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STEP1 > 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 transporter 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 into the blood and two potassium ions in across that surface into the lumen

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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 ascending loop of henle 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?

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 since creatinine is mainly filtered while urea is filtered and reabsorbed
  • the normal value is roughly 15
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17
Q

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

A

FF = GFR/RPF = 0.2

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18
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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19
Q

What triggers the release of ADH? What are it’s effects? Explain the receptor and cascade types involved.

A
  • a rise in ECF osmolarity is detected by osmoreceptors in the supraoptic and paraventricular nuclei of the hypothalamus, which induce thirst and release ADH
  • ADH binds V2 receptors on principal cells in the collecting tubules, activating Gs and AC to induce expression of additional aquaporin2
  • aquaporin2 promotes reabsorption of water from the hypotonic fluid passing through the collecting tubule
  • ADH has a lower affinity for V1 receptors found in the periphery on endothelial cells and works through a Gq signal transduction mechanism to induce vasoconstriction
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20
Q

Describe the countercurrent mechanism of the Loop of Henle

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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21
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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22
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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23
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 distention of those walls
  • they work via cGMP second messenger systems
  • reduces aldosterone and ADH secretion while promoting closure of ENaC sodium channels in the collecting tubule
  • inhibits sympathetic input to the kidneys and increases GFR through via efferent constriction and afferent dilation, which both reduce renin release
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24
Q

What names are given to brain and renal natriuretic peptides?

A

CNP and urodilatin, respectively

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25
Q

Describe five effects elicited by angiotensin II.

A
  • peripheral vasoconstriction
  • increase FF while increasing GFR
  • increase aldosterone and ADH production
  • increases Na/H pump activity in the PCT
  • stimulates the thirst center
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26
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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27
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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28
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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29
Q

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

A
  • secreted by the adrenal gland in response to low volume states
  • activates and increases expression of Na/K-ATPases as well as expression of ENaC channels in principal cells of the collecting tubules
  • activates H-ATPase activity in alpha-intercalated cells
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30
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)
  • alpha1 receptors mediate an increase in tubular reabsorption
  • beta1 receptors on granular cells in the juxtamedullary apparatus induce an increase in renin release
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31
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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32
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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33
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
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34
Q

What role does carbonic anhydrase play in the tubules?

A

it catalyzes CO2 + H2O H2CO3, important for urine acidification

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35
Q

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

A
  • bicarbonate
  • phosphate
  • ammonium
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36
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
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37
Q

What is the equation for the urine anion gap?

A

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

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38
Q

What is the equation for plasma anion gap?

A

PAG = [Na] - [Cl] - [HCO3]

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39
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

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40
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

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41
Q

What induces the release of EPO by the kidneys?

A

reduced oxygen tension in the kidneys

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42
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 by activating Ca/Na exchange
  • reduces phosphate reabsorption in the PCT by inhibiting the Na/PO4 cotransporter
  • increases calcitriol production
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43
Q

What is calcitriol?

A

the active, dihydroxy form of VitD

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44
Q

What is calciferol?

A

the inactive form of VitD

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45
Q

Describe the timeline for kidney development in utero.

A
  • the pronephros appears at week 4 but degenerates
  • the mesonephros functions as the interm kidney for the first trimester before contributing to the male genital system
  • the metanephros appears in week 5, but isn’t fully canalized until week 10
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46
Q

What is the mesonephros?

A

a functional kidney that works during the first trimester and later contributes to the male genital system

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47
Q

Describe formation of the metanephros.

A
  • the ureteric bud, derived from mesoderm, specifically the caudal end of the mesonephric duct, gives rise to the ureter, pelvises, calyces, and collecting ducts
  • it interacts with the metanephric mesenchyme and, dependent on WT1, induces differentiation and formation of the glomerulus through to the distal convoluted tubule
  • the system is fully canalized by week 10
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48
Q

What is the most common site of urinary obstruction in a developing fetus? Why?

A

the ureteropelvic junction because it is the last thing to canalize

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49
Q

Describe Potter’s syndrome.

A
  • renal insufficiency in the developing fetus for one reason or another causes oligohydramnios
  • this leads to compression of the developing fetus
  • the end result is limb deformities and facial anomalies (flat nose, recessed chin, infraorbital folds, low ears)
  • the real problem, however, is that compression of the chest and lack of amniotic fluid aspiration into fetal lungs contributes to pulmonary hypoplasia
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50
Q

Duplex Collecting System

A
  • a congenital renal anomaly in which the ureteric bud bifurcates before interacting with the metanephric blastema, creating a bifid ureter
  • can also arise if two ureteric buds interact with the same metanephric blastema
  • strongly associated with vesicoureteral reflux and ureteral obstruction, increasing the risk of UTI
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51
Q

Describe the route of blood flow through the kidney.

