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Step1 > Renal > Flashcards

Renal Flashcards

1
Q

Pronephros

A

week 4

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2
Q

Mesonephros

A

interim kidney in first trimester

becomes male genital system

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3
Q

Metanephros

A

permanent kidney

appears in 5th week

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4
Q

Ureteric bud gives rise to

A

ureter, pelvises, calyces, collecting ducts, fully canalized by week 10

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5
Q

metanephric mesenchyme

A

interacts with ureteric bud

induces differentiation and formation of glomerulus through to distal convoluted tubule

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6
Q

Ureteropelvic junction is last to canalize and most common site of ______

A

obstruction

can lead to hydronephrosis

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7
Q

Babies who cant pee in utero develop the potter sequence which consists of:

A 
pulmonary hypoplasia
oligohydramnios
twisted face
twisted skin
extremity defects
renal failure (in utero)

oligohydramnios causes the other problems due to compression

caused by aut. recessive polycystic kidney disease, obstructive uropathy, bilateral renal agenesis, chronic placental insufficiency

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8
Q

horseshoe kidney

A

inferior poles of both kidneys duse abnormally and get trapped under the inferior mesenteric artery. This results in them remaining low in the abdomen

kidney functions normal

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9
Q

Patient is born with only one functioning kidney.

A

congenital solitary functioning kidney

hypertrophy of contralateral kidney

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10
Q

unilateral renal agenesis

A

ureteric bud fails to develop and induce differentiation of metanephric mesenchyme

complete absence of kidney and ureter

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11
Q

multicystic dysplastic kidney

A

ureteric bud fails to develop and induce differentiation of metanephric mesenchyme

results in nonfunctioning kidney consisting of cysts and connective tissue

unilateral

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12
Q

bilateral multicystic dysplastic kidney can result in

A

potters syndrome

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13
Q

Duplex collecting system

A

bifurcation of ureteric bud before it enters the metanephric blastema creates a Y shaped bifid ureter

OR

two ureteric buds reaching and interacting with metanephric blastema

strongly associated with vesicoureteral reflux and or ureteral obstruction which increases risk of UTI

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14
Q

Posterior urethral valves

A

Membrane remnant in the posterior urethra in males

persistence and lead to urethral obstruction

presents prenatally by hydronephros and dilated or thick walled bladder on ultrasound

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15
Q

What is the most common cause of bladder outlet obstruction in male infants

A

Posterior urethral valves

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16
Q

What kidney is used for donor transplantation

A

Left kidney because of its longer renal vein

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17
Q

Renal blood flow

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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18
Q

Course of ureters

A

renal pelvis –> under gonadal arteries –> over common iliac artery –> under uterine artery/vas deferns (retroperitoneal)

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19
Q

Three points of constriction of the ureter

A

ureterovesical junction
ureteropelvic junction
pelvic inlet

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20
Q

In a 70 kg person what is the total body water and the ICF and ECF

A

total body water is 60% or 42 kg
ICF is 40% (2/3) or 28 kg
ECF is 20% (1/3) or 14 kg

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21
Q

ECF is composed of

A

plasma 25% of ECF

Interstitial fluid 75% of ECF

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22
Q

There is a ______ K concentration intracellularly

A

high

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23
Q

plasma volume can be measured by radiolabeling ____

A

albumin

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24
Q

extracellular volume can be measured by

A

inulin and mannitol

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25
Q

The glomerular filtration barrier

A

composed of

  • Fenestrated capillary endothelium
  • Basement membrane with type 4 collagen chains and heparan sulfate
  • Epithelial layer consisting of podocyte foot processes
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26
Q

how does the glomerular filtration barrier work according to size and charge

A
  • all three layers are neg charge and prevent entry of other neg charged molecules like albumin
  • fenestrated capillary endothelium prevent entry of >100 nm molecules/blood cells
  • podocyte foot processes interpose with basement membrane
  • slit diaphragm which prevent entry of molecule >50-60 nm
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27
Q

