Water-pumping turbulent flow in thin segments of the loop of Henle concentrates urine

322 loop of henle

In the mammalian kidney, urine is concentrated by passing through the thin descending limb (TDL) of Henle’s loop, correlated with an osmotic gradient in the interstitial fluid that is increased from the outer medulla (OM) to the tip of the inner medulla (IM).

The “water-pumping turbulence” hypothesis states that both the urinary concentrating and the osmotic gradient of the renal medulla result from turbulent urine flow in the TDL. In turbulent flow, molecules move crosswise as well as along the tubule so H2O molecules are driven out through aquaporins; this concentrates urine. Since the TDL has fewer aquaporins in the IM than in the OM, the IM interstitium receives less water; this can establish an osmotic gradient. Turbulence in thin segments results from a greater Reynolds’ number (RN), the measure of tendency for turbulence, calculated based on velocity, density, and viscosity of urinary flow and tubule diameter. RN (and the tendency for turbulence) of urinary flow in the TDL is approximately 2 times the RN in a thick segment. It makes the flow a water-pump and results in urinary concentration and the osmotic gradient of the renal medulla.

_________________________________________________________________________________

Introduction
The mammalian kidney continuously changes water excretion and urinary concentration depending on different conditions in order to maintain a nearly constant blood plasma osmolality. For most mammals that do not have free access to water, the ability to change water excretion is essential for survival (1).

In order to change urinary concentration, nephrons have several mechanisms, the best known of which is urinary concentration through the generation of a progressive osmotic gradient extending from the cortico-medullary boundary to the inner medullary tip (2) and a hyperosmotic medulla (Figure 1). Many hypotheses have been proposed to explain how this gradient is established. Most of these hypotheses are designed based on “counter-current multiplication of a single effect” (Figure 2). The single effect is a small transepithelial osmolality difference between fluid flows in the ascending and descending limbs of the loop of Henle at each level of the medulla (1).

 

Figure 1: A brief review on kidney structure, nephron components, and the physiology of the loop of Henle (water and solutes transportation):

Kidney Structure

1. Afferent arteriole, 2. Glomerulus, 3. Bowman’s capsule, 4. Proximal convoluted tubule, 5. Efferent arteriole, 6. Thin descending limb of the loop of Henle, 7. Thin ascending limb of the loop of Henle, 8. Thick ascending limb of the loop of Henle, 9. Distal convoluted tubule, 10. Cortical collecting duct, 11. Outer medullary collecting duct, 12. Inner medullary collecting duct, 13. Renal cortex, 14. Renal medulla, 15. Renal capsule 16. Ureter 

The kidney’s structural and functional units are nephrons. Every nephron has the segments 3, 4, 6, 7, 8, and 9. The filtrate (blood that is filtered through a network of capillaries called the glomerulus to the Bowman’s capsule) passes through them respectively. Urine is formed by active and passive transportations. Nephrons empty into the collecting ducts. The collecting duct system has a wide variation in water reabsorption level depending on the presence of antidiuretic hormone. The collecting duct system is emptied into the ureter and the final product, urine, is excreted.

In 1942, Kühn and Ryffel (2) proposed that a small concentration difference between two compartments of the loop of Henle (single effect) can be multiplied in a counter-current system if the membranes separating the compartments have the required permeabilities (2). In their hypothesis, a loop-shaped segment of the mammalian nephron called the loop of Henle creates a counter-current system by directing the fluid in two opposite directions, making urine flow in the descending and ascending limbs of Henle’s loop. Single effect originates from outward active transportation of NaCl, but not water, along the ascending limb of the loop. This small difference is then multiplied by the counter-current circulation of the fluid in the loop, resulting in a progressive osmotic gradient extending from the cortico-medullary boundary to the inner medullary tip.