A
  • renal artery
  • segmental artery
  • interlobar artery
  • arcuate artery
  • interlobular artery
  • afferent arteriole
  • glomerulus
  • efferent arteriole
  • vasa recta
  • peritubular capillaries
  • venous outflow
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52
Q

Which portion of the tubule contains the macula densa and is position in proximity to the glomerulus?

A

the distal convoluted tubule

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53
Q

What important relationship exists between the ureters and the female/male reproductive anatomy? Why is this clinically important?

A
  • the ureters pass under the uterine artery or under the vas deferens
  • this is important because gynecologic procedures like ligation of uterine vessels may damage the ureter, contributing to an obstruction or leakage
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54
Q

Is potassium high in the intracellular or extracellular space?

A
  • it is high intracellularly

- HIKIN: HIgh K INtracellularly

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55
Q

How can we estimate TBW, ICF, ECF, interstitial fluid, and plasma.

A
  • TBW is roughly 60% total body mass or 75% lean mass
  • ICF is 40% of total body mass (⅔ TBW)
  • ECF is 20% of total body mass (⅓ TBW)
  • ECF is divided into 75% interstitial fluid and 25% plasma volume
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56
Q

How is the renal clearance of a substance calculated? What does it mean if clearance exceeds the GFR or is less than the GFR?

A

C = (urine concentration)(urine flow rate)/(plasma concentration)

  • when C > GFR it suggests a degree of tubular secretion
  • when C < GFR it suggests a degree of tubular reabsorption
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57
Q

What inflammatory mediates cause afferent arteriole dilation?

A

prostaglandins

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58
Q

What is the effect of NSAIDs on renal blood flow?

A
  • they inhibit prostaglandins, which would otherwise, cause afferent arteriole vasodilation
  • NSAIDs, then, promote afferent arteriole constriction
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59
Q

What is the effect of angiotensin II on afferent and efferent arteriole dilation?

A
  • causes efferent vasoconstriction that exceeds afferent vasoconstriction
  • the net effect is a decrease in RPF, an increase in GFR, and an increase in FF
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60
Q

How does afferent arteriole constriction affect GFR, RPF, and FF?

A
  • GFR is reduced
  • RPF is reduced
  • FF is unchanged
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61
Q

How does efferent arteriole constriction affect GFR, RPF, and FF?

A
  • GFR is increased
  • RPF is reduced
  • FF is increased
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62
Q

How does dehydration affect GFR, RPF, and FF?

A
  • RPF is reduced
  • GFR is reduced
  • FF is increased
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63
Q

Describe reabsorption of glucose in the tubules? What happens in states of hyperglycemia?

A
  • normally, 100% is reabsorbed in the PCT via the Na/glucose-cotransporter (SGLT2)
  • when serum glucose exceeds 200 mg/dL, glucosuria begins
  • when glucose transport reaches 375 mg/min, all transporters are fully saturated
  • “splay” refers to the difference between urine threshold at which glucose appears in the urine, and receptor saturation and is a function of heterogeneity between nephrons
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64
Q

How does pregnancy affect tubular reabsorption?

A

it decreases the ability of the PCT to reabsorb glucose and amino acids

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65
Q

How are drugs secreted in the renal tubules?

A

via non-specific anion and cation transporters coupled to Cl- and H+ movement, respectively

66
Q

What is the difference between alpha- and beta-intercalated cells of the collecting tubule?

A
  • alpha cells secrete protons
  • beta cells secrete bicarbonate
  • both function in the maintenance of physiologic pH
67
Q

What is Fanconi syndrome?

A
  • a renal tubular defect characterized by a generalized reabsorptive defect in the proximal convoluted tubule
  • loss of various solutes often results in a metabolic acidosis
  • can be acquired or hereditary
68
Q

What is Bartter syndrome?

A
  • an autosomal recessive reabsorptive defect in the ascending loop of Henle due to an NKCC defect
  • presents similarly to chronic loop diuretic use
  • results in hypokalemia and metabolic alkalosis with hypercalciuria
69
Q

What is Gitelman syndrome.

A
  • an autosomal recessive reabsorptive defect of NaCl in the DCT
  • presents like chronic thiazide diuretics
  • hypokalemia, hypomagnesemia, metabolic alkalosis, and hypocalciuria
70
Q

What is Liddle syndrome?

A
  • an autosomal dominant gain of function mutation that increases ENaC activity in the collecting tubules
  • presents like hyperaldosteronism, but aldosterone levels are appropriately low
  • results in hypertension, hypokalemia, and metabolic alkalosis
  • treat with amiloride (an ENaC inhibitor)
71
Q

What is Syndrome of Apparent Mineralocorticoid Excess?

