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IC 1.0 > Renal > Flashcards

Renal Flashcards

1
Q

Where in the renal vasculature are the major sites of resistance?

A

the afferent and efferent arterioles

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2
Q

What is the effect of a pre-renal problem on GFR? A post-renal problem?

A
  • both will lower GFR, but by different mechanisms
  • a pre-renal problem lowers the hydrostatic pressure of plasma
  • a post-renal problem increases the hydrostatic pressure of bowman’s space
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3
Q

What is the ultrafiltration coefficient? What is it’s utility?

A
  • the ultrafiltration coefficient, K(uf), reflects the surface area and permeability of the glomerular membrane
  • in conjunction with the filtration forces, it defines GFR
  • GFR = K(uf) x P(uf)
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4
Q

Describe the layers of the glomerular filtration membrane.

A
  • fenestrated endothelium
  • atop a basement membrane
  • under which podocyte foot processes, called pedicels, form the epithelial layer
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5
Q

What component of the glomerular filtration membrane forms the charge barrier? What sorts of ions pass through most easily?

A

negatively charged glycoproteins in the basement membrane allow small cations to pass through more readily than anions of the same size

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6
Q

What transport drives nearly all absorption and secretion in the renal tubules? Describe it’s action.

A

Na/K-ATPases pump three sodium ions out of the basal surface of the epithelial cells and two potassium ions in across that surface

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7
Q

What electrical gradient exists across the tubular epithelium?

A

-50mV, with the tubular lumen more negative (makes sense because the gradient is set up by the Na/K-ATPase which pumps three cations out of the cell and two into it)

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8
Q

Where is most calcium reabsorbed in the kidney? Through what mechanism?

A

most is reabsorbed in the proximal tubule via the paracellular pathway

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9
Q

What substance is used to estimate GFR? Why is it a good marker of GFR?

A
  • creatinine is used because it is freely filtered, not reabsorbed, and minimally secreted
  • furthermore, unlike inulin, it requires no infusion or emptying of the bladder beforehand
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10
Q

What is a normal value for GFR?

A

roughly 100-125 mL/min

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11
Q

What equation is used to calculate GFR from creatinine?

A

GFR = (urine creatinine)(rate of flow of urine)/(plasma creatinine)

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12
Q

How is fractional excretion of a solute calculated?

A

FE = (solute excreted)/(solute filtered) = (urine solute)(urine flow rate)/(GFR x plasma solute) = (plasma creatinine x urine solute)/(urine creatinine x plasma solute)

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13
Q

What is the normal value for fraction excretion of sodium?

A

1-3 percent

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14
Q

What substance is used to calculate renal plasma flow? What characteristics make this a good marker?

A

para-amniohippuric acid (PAH) is used because between filtration and secretion, there is nearly 100% excretion of all PAH that enters the kidney

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15
Q

What equation is used to calculate renal plasma flow? How about renal blood flow? What are normal values for these two measures?

A
  • RPF =(urine PAH)(urine flow rate)/(plasma PAH) = 660 mL/min
  • RBF = RPF/(1-Hct) = 1.2 L/min
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16
Q

What is the normal BUN/Cr ratio? What does it represent?

A
  • it is an important indicator of both glomerular and tubular function (creatinine is mainly filtered while urea is filtered and reabsorbed)
  • the normal value is roughly 15
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17
Q

How does the BUN/Cr ratio and FE(sodium) change in someone with prerenal, intrarenal, or post-renal failure? In which cases is the kidney’s ability to concentrate urine affected?

A
  • BUN/Cr > 15, and FE is normal in someone with pre-renal failure
  • BUN/Cr < 15, and FE > 3% in someone with intra-renal failure
  • BUN/Cr is not a particularly good indicator for post-renal failure, but the FE > 3%
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18
Q

What is filtration fraction? How is it calculated? What is a normal value?

A

FF = GFR/RPF = 0.2

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19
Q

How do control of ECF osmolarity and ECF volume differ?

A
  • for volume, the system changes urinary excretion of sodium

- for osmolarity, the system changes the urinary excretion of water

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20
Q

What causes the release of ADH? What are it’s overall effects? Through what mechanisms does it elicit these changes?