This counter-current multiplier system produces a favorable hyperosmotic renal medulla for urinary concentrating. In the presence of antidiuretic hormone and a hyperosmotic renal medulla, water is reabsorbed from the inner medullary collecting ducts to the interstitial fluid and subsequently to the peritubular capillaries (3). In other words, water moves from a hypotonic inner tubular fluid to the hypertonic interstitial fluid, and urine is progressively concentrated while flowing in the medullary collecting ducts.

In the outer medulla, single effect originates from active transportation of NaCl from the thick ascending limb to the interstitium. This single effect is multiplied by the counter-current flow configuration to establish a large axial osmolality difference. In the inner medulla the counter-current multiplication of a single effect may also be the source of this gradient but the single effect in this part has not been definitively identified (1).

 

Figure 2: Countercurrent multiplication of a single effect in the loop of Henle for producing a hyperosmotic renal medulla.

Step 1: process begins with isomolar fluid entering the limbs. 

Step 2: active solute transport establishes a 80 mOsm/kg H2O transepithelial osmolality difference between fluid flows in ascending and descending limbs of the loop of Henle at each level (single effect). 

Step 3: passive transportation of H2O molecules from the tubule to the interstitium. 

Step 4: fluid flows half-way down the descending limb and up the ascending limb. 

Step 5: active transport reestablishes another 80 mOsm/kg H2O transepithelial osmolality gradient. 

Note that the luminal fluid near the bend of the loop achieves a higher and higher osmolality as the process is repeated. This establishes a large axial osmotic gradient.

Kokko and Rector (4) and Stephenson (5) proposed that a passive mechanism provides the single effect for countercurrent multiplication in the inner medulla. In their hypothesis, progressively passive water reabsorption from descending limbs of the loops of Henle and inner medullary collecting ducts concentrates NaCl and urea respectively. This increased concentration of NaCl and urea is responsible for progressive inner medullary osmotic pressure, and the osmotic pressure accounts for passive water reabsorption from the descending limb of the loop of Henle and the inner medullary collecting duct. It means that in their hypothesis “the consequences are themselves the causes!”, as de Rouffignac states (3).

Knepper and colleagues (6,7,8) considered a key role for peristalsis of the papilla in the inner medullary urinary concentrating mechanism but when the measured transepithelial permeabilities were incorporated into mathematical models, the significant concentrating effect of the inner medulla was not predictable by the models (9,10,11).

It seems that “counter-current multiplication of a single effect” can’t explain how the osmotic gradient is produced in the inner medulla, and subsequently this hypothesis can’t explain how urine is passively concentrated by entering the inner medulla and passing through the thin descending segment of the loop of Henle, or while it flows in the inner medullary collecting ducts in the presence of antidiuretic hormone (3).

The purpose of this study is to apply physical rules in answering the following questions: Why is water passively diffused from the thin descending segment of the loop of Henle to the interstitial fluid without any energy consumption? Could special morphology of the nephron or special properties of urinary flow in this segment have a role? Urine is concentrated by passing through the thin descending segment of the loop of Henle and is correlated to an osmotic gradient in the interstitial fluid which is increased from the outer medulla to the inner medulla. They are correlated; but is osmotic gradient the original cause of urinary concentration? Or do both have a common cause?

The hypothesis: “water-pumping turbulence”
To identify the mechanisms of urine concentration, what has received less consideration is the role of the morphology of a special segment of nephrons called “the loop of Henle” which is located in the medulla. In my hypothesis, there is a key role for this morphology and particularly, for the diameter difference between thin and thick segments of the loop of Henle. In the “water-pumping turbulence” hypothesis, mechanisms and physical forces which arise from this special morphology of the nephron and also special properties of urinary flow in this segment can explain why urine is concentrated by entering the medulla.

The water-pumping turbulence hypothesis is defined in 2 steps:

STEP 1: first it demonstrates that laminar urinary flow has the tendency to be turbulent in the thin segments of the loop of Henle because of the special morphology of the tubule. Also, turbulence of urinary flow in the thin segments is more probable because of a greater Reynolds’ number of the flow compared to the urine flow in the thick segment.