A
  • a hereditary deficiency of 11B-hydroxysteroid dehydrogenase, which would normally convert cortisol to cortisone (unable to bind mineralocorticoid receptors)
  • can also be acquired from licorice, which contains glycyrrhetinic acid and inhibits the same enzyme
  • excess cortisol results in increased mineralocorticoid receptor binding and activity
  • presents with hypertension, hypokalemia, metabolic alkalosis, low serum aldosterone levels
  • treat with corticosteroids, which feedback and reduce endogenous cortisol production
72
Q

Under what circumstances is renin secreted by granular JG cells?

A
  • low renal arterial pressure
  • low sodium delivery to the macula densa
  • increased B1 activation of granular cells
73
Q

What are juxtaglomerular cells?

A

modified smooth muscle cells of the afferent arteriole, which detect stretch among other things

74
Q

How do macula densa cells respond to low sodium delivery?

A
  • increase renin release, which elicits vasoconstriction of the efferent arteriole
  • release NO to elicit vasodilation of the afferent arteriole
75
Q

The macula densa uses what transporter to measure Na/Cl delivery?

A

an NKCC transporter

76
Q

How does PTH affect calciferol and calcitriol levels?

A
  • PTH activates 1a-hydroxylase, which converts calciferol (inactive VitD) to calcitriol (active VitD)
77
Q

Prostaglandins have what effect on the kidneys?

A

they cause vasodilation to the afferent arterioles

78
Q

List six things that shift potassium out of cells, causing a hyperkalemia.

A

“DO LABS”

  • digitalis (blocks Na/K-ATPase)
  • hyperosmolarity
  • lysis of cells (tumor lysis syndrome, crush injury, rhabdo)
  • acidosis (protons displace K bound to proteins and direct inhibits Na/K-ATPase)
  • B-blocker
  • high blood Sugar (low insulin)
79
Q

What effect does insulin have on potassium levels?

A

insulin shifts potassium into cells

80
Q

What are the consequences of low and high serum sodium?

A
  • low: stupor, coma, seizures, nausea, malaise,

- high: stupor, coma, irritability,

81
Q

What are the consequences of low and high serum potassium?

A
  • low: U waves, flat T waves, arrhythmias, muscle cramps, spasm, weakness
  • high: wide QRS, peaked T waves, arrhythmias, muscle weakness
82
Q

What are the consequences of low and high serum calcium?

A
  • low: tetany, seizures, prolonged QT, twitching (Chvostek sign), spasm (Trousseau sign)
  • high: stones (renal), bones (pain), groans (abdominal pain), thrones (urinary frequency), and psychiatric overtones (anxiety, altered status)
83
Q

What are the consequences of low and high serum magnesium?

A
  • low: tetany, torsades de pointes on ECG, hypokalemia

- high: low DTR, lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia

84
Q

What are the consequences of low and high serum phosphate?

A
  • low: bone loss, osteomalacia, rickets

- high: renal stones, metastatic calcifications, hypocalcemia

85
Q

What is primary hyperaldosteronism?

A

excess aldosteronism causes hypertension, which subsequently induces less renin release

86
Q

What effect will a renin-secreting tumor have on BP?

A

it will induce hypertension

87
Q

How do pH, PCO2, and HCO3 compare in metabolic versus respiratory acidosis?

A
  • pH is low in both
  • PCO2 and HCO3 are low in a metabolic acidosis
  • PCO2 and HCO3 are high in a respiratory acidosis
88
Q

What is winter’s formula? How is it used?

A
  • It is a formula for predicting respiratory compensation for a simple metabolic acidosis
  • if measured PCO2 is greater than predicted, there is a concomitant respiratory acidosis
  • if measured PCO2 is less than predicted, the lungs are attempting to compensate
  • Predicted PCO2 = 1.5[bicarb] + 8 +/- 2
89
Q

List the four major causes of metabolic alkalosis.

A
  • loop diuretics
  • vomiting
  • antacid use
  • hyperaldosteronism (Liddle syndrome)
90
Q

List five major causes of respiratory alkalosis.

A
  • hyperventilation (hysteria)
  • hypoxemia (e.g. high altitude)
  • salicylates (early)
  • tumor
  • pulmonary embolism
91
Q

What are the most significant causes of an anion gap metabolic acidosis?

A

MUDPILES

  • methanol
  • uremia
  • diabetic ketoacidosis
  • propylene glycol
  • iron tablets
  • lactic acidosis
  • ethylene glycol
  • salicylates (late)
92
Q

What are the most significant causes of non-anion gap metabolic acidosis?