Renal clearance formula

A

Cx=(UxV)/P

Ux= Urine concentration of X
Px= Plasma concentration of X
V=Urine flow rate
Cx=Clearance of X

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28
Q

If Cx is ____ than GFR

A

less than GFR

net reabsorption of X

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29
Q

If Cx is ____ than GFR

A

greater than GFR

net tubular secretion of X

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30
Q

If Cx is _____than GFR

A

equal to GFR

no net secretion or reabsorption

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31
Q

____ clearance can be used to measure GFR. Why?

A

Inulin

because it is freely filtered and is neither reabsorbed nor secreted

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32
Q

GFR equation

A

Uinulin x V/Pinulin = Cinulin

= Kf[(Plasma concentration of glomerular capillary - plasma concentration of bowman space)-(Osmotic concentration of glomerular capillary)]

= (Pcr x Una) / (Ucr x Pna)

V=urine flow rate

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33
Q

_____ clearance is an approximate measure of GFR. Why only an estimate?

A

creatinine

Slightly overestimates the GFR because creatinine is moderately secreted by renal tubules

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34
Q

Effective renal plasma flow (eRPF) can be estimated using ______

A

para-aminohippuric acid (PAH) clearance

100% excretion of all PAH that enters the kidney

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35
Q

Effective renal plasma flow equation

A

eRPF=UpahxV/Ppah=Cpah

underestimates true renal plasma flow slightly

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36
Q

renal blood flow =

A

RPF/(1-Hct)

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37
Q

plasma volume

A

TBVx(1-Hct)

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38
Q

Filtration fraction

A

FF= GFR/RPF

normal filtration fraction is 20%

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39
Q

Filtered load

A

GFR x plasma concentration

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40
Q

Prostaglandins _______ afferent arterioles

A

dilate

“PDA”

This causes increased renal plasma flow and increased GFR. Therefore no change in filtration fraction (GFR/RPF)

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41
Q

Angiotensin II ___ efferent arterioles

A

constrict

“ACE”

This causes a drop in GFR but an increase in GFR, therefore there is an increase in FF (GFR/RPF)

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42
Q

Filtered load

A

GFR x Px

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43
Q

Excretion rate

A

V x Ux

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44
Q

Reabsorption rate

A

filtered-excreted

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45
Q

Secretion rate

A

excreted - filtered

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46
Q

Fractional excretion of sodium (Fe na)

A

Fe Na= Na excreted/Na filtered= (VxUna)/(GFRxPna)

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47
Q

At what plasma level does glucosuria begin

A

~200 mg/dL

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48
Q

At what plasma level are transporters fully saturated (Tm)

A

~375 mg/dL

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49
Q

At normal glucose levels (60-120) glucose is ______ reabsorbed in ________ tubule by Na/Glucose cotransport

A

completely

proximal convoluted tubule (PCT)

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50
Q

What part of the nephron do you reabsorb all glucose and amino acids.

A

early proximal convoluted tubule

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51
Q

what part of the nephron is most HCO3-, Na+, Cl-, PO4, K+, H2O, Uric Acid reabsorbed

A

early proximal convoluted tubule

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52
Q

what part of the nephron is there a brush border and isotonic absorption. It generates and secretes NH3 which enables the kidney to secrete more H+

A

early proximal convoluted tubule

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53
Q

Where does PTH act to inhibit Na/PO4 cotransport ? And what does it result in?

