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KBF- Kidney and Body Fluids > S2: Structure and Function of a Renal Tubule > Flashcards

S2: Structure and Function of a Renal Tubule Flashcards

1
Q

Compare glomerular filtrate

A

It is the same composition as plasma except it contains no cells and very little protein (GF is a ultrafiltrate of the plasma)

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2
Q

Briefly explain modification of glomerular filtrate

A
  • Filtration occurs at glomerulus which is relatively non selective.
  • Modification of the filtrate occurs along the renal tubule where re-absorption and secretion of water and various solutes occurs and this changes the composition of the filtrate.
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3
Q

What is reabsorption?

A

It is movement from the tubular lumen into the peritubular capillary/interstitial fluid. Wanted substances are reabsorbed.

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4
Q

What is secretion?

A

Movement from the peritubular capillary plasma into the tubular lumen

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5
Q

What is excretion?

A

The clearance of unwanted substances in the urine through the tubule.
A substance can enter into the tubule and be excreted by being filtered through at the glomerulus or by being secreted in the tubule.

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6
Q

Explain the structure of a renal tubule and how this allows reabsorption and secretion

A
  • The tubular lumen is surrounded by tubular epithelial cells. There are tight junctions between adjacent cells.
  • Between the cells is interstitial fluid and also between the peritubular capillaries and tubule although this is sometimes called the peritubular fluid
  • The apical/luminal membrane faces the lumen
  • The basolateral membrane towards the blood

For a substance to be reabsorbed it must first cross the luminal membrane – diffuse through the cytosol – across the basolateral membrane and into the blood (transcellular transport). Vice versa for secretion.

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7
Q

What physiological processes are involved in reabsorption and secretion?

A
  • Active transfer/ Primary active transport (often against electrochemical gradient as well as conc)
  • Passive transfer ( can be a cosequence of AT due to AT concentrating a component to due active removal)
  • Co transport/Secondary (One substance down conc, one substance against conc - requires either a symport or antiport)
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8
Q

Explain Na+ and Glucose reabsorption

A

Na+ is freely filtered at the glomerular capillaries so is at much higher concentration in glomerular filtrate than in the tubular cells. It therefore passively moves down its concentration gradient into the tubular cell, aided by electrochemical gradient.

As it moves down through the symport protein, it generates energy to transport glucose. Glucose is lower in the tubular fluid than it is in the cell so it is taken up against its concentration gradient through symporter SGLT2 (similar to SGLT1 in small intestine responsible for glucose and galactose).

As glucose builds up in the cell, it can move passively by facilitated diffusion into the peritubular capillaries through GLUT-2 transporter.

To prevent the concentration of intracellular Na+ equilibrating with extracellular Na+ (this would stop glucose and Na+ transport) , we have the 2Na+/2K+ ATPase pump on the basolateral membrane pumping Na+ into the blood keeping the concentration in the cell low.

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9
Q

What causes familial renal glycosuria?

A

Mutations of the genes coding for SGLT2 symporter.

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10
Q

What can SGLT2 inhibitors be used to treat?

A

Diabetes

This is helpful because it just dumps out a lot of the excess glucose, rather than reabsorbing it.

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11
Q

What mode of transport is glucose and Na+ reabsorbed by?

A

Transcellular mode of transport

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12
Q

What other molecules (apart from glucose) are transported along with Na+?

A 
Amino acids (symporter)
 H+ (antiporter)
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13
Q

What are the 3 techniques to investigate tubular function?

A
  1. Clearance studies
  2. Micropucture and isolated perfused tubule
  3. Electrophysiological analysis + Patch clamping
1 = humans
2+3 = lab animals
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14
Q

Describe micropuncture (human technique to investigate tubular function)

A

It is direct sampling of tubular fluid in different parts of the nephron

  1. Puncture
  2. Inject viscous oil
  3. Inject fluid for study
  4. Sample and Analyse
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15
Q

Describe electrical potential and patch clamping (animal technique to investigate tubular function)

A

ELECTRICAL POTENTIAL:

  • Micropipette inserted into cell
  • Combine with microperfusion to alter potential difference (PD) across whole cell epithelium
  • Measure whether ion moving with or against electrochemical gradient

PATCH CLAMPING:
- Insert microelectrode through membrane , a blunt tip pipette is pressed against the cell
- Current flow through individual ion channel measured
- Measure electrical resistance: across patch of cell membrane and changes when channel open/close
Types of channels and response to drugs and hormones

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16
Q

List the 7 segments of the tubule

A
  1. Proximal convoluted tubule (PCT)
    1. Thin descending limb, loop of Henle
    2. Thin ascending limb, LoH
    3. Thick ascending limb, LoH
    4. Distal convoluted tubule (DCT)
    5. Collecting/Connecting tubule
      7.
      Medullary collecting duct
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17
Q

What are the two types of nephron?

A
  1. Cortical nephrons (85%) have short LoH that just passes the corticomedullary junction but does not extend into the medulla
  2. Juxta-medullary (15%) have a very long LoH goes deep into the medulla. These nephrons are involved in concentrating urine.
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18
Q

How is the vascular system for cortical and juxa-medullary nephron different?