A
  • a rise in ECF osmolarity is detected by osmoreceptors in the hypothalamus (supraoptic and paraventricular nuclei)
  • these sensors trigger the thirst mechanism and release of ADH from the pituitary
  • secondarily, ADH can be released in response to low volume to a lesser degree
  • ADH has a high affinity for V2 receptors on the basolateral surface of principal cells in the epithelium of the collecting tubules
  • binding to V2 activates Gs and rising cAMP levels trigger expression of aquaporin2 molecules in the apical surface
  • these aquaporin2 molecules promote reabsorption of water from the hypotonic fluid passing the the collecting tubule
  • ADH has a lower affinity for V1 receptors found in the periphery on endothelial cells
  • when it binds V1 receptors, it works through a Gq signal transduction mechanism to induce vasoconstriction
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21
Q

Describe the countercurrent mechanism of the LoH.

A
  • the descending limb is permeable to water and the medulla becomes more hypertonic as you descend, drawing fluid out of the tubular lumen
  • the result is an extremely hypertonic solution at the bottom of the LoH
  • the ascending limb is permeable only to salt, so as the fluid rises, solutes are drawn out
  • the resulting fluid is hypotonic as it enters the distal tubule
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22
Q

What is the purpose of the vasa recta countercurrent exchange? Describe the characteristics of the vasa recta that allow it to carry out this purpose.

A
  • it is essential for conserving the composition of the medullary interstitium, which provides the foundation for the Loop of Henle’s countercurrent mechanism
  • the hairpin structure and slow rate of blood flow allow minimal disruption of the medulla’s gradient while still allowing the vessel to supply nutrients to cells
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23
Q

How does the rate of blood flow in the vasa recta or the length of the loop of hence affect the ability of the kidney’s to concentrate urine?

A
  • slow blood flow in the vasa recta prevents it from disturbing the medullary salt gradient and diminishing the countercurrent effect of the LoH
  • the length of the LoH lowers or extends the vertical osmotic gradient to which the fluid is subjected, changing the degree to which it is concentrated
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24
Q

What triggers the release of ANP and BNP? What are it’s effects? What mechanisms elicit these effects?

A
  • ANP and BNP are released from the atrial and ventricular walls in response to increased blood volume and distension of those walls
  • in the adrenal cortex, ANP reduces aldosterone production
  • in the hypothalamus, it reduces ADH secretion
  • in the tubules it promotes closure of ENaC sodium channels, inhibiting Na reabsorption, thus promoting elimination of water
  • it reduces sympathetic input to the kidneys, causing vasodilation of the afferent arteriole while also inducing vasoconstriction of the efferent arteriole
  • the net effect of this is increased GFR, which increases sodium delivery to the macula densa and impairs renin release
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25
Q

What is CNP?

A

brain natriuretic peptide

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26
Q

What is urodilatin?

A

renal natriuretic peptide

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27
Q

Describe the six changes elicited by the renin-angiotensin system.

A
  • ATII binds receptors on vascular smooth muscle in the periphery, inducing vasoconstriction to increase BP
  • ATII causes constriction of efferent arterioles, increasing FF in low-volume states to preserve GFR and renal function
  • ATII induces an increase in aldosterone which increases sodium channel and Na/K pump activity and expression, potassium excretion, and proton excretion in the collecting tubules, favoring water reabsorption
  • ATII induces ADH secretion, which increases water reabsorption from the collecting tubules
  • ATII increases Na/H pump activity in the PCT, increasing water, bicarb, and sodium reabsorption
  • ATII stimulates the thirst center, driving water intake
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28
Q

What triggers the release of renin? What senses each change?

A
  • low BP, sensed by the juxtaglomerular apparatus, which detects reduced tension on the afferent arteriole
  • low Na delivery, sensed by the macula densa
  • increased sympathetic tone (B1)
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29
Q

What role does renin play in the renin-angiotensin system?

A
  • renin catalyzes the conversion of angiotensinogen produced in the liver to angiotensin I
  • angiotensin I is then converted to angiotensin II by ACE
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30
Q

ACE is an enzyme with what two catalytic functions?

A
  • conversion of angiotensin I to angiotensin II

- breakdown of bradykinin

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31
Q

What adrenergic receptor is expressed by juxtaglomerular cells?

