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Renal Exam > Tubular Transport > Flashcards

Tubular Transport Flashcards

1
Q

tight junctions

A

*composed mostly of zona occludens
*variable barrier to passive diffusion
*separates luminal from basolateral membrane segments

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2
Q

solute transport - key concepts

A

*transcellular reabsorption or secretion is mediated by protein carriers or ion channels to allow passage through lipid bilayer cell membrane
*basolateral Na+/K+ ATPase pump (3 Na+ out, 2 K+ in) maintains low Na+ and electronegative charge inside the cell
*Na+ enters the cell down a favorable gradient via a variety of mechanisms at different nephron sites
*tubular SECRETION happens via similar mechanisms, in reverse

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3
Q

solute transport - key sodium transporters

A
  1. proximal tubule:
    -Na+ cotransporters with glucose, phosphate, and amino acids
    -Na+/H+ antiporter
  2. Loop of Henle:
    -Na+/K+/2Cl- cotransporter
  3. distal tubule:
    -Na+/Cl- cotransporter
  4. collecting tubule:
    -epithelial Na+ channel (ENaC)
    -ROMK K+ channel
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4
Q

glomerulus functions (overview)

A

*forms ultrafiltrate

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5
Q

proximal tubule functions (overview)

A

*reabsorbs majority of filtered NaCl/water
*reabsorbs majority of filtered bicarbonate
*site of ammonia production
*reabsorbs almost all filtered glucose and amino acids
*reabsorbs K, phosphate, calcium, magnesium, urea, and uric acid
*secrete organic anions (urate) and cations (protein-bound drugs)

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6
Q

loop of henle functions (overview)

A

*reabsorbs additional filtered NaCl
*counter current multiplier as NaCl is absorbed in excess of water
*magnesium excretion

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7
Q

distal convoluted tubule functions (overview)

A

*reabsorbs a small fraction of filtered NaCl
*active regulation of calcium excretion

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8
Q

connecting segments and cortical collecting tubule functions (overview)

A

*principal cells: reabsorb Na/Cl and secrete K (aldosterone)
*intercalated cells: secrete H+, reabsorb K, secrete bicarbonate in metabolic alkalosis
*reabsorb water (ADH)

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9
Q

medullary collecting tubule functions (overview)

A

*site of final modification of urine
*reabsorb Na/Cl
*reabsorb water (ADH) and urea, causing a dilute or concentrated urine to be excreted
*secrete H+ and NH3; urine pH can be lowered to 4.5-5
*reabsorption or secretion of K

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10
Q

early PCT (first aid)

A

*contains brush border
*reabsorbs all glucose & amino acids and most HCO3-, Na+, Cl-, PO43-, K+, H2O, and uric acid
*isotonic absorption
*generates and secretes NH3, which enables the kidney to excrete (via secretion) more H+

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11
Q

PTH and early PCT (first aid)

A

*PTH (parathyroid hormone) inhibits Na+/PO43- cotransport → increased excretion of PO43-

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12
Q

Angiotensin II & early PCT (first aid)

A

*Ang II stimulates Na+/H+ exchange → increased Na+, H2O, and HCO3- reabsorption (permitting contraction alkalosis)

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13
Q

diuretics & early PCT

A

*acetazolamide: blocks CA (carbonic anhydrase)
*SGLT2 inhibitors: block SGLT2

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14
Q

early PCT: Na+/H+ antiporter

A

*directly promotes bicarb reabsorption
*Ang II and NE increase activity of the exchanges (these increase in response to volume depletion)

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15
Q

glucose transport in PCT

A

*2 cotransporters:
-SGLT1: high affinity, low capacity
-SGLT2: low affinity, high capacity
*transport maximum: concentration above which tubule can no longer completely reabsorb glucose (occurs when plasma glucose ~ 300 mg/dL; results in excretion of glucose in urine)