A

HARDASS

  • hyperalimentation
  • addison disease
  • renal tubular acidosis
  • diarrhea
  • acetazolamide
  • spironolactone
  • saline infusion
93
Q

What are normal serum pH, [bicarb], and PCO2?

A
  • pH = 7.4
  • [bicarb] = 24 mEq/L
  • PCO2 = 40 mmHg
94
Q

Horseshoe Kidney

A
  • a most common congenital renal anomaly, in which the kidneys are conjoined, usually at the inferior pole
  • ascent of the kidneys is stopped by the inferior mesenteric artery, and they end up located in the lower abdomen
95
Q

Renal Agenesis

A
  • unilateral or bilateral absent kidney formation
  • unilateral leads to hypertrophy of the existing kidney and increases risk of renal failure later in life
  • bilateral leads to Potter sequence
96
Q

Dysplastic Kidney

A
  • a non-inherited, congenital malformation of renal parenchyma with cysts and abnormal tissue
  • failure of metanephric mesenchyme to differentiate
  • usually unilateral, but the bilateral form must be distinguished from inherited polycystic kidney disease
97
Q

Polycystic Kidney Disease

A
  • an inherited defect leading to bilaterally enlarged kidneys with cysts in the renal cortex and medulla
  • autosomal recessive presents in infants as worsening renal failure with hypertension, and possibly Potter sequence
  • autosomal recessive is associated with congenital hepatic fibrosis, leading to portal hypertension and hepatic cysts
  • autosomal dominant (due to APKD1 or APKD2 mutation) presents in young adults as hypertension, hematuria, and worsening renal failure with cysts developing over time
  • autosomal dominant is associated with berry aneurysm, hepatic cysts, and mitral valve prolapse
98
Q

Medullary Cystic Kidney Disease

A
  • an autosomal dominant defect leading to cysts in the medullary collecting ducts
  • fibrosis of the parenchyma results in shrunken kidneys (as opposed to the enlarged, cystic kidneys of PKD)
99
Q

How is acute renal failure defined? What is the hallmark?

A
  • define as an acute, severe decrease in renal function

- hallmark is azotemia (increased BUN and Cr, which are both nitrogenous waste products), often with oliguria

100
Q

What is azotemia?

A

a hallmark of acute renal failure, it is an increase in nitrogenous products (BUN and creatinine) in the blood

101
Q

What is prerenal azotemia?

A

an acute renal failure due to problems in renal blood flow

102
Q

What happens to BUN:Cr, FENa, and urine osmolality in someone with pre-renal azotemia?

A
  • when RBF decreases, BUN reabsorption is enhanced and the BUN:Cr increases > 15
  • since tubular function is intact, FENa is normal (<1%) and urine osmolarity is normal (>500 mOsm/kg)
103
Q

What happens to BUN/Cr, FENa, and urine osmolality in someone with post-renal azotemia?

A
  • in the early stage, increased tubular pressure enhances BUN reabsorption, and the BUN/Cr increases > 15
  • in the early stage, tubular function is also normal with FENa < 1% and urine osmolarity > 500mOsm/kg
  • with long-standing obstruction, tubular damage ensues and the BUN/Cr falls, FENa rises, and there is an inability to concentrate urine
104
Q

Acute Tubular Necrosis

A
  • the most common cause of acute renal failure
  • due to ischemia or nephrotoxicity in the form of aminoglycosides, heavy metals, myoglobinuria as in crush injury, ethylene glycol, radio contrast dye, or urate from tumor lysis syndrome, cisplatin, amphotericin
  • injury results in necrosis of tubular epithelial cells, which form brown, granular casts and diminish GFR
  • tubular dysfunction leads to elevated BUN and Cr, though the BUN/Cr is < 15, FENa > 1%, and Osm < 500
  • clinical features include oliguria as well as hyperkalemia and acidosis due to the inability to secrete these cations
  • reversible but requires supportive dialysis since electrolyte imbalances can be fatal
  • recovery takes 2-3 weeks as tubular cells are stable and take time to re-enter the cell cycle
105
Q

What portions of the nephron are most susceptible to ischemia and to nephrotoxicity?

A
  • ischemia: the proximal tubule and the medullary segment of the thick ascending limb
  • nephrotoxicity: the proximal tubule
106
Q

How does tumor lysis syndrome affect the kidneys? Describe the mechanism and prevention.