STEP 2: then it proves that turbulent flow can make small H2O molecules leave the tubule through aquaporins (AQs) and result in urine concentrating. Also, different distribution of AQs all over the tubule make turbulent flow result in an osmotic gradient in the interstitial fluid, which is increased from the outer medulla to the tip of the inner medulla. In the presence of antidiuretic hormone and a hyperosmotic renal medulla, water is reabsorbed from the inner medullary collecting ducts to the hyperosmotic interstitial fluid and subsequently, to the peritubular capillaries. So, in the presence of antidiuretic hormone, a concentrated urine is excreted.

Definitions
Before explaining the water-pumping turbulence hypothesis, it seems necessary to define some terms: [These are adopted from chapter 14 “Overview of the Circulation; Medical Physics of Pressure, Flow, and Resistance” of “Guyton and Hall Textbook of Medical Physiology”(12); so, the terms are defined in the area of blood circulation.]

“Laminar flow of blood in vessels:

When blood flows at a steady rate through a long, smooth blood vessel, it flows in streamlines, with each layer of blood remaining the same distance from the vessel wall. This type of flow is called laminar flow or streamline flow, and it is the opposite of turbulent flow, which is blood flowing in all directions in the vessel and continually mixing within the vessel, as discussed subsequently.

Turbulent flow of blood under some conditions:

When the rate of blood flow becomes too great, when it passes by an obstruction in a vessel, or when it makes a sharp turn, the flow may then become turbulent, or disorderly, rather than streamline. Turbulent flow means that the blood flows crosswise in the vessel as well as along the vessel, usually forming whorls in the blood called “eddy currents”. These are similar to the whirlpool that one frequently sees in a rapidly flowing river at a point of obstruction.

The tendency for turbulent flow increases in direct proportion to the velocity of blood flow, the diameter of the blood vessel, and the density of the blood, and is inversely proportional to the viscosity of the blood, in accordance with the following equation:

Where Re is Reynolds’ number and is the measure of the tendency for turbulence to occur, v is the mean velocity of blood flow (in centimeters/second), d is the vessel diameter (in centimeters), ρ is density, and η is the viscosity (in poise)” (12).

Application of Reynolds’ number in explaining STEP 1 of the water-pumping turbulence hypothesis:

If we consider 3 segments for the loop of Henle (thin descending, thin ascending, and thick ascending), Reynolds’ number can be used in analyzing the urinary flow in these segments, and it can be concluded that the tendency and the possibility of turbulence to occur in thin segments of the loop of Henle (ascending and descending) is much more than in the thick ascending segment of the loop of Henle for several reasons:

1) Although thin segments have a smaller diameter and radius than the thick segment, both have equal input, because every minute the urine input of thin segments is equal to their own urine output, and subsequently is equal to the input of the thick ascending segment (if we ignore transportation between tubules and peripheral interstitium). Note that for a given length, thin segments can contain a lower volume of fluid, so urine displacement in thin segments is more per minute. The urine displacement is inversely proportional to the volume of tubules. The volume of the tubule is directly proportional to r2. The displacement and subsequently the velocity of the urinary flow  in tubules is inversely proportional to r2.

L: Length            r: radius

Reynolds’ number is directly proportional to the diameter (and the radius) of tubules; it is also directly proportional to the velocity of urinary flow. So, Reynolds’ number in thin segments is decreased in proportion to , and is increased in proportion to .  Altogether, Reynolds’ number in thin segments rises in direct proportion to . The radius of thin and thick segments are respectively 12μm and 60μm (13). This means that the radius in the thick segment is 5 times the radius in the thin segments.