A

B1-adrenergic receptors

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32
Q

What is the net effect and mechanism of aldosterone. From where is it secreted?

A
  • secreted by the adrenal gland
  • responds to low blood volume states by increasing Na/K pump activity and expression in principal cells of the collecting duct, enhancing K excretion, and raising H+ ATPase activity in a-principal cells of the collecting duct
  • net effect is sodium and water reabsorption
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33
Q

How does efferent sympathetic nerve activity affect the functions of the kidney?

A
  • alpha receptors mediate afferent and efferent arteriole constriction (lower GFR, lower RBF, but higher FF)
  • alpha receptors mediate an increase in tubular reabsorption
  • beta receptors on granular cells in the juxtamedullary apparatus induce an increase in renin release
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34
Q

Where in the nephron is urea reabsorbed and secreted?

A
  • 50% reabsorbed in the proximal tubule via paracellular route
  • 60% secreted in the LoH via UT2
  • 50% reabsorbed in the collecting tubule via UT1 and UT4
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35
Q

Which class of diuretic is most effective? Why is this the case and how does it work?

A
  • loop diuretics (e.g. furosemide) work in the LoH by blocking the NKCC transporter
  • they are very potent because there is very little nephron after the LoH to compensate for its effects
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36
Q

Where in the tubule are protons and bicarbonate secreted? Absorbed?

A
  • in the proximal tubule, protons are secreted while bicarbonate is reabsorbed
  • in the collecting tubules, a-intercalated cells secrete protons and reabsorb bicarbonate
  • in the collecting tubules, B-intercalated cells secrete bicarbonate and reabsorb protons
37
Q

What role does carbonic anhydrase play in the tubules?

A

it catalyzes CO2 + H2O H2CO3, important for urine acidification

38
Q

What three molecules are used to buffer acid in the renal tubules?

A
  • bicarbonate
  • phosphate
  • ammonium
39
Q

How is ammonium produced in the renal tubules?

A
  • an ammonia group is removed from glutamate, forming a-ketoglutarate and NH3
  • NH3 diffuses into the tubule lumen and binds to protons, forming ammonium, which associates with chloride ions
40
Q

What is the equation for the urine anion gap?

A

UAG = [Na] + [K] - [Cl]

41
Q

What is the equation for plasma anion gap?

A

PAG = [Na] - ([Cl] + [HCO3])

42
Q

How is urine anion gap interpreted?

A
  • a negative UAG indicates normal ammonium production

- a positive UAG or value of zero indicates low ammonium production

43
Q

How is the equation for plasma anion gap interpreted?

A
  • normal ranges between 8-16 mEq/L

- it increases in metabolic acidosis when the HCO3 concentration in blood lowers

44
Q

What induces the release of EPO by the kidneys?

A

reduced oxygen tension in the kidneys

45
Q

What effect does PTH have in the kidneys? What triggers it’s release?

A
  • secreted in response to diminishing plasma calcium, increasing plasma phosphate, or diminishing calcitriol
  • increases calcium reabsorption in the DCT, reduces phosphate reabsorption in the PCT, and increases calcitriol production
46
Q

What is calcitriol?

A

the active form of VitD, which increases reabsorption of calcium from the intestine, bone, and renal tubules

47
Q

What is calciferol?

A

the inactive form of VitD

48
Q

What is the most common cause of acute renal failure?

A

shock

49
Q

Why is rapidly progressive glomerulonephritis a unique renal pathology?

A

because it is essentially the only glomerular disease that can cause acute renal failure (others are prerenal or tubular)

50
Q

How many nuclei should you expect in a normal, healthy glomerulus?

A

50-100

51
Q

What are the features of nephrotic syndrome?

A
  • a massive proteinuria (>3.5 gm/day)
  • hypoalbuminemia
  • generalized edema
  • hyperlipidemia and lipiduria
52
Q

Nephrotic syndromes typically indicate a defect in what part of the nephron?

A

a malfunction of the glomerular filtration barrier (rather than destruction of the filter by an inflammatory process)

53
Q

Most nephrotic syndromes are characterized by a selective proteinuria of which protein?

A

albumin

54
Q

What is the most common cause of chronic renal failure in the US?

A

diabetic glomerulosclerosi

55
Q

Describe Diabetic glomerulosclerosis.