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16
Q

urea transport

A

*reabsorption of water in proximal segments results in gradually increasing urea concentrations in the tubule, favoring passive reabsorption further down the road

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17
Q

Fanconi syndrome

A

*generalized reabsorption defect in PCT
*a clinical condition marked by urinary losses of molecules normally reclaimed by the PCT (proximal tubule):
-phosphaturia, amino aciduria, uric aciduria, glycosuria
*can be caused by a variety of diseases that damage proximal tubular cells (ex. multiple myeloma)

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18
Q

secretory pathways of organic cations in the PCT

A

*endogenous: creatinine
*exogenous: cimetidine, trimethoprim, quinidine
*enter the cell via the Organic cation transporter 1 (OCT1)

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19
Q

secretory pathways of organic anions in the PCT

A

*endogenous: urate, hippurate, ketoacids
*exogenous: PAH, penicillin, cephalosporins, salicylates, diuretics, radiocontrast media
*transported through the organic anion transporter 1 (OAT1)

20
Q

ammoniagenesis in the PCT

A

*ammonia is produced in the proximal tubule
*key factor in acid secretion
*glutamine → alpha-keto gluturate & ammonia (NH3)
*NH3 + H+ → NH4+ (ammonium)
*NH4+ can be excreted from the cell

21
Q

cortical vs. cortico-medullary nephrons

A

*based on the length of the loop of Henle
*outer cortical nephrons have no thin ascending limb

22
Q

descending loop of Henle (first aid)

A

*thin, WATER PERMEABLE
*passively reabsorbs H2O via medullary hypertonicity (impermeable to Na+)
*concentrating segment
*makes urine hypertonic

23
Q

ascending loop of Henle (first aid)

A

*thick, NaCl permeable
*reabsorbs Na+, K+, and Cl- via NKCC channel
*indirectly induces paracellular reabsorption of Mg2+ and Ca2+ through positive lumen potential generated by K+ backleak
*impermeable to H2O
*makes urine less concentrated as it ascends

24
Q

Loop of Henle - general functions

A

*descending limb = water permeable
*ascending limb = NaCl permeable
*concentrates filtrate in loop as it goes down
*allows for efficient passive NaCl reabsorption as it ascnends
*NaCl contributes to gradient
*gradient assists with maximal urine concentration later in the collecting duct

25
Q

countercurrent multiplier in the loop of henle

A

*allows for maximum urine concentration in the collecting duct
*water can be reabsorbed efficiently due to high gradient
*in the collecting duct: ADH required for water reabsorption even though there is a high gradient

26
Q

sodium transport in the thick ascending limb of the loop of Henle

A

*Na+/K+/2Cl- cotransporter allows influx (reabsorption) of sodium, potassium, and chloride into the cells
*potassium leaks back out via a potassium channel
*site of loop diuretic action

27
Q

calcium handling in the thick ascending limb

A

*potassium leaking out of the cell results in a slight electropositive charge
*this charge is used to transport calcium down the gradient para-cellularly

*high calcium detected by CaSR (calcium-sensing receptor) and inhibits the NaK2Cl channel to stop the reabsorption of calcium

28
Q

Bartter’s syndrome

A

*mutations resulting in defective NKCC (Na+/K+/2Cl- cotransporter in loop of Henle)
*phenotype: child with hypokalemia, volume depletion (with low BP), hypercalciuria, and metabolic acidosis

presents similarly to chronic LOOP diuretic use: metabolic alkalosis + hypokalemia + hypercalciuria (loops LOSE calcium in the urine

29
Q

early DCT (first aid)

A

*reabsorbs Na+ , Cl- (via Na+/Cl- cotransporter)
*impermeable to water
*makes urine fully dilute (hypotonic)
*site of action of thiazide diuretics

30
Q

antidiuretic hormone (ADH)

A

*ADH is made in the hypothalamus & stored in the posterior pituitary
*released in response to blood hypovolemia & hypertonicity
*ADH binds V2 receptors and causes increase in insertion of aquaporins in the cortical collecting duct, which function exclusively as water transporters, in the luminal membrane