2) The density of solutions is in direct proportion to their concentration. The density-concentration relationship is fitted with a 1st order polynomial (14). When urine enters the thin descending segment of the loop of Henle, it has a concentration of 285 mOsm/kg H2O and extends to 1200 mOsm/kg H2O at the tip of the medulla (in conditions where the maximum water reabsorption is essential); then, it is decreased gradually to 400 mOsm/kg H2O while passing through the thin ascending limb (15). So, the mean urine concentrations in thin segments is approximately 676 mOsm/ kg H2O [this is the mean of different urinary concentrations at different points of the loop mentioned in (15)]. On the other hand, the concentration of the input and the output of the thick ascending limb is respectively 400 mOsm/kg H2O and 100 mOsm/kg H2O (15). So, the mean urine concentration in the thick segment is approximately 250 mOsm/kg H2O. This means that (in conditions with the maximum water reabsorption) the mean urine concentration in thin segments is about 2.7 times the mean urine concentration in the thick segment.

(Note that approximations used to get this result won’t act as a disturbance factor in conclusions, because in conditions where the maximum water reabsorption is not essential, the mean urine concentration difference between urine flows in thin and thick segments is even less than what was mentioned before and it does not disturb the result of the mathematical part coming in the section “Conclusion of 1-4”). These concentration differences are caused by:

2-a) Efflux of water from the thin descending limb (16) which concentrates urine and increases the density of urine.

2-b) Passive NaCl reabsorption from the thin ascending limb (15) which dilutes urine and decreases the density of urine.

2-c) Active reabsorption of K+, Na+, Ca2+, Mg2+, HCO3, Cl-, and other ions in the thick ascending limb (17) which dilutes urine and decreases the density of urine.

Since the density of solutions is in direct proportion to their concentration, it can be concluded that the mean urine density in thin segments is 2.7 times the mean urine density in the thick segment.

3) Urine viscosity, like other solutions, depends on different factors such as:

3-a) Concentration of ions in solution: Viscosity-concentration relationship is fitted with a 2nd order polynomial (18). So, the mean urine viscosity in thin segments is approximately 2.72 times the mean urine viscosity in the thick segment (if we ignore ions with a viscosity changing coefficient as mentioned below).

3-b) Ion type that has been dissolved in solution: every ion has a coefficient in changing solution viscosity. Some of these coefficients are:

K+ : -0.007    Na+ : 0.086    Cl- : -0.007    Mg2+ : 0.385 Ca2+ : 0.28518

Concentration of both ions with positive coefficient (which can increase urine viscosity) and ions with negative coefficient (which can reduce urine viscosity) is higher in thin segments (descending and ascending); thus, their effects are in competition.

Altogether it can be concluded that the mean urine viscosity in thin segments is approximately less than 2.72 times the mean urine viscosity in the thick segment.

4) Bending of nephrons between thin descending and thin ascending segments makes urinary flow turn sharply, thereby increasing the tendency of urinary flow to be turbulent in thin segments.

Conclusion of 1-4:

Based on the formula , Reynolds’ number of urinary flow in thin segments can be calculated as (in all calculations below, n stands for thin segments and k stands for the thick segment):

AND

 

 

 

 

SO:

IN SUMMARY:

As a result, it can be concluded that Reynolds’ number of urinary flow in thin segments (n) and subsequently the tendency of urinary flow to be turbulent is approximately 2 times the tendency in the thick segment (k).

(Note that in conditions where the maximum water reabsorption is not essential, the mean urine concentration difference between urine flow in thin and thick segments is much less than 2.7, subsequently    is increased).

 

Figure 2: Turbulent flow in comparison with laminar flow

Left: In laminar flow, molecules move just along the tubule, so small H2O molecules pass along the tubule’s pores. Laminar flow occurs in the thick segment of the loop of Henle. Right: In turbulent flow, molecules move crosswise as well as along the tubule, so small H2O molecules are more likely to be driven out through pores. Turbulent flow is more likely in the thin segment of the loop of Henle.

Application of STEP 1 conclusions in STEP 2:

In STEP 2, the water-pumping turbulence hypothesis states that turbulence in urine flow can result in an osmotic gradient in the medullary interstitial fluid, as well as the concentration of urine:

In turbulent flow different forces make molecules move in different directions. Some of these forces have the power to jet and drive small H2O molecules out of the urinary tubules through special pores called AQs. So, turbulence can pump H2O molecules into the interstitium (Figure 3).

