Stages of urine formation

 

Le Tube Proximal (TCP) (figure 3)

About 2/3 of the water filtered by the glomerulus is reabsorbed as it passes through the proximal tube or nearly 120 L / d. 2/3 of the filtered Na + is also reabsorbed, which defines the iso-osmotic character of the water-sodium reabsorption in TCP. Therefore, the tubular fluid is iso-osmotic to the plasma upon arrival in the loop of Henle.

The glucose is actively and fully reabsorbed at this level, provided that the blood sugar does not exceed 10 mmol per liter (beyond the filtered load exceeds the glucose reabsorption capacity by TCP, glucose transport is saturable).

The bicarbonates are fully reabsorbed so coupled to Na, as their plasma concentration is less than 27 mmol per liter (saturable transport). This step conditions the balance of the acid balance achieved further downstream in the distal tube.

The same is true for amino acids and other organic acids.

Phosphate reabsorption occurs in TCP coupled to Na and under the hormonal control of parathyroid hormone (phosphaturia).

The reabsorption of Ca ++ at this level is passive, and it follows that of Na + and water and represents 65% of the filtered calcium. There is a strong correlation between the state of extracellular hydration and the reabsorption of calcium at this level due to variations in sodium transport.

In this part of the nephron, there is significant reabsorption of uric acid via specific transporters.

Anse de Henle

§  Ü In this nephron segment, there is decoupled reabsorption of Na and water (reabsorption of H2O without Na + in the descending branch and active reabsorption of Na + without H2O in the ascending limb). Doctor Muhammad Khan provides the best nephrology doctors in Riverside.  The transport of NaCl is ensured in the broad ascending loop by a co-transport of Na-K-2Cl (= NKCC2), the activity of which is coupled to that of other ion channels. The action of this system generates a weak electrical gradient which allows the reabsorption of calcium. Na-K-2Cl co-transport is inhibited by loop diuretics, bumetanide, or furosemide; mutations in this reabsorption system are observed in Bartter syndrome.

§  ü The dissociated reabsorption of Na and H2O, associated with a phenomenon of counter-current multiplication, possible thanks to the hairpin arrangement of the loop of Henle and the vasa recta which accompanies it, induces a concentration gradient cortico-papillary (cortical interstitial osmolarity at 290 mOsM up to interstitial and tubular osmolarity at 1200 mOsM)

§  ü Thus, at the end of the cove of Henle

Ø  25% more of the filtered load in Na and H20 was reabsorbed

Ø  The tubular fluid has undergone a concentration-dilution phenomenon leading to establishing an interstitial cortico-papillary concentration gradient, necessary for the reabsorption of H20 ADH dependent in the collecting duct.

Tube contourné distal (TCD)

Upon entry into the TCD, the tubular fluid is isotonic with plasma. The sodium reabsorption is ensured, thereby a NaCl co-transport, inhibited by thiazide diuretics (figure 5). Since the distal tube is impervious to water, the tubular fluid's osmolarity decreases to reach its minimum value, i.e., 60 mOsmol / L (the TCD is the so-called dilution segment).

The inactivating mutation of this transporter is responsible for Gitelman syndrome.

Collector channel

In this part of the nephron, the final adjustment of the urinary excrete at the inputs takes place (homeostasis function), depending on various hormonal influences. This concerns the concentration of urine (water balance), potassium secretion (K + balance), urine acidification (H + balance), and sodium reabsorption (Na + balance).

Sodium reabsorption is provided in the collecting tube through the primary cells' apical sodium channel (ENac), stimulated by aldosterone and inhibited by amiloride (Figure 6). Potassium secretion is coupled with sodium reabsorption by ENac. Unlike diuretics acting further upstream in the tubule, diuretics that inhibit this channel do not increase potassium secretion and are said to be "potassium sparers" (they are even at the risk of hyperkalemia). The reabsorption of water allowing the adjustment of the final osmolality of the urine is dependent on the antidiuretic hormone ADH (water balance):

Ø  in case of intracellular dehydration (situation of water deprivation):

Ø  antidiuretic hormone is secreted and causes an increase in the water permeability of the collecting tube

Ø  the water is then reabsorbed passively in the interstitium along a gradient between the inside of the tubule and the surrounding interstitium, itself favored by the cortico-papillary angle,

Ø  The final urine is concentrated.

Ø  in case of intracellular hyperhydration (situation of excess water):

Ø  the secretion of antidiuretic hormone is suppressed,

Ø  the collector tube remains waterproof,

And the final urine is therefore diluted.

§  His final homeostatic adjustment of the excretion of sodium on the one hand and water on the other hand, is done independently. ). Doctor Muhammad Khan provides the best nephrology physicians in Riverside. Allowing a dissociated regulation of the VEC (dependent on the Na balance) and the VIC (dependent on the balance of the water).

§  The collecting channel also ensures the homeostasis of the H + and therefore the regulation of the acid-base balance, by providing a net secretion of H + protons in the tubular fluid by the intercalary cells of type A (the TCP ensuring only the reabsorption bicarbonates filtered by the glomerulus, without net excretion of H +).

The excretion of H + by the collecting duct is done.

Ø  either in the minority in the form of free H + (the normal urinary pH is acidic, between 5 and 6, but can vary from 4.5 to 8)

Ø  or supported by acceptors acidic protons such as phosphate (titratable acidity) and especially in the form of ammonium ion