A
  • the most common cause of chronic renal failure in the US
  • begins with GBM thinkening, but with poor control it may progress to classic Kimmelsteil-Wilson nodular sclerosis
  • light microscopy reveals acellular, spherical nodules of matrix situated in the periphery of the glomerulus that are PAS-positive
56
Q

What features are characteristic of a nephritic syndrome?

A

usually seen with acute inflammatory conditions

  • mild to moderate hypertension
  • proteinuria (< 3.5 gm/day)
  • hematuria (and red cell casts)
  • azotemia
  • oliguria
57
Q

Describe the pathogenesis of nephritic syndromes.

A
  • usually seen with an acute inflammatory condition

- severe damage to the glomerular basement membrane allows leakage of large proteins and RBCs into the urinary space

58
Q

Most often, what are RBC, WBC, and epithelial cell casts indicative of?

A
  • RBCs: glomerulonephritis
  • WBCs: acute pyelonephritis
  • epithelial: acute tubular necrosis
59
Q

How does chronic glomerulonephritis present?

A
  • it is the end-stage of most glomerular diseases but in rare cases may also arise without any antecedent history
  • slowly progresses with the development of chronic renal failure, uremia, and hypertension
  • glomeruli reflect the changes associated with the underlying disease but eventually become acellular, eosinophilic PAS-positive masses
60
Q

What are the main clinical applications for diuretics?

A
  • heart failure
  • hypertension
  • acute and chronic renal failure
  • nephrotic syndrome and cirrhosis
61
Q

Drugs ending in the suffix “-zolamide” have what function?

A

they are carbonic anhydrase inhibitors (diuretics)

62
Q

Why are most diuretics potassium wasting?

A

most block sodium reabsorption, and when more sodium reaches the collecting duct, more potassium is secreted in an effort to reabsorb more sodium than usual

63
Q

What is the clinical use of an SGLT2 inhibitor?

A
  • potentially a diuretic but not used as such
  • third-line therapy for type 2 diabetes because they block glucose reabsorption in the proximal tubule and can reduce A1C by 0.5-1%
64
Q

Drugs ending in the suffix “-agliflozin” function in what way?

A

they are SGLT2 inhibitors

65
Q

Through what mechanism does the macula densa sense sodium delivery and induce renin release form granular cells?

A
  • an NKCC detects Na and Cl concentrations
  • when levels fall, activation of COX-2 induces PG formation and there is also an elevated production of adenosine
  • adenosine binds a receptor on the granular cell as does prostaglandin
  • both serve to regulate cAMP levels, which control renin release
66
Q

Which diuretic is used clinically for hypertension?

A

thiazides

67
Q

Which group of diuretics is still effective, even when GFR is low?

A

loop diuretics because they can also have a vascular effect mediated by prostaglandins and their effect on the renin system

68
Q

Drugs ending in “-vaptan” have what mechanism of action?

A

they are ADH antagonists

69
Q

How are the ADH antagonists conivaptan and tolvaptan clinically used?

A
  • management of Syndrome of Inappropriate ADH Secretion when water restriction isn’t sufficient
  • congestive heart failure when ADH is elevated due to low blood volume
70
Q

What is the primary osmotic diuretic?

A

mannitol

71
Q

How does mannitol function as a diuretic? How is it used clinically?

A
  • it is filtered by not reabsorbed, increasing the osmolarity of the ultra filtrate and promoting water diuresis
  • greatest effect is in PCT and descending limb where the tubules are freely permeable to water
  • used primarily for rapid reduction of intracranial pressure
72
Q

What are the adverse effects of mannitol and other osmotic diuretics?

A
  • may cause osmotic diarrhea since they are poorly absorbed

- can cause severe dehydration, hypernatremia, headache, nausea, and vomiting

73
Q

What is the first choice diuretic for patients with CHF? Why?

A
  • loop diuretics (furosemide or athacrynic acid if allergic to sulfonamides)
  • this is because other diuretics lose efficacy when combined with a vasodilator which reduces renal blood flow
74
Q

What is the preferred thiazide-like diuretic?

A

chlorthalidone because of it’s long-half life and proven reduction of CV disease

75
Q

What is the clinical benefit of potassium-sparing diuretics?