A
  • rapid lysis of tumor cells following chemotherapy may release lots of urate, which is particularly nephrotoxic
  • the result is often intra-renal azotemia (acute renal failure)
  • to prevent this, hydration and allopurinol are used prior to initiating chemotherapy
107
Q

Acute Interstitial Nephritis

A
  • an intra-renal azotemia (acute renal failure)
  • characterized as a drug-induced hypersensitivity affecting the interstitium and tubules
  • most commonly due to the 5 P’s: Pee (diuretics), Pain-free (NSAIDS), Penicillins, Proton pump inhibitors, and rifamPin
  • presents with oliguria, fever, and rash lasting days to weeks
  • uniquely, eosinophils may be seen in urine
  • biopsy will reveal an inflammatory infiltrate in the interstitium
  • may progress to renal papillary necrosis
108
Q

Renal Papillary Necrosis

A
  • necrosis of renal papillae
  • due to chronic analgesic abuse, diabetes mellitus, sickle cell disease/trait, or severe acute pyelonephritis
  • presents with gross hematuria and flank pain
109
Q

What are the signs and symptoms of nephrotic syndrome?

A
  • a syndrome of hypoalbuminemia, hypogammaglobulinemia, a hyper coagulable state, and hyperlipidemia/hypercholesterolemia due to glomerular dysfunction
  • protein loss contributes to pitting edema, loss of Ig increases the risk of infection, antithrombin III loss increases coagulability, and lipids may result in fatty casts in urine
110
Q

Minimal Change Disease

A
  • the most common cause of nephrotic syndrome in children
  • usually idiopathic, but may be associated with Hodgkin lymphoma
  • glomeruli appear normal on light and electron microscopy, but effacement of foot processes can be seen on EM
  • proteinuria is selective (only albumin)
  • respond extremely well to steroids, suggesting damage is mediated by cytokines
111
Q

Focal Segmental Glomerulosclerosis

A
  • the most common cause of nephrotic syndrome in Hispanics and African Americans
  • often idiopathic but may be associated HIV, IV drug use, or sickle cell disease
  • sclerosis involving part of some glomeruli is visible on light microscopy and effacement of foot processes can be seen on EM
  • don’t respond well to steroids and progress to chronic renal failure
112
Q

Membranous Nephropathy

A
  • the most common cause of nephrotic syndrome in Caucasian adults
  • usually idiopathic but may be associated with HBV, HCV, solid tumors, or SLE
  • light microscopy reveals thick glomerular basement membranes, IF shows granular immune complex deposits, and EM shows sub epithelial deposits
113
Q

Membranoproliferative Glomerulonephritis

A
  • a mix of nephritic and nephrotic syndrome
  • type I is characterized by subendothelial deposits and an associated with HBV and HCV
  • type II is characterized by intramembranous, “ribbon-like” deposits and C3 nephrotic factor (an antibody that stabilizes C3 convertase; see low levels of C3 in patient)
  • light microscopy reveals a “tram-track” appearance
  • IF reveals granular immune complex deposition
114
Q

Diabetic Glomerulonephropathy

A
  • nonenzymptic glycosylation of the vascular basement membrane results in hyaline arteriolosclerosis, reducing lumen diameter
  • efferent arteriole more affected than afferent, increasing the GFR, and this hyperfiltration injury leads to microalbuminuria
  • eventually progresses to nephrotic syndrome characterized by sclerosis of the mesangium with formation of Kimmelstiel-Wilson nodules
  • ACE inhibitors slow the progression by inhibiting efferent arteriolar constriction
115
Q

Systemic amyloidosis affecting the kidneys leads to what sort of syndrome?

A

a nephrotic syndrome

116
Q

What is a nephritic syndrome? What is the cause? How does it manifest?

A

characterized by glomerular damage due immune complex deposition, activation of complement, C5a-mediated neutrophil chemotraction

  • proteinuria is limited (< 3.5 g/day)
  • oliguria and azotemia
  • salt retention with periorbital edema and hypertension
  • RBC casts
117
Q

IgA Nephropathy

A
  • the most common nephropathy worldwide
  • it is due to IgA complex deposition in the mesangium
  • presents during childhood with episodic hematuria with RBC casts present in urine, typically following mucosal infections
  • it is the real pathology of Henoch-Schonlein purpura
118
Q

Alport Syndrome

A
  • an X-linked dominant type IV collagen defect
  • results in thinning and splitting of the glomerular basement membrane
  • presents with hematuria, sensory hearing loss, and ocular disturbances
119
Q

Poststreptococcal glomerulonephritis

A
  • also known as acute proliferative glomerulonephritis
  • a nephritic syndrome arising 2-3 weeks after a group A, beta-hemolytic strep infection
  • glomeruli appear hyper cellular
  • granular, subepithelial deposits of IgG, IgM, and C3
  • treatment is supportive as children rarely progress to renal failure
120
Q