A
  • The cortical nephrons have them intwined all across the tubule apart from LoH (extensive network of capilaries).
    In the juxta-medullary ones, the capillary tubules are in a pattern of vasa recta.
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19
Q

What are the special cellular characteristics of PCT and how do they aid function?

A

PCT is designed for reabsorption

  • Large number of transporters
  • Large number of mitochondria for AT
  • Extensive brush border on luminal side - large surface area for rapid exchange
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20
Q

How are protein reabsorbed at PCT?

A

Glomerular filtrate is protein free but some small proteins do get through, these proteins are taken up by endocytosis into the tubular cells and are degraded by lysosomal enzymes into amino acids and simple sugars which can then be reabsorbed into plasma.

21
Q

What is reabsorbed at PCT?

A

The majority of substances that we would want to keep in the blood are reabsorbed here, driven by the Na+/K+ ATPase pump on the basolateral membrane. So you get a lot of the glucose, amino acids and certain ions moving across. As a result a fair amount of water follows Na+ by osmosis and moves out of the tubule into the blood.

By the end of the PCT, essentially all of the glucose and AA and most of the HCO3- has been reabsorbed.

22
Q

What is Fanconi’s syndrome?

A

A condition where all PCT reabsorptive mechanisms are defective so subtances e.g. glucose, AA are detected in urine.

23
Q

Explain the structure of the thin descending limb, thin ascending limb and thick ascending limb

A

Thin descending limb and thin ascending limb

  • Thin epithelial cells
  • No brush border
  • Few mitochondria
  • Low metabolic activity

Thick ascending limb

  • Thick epithelial cells
  • Extensive intracellular folding
  • Few microvilli
  • Many mitochondria]
  • High metabolic activity
  • Virtually impermeable to water and actively pumps out Na+ and Cl-
24
Q

What is the role of LoH?

A

The LoH has a critical role in concentrating/diluting urine and it does this by adjusting the rate of water reabsorption.

The descending limb is very permeable to water, while the ascending limb is virtually impermeable to water.
These characteristics of the LoH result in it creating an osmotic gradient, with the osmolality being very high in the medulla (it is hypertonic).
The collecting duct also transverses the medulla, the urine gets even more concentrated as water moves out by osmosis.

25
Q

What is the role of loop diuretics e.g. furosemide at thick ascending limb?

A

Loop diuretics act here causing 20% of filtered Na to be excreted in urine, by blocking Na-transport out of LoH.

26
Q

What is counter current flow?

A

One of the first most important things about the LoH is the parallel arrangement of the limbs. As the tubular fluid moves down in the descending limb, it is moving up in the other, this is the countercurrent flow

27
Q

Explain how the LoH makes the tubular fluid hypoosmotic to plasma

A

On the thick ascending limb, NaCl is pumped out of tubular fluid into the interstitial fluid between two limbs. It is impermeable to water so water doesn’t move out of the limb, so as the solute build up in interstitium as you move down it, it becomes hyperosmotic.

There is an hyperosmotic gradient between medulla and tubular fluid so as fluid enters the descending limb its osmolality is roughly the same as plasma. As it moves down, water starts to leave and tubular fluid starts becoming hyperosmolar.

As the fluid moves up, water is trapped within as this part is impermeable to water. As a result the osmolality of the tubular fluid starts to change and it becomes more dilute, hypoosmotic as NaCl is pumped out.

So when tubular fluid leaves the LoH it is quite hypo-osmotic i.e. it is more diluted than plasma.

28
Q

What happens at thick ascending LoH?

How does it contribute to the osmotic gradient between the tubule and interstitial space?

A
  • Thick ascending limb reabsorbs approx 25% filtered Na+
  • Na+ enters tubular cell from lumen via Na+/2Cl-/K+ symporter. On the basolateral side, Na+/K+ ATPase pump moves Na+ to peritubular capillary and K+ into cell. here, K+ and Cl- diffuse passively out.
    Together, the Na+/2Cl-/K+ all contribute to the osmotic gradient between the tubule and interstitial space.
29
Q

How does loop diuretics affect Na+/2Cl-/K+ symporter at thick ascending LoH?

A

The loop diuretics work at the symporter, inhibiting it so that these ions cannot be reabsorbed and transferred into the peritubular space. Therefore they prevent the generation of the medullary osmotic gradient.
Without a concentrated medulla, water will have less of a driving force out of the collecting duct system, resulting in increased water excretion and urine production.

30
Q

What is the medullary osmotic gradient maintained by?

A

The answer is the vasa recta. These also flow in a counter-current, in an opposite direction to the tubular fluid flow

  • VR freely permeable to solutes and H2O
    As the vasa recta descends into the renal medulla, passing the ascending LoH, water diffuses out into the interstitial space and salts diffuse into the vasa recta.
    As the vasa recta ascends, the reverse occurs and water moves into the vasa recta and salts move out into the interstitial space.
31
Q

Why is blood flow in the vasa recta slow?

