule is illustrated in Fig. 34.3.
Fig. 34.2 ). Reabsorption of NaHCO3 and Na+–organic solutes across the proximal tubule establishes a transtubular osmotic gradient (i.e., the osmolality of the interstitial fluid bathing the basolateral side of the cells is a few mOsm/L higher than the osmolality of tubule fluid) that provides the driving force for the passive reabsorption of water by osmosis. Because more water than Cl− is reabsorbed in the first half of the proximal tubule, the [Cl−] in tubular fluid rises along the length of the proximal tubule (see
Fig. 34.2
In the second half of the proximal tubule, Na+ reabsorption is largely accompanied by Cl− reabsorption via both transcellular and paracellular pathways (
Fig. 34.3 ). Na+ is primarily reabsorbed with Cl− rather than organic solutes or HCO3 − as the accompanying anion because the Na+ transport mechanisms in the second half of the proximal tubule
There are over 300 different solute transporter genes that form the so-called SLC (solute carrier) family of genes.AD, autosomal dominant; AR, autosomal recessive; TAL, thick ascending limb of Henle’s loop; XLR, X-linked recessive.Modified from Nachman RH, Glassock RJ. NephSAP 2010;9(3).
differ from those in the first half, and because the tubular fluid that enters the second half contains very little glucose or amino acids. In addition the high [Cl−] (140 mEq/L)
Fanconi syndrome, a renal disease that is either hereditary in tubule fluid, which is due to preferential reabsorption − or acquired, results from an impaired ability of the proximal of Na+ with HCO3 and organic solutes in the first half − tubule to reabsorb HCO3, Pi, amino acids, glucose, and of the proximal tubule, facilitates reabsorption of Cl− low-molecular-weight proteins. Because other downstream with Na+ . nephron segments cannot reabsorb these solutes and
The mechanism of transcellular Na+ reabsorption in the protein, Fanconi syndrome results in increased urinary excretion of HCO3− , amino acids, glucose, Pi, and low- second half of the proximal tubule is shown in
Fig. 34.3 molecular-weight proteins.