Note that the thin ascending segment is relatively water-impermeable in comparison with the thin descending limb, which is highly water-permeable (1).

By these forces, small H2O molecules leave the thin descending limb and exit through the AQs, because the thin descending limb of the loop of Henle has so many AQs (19). Subsequent to passage of urine from the thin descending limb, urine is concentrated and the medullary interstitial fluid is diluted. This water leakage continues until the number of H2O molecules (which are driven out of the tubule because of the forces arising from turbulent flow in the thin segment) becomes equal to the number of H2O molecules which return to the thin segment (because of the osmolality difference between concentrated urinary flow and diluted interstitial fluid).

This excess water is reabsorbed by the peritubular capillaries and is continuously removed from the medulla.

Studies have revealed that the descending thin limb of the loop of Henle turning below the first upper millimeter has two different functional parts: the upper 40% expresses AQP-1, whereas the lower 60% does not (19). So, the leakage of water from the thin descending limb in the outer medulla is much more than the water leakage in the inner medulla. Thereby, in the outer medulla the equilibrium between H2O molecules which return to the thin segment (because of the osmolality difference) and H2O molecules which are driven out of the tubule (because of the forces arising from turbulent flow in the thin segment) is established in a lower osmolality of interstitial fluid compared to the inner medulla (note that AQP-1s in the upper 40% that is located in the outer medulla make the forces more effective for pumping the water to the interstitial fluid). It can be what is known as an axial osmotic gradient which is increased progressively from the cortico-medullary boundary to the inner medullary tip.

Subsequent to the withdrawal of water in the outer medulla, a hyperosmotic urine flows in the thin descending segment in the inner medulla. After that, urine enters the thin ascending segment and is diluted while nearing the outer medulla, by passive transportation of NaCl to the interstitium. Note that the thin ascending segment is water-impermeable. Then urine enters the thick ascending segment, where urine is more diluted by active transportation of ions from the tubule to the interstitium.

Supporting arguments and discussion:

So far mathematical models have failed to predict a significant role for the inner medulla in urine concentration (1). This failure could be from ignoring the forces arising from turbulent flow in the thin segments and acting as a water pump. These forces can drive H2O molecules out through the AQP-1s.

In comparison with the passive mechanism hypothesis, which is described in a stepwise fashion (4,5), the water-pumping turbulence hypothesis has a continuous, steady-state fashion and is more similar to the natural mechanisms. Also, the water-pumping turbulence hypothesis can identify what is happening in the inner medulla as well as in the outer medulla, while the counter-current multiplication of a single effect hypothesis can’t, because the single effect in the inner medulla has not been definitively identified (1).

Many observations are predictable and compatible with the water-pumping turbulence hypothesis. For example, Keye et al. showed that tachycardia is accompanied by a significant increase in urine output, independent of the plasma level or level of activity of hormones which can regulate water excretion and urine concentration (like arginine-vasopressin or renin) (20). This observation is compatible with the water-pumping turbulence hypothesis because tachycardia enhances the cardiac output and increases the volume of blood which enters the kidney and subsequently the volume of plasma which is filtered in Bowman’s capsule. Note that complete blood volume entering the kidney is made up of plasma that can be filtered and blood cells that can’t be filtered.

Hematocrit is a blood parameter that measures the percentage of the volume of whole blood that is made up of red blood cells. As normal hematocrit range is 37 to 48 percent for women and 42 to 52 percent for men (21), most of complete blood volume entering the kidney is made up of plasma (approximately 60%). As blood flows in the peritubular capillaries after filtration and after losing most of its plasma (which makes up most of its volume), urinary flow velocity in nephrons and subsequently in the loops of Henle is increased more than the blood flow velocity in the peritubular capillaries, while the volume of blood which enters the kidney is increased. So, blood flow (that plays the role of reabsorbant) is unable to reabsorb all of the water which leaks into the interstitium. In this condition, although H2O molecules are more likely to be driven out of the urinary tubules because of stronger forces arising from a more intensive turbulent urinary flow and a greater Reynolds’ number, all of these molecules can’t be reabsorbed by the peritubular capillaries and will return to the urinary tubules again. Therefore the final urine output of nephrons is watery and attenuate.