A

they are weak and only used in combinations with other diuretics to avoid hypokalemia

76
Q

What is normal pH, PCO2, and [HCO3-]?

A
  • pH = 7.4
  • PCO2 = 40 mmHg
  • [HCO3-] = 24 mEq/L
77
Q

Which acids and bases are eliminated via the lungs? Which via the kidneys?

A
  • lungs: volatile acids as CO2

- kidneys: non-volatile acids and bases

78
Q

Describe acid-base regulation within the PCT.

A
  • CO2 diffuses into epithelial cells and is converted to bicarb by the action of carbonic anhydrase
  • bicarb is broken down into a proton and HCO3-
  • the proton is secreted via a Na/H exchanger in the apical membrane
  • bicarb is reabsorbed via a Na/HCO3 cotransporter on the basolateral surface
79
Q

Describe acid-base regulation in the DCT.

A
  • CO2 diffuses into epithelial cells and is converted to bicarb by the action of carbonic anhydrase
  • bicarb is broken down into a proton and HCO3-
  • the proton is secreted by either an H-ATPase or via a H/K exchanger in the apical membrane
  • the bicarb molecule is reabsorbed via a bicarb/Cl exchanger in the basolateral membrane
  • this process occurs in the DCT epithelium and alpha-intercalated cells of the collecting duct but is flipped in the beta-intercalated cells to facilitate wasting of bases and reabsorption of acids
80
Q

What compounds are used as buffers in the urine?

A
  • H2PO4-

- HCO3-

81
Q

Describe ammonium production in the renal tubules.

A
  • in the tubular epithelium, cells convert glutamine to glutamate and then alpha-ketoglutarate with the production of an ammonia molecule
  • ammonia is then able to diffuse into the lumen where it combines with a proton
  • or it can combine with a proton in the epithelial cell and be pumped into the lumen via a ammonium/sodium exchanger
82
Q

What are possible causes of a respiratory acidosis?

A
  • airway obstruction
  • acute lung injury
  • chronic lung disease (COPD)
  • obesity hypoventilation syndrome
  • opioids or sedatives
  • wearing of respiratory muscles (neuromuscular disease like MG, muscular dystrophy, or Guillain-Barre)
83
Q

What are possible causes of an anion gap metabolic acidosis?

A

MUDPILES (some additional anion or loss of a cation)

  • methanol (formic acid)
  • uremia
  • diabetic ketoacidosis
  • propylene glycol
  • iron tablets or INH
  • lactic acidosis
  • ethylene glycol
  • salicylates (late)
84
Q

What are possible causes of non-anion gap metabolic acidosis?

A

HARDASS

  • hyperalimentation
  • addison disease
  • renal tubular acidosis
  • diarrhea
  • acetazolamide
  • spironolactone
  • saline infusion
85
Q

What are possible causes of respiratory alkalosis?

A
  • hysteria and hyperventilation
  • hypoxemia
  • salicylates (early)
  • tumor
  • pulmonary embolism
86
Q

What are possible causes of metabolic alkalosis?

A
  • loop or thiazide diuretics
  • hyperaldosteronism
  • Cushing’s syndrome
  • antacid ingestion
  • vomiting
87
Q

Describe the changes along a Davenport diagram that occur during a compensated respiratory acidosis.

A
  • initially, there is a shift to the left along the non-bicarbonate buffer line
  • then with renal compensation, there is an increase in HCO3- made available and there is a shift up the PCO2 curve
88
Q

Describe the changes along a Davenport diagram that occur during a respiratory and renal compensated metabolic acidosis.

A
  • initially, there is a shift down the PCO2 curve
  • then with respiratory compensation, there is a shift to the right along the non-bicarbonate buffer line
  • finally with renal compensation, there is a shift back up the PCO2 curve as more HCO3- is retained
89
Q

What is winter’s formula?

A
  • a formula used to predict respiratory compensation for a simple metabolic acidosis
  • If PCO2 = 1.5[HCO3-] + 8 +/- 2, then there is appropriate compensation, if PCO2 is less than predicted, there is a concomitant respiratory alkalosis, and if PCO2 is more than predicted, there is a concomitant respiratory acidosis

IC 1.0 (24 decks)

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