A

early proximal convoluted tubule

PO4 excretion

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54
Q

Where does AT II act to stimulate Na/H exchange? and what does it result in

A

early proximal convoluted tubule

increase Na, H2O, and HCO3 reabsorption

contraction alkalosis

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55
Q

Where is 65-80% of Na reabsorbed

A

early proximal convoluted tubule

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56
Q

Where is H20 passively reabsorbed in the nephron and how

A

Thin descending loop of henle
via medullary hypertonicity
It is impermeable to Na

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57
Q

what part of the nephron is the concentrating segment that makes urine hypertonic

A

Thin descending loop of henle

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58
Q

What part of the nephron reabsorbs Na, K , and Cl. Indirectly induces paracellular reabsorption of Mg and Ca through a positive lumen potential generated by K backleak

A

Thick ascending loop of henle

10-20% of Na reabsorbed

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59
Q

What part of the nephron is important for making the urine less concentrated and is impermeable to H20

A

Thick ascending loop of henle

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60
Q

What part of the nephron is important for reabsorbing Na, Cl and is impermeable to H20. It is important for fully diluting (hypotonic) the urine.

A

Early distal convoluted tubule

5-10% Na reabsorbed

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61
Q

PTH effect on early distal convoluted tubule

A

increases Ca/Na exchange which results in Ca reabsorption

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62
Q

What part of the nephron is regulated by aldosterone and it reabsorbs Na in exchange for secreting K+ and H+

A

Collecting tubule

3-5% Na reabsorbed

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63
Q

Effect of aldosterone on the collecting tubule

A

acts on mineralocorticoid receptor to induce protein synthesis

in principal cells: increase apical K conductance, increase Na/K pump, increase epithelial Na channel (ENaC) activity –> lumen negativity –> increases H+ ATPase activity –> H+ secretion –> increases HCO3/Cl exchanged activity

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64
Q

Effect of ADH on the collecting tubule

A

acts at V2 receptor to insert aquaporin H2O channels on apical side

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65
Q

What renal syndrome is due to a defect in the general reabsorption within the PCT

A

Fanconi syndrome

results in excretion of AA, glucose, HCO3, PO4, and all substances reabsorbed by the PCT

may lead to metabolic acidosis, hypophosphatemia, osteopenia

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66
Q

What renal syndrome is due to a resorptive defect in the thick ascending loop of henle that affects Na/K/2Cl cotransporter

A

Bartter syndrome

results in metabolic alkalosos, hypokalemia, hypercalciuria

increased renin, aldosterone, urine Ca

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67
Q

What renal syndrome is due to reabsorption defect of NaCl in DCT

A

Gitelman syndrome

results in metabolis lakalosis, hypokalemia, hypocalciuria

Increased renin, aldosterone
Decreased serum Mg and Urine ca

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68
Q

What renal syndrome is due to gain of function mutation that increases activity of Na channel and thus increased Na reabsorption in collecting tubules

A

Liddle syndrome

results in metabolic alkalosis, hypokalemia, hypertension, decreased aldosterone

Increased BP
Decreased plasma renin and aldosterone

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69
Q

What renal syndrome present similar to hyperaldosteronism ? how do you treat it?

A

liddle syndrome

treat with amiloride

“it is a liddle like hyperaldosteronism”

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70
Q

What renal syndrome is due to a hereditary deficiency of 11beta hydroxysteroid dehydrogenase.

A

Syndrome of Apparent Mineralocorticoid excess

This results in excess cortisol (usually the enzyme would convert it to cortisone) and ultimately increased mineralocorticoid receptor activity

Metabolic alkalosis, hypokalemia, hypertension, decreased serum aldosterone level

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71
Q

Syndrome of Apparent Mineralocorticoid excess can be caused from _____ acid present in licorice which blocks activity of 11beta hydroxysteroid dehydrogenase

A

glycyrrhetinic acid

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72
Q

How can you best treat Syndrome of Apparent Mineralocorticoid excess

A

treat with K sparing diuretics which decrease mineralocorticoid effects

or treat with corticosteroids which result in decrease of endogenous cortisol production. Ultimately decreasing mineralocorticoid receptor activation

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73
Q

TF/P > 1

A

Tubular fluid concentration/plasma concentration

when solute is reabsorbed less quickly than water or when solute is secreted

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74
Q

TF/P = 1

A

Tubular fluid concentration/plasma concentration

When solute and water are reabsorbed at the same rate

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75
Q

TF/P<1

A

Tubular fluid concentration/plasma concentration

when solute is reabsorbed more quickly than water

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76
Q

What cells secrete renin?