In other words, in spite of normal conditions, the equilibration between the number of H2O molecules which are driven out of the tubules and the number of H2O molecules which are reabsorbed by the peritubular capillaries is disturbed and peritubular capillaries are unable to reabsorb all of this excess water.

This is exactly what Lote and Snape concluded from their study: Collecting duct flow rate is an important determinant of final urine concentration, because the osmotic equilibration between urine and renal papilla is restricted by tubular flow rate (22). Different collecting duct flow rates were made by different rates of infusion of a hypotonic fluid over an infusion period of 4 hours. They measured urine concentration in the presence of an effectively constant high circulating level of antidiuretic hormone (resulting from exogenous infusion), because the concentration of fluid within the inner medullary collecting ducts (that makes the final urinary concentration) may be affected by the circulating level of antidiuretic hormone (22).

Lote and Snape’s findings can be explained based on the water-pumping turbulence hypothesis. In this hypothesis, eddy current throws small H2O molecules out of tubules through the AQP-1s. In normal conditions these H2O molecules will be reabsorbed by the peritubular capillaries. This process concentrates the inner tubular fluid. Increased tubular flow rate makes a more intensive turbulent urinary flow with a greater Reynolds’ number, which throws H2O molecules out even more than normal conditions, but can’t concentrate urine more than normal conditions because the capability of peritubular capillaries for reabsorption of these H2O molecules has not been increased to equal the turbulence water-pumping power. When the concentration of H2O molecules in the interstitium is increased, they will return to the urinary tubules again, because in this condition, while the inner tubular fluid loses its water, the power of osmotic pressure (which makes water return to the tubule) grows so that it can overcome the turbulent pump. As a consequence, collecting duct flow rate can be an important determinant of final urine concentration.

Following is a detailed explanation of Lote and Snape’s findings and what is expected by the water-pumping turbulence hypothesis:

a) Lote and Snape concluded that the rate and the extent of the increase in urine flow rate is related to the volume rate of infusion and is due almost entirely to an increase in free water clearance. This increased urine flow rate is accompanied by no change in osmolal clearance. In the water-pumping turbulence hypothesis, increased velocity of the fluid flowing in the nephrons decreases water reabsorption, without any changes in the osmolal clearance, and makes an attenuate urine.

b) Lote and Snape concluded that urine osmolality tends to decline toward a steady state. The rate and extent of the decline is related to the rate of infusion. Also the time course (the time that is taken for decreasing the interstitial fluid and final urine osmolality) is identical for every group with a different rate of infusion. In the water-pumping turbulence hypothesis, this time is taken for the turbulence pump to throw small H2O molecules out of tubules until peritubular capillaries become unable to reabsorb all of this excess water and H2O molecules will return to the urinary tubules and reduce urine osmolality.

c) Lote and Snape concluded that papillary and medullary interstitial fluid concentrations are progressively reduced at the higher rates of infusion. In the water-pumping turbulence hypothesis, as Reynolds’ number grows because of increased urine flow velocity in the higher rates of infusion, the turbulence pump achieves more power to throw small H2O molecules out of tubules through AQP-1s. So in the water-pumping turbulence hypothesis, the result of infusion with a higher rate is a progressive reduction in papillary and medullary interstitial fluid concentrations too.

d) Lote and Snape concluded that as urine flow velocity increases, there is a progressive reduction in the osmotic gradient between the final urine and the papillary tip. In the water-pumping turbulence hypothesis, as renal blood flow and subsequently urine flow velocity increases, the turbulence pump overcomes the blood flow of peritubular capillaries (which play the role of reabsorbant) and peritubular capillaries become unable to reabsorb all of the water which leaks into the interstitium. As a result, the osmotic gradient between the final urine and the papillary tip is reduced.

