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Renal > Renal Physiology 3 > Flashcards

Renal Physiology 3 Flashcards

1
Q

How does chloride typically move in relation to sodium in the nephron?

A

chloride is the principal extracellular anion, dictates tonicity with sodium

Sodium and chloride usually move in parallel and to the same degree - if changes in plasma chloride are opposite to those of sodium or disproportionate in magnitude, an acid base disorder is probable

unless specifically indicated, assume sodium movement means NaCl movement

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2
Q

what effect does metabolic acidosis have on chloride levels?

A

Hyperchloremia can be induced as a compensatory mechanism during metabolic acidosis (normal anion gap)

Cl- is retained to balance the HCO3- that is lost (negative charge for a negative charge)

notice that buffering of H+ (HCl) by HCO3- (NaHCO3) retains the negative charge via Cl- (NaCl):

HCl + NaHCO3 —> H2CO3 + NaCl

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3
Q

what is the effect of alpha versus beta adrenoceptor activation by norepinephrine in the nephron?

A

NE binds beta1 in JG apparatus —> renin secretion and RAAS activation

NE binds alpha within tubule epithelium —> activation of Na+/H+ exchangers and Na+/K+ ATPases

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4
Q

the majority of K+ is reabsorbed in which compartment of the nephron? How does this reabsorption occur?

A

most K+ reabsorbed in proximal tubule via 1. passive reabsorption through paracellular junctions and 2. active reabsorption through basolateral K+ pumps/channels

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5
Q

what 2 factors regulate K+ secretion in the cortical collecting tubule (CCT)?

A
  1. principal cells secrete K+ due to favorable electrochemical gradient, established by lumen-negative transepithelial voltage (Na+ reabsorbed more rapidly than Cl-)
  2. increased flow causes decrease in luminal [K+], creating favorable gradient for K+ secretion
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6
Q

what channels are responsible for K+ secretion in the cortical collecting tubules (CCT)?

A

apical:
1. ROMK2
2. K+/Cl- symporters

basolateral:
3. K+ channels
4. Na+/K+ ATPases

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7
Q

which cells in the cortical collecting tubules (CCT) mediate K+ secretion and reabsorption, respectively?

A

principal cells - secrete K+

intercalated cells - reabsorb K+

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8
Q

what happens to K+ levels during episodes of volume hyponatremia or volume reduction?

A

usually, the trade-off for aldosterone-dependent Na+ reabsorption is K+ secretion within the ASDN (aldosterone-sensitive distal nephron)

during volume hyponatremia or volume reduction, RAAS is activation —> decreased GFR/ luminal flow

this triggers Na+ reabsorption, but actually decreases K+ secretion because the influence of low luminal flow (dampening K+ secretion) is greater than that of aldosterone (promoting K+ secretion)

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9
Q

explain how HCO3- is reclaimed for reabsorption in the nephron (5 steps)

A
  1. filtered HCO3- reacts with carbonic anhydrase type IV (CAIV), which causes its dissociation into OH- and CO2
    2a. CO2 rapidly diffuses into epithelium
    2b. luminal OH- reacts with secreted H+ to form H2O
  2. H2O rapidly diffuses into tubule epithelium and dissociates into H+ and OH-
  3. CA type II catalyzes formation of HCO3- from OH- and CO2
  4. HCO3- is reabsorbed into interstitium and back into circulation
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10
Q

which two forms of carbonic anhydrase are required in the process of HCO- reclamation? what do they do?

A
  1. filtered HCO3- reacts with carbonic anhydrase type IV (CAIV), which causes its dissociation into OH- and CO2
    2a. CO2 rapidly diffuses into epithelium
    2b. luminal OH- reacts with secreted H+ to form H2O
  2. H2O rapidly diffuses into tubule epithelium and dissociates into H+ and OH-
  3. CA type II catalyzes formation of HCO3- from OH- and CO2
  4. HCO3- is reabsorbed into interstitium and back into circulation
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11
Q

what is the mechanism by which H+ is buffered in the distal nephron? (4 steps)

A
  1. H+ combines with ammonia (NH3, byproduct of glutamine metabolism) to produce ammonium (NH4+)
  2. NH4+ travels to thick ascending limb where it is reabsorbed (competes for K+ binding site on NKCC)
  3. within tubule epithelium, NH4+ dissociates into NH3 and H+
  4. NH3 freely diffuses into renal medullary interstitium - some returns to proximal tubule (area of low concentration) to buffer more H+, some goes to collecting tubule to combine with secreted H+ there (this NH4+ is excreted to reduce acid load)
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12
Q

how do the kidneys respond to a high alkaline load (such as loss of H+ via severe vomiting or ingestion of an alkali)?