A

juxtaglomerular cells in response to decreased renal blood pressure and increased sympathetic tone (beta 1)

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77
Q

What is reaction is renin important for

A

converting angiotensinogen to angiotensin I

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78
Q

What enzyme converts angiotensin I to angiotensin II

A

ACE

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79
Q

Renin

A

responds to decreased renal perfusion pressure that is detected by renal baroreceptors in the afferent arterioles.

It increases renal sympathetic discharge (beta 1 effect) and decreases NaCl delivery to macula densa cells

80
Q

Angiotensin II

A

helps maintain blood volume and blood pressure. Net effect of preservation of renal function with increased FF in low volume state with simultaneous Na reabsorption to maintain circulating volume

responds to drop in BP by causing efferent arteriole constriction which increases GFR and increases FF but with compensatory Na reabsorption in proximal and distal nephron

limits reflex bradycardia which would normally accompany its pressor effects

81
Q

ANP/BNP

A

released from atria (ANP) and ventricles (BNP) in response to increase volume –> relaxes vascular smooth mm via cGMP and increases GFR –> decrease in renin

ANP : secreted in response to increased atrial pressure which causes increased GFR and increased Na filtration with no compensatory Na reabsorption in distal nephron. Net effect: Na loss and volume loss

“check” on the renin-angiotensin-aldosterone system

82
Q

What is the effect of ANP/BNP on the afferent and efferent arterioles

A 
Afferent dilates
Efferent constriction
Promotes natriuresis (excretion of Na in urine)
83
Q

ADH

A

responds to increased plasma osmolality and responds to low blood volume states

stimulates reabsorption of water in collecting ducts

Also stimulates reabsorption of urea in collecting ducts to maintain corticopapillary osmotic gradient

84
Q

Aldosterone

A

primarily regulated ECF volume and Na content

responds to low blood volume states and increased plasma [K]

Causes increased Na reabsorption, K secretion, H secretion

85
Q

What responds to hyperkalemia by increasing K excretion

A

Aldosterone

86
Q

Angiotensin II effects

A

vasoconstriction –> increased BP

Constrict efferent arteriole –> Filtration fraction increase –> preserves GFR when RBF is low

Increase kidney Na/H activity at the PCT cell –> Na, HCO3, H20 reabsorption –> contraction alkalosis

Causes aldosterone secretion which causes the alpha intercalated cells to secrete H+ by increase in H+ ATPASE activity

Aldosterone secretion also causes principal cells to reabsorb Na nd secrete K

ADH release from posterior pituitary causes principal cells to reabsorb H20 by increasing aquaporins

87
Q

Juxtaglomerular apparatus

A

consists of mesengial cells, juxtaglomerular cells, and macula densa

maintains the GFR via renin-angiotensin aldosterone system

88
Q

Juxtaglmerular cells

A

modified smooth muscle of afferent arteriole

89
Q

Macula densa

A

NaCl sensor
Located at distal end of loop of Henle

sense decrease NaCl delivery to DCT and increase renin release –> efferent arteriole vasoconstriction –> increases GFR

90
Q

How can beta blockers impact the juxtaglomerular apparatus

A

they decrease BP by inhibiting Beta 1 receptors of the JGA and thus decreasing renin release

91
Q

Released by interstitial cells in peritubular capillary bed in response to hypoxia

A

erythropoietin

this is why it is supplemented in patients with chronic kidney disease

92
Q

_____ cells convert 25-OH vitamin D3 to 1,25-(OH)2 vitamin D3 (calcitriol, active form). What enzyme is important for this?