e) Lote and Snape concluded that the osmolality difference between the outer medulla and the papillary tip is decreased at the higher rates of infusion, largely owing to reduction in the papillary interstitial concentration. In the water-pumping turbulence hypothesis, turbulence is more probable and more intensive in thin segments that are located in the inner medulla. It reduces inner medullary interstitial fluid concentration more than outer medullary interstitial fluid concentration, so the axial osmotic gradient is reduced as renal blood flow and subsequently urine flow velocity increase.

As mentioned above, it can be stated that changes in urine concentration in this experiment are attributable to changed water excretion. From this experiment, it can be concluded that changes in water excretion (while the rate of infusion is increased) are almost entirely because of something happening in the inner medulla and papilla that reduces medullary interstitial fluid concentration, something that is more effective in the inner medulla than in the outer medulla. Since all of the factors are similar in the groups of this study (like the period of infusion, the osmolality of the infused fluid, the concentration of antidiuretic hormone, osmotic clearance, etc.), the findings can be attributed to the urine flow velocity because it is increased by a higher rate of infusion and is more increased in the inner medulla because the inner medulla contains the thin segments and urine flow velocity grows in the thin segments.

Conclusion

In summary, the water-pumping turbulence hypothesis explains that both the urinary concentrating and presence of an osmotic gradient in the renal medulla result from turbulent urine flow in the thin descending limb of the loop of Henle. In turbulent flow, molecules move crosswise as well as along the tubule, so small H2O molecules are more likely to be driven out through AQs. This concentrates urine. Turbulence in the thin segment results from a greater Reynolds’ number (the measure of the tendency for turbulence, calculated based on the velocity, density, and viscosity of urinary flow and tubule diameter). Since the thin descending limb has fewer AQs in the inner medulla than in the outer medulla (19), the inner medulla interstitium receives less water. This can establish an osmotic gradient.

Based on this hypothesis, turbulence can be present in both the thin descending and thin ascending limbs of the loop of Henle, but in the thin ascending limb, turbulence forces are not efficient and can’t throw H2O molecules out of the tubule, because the thin ascending segment is relatively water-impermeable in comparison to the thin descending limb that is highly water-permeable (1).

Finally, we need more experimental studies to examine if this hypothesis and its concluded rules can be applied in dialysis instruments, in order to make them more efficient and a better replacement for kidneys (for example, using tubules with different diameters in different segments, like the loop of Henle, in order to get desirable water excretion). H

Acknowledgements

I am very grateful to my family (my father, my mother, and my brother) for their valuable emotional, technical, and scientific support. I am very thankful to Parisa Khosravi for her kind help in proofreading.

Author declares no conflicts of interest.

________________________________________________________________________________

About the author

Niloufar Shabanikia is a student in the medical faculty of Isfahan University of Medical Sciences (IUMS). Her area of interest is physical systems of organs. She has been involved in several research projects and is a member of Isfahan Medical Student Research Committee (IMSRC).