A

renal response is not to increase HCO3- excretion but to lower excretion of titratable acid and NH4+

recall NH4+ and H2PO4- are used to generate HCO3- for reabsorption - by dampening urinary acid excretion, the renal system effectively suppresses HCO3- reclamation

over time this allows products of endogenous basal acid production to lower blood pH

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13
Q

explain these statements:
a. metabolic alkalosis and hypokalemia are often coupled
b. metabolic acidosis and hyperkalemia are often coupled

A

a. hypokalemia (such as by increased K+ excretion) promotes renal H+ secretion… because the trade-off for H+ secretion is generation of reclaimed HCO3-, hypokalemia may induce metabolic alkalosis

b. acidosis causes an increase in extracellular K+ as it swaps places with H+ that is following its concentration gradient into cells (to maintain electroneutrality) - but K+ secretion is decreased because hyperkalemia suppresses H+ secretion within the renal tubules (it’s a charge thing), so acidosis and hyperkalemia are coupled

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14
Q

what is the effect of aldosterone on the principal cells vs intercalated cells in the distal nephron?

A

principal cells - aldosterone induces Na+ reabsorption to create a lumen-negative potential to drive H+ secretion

intercalated cells - aldosterone stimulates H+/K+ exchanger and H+ ATPase which both mediate H+ secretion

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15
Q

how is urine anion gap calculated?

A

urine anion gap (UAG) =
U(Na+) + U(K+) - U(Cl-)

because Na+ and K+ are major urinary cations and Cl- is major urinary anion

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16
Q

how is urine [Cl-] affected by metabolic acidosis caused by diarrhea vs that caused by renal dysfunction?

A

in metabolic acidosis caused by diarrhea (normal AG metabolic acidosis due to GI loss of HCO3-), kidneys respond to low pH by excreting H+ in the form of NH4+ (distal acidification)… urine [Cl-] is high because it is excreted as well to maintain electroneutrality (as NH4Cl)

in renal dysfunction, H+ cannot be effectively secreted, so urine [Cl-] is low

17
Q

describe the process of urea recycling, and the transporters involved in the nephron

A
  1. urea generated from NH4+ (via amino acid metabolism)
  2. about half reabsorbed in PCT
  3. secreted via UT2 transporter in thin descending and ascending limbs
  4. reabsorbed via UT1 and UT4 in collecting ducts

urea is freely filtered/reabsorbed/secreted, but it is trapped in medullary interstitium, where it maintains hyperosmotic gradient (important for formation of concentrated urine)

18
Q

fill in the blanks regarding urea recycling:

  1. urea generated from ____
  2. about half reabsorbed in PCT
  3. secreted via ___ transporter in thin descending and ascending limbs
  4. reabsorbed via ___ and ___ in collecting ducts
A
  1. urea generated from NH4+ (via amino acid metabolism)
  2. about half reabsorbed in PCT
  3. secreted via UT2 transporter in thin descending and ascending limbs
  4. reabsorbed via UT1 and UT4 in collecting ducts

urea is freely filtered/reabsorbed/secreted, but it is trapped in medullary interstitium, where it maintains hyperosmotic gradient (important for formation of concentrated urine)

19
Q

In which part of the nephron does gluconeogenesis take place?

A

proximal tubule cells utilize lactate (predominant), glutamine, and glycerol for gluconeogenesis

Kidneys can account for as much as 20% of gluconeogenesis under conditions of prolonged fasting, hypoglycemia, and acidosis

Glucagon, glucocorticoids, and norepinephrine/upper nephron all stimulate renal gluconeogenesis

20
Q

Which transporters in the nephron are responsible for glucose reabsorption?