A

PCT cells

via 1alpha hydroxylase ( + by PTH)

93
Q

Paracrine secretion of ______ vasodilates the afferent arterioles to increase RBF

A

prostaglandins

94
Q

NSAIDs block ________and thus constriction of afferent arterioles and decreased GFR. This may result in acute renal failure in low renal blood flow states

A

prostaglandins

95
Q

______ is secreted by PCT cells and promotes natriuresis. At low doses it ______ the interlobular arteries, afferent arterioles, efferent arterioles and thus increases RBF (little or no change to GFR). At higher doses it acts as a _______

A

Dopamine
Dilates
Vasoconstrictor

96
Q

Parathyroid hormone effect on kidney

A

Secreted in response to a drop in plasma Calcium concentrations, increase in PO4, or decrease in plasma 1,25-(OH)2D3

Causes increase in Ca reabsorption (DCT), decrease in PO4 reabsorption (PCT), and increase 1,25(OH)2D3 production

increased Ca and PO4 absorption from gut via vitamin D

97
Q

Insulin shifts K out or into cells?

A

INsulin therefore INto cells –> hypokalemia

98
Q

What causes hypokalemia due to shift of K into cells

A

Hypoosmolarity
Alkalosis
Beta adrenergic agonist ( increase Na/K ATPase)
Insulin (increase Na/K ATPase)

99
Q

What causes hyperkalemia due to shift of K out of cells?

A 
Digitalis (blocks Na/K ATPase)
Hyperosmolarity
Lysis of cells
Acidosis
Beta blockers
High blood sugar
Succinylcholine

“DO LABSSS”

100
Q

Hypokalemia effects

A

U waves and flattened T waves on ECG

Arrhythmias, mm cramps, spasm, weakness

101
Q

Hyperkalemia effects

A

Wide QRS, peaked T waves, arrhythmias, mm weakness

102
Q

Hypocalemia effects

A

Tetany, seizures, QT prolongation, twitching (Chvostek sign), spasm (trousseau sign)

103
Q

Hypercalemia effects

A 
Stones --> renal stones
Bones --> Bone pain
Groans --> abdominal pain
Thrones --> increased urinary frequency
Psychiatric overtones --> anxiety, altered mental status
104
Q

Hypomagnesia effects

A

Tetany
Torsades de pointes
hypokalemia
hypocalcemia

105
Q

Hypermagnesia effects

A 
Decreased DTRs
Lethargy
Bradycardia
Hypotension
Cardiac Arrest
Hypocalcemia
106
Q

hypophosphatemia effects

A

Bone loss
osteomalacia in adults
rickets in children

107
Q

Hyperphosphatemia effects

A

renal stones
metastatic calcifications
hypocalcemia

108
Q

SIADH effects on BP, Renin, aldosterone

A

normal or increased BP
Decreased Plasma renin
decreased aldosterone

109
Q

Primary hyperaldosteronosim (Conn syndrome)

A

Increased BP and aldosterone

Decreased plasma renin

110
Q

Renin secreting tumor

A

Increased BP, increased plasma renin, increased aldosterone

111
Q

Metabolic acidosis

A

decreased pH due to decreased [HCO3] or <20

compensate by decreasing PCO2 by hyperventiation

immediate compensation

112
Q

Metabolic alkalosis

A

increased pH due to increased [HCO3] or >28

immediate compensation by increasing PCO2 by hypoventiation

113
Q

Respiratory acidosis

A

Decreased pH due to increased PCO2 or >44

delayed compensation by increasing [HCO3] reabsorption

114
Q

Respiratory alkalosis

A

Increased pH due to decreased PCO2 or < 36

delayed compensation by decreasing [HCO3] reabsorption

115
Q

Winters formula

A

PCO2=1.5[HCO3]+8 +/- 2

predicted respiratory compensation for a simple metabolic acidosis

if predicted< measured PCO2 respiratory acidosis

if predicted> measured PCO2 respiratory alkalosis

116
Q

Henderson Hasselbach equation

A

pH= 6.1 + log((HCO3)/(0.03PCO2))