A

This minimises solute loss from the intersitium and maintains medullary interstitial gradient. It is also slow enough to provide nutrients and O2 to the cell of LoH

An alteration in blood flow in the VR can change the gradient.

32
Q

Describe the macula densa

A
  • Found in first part of DCT
  • Specialised cell in contact with afferent and efferent arteriole and linked to the juxtaglomerular complex

The macula densa allows communication of what is going on in the lower part of the tubule to the GFR and tubular fluid flow allowing feedback control

33
Q

What is the connecting tubule?

A

This connects the end of the DCT to the collecting duct, it is mainly in the outer cortex and it is very similar in its functional characteristics to the 2nd part of the DCT.

34
Q

Functions of DCT

A
  • No water reabsorption but solute reabsorption occurs so there is high Na+/K+ ATPase activity
  • Low H2O permeability hence further dilution of tubular fluid (solutes move out)
  • ADH can increase permeability to H2O
  • DCT also has an important role in acid base balance via secretion of NH3
35
Q

What are the two cells in the collecting duct?

A

Collecting duct is made out of cuboidal epithelia and there are few mitochondria.

  1. Intercalated cells which are involved in acidification of urine and acid-base balance
  2. Principle cells which have a role in Na+ balance and ECF volume regulation
36
Q

Describe collecting duct

Include function

A

The collecting duct is the final site for processing urine

  • Made very permeable to H2O by ADH
  • Permeable to urea
  • These factors contribute to the counter-current mechanism. (H2O can move out due to the high medullary osmolality)
37
Q

What is the collecting duct divided into?

A

The collecting duct is divided into the cortical collecting duct and the medullary collecting duct based on location

38
Q

Explain effect of ADH on collecting duct

A
  • ADH is secreted from posterior pituitary when triggered by an increase in plasma osmolarity sensed by osmoreceptors in
  • ASH binds to receptors AVP-2 on collecting ducts
  • Gs - cAMP - PKA
  • Increased synthesis and insertion of aquaporin onto the luminal surface of cells
  • Water moves out through pore to be reabsorbed into blood
39
Q

Explain Urea Metabolism

A

The majority of urea is removed from the body via urine but a small amount is reabsorbed into the circulation. This is because it contributes to the medullary-interstital osmotic gradient.

The medullary collecting duct is permeable to urea, so as water is reabsorbed into blood from the collecting duct (e.g. in presence of ADH), urea gets concentrated in it and so will start to move out. It moves out into both surrounding capillaries and the interstitum of the medulla where it contributes to the osmotic gradient around the LoH.

40
Q

How are urea levels monitored?

A

Clinically it is useful to know about urea levels in kidney as they tell us about kidney state

Urea levels are monitored using BUN (blood urea nitrogen) test

41
Q

What is the osmolarity of tubular fluid that enters collecting duct?

A

The tubular fluid that enters into the CD system is always hypo-osmotic (i.e. more dilute than blood)

42
Q

How is urine concentration and volume affected by water deprivation?

A
  • ADH increases
  • Increased water reabsorption
  • Increase Urea reabsorption contributing to medullary-intersitial conc. gradient
  • NaCl is reabosorped into ISF
  • Final urine volume is small and concentrated
43
Q

How is urine concentration and volume affected by water deprivation?

A
  • ADH increases
  • Increased water reabsorption
  • Increase Urea reabsorption contributing to medullary-intersitial conc. gradient
  • NaCl is reabosorped into ISF
  • Final urine volume is small and concentrated
44
Q

How is urine concentration and volume affected by excess water?

A

Alternatively in the absence of ADH, the CD becomes virtually impermeable to water and urea, Na+ reabsorption still continues in the CD (into ISF) and so tubular fluid becomes more dilute in this progress. Water is retained and excreted out.
Therefore, we will end up producing very large urine volume of low osmolality, as low as 50Osm/L (very hypo-osmotic)

45
Q

What is PKD - Polycystic kidney disease?

A

Genetic disorder characterised by growth of numerous cysts in the kidney

46
Q

What is glomerulonephritis?

A

This is inflammation of glomeruli or some or all of the million nephrons in the kidney. It can be primary, or could be secondary to systemic disease such as diabetes mellitus.

47
Q

List some diseases of tubules

A
  • There could be obstruction of them, which would reduce glomerular filtration
    Or there could be impairment of transport functions (reducing water and solute reabsorption), e.g. Fanconi’s syndrome
48
Q

List some acquired kidney diseases

A

Hypertension
- The kidneys regulate ECF volume and hence influence blood pressure

Congestive Cardiac Failure
- A fall in CO, can lead to renal hypoperfusion, registred as hypovolemia and the kidneys compensation for this results in pulmonary odema

Diabetic nephropathy
- As a consequence of diabetes, the filtering system of the kidneys gets destroyed over time

Lithium treatment (often in past used for bipolar disorder)
- has a side effect of acquired nephrogenic diabetes insipidus (due to reduced expression of aquaporin receptor 2 expression.

KBF- Kidney and Body Fluids (14 decks)

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