A

in the proximal tubule:

apical: SGLT1 and SGLT2 - Na+/glucose cotransporter driven by Na+ gradients

basolateral: GLUT1 and GLUT2 - facilitated diffusion

21
Q

why is glycated albumin a problem for a diabetic patients?

A

In diabetics albumin exists in a glycosylated state which functions as an antigen, and causes immune and cellular responses within the nephron (like generation of ROS)

22
Q

how does glomerulosclerosis develop from excess urinary proteins?

A

Elevated concentrations of urinary proteins induce:
1. Overloading of tubule intracellular lysosomes.
2. Local production of inflammatory cytokines.
3. Increased synthesis of extra cellular matrix proteins within the tubular tissues.

—> glomerulosclerosis, fibrosis, renal failure

23
Q

How does diabetes cause remodeling of the nephron and how does this affect glomerular function?

A

glomerulus and tubular epithelium can hypertrophy due to thickening of the cellular basement membranes —> This causes hyperfiltration (high GFR) and microalbuminuria (*note over time GFR eventually begins to decrease due to damage)

diabetic hypertension also taxes the vascular endothelium by pressure induced capillaries stretch —> increased vascular permeability —> increased reabsorption by the proximal tubule and further stimulation of GFR

24
Q

describe the effects of hyperglycemia on the proximal tubule of the nephron

A

Excess glucose in glomerular filtrate induces up regulation of SGLT2 —> increase in proximal Na+ reabsorption, resulting in decreased Na+ delivery to the macula densa

The TGF mechanism perceives low perfusion and induces secretion of vasodilators at the afferent arterial

afferent dilation increases glomerular pressure and hyperfiltration

25
Q

what is the function of nephrin in the nephron and how is it affected by up-regulated RAAS, as seen in the diabetic kidney?

A

nephrin: structural transmembrane protein within slit diaphragms of glomerular podocytes, restricts protein filtration across the glomerulus

high RAAS activity impairs the expression of nephrin, resulting in leaky glomerulus (hyperfiltration)

26
Q

what stimulates the production of calcitriol and what is the effect of calcitriol on renal function?

A

Kidney tubular cells catalyze hydroxylation of calcidiol (25-hydroxyl vit. D) to calcitriol (1,25-dihydroxy vit. D) - stimulated by PTH and hypophosphatemia

Calcitriol stimulates Ca2+ reabsorption and blocks PO4 excretion

Calcitriol is also a powerful stimulant of Ca2+/PO4 Absorption from the small intestine and induces Ca2+/PO4 reabsorption from the bone

—> the function of calcitriol is to maintain plasma Ca2+ and PO4 levels

27
Q

what is the effect of parathyroid hormone (PTH) vs calcitriol on PO4 levels?

A

PTH - promotes PO4 excretion (phosphaturia)

calcitriol - antagonizes the effect of PTH on PO4 excretion

however, the effect of PTH is much more powerful than that of calcitriol on PO4 reabsorption

28
Q

how would the phosphate and calcium urinary levels in a healthy patient respond to a parathyroid challenge?

A

PTH increases blood Ca2+ by mobilizing it from bone and promoting its reabsorption in the kidneys

PTH also blocks PO4 reabsorption in the proximal tubule

therefore, PTH challenge in a healthy patient would result in phosphaturia (increased PO4 in urine) and hypocalciuria (decreased Ca2+ in urine)

29
Q

Describe the cause of secondary hyperparathyroidism

A

aka high bone turnover renal osteodystrophy

  1. In chronic renal disease, calcitriol synthesis (produced in kidney) is impaired —> decreased calcium reabsorption from the kidney and GI tract —> hypocalcemia
  2. Hypocalcemia stimulates PTH secretion, which is exacerbated by diminished calcitriol (blocks PTH secretion) —> Ca2+ reabsorption from bone
  3. extra-skeletal calcifications form in heart, skeletal muscle, lungs, blood vessels
30
Q

What is the function of the vasa recta in the kidneys?

A

vasa recta: microvascular network intertwined among loop of Henle, establishes the countercurrent exchange that maintains hypertonicity of the medullary interstitium

Recycles NaCl, H2O, and some urea back into systemic circulation (but cannot perform active transport)

Renal (28 decks)

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