Reabsorption from the proximal tubule

Reabsorption affects all the glucose of the filtrate, up to 70 percent of its water and sodium (the remainder is absorbed in the distal tubule), most of the potassium and chloride ions, some of the uric acid, 40 percent of the urea, and little or none of the sulfate. Of the total solids 75 percent are reabsorbed in the proximal tubule. The first part of the tubule absorbs amino acids, glucose, lactate, and phosphate; the whole convolution absorbs sodium, potassium, calcium, and chloride and, by removing bicarbonate, acidifies the fluid slightly.

The tubule has only a certain capacity for reabsorption. Thus, normally all the glucose arriving in the filtrate is absorbed; but if plasma glucose is increased to high enough levels, the glucose arrives at the tubule cells faster than it can be absorbed—a condition that occurs in diabetes. In other words, there is a critical rate of delivery determined by plasma concentration and filtration rate, and a maximum reabsorptive capacity for each substance in the filtrate. The rate of tubular reabsorption has an upper maximum value that is constant for any given substance. Consequently, if the plasma level rises sufficiently, all surplus of the substance will pass out in the urine; this is true even for glucose, which is totally reabsorbed under normal conditions. On the other hand, the upper maximum value is much lower for phosphate, so there is normally always some phosphate in the urine. The proximal tubular reabsorption of phosphate is also affected by the phosphate content of the filtrate and is influenced by parathyroid hormone. Phosphate competes with glucose for reabsorption, and its reabsorption is reduced by parathyroid hormone and by vitamin D and is increased, at least for some time, by a high dietary phosphate intake. The amino acids also have their own maximum tubular reabsorption values, but these are high enough to ensure that they are entirely reabsorbed under normal conditions; in certain rare inherited disorders such as cystinuria, in which there is excessive excretion of cystine, their reabsorption is reduced.

The reabsorption of about 70 percent of the sodium ions in the filtrate means that a similar value of water in the filtrate must accompany these ions as a vehicle to prevent a rising osmotic gradient (i.e., to prevent a rising difference in the concentration of the sodium solution inside and outside the tubule). The energy required for the reabsorption of sodium into the blood uses 80 percent of the oxygen consumed by the kidney and represents one-eighth of the oxygen consumption of a person at rest. There is no evidence for active water transport, and the large volume of water reabsorption occurs passively in response to the movement of sodium. Since sodium is quantitatively the major osmotically active solute, the overall effect is to keep the fluid that remains in the tubular lumen, though much reduced in volume, roughly isosmotic with the original glomerular filtrate.

The active reabsorption of sodium (a positively charged ion) into the blood leaves the fluid remaining in the proximal tubule electronegative with respect to the peritubular fluids. This provides a driving force for the reabsorptive transport of negatively charged ions such as chloride, bicarbonate, and organic solutes. Reabsorption of neutral molecules such as urea into the blood is also driven by active sodium transport. Because the tubular epithelium is less permeable to urea and creatinine than it is to water or chloride, however, the free passive movement of water out of the tubular lumen leads to a rising luminal concentration of urea (i.e., above the concentration in the original filtrate with plasma). As a result, a smaller proportion of filtered urea or creatinine than of sodium or water is reabsorbed into the blood, resulting in the elimination of a considerable amount in the urine.

Reabsorption from the loop of Henle

About one-third of the volume of the glomerular filtrate enters the descending limb of the loop of Henle. This fluid is isosmotic with plasma. The reabsorptive characteristics of the descending thin limb and those of the bend of the loop differ greatly from those of the ascending thick limb. The thin epithelium lining the thin limb is permeable to water and solute and has no power of active transport. Accordingly, the fluid entering the limb and the bend of the loop acquires the concentration of the fluid of the surrounding interstitial peritubular fluid. In contrast, the thick ascending limb lined by taller cells has low permeability to water and to urea but actively transports sodium and chloride into the peritubular fluid around both limbs. As a result this fluid in the medullary and deep cortical regions of the kidney becomes highly concentrated, reaching concentrations of up to four times that of the plasma (1,200 mosmoles per litre), mainly owing to the accumulation of sodium and chloride. This accumulation of solute, essential to the formation of a concentrated urine, is discussed in further detail below.

Reabsorption from the distal convoluted tubule

The active transport of sodium out of the ascending limb renders the fluid entering the distal convoluted tubule less concentrated than plasma. Active sodium reabsorption continues throughout the whole of the distal tubule, and this extends to the early part of the collecting duct. As this part of the nephron is relatively impermeable to water, a large concentration gradient of sodium and chloride between the luminal fluid and the plasma is maintained, the concentration of sodium in the tubule being kept well below that of the plasma. The luminal fluid here is also markedly electronegative to the surrounding tissues. The mechanism of sodium reabsorption appears to be directly linked to the secretion of potassium and of hydrogen ions into the tubule from the blood and is greatly influenced by the hormone aldosterone, which is secreted by the adrenal gland when the body’s sodium level is deficient.