References

  1. Sands JM, Layton HE. The Physiology of urinary concentration: an update. Seminars in Nephrology. 2009; 29(3):178-195.
    http://dx.doi.org/10.1016/j.semnephrol.2009.03.008
    PMid:19523568
  2. Kuhn W, Ryffel K. Herstellung konzentrierrter Losungen aus verdunnten durch blosse Membranwirkung: Ein Modellversuch zur Funktion der Niere. Hoppe-Seylers. Z Physiol Chem 1942; 276:145-178.
    http://dx.doi.org/10.1515/bchm2.1942.276.4-6.145
  3. de Rouffignac C. The urinary concentrating mechanism: A model of integrative physiology. Nephrol Dial Transplant. 2001; 16(11):2127-2130.
    http://dx.doi.org/10.1093/ndt/16.11.2127
  4. Kokko JP, Rector FC. Countercurrent multiplication system without active transport in inner medulla. Kidney Int. 1972; 2:214-223.
    http://dx.doi.org/10.1038/ki.1972.97
  5. Stephenson JL. Concentration of urine in a central core model of the renal counterflow system. Kidney Int. 1972; 2:85-94.
    http://dx.doi.org/10.1038/ki.1972.75
    PMid:4671532
  6. Chou CL, Knepper MA, Layton HE. Urinary concentrating mechanism: the role of the inner medulla. Semin. Nephrol. 1993; 13:168-181.
  7. Knepper MA, Chou CL, Layton HE. How is urine concentrated by the renal inner medulla? Contrib. Nephrol. 1993; 102:144-160.
  8. Knepper MA, Saidel GM, Hascall VC, Dwyer T. Concentration of solutes in the renal inner medulla: interstitial hyaluronan as a mechano-osmotic transducer. Am J Physiol Renal Physiol. 2003; 284:F433-F446.
    PMid:12556362
  9. Layton HE, Knepper MA, Chou CL. Permeability criteria for effective function of passive countercurrent multiplier. Am J Physiol Renal Physiol. 1996; 270:F9-F20.
  10. Moore LC, Marsh DJ. How descending limb of Henle’s loop permeability affects hypertonic urine formation. Am J Physiol Renal Physiol. 1980; 239: F57-F71.
  11. WexlerAS, Kalaba RE, Marsh DJ. Passive, one-dimensional countercurrent models do not simulate hypertonic urine formation. Am J Physiol Renal Physiol. 1987; 253:F1020-F1030.
  12. Guyton AC, Hall JE. Guyton and Hall textbook of medical physiology, 11th edition. Philadelphia: Elsevier Saunders; 2006; p 165-166.
  13. Junqueira LC, Carneiro J. Basic Histology: Text & Atlas (Junqueira’s Basic Histology), 11th edition. USA: McGraw-Hill Companies; 2005. Available at:   http://www.engineeringtoolbox.com/sodium-chloride-water-d_1187.html Accessed May 17, 2012.
  14. Rhoades RA, Bell DR. Medical Physiology: Principles for Clinical Medicine (MEDICAL PHYSIOLOGY (RHOADES)) 3rd edition. China: Lippincott Williams & Wilkins, a Wwolterskluwer business; 2009; Part VI, chapter 22.
  15. Kokko JP. Sodium chloride and water transport in the descending limb of Henle. J Clin Invest. 1970; 49:1838-1846.
    http://dx.doi.org/10.1172/JCI106401
    PMid:5460286PMCid:PMC322672
  16. Guyton AC, Hall JE. Guyton and Hall textbook of medical physiology, 11th edition. Philadelphia: Elsevier Saunders; 2006: p 335.
  17. Kwak HT, Zhang G, Chen S. The effect of salt type and salinity on formation water viscosity and NMR responses. In: Int Symp Society Core Analysts: Toronto, Canada; 21-25 August 2005, 1-13.
  18. Pannabecker TL, Dantzler WH, Layton HE, Layton AT. Role of three-dimensional architecture in the urine concentrating mechanism of the rat renal inner medulla. Am J Physiol Renal Physiol. 2008; 295(5):F1271-F1285
    http://dx.doi.org/10.1152/ajprenal.90252.2008
  19. Kaye GC, Bayliss P, Lowry PJ, Drury PL, Camm AJ. Effect of induced supraventricular tachycardias on changes in urine output and plasma hormone levels in man. ClinSci (Lond). 1992; 82(1):33-37.
  20. Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Normal reference laboratory values. N Engl J Med. 1992; 327(10):718-724.
  21. Lote CJ, Snape BM. Collecting duct flow rate as a determinant of equilibration between urine and renal papilla in the rat in the presence of a maximal antidiuretic hormone concentration. J Physiol. 1977; 270(2):533-544.
    PMCid:PMC1353528

Share your thoughts



Leave a Reply

You must be logged in to post a comment.