Rapidly Progressive Glomerulonephritis

A
  • a nephritic syndrome that progress to renal failure in weeks to months
  • a description, not a disease
  • cases are split into three groups (anti-GBM disease, RPGN related to systemic disease, and Pauli-Immune type) based on the pattern of immunofluorescence and other features
  • all share the light microscope finding of crescents in Bowman space comprised of fibrin and macrophages
121
Q

Anti-GBM Disease

A
  • a type of RPGN known as goodpasture syndrome
  • a type II hypersensitivity mediated by antibodies directed against the basement membrane of alveoli and glomeruli
  • most common in males between 20-40 with hemoptysis preceding hematuria
  • strongly associated with the HLA-DR2 haplotype
  • light microscopy finds hyper cellular glomeruli surrounded by a fibrin/macrophage crescent
  • immunofluorescence confirms a linear pattern of IgG and C3
122
Q

Diffuse Proliferative Glomerulonephritis

A
  • a type of RPGN secondary to systemic disease; in particular it is the most common type of renal disease seen in patients with SLE
  • mediated by antigen-antibody complex deposition
  • light microscope finds hyper-cellular glomeruli surrounded by a fibrin/macrophage crescent and “wire looping” of capillaries
  • IF confirms granular complex deposits of IgG and C3 and EM finds sub-endothelial deposits
123
Q

Pauci-Immune Rapidly Progressive Glomerulonephritis

A
  • a type of RPGN associated with various types of vasculitis, particularly Wegener granulomatosis, polyangiitis, and Churg-Strauss syndrome
  • IF is negative but ANCA (anti-neutrophil cytoplasmic antibodies) are present in serum; c-ANCA for wegener granulomatosis and p-ANCA for Churg-Strauss
  • light microscopy finds hyper-cellular glomeruli surrounded by a fibrin/macrophage crescent
124
Q

What are the risk factors for urinary tract infection?

A
  • sexual intercourse
  • urinary stasis
  • catheters
125
Q

Cystitis

A
  • a infection fo the bladder
  • most often due to E. coli; Staph saprophyticus is characteristically seen in young, sexually active women; K. pneumoniae is a common agent; Proteus mirabilis is likely if the urine is alkaline with an ammonia scent
  • presents with dysuria, urinary frequency, urgency, and suprapubic pain, but systemic symptoms are absent
  • urine is cloudy with WBC, dipstick is positive for leukocyte esterase and nitrites, culture grows greater than 100K colonies
  • sterile pyuria (cystitis with a negative urine culture) suggests urethritis due to Chlamydia trachoma’s or Neisseria gonorrhoeae
126
Q

Sterile Pyuria

A
  • the presence of pyuria (WBCs in urine and positive dipstick for leukocyte esterase)
  • with a negative urine culture
127
Q

A patient presents with the symptoms of cystitis what etiologic agents do you suspect? What about if the the urine culture is negative (i.e. sterile pyuria)?

A
  • E. coli is most common
  • Staph saprophyticus is common in young, sexually active women
  • K. pneumoniae is possible
  • Proteus mirabilis is likely if the urine is alkaline with an ammonia scent
  • sterile pyuria suggests either Chlamydia trachomatis or Neisseria gonorrhoeae
128
Q

Acute Pyelonephritis

A
  • an infection of the kidney
  • usually due to ascending infection secondary to vesicoureteral reflux
  • presents with fever, flank pain, WBC casts, and leukocytosis in addition to the symptoms of cystitis
  • most commonly due to E. coli, Enterococcus faecalis, or Klebsiella
129
Q

Chronic Pyelonephritis

A
  • recurrent pyelonephritis, usually due to vesicoureteral reflux or obstruction
  • leads to interstitial fibrosis and atrophy of the tubules
  • atrophic tubules contain eosinophilic proteinaceous material and resemble thyroid follicles (referred to as thyroidization of the kidney)
  • cortical scarring at the upper and lower poles with blunted calyces is indicative of vesicoureteral reflux
130
Q

Nephrolithiasis

A
  • a precipitation of a urinary solute as a stone
  • presents with colicky pain, hematuria, and unilateral flank tenderness
  • high concentration of solute and low urine volume are risk factors
  • usually passed within hours but may require surgical intervention
  • typically calcium oxalate, calcium phosphate, ammonium magnesium phosphate, uric acid, or cystine in nature
131
Q

Calcium Oxalate/Calcium Phosphate Nephrolithiasis

A
  • the most common type of kidney stone
  • the urine crystals have an envelope shape
  • usually due to idiopathic hypercalciuria
  • treatment is HCTZ, a calcium-sparing diuretic that enhances calcium reabsorption
132
Q