31
Q

water reabsorption (antidiuresis) in the cortical collecting duct - ADH active

A

*active NaCl transport in thick ascending loop
*ADH allows for passive water diffusion down the steep gradient (aquaporins inserted)
*osmolality of urine INCREASES

32
Q

water excretion (diuresis) in the cortical collecting duct - ADH absent

A

*active NaCl transport in thick ascending loop
*more NaCl absorption in DCT
*no ADH, so no water movement in collecting ducts
*osmolality of urine DECREASES

33
Q

role of urea in the medullary gradient

A

*ADH helps urea concentrate in tubule
*high urea gradient promotes absorption
*if ADH has been absent, urea gradient dissipates

34
Q

when the body needs to conserve water, what response occurs in the kidney?

A

*ADH production increases → the cortical collecting duct reabsorbs more water, producing a concentrated urine

35
Q

diuretics & DCT

A

*thiazide diuretics: inhibit Na+/Cl+ co-transporter in DCT

36
Q

calcium handling in the DCT

A

*major site of active calcium transport
*PTH and calcitriol increase calcium reabsorption here
*NaCl channel activity separate, but inhibition of this channel increases calcium reabsorption
*thiazide diuretics thus increase calcium reabsorption

recall: loops lose calcium, so thiazides retain calcium

37
Q

Gitelman’s Syndrome

A

*mutations resulting in defective NaCl cotransporter in DCT (acts like a thiazide diuretic)
*phenotype: young adult with hypokalemia, hypomagnesemia, metabolic alkalosis, hypocalciuria

38
Q

familial hyperkalemic hypertension (FHH)

A

*an activating mutation of NaCl channel
*sx: hypertension, hyperkalemia, metabolic acidosis, normal kidney function
*cause: inherited defect of kinases in DCT that control turning off NaCl channel; defect prevents ability to turn off, so constitutively activated
*result: increase in NaCl absorption → volume expansion, suppression of RAAS, decrease in delivery of Na+ and Cl- to collecting duct, and decrease in K+ secretion
*treatment: thiazide diuretic

39
Q

principal cells in cortical collecting tubule

A

*primary site of K+ excretion
*electrogenic Na+ transport via ENaC (epithelial sodium channel)
*creates an electronegative gradient in the lumen, which favors K+ excretion through ROMK channels
*aldosterone binds to mineralocorticoid receptor (MR) intracellularly, where it:
-increases # of ENaC and probability of being open
-increases # of ROMK

40
Q

diuretics & cortical collecting tubule

A

*potassium sparing diuretics
*examples: spironolactone, amiloride, triamterene

41
Q

Liddle’s Syndrome

A

*constitutive activation of the ENaC channels (gain-of-function of ENaC) in he cortical collecting duct
*results in:
-excessive Na+ reabsorption
-excessive K+ excretion
*phenotype: HTN, low renin/aldosterone, hypokalemia, metabolic alkalosis

42
Q

intercalated cells type A (alpha) in cortical collecting tubule

A

*main job = acid handling
*excrete H+
*can also reabsorb K+ in response to hypokalemia

43
Q

intercalated cells type B (beta) in cortical collecting tubule

A

*shows reverse polarity of alpha type
*excrete bicarbonate

44
Q

medullary collecting tubule

A

*main job is to fine tune NaCl, H+, and water absorption
*amiloride sensitive Na+ channel
*aldosterone sensitive
*in volume expansion: ANP causes natriuresis
*water: ADH responsive
*highly permeable to urea

45
Q

renal pelvis, ureters, and bladder

A

*renal pelvis is modestly permeable to urea and water
*urea may move from pelvis to medulla, water opposite direction
*changes of 7-15% in urine composition can occur in ureters and bladder, depending on flow state/contact time

Renal Exam (44 decks)

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