Ammonium Magnesium Phosphate Nephrolithiasis

A
  • the second most common type of kidney stone
  • usually due to infection with a urease-positive organism like Proteus vulgaris or Klebsiella
  • alkaline urine also increases one’s risk
  • the urine crystals are coffin lid shaped
  • forms a stag horn calculi, which increases one’s risk for UTI and requires surgical removal
133
Q

Uric Acid Nephrolithiasis

A
  • the only radiolucent (not visible) kidney stone
  • it is the most common stone seen in patients with gout and in those with a myeloproliferative disorder
  • hot, arid climates, low urine volume, and acidic pH are all risk factors
  • the urine crystals are rhomboid in shape
  • treatment involves hydration, alkalinization of urine, and allopurinol
134
Q

Cystine Nephrolithiasis

A
  • a rare form of kidney stone that most commonly presents in children
  • associated with cystinuria, a genetic tubule defect resulting in poor cysteine reabsorption as well as poor reabsorption of ornithine, lysine, and arginine
  • the urine crystals are hexagonal
  • may form a staghorn calculi
  • treatment involves hydration and alkalinization of urine
135
Q

What are the simple ways to distinguish between the various kidney stones?

A
  • staghorn in adult: ammonium magnesium phosphate
  • staghorn in child: cystine
  • radiolucent: uric acid
136
Q

What are the three most common causes of chronic renal failure?

A
  • diabetes mellitus
  • hypertension
  • glomerular disease
137
Q

Chronic Renal Failure

A
  • end-stage kidney failure, most often due to diabetes, hypertension, or glomerular disease
  • presents with uremia, salt and water retention (causing hypertension), hyperkalemia with metabolic acidosis, anemia (low EPO production), hypocalcemia and hyperphosphatemia (decreased vitamin D activation), renal osteodystrophy (secondary hyperparathyroidism, osteomalacia, and osteoporosis)
  • treated with dialysis and transplant
  • cysts often develop within shrunken, end-stage kidneys during dialysis, increasing the risk for RCC
138
Q

What are the symptoms of uremia?

A
  • nausea
  • anorexia
  • pericarditis
  • platelet dysfunction
  • encephalopathy with asterisks
  • deposition of urea crystals in skin
139
Q

Which renal cells produce EPO?

A

the peritubular interstitial cells

140
Q

What is renal osteodystrophy?

A
  • a secondary hyperparathyroidism due to the effects of chronic renal failure, including poor VitD activation, hyperphosphatemia, and hypocalcemia
  • hyperparathyroidism leads to bone reabsorption, burn out, and bone fibrosis
  • characterized by osteomalacia
  • and osteoporosis since the metabolic acidosis leaches calcium out of bones
141
Q

Angiomyolipma

A

a renal hamartoma comprised of blood vessels, smooth muscle, and adipose tissue with increased frequency in those suffering tuberous scelerosis

142
Q

Renal Cell Carcinoma

A
  • a malignant epithelial tumor arising from the tubules
  • presents with a classic triad of hematuria, palpable mass, and flank pain
  • paraneoplasic syndromes derived from increased EPO, renin, PTHrP, or ACTH (polycythemia vera, HTN, hypercalcemia, or Cushing syndrome)
  • gross exam reveals a yellow mass, while microscopically, you see cells with abundant clear cytoplasm
  • pathogenesis involves loss of VHL, a tumor suppressor, which increases IGF-1 release and HIF transcription factor, increasing VEGF an PDGF expression
  • may be sporadic (often a male over 60 with history of smoking and a single tumor in the upper pole) or hereditary (bilateral and earlier age of onset)
  • one of few carcinomas that utilize hematogenous spread (T staging takes into account involvement of the renal vein)
  • most likely to spread to lung and bone
143
Q

Why does renal cell carcinoma occasionally cause a varicocele? In which side is it most likely?

A
  • the left side is most likely because involvement of the left renal vein by the carcinoma can block drainage of teh eft spermatic vein
  • the right spermatic vein, however, drains directly into the IVC
144
Q

On which chromosome is the VHL gene located?

A

chromosome 3

145
Q

Von Hippel-Lindau disease

A
  • autosomal dominant disorder associated with inactivation for the VHL gene
  • increases the risk for hemangioblastoma of the cerebellum and renal cell carcinoma
146
Q

Wilms tumor

A
  • a malignant tumor comprised of blastema, primitive glomeruli and tubules, and stormal cells
  • the most common malignant renal tumor in children
  • presents as a large, unilateral flank mass with hematuria and hypertension
  • usually sporadic but may be seen as part of WAGR, Denys-Drash, and Beckwiith-Weidemann syndromes
147
Q

WAGR syndrome

A
  • a syndrome associated with deletion of the WT1 tumor suppressor gene
  • presents with Wilms tumor, Aniridia, Genital abnormalities, and mental/motor Retardation
148
Q

Denys-Drash syndrome

A
  • a syndrome association with mutations of WT1

- presents with Wilms tumor, progressive renal disease, and male pseudohermaphroditism

149
Q

Beckwith-Wiedemann syndrome

A
  • a syndrome associated with mutations in the WT2 gene cluster, particularly IGF-2
  • presents with Wilms tumor, neonatal hypoglycemia, muscular hemihypertrophy, and organomegaly including the tongue
150
Q

On what chromosome are the WT1 and WT2 genes located? With what are they associated?

A
  • found on chromosome 11
  • they are necessary for proper induction of the the metanephros parenchyma by the ureteric bud
  • WT1 deletion associated with WAGR syndrome, WT1 mutation associated with Denys-Drash syndrome, WT2 mutation associated with Beckwith-Wiedemann syndrome
151
Q

Adenocarcinoma of the Bladder

A
  • a malignant proliferation of glands, usually involving the baldder
  • can arise from three etiologies: tracheal remnant (tumor develops in the dome of the bladder), cystitis glandular (chronic inflammation leads to columnar metaplasia then adenocarcinoma), or exstrophy (congenital failure to form the caudal anterior abdominal and bladder walls exposes the bladder increases risk for malignancy)
152
Q

Describe the urachus. What risk does it carry with it?

A
  • a fetal structure that connects the fetal bladder to the yolk sac and allows waste drainage
  • lined by glandular cells
  • failure to involute is likely to lead to an adenocarcinoma developing in the dome of the bladder
153
Q

Squamous Cell Carcinoma of the Bladder

A
  • a malignant proliferation of squamous cells
  • arises in a background of squamous metaplasia
  • risk factors include chronic cystitis (patient is likely an older woman), Schistosoma haematobium infection (patient is usually an Egyptian male), or long-standing nephrolithiasis
154
Q

Urothelial Carcinoma

A
  • a malignancy arising form the lining of the renal pelvis, ureter, or urethra but most often the bladder
  • generally seen in older adults with painless hematuria
  • risk factors include cigarette smoke, naphthylamine, azo dyes, and long-term cyclophosphamide or phenacetin use
  • tumors arise via two pathways: flat develop as a high grade flat tumor and then invades (associated with early p53 mutations) while papillary develop as a low-grade papillary tumor that progresses to a high-grade papillary tumor and then invades (no p53 association)
  • often multifocal and recur
155
Q

Renal Oncocytoma

A
  • a bening epithelial cell tumor arising from the collecting ducts
  • gross examination reveals a well-circumscribed mass with a central scar
  • microscopic examination reveals large, eosinophilic cells
  • presents with painless hematuria, flank pain, and an abdominal mass
156
Q

Stress Incontinence

A
  • an outlet incompetence defined by leakage with an increase in intra-abdominal pressure
  • risk increases with obesity, vaginal delivery, or prostate surgery
  • treat with pelvic floor muscle strengthening exercises (Kegels), weight loss, or pessaries
157
Q

Urgency Incontinence

A
  • an overactive bladder due to detrusor instability
  • leakage is accompanied by the urge to void immediately
  • treatment with Kegel exercises, bladder training (e.g. timed voiding, distraction/relaxation techniques, etc.), or antimuscarinics
158
Q

Mixed incontinence

A

a combination of stress and urgency incontinence

159
Q

Overflow Incontinence

A
  • an incontinence defined by incomplete emptying due to either detrusor under activity or outlet obstruction
  • leakage is due to overfilling secondary to an increase in post-void residual volume
  • treat with catheterization or by relieving the obstruction (a-blockers work particularly well for patients with BPH)
160
Q

Diffuse Cortical Necrosis of the Kidneys

A
  • an acute, generalized cortical infarction of both kidneys
  • likely due to a combination of vasospasm and DIC
  • associated with obstetric catastrophes and septic shock
161
Q

What are the consequences of renal failure, acute or chronic?

A

MAD HUNGER

  • metabolic acidosis
  • dyslipidemia
  • hyperkalemia
  • uremia (nausea, anorexia, pericarditis, platelet dysfunction, encephalopathy with asterixis)
  • Na/H2O retention (HF, pulmonary edema, HTN)
  • Growth retardation and developmental delay
  • Erythropoietin failure (anemia)
  • Renal osteodystrophy
162
Q

What is the difference between simple and complex renal cysts?

A
  • simple are filled with ultra filtrate, are typically asymptomatic, and require no action
  • complex are those that are separated, enhanced, or have solid components, which require follow-up and removal due to the risk for RCC

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