117
Q

Check the anion gap when there is

A

metabolic acidosis

118
Q

anion gap formula

A

Na- (Cl+HCO3)

if >12 anion gap
if 8-12 normal anion gap

119
Q

anion gap metabolic acidosis (AGMA)

A

MUDPILES

Methanol (formic acid)
Uremia
Diabetic Ketoacidosis
Propylene Glycol
Iron tablets or INH
Lactic Acidosis
Ethylene glycol (oxalic acid)
Salicylates (late)
120
Q

Normal anion gap metabolic acidosis (NAGMA)

A 
HARDASS
Hyperalimentation
Addison disease
Renal tubular acidosis
Diarrhea
Acetazolamide
Spironolactone
Saline infusion
121
Q

Metabolic alkalosis caused by

A

Loop diuretics
Vomiting
Antacid Use
Hyperaldosteronism

122
Q

Distal renal rubular acidosis

A

Type 1

NAGMA

inability of alpha intercalated cells tos ecrete H+ –> no new HCO3 is generated –> metabolic acidosis

urine ph >5.5 and low serum K

increased risk for calcium phosphate kidney stones (due to increased urine pH and increased bone turnover)

123
Q

Proximal renal tubular acidosis

A

Type 2

NAGMA

defect in PCT HCO3 reabsorption which increases excretion of HCO3- in urine resulting in metabolic acidosis

urine pH <5.5 and decreased serum K

Increased risk for hypophosphatemic rickets (in fanconi syndrome)

124
Q

Hyperkalemic tubular acidosis

A

type 4

NAGMA

hypoaldosteronism or aldosterone resistance; hyperkalemia –> drop in NH3 synthesis in PCT –> decrease in NH4 excretion

125
Q

Amphotericin B toxicity can cause what type of renal tubular acidosis

A

Distal renal tubular acidosis

type 1

126
Q

Fanconi syndrome, multiple myeloma, carbonic anhydrase inhibitors can cause what type of renal tubular acidosis

A

Proximal renal tubular acidosis

type 2

127
Q

Decreased aldosterone production or increased aldosterone resistance can cause what type of renal tubular acidosis

A

Hyperkalemic tubular acidosis

type 4

128
Q

Hematuria with no casts

A

bladder cancer or kidney stones

129
Q

Pyuria with no casts

A

Acute cytitis

130
Q

RBC casts

A

Glomerulonephritis, hypertensive emergency

131
Q

WBC casts

A

Tubulointerstitial inflammation, acute pyelonephritis, transplant rejection

132
Q

Fatty casts (oval fat bodies)

A

Nephrotic syndrome. Associated with Maltese cross sign)

133
Q

Granular muddy brown casts

A

acute tubular necrosis

134
Q

Waxy casts

A

end stage renal disease/chronic renal failure

135
Q

Hyaline casts

A

nonspecific, can be a normal finding, often seen in concentrated urine samples

136
Q

Nephrotic syndrome

A

Massive proteinuria (>3.5 g/day), with hypoalbuminemia. hyperlipidemia, edema, frothy urine with fatty casts

podocyte disruption results in impaired charge barrier

associated with hypercoagulable state due to antithrombin (AT) III loss in urine and increased risk of infection (loss of immunoglobulins in urine and soft tissue compromise by edema)

137
Q

Nephritic syndrome

A

Inflammatory

RBC casts in urine and hematuria if glomeruli involved

due to GBM disruption

can see hypertension (due to salt retention), increased BUN and creatinine, oliguria, hematuria, azotemia

138
Q

Nephrotic-Nephritic syndrome

A

severe nephritic syndrome with profound GBM damage that damages the glomerular filtration charge barrier causing nephrotic range proteinuria (>3.5) and concomitant features of nephrotic syndrome

139
Q

What nephritic syndromes are commonly seen in nephrotic-nephritic syndrome

A

Diffuse proliferative glomerulonephritis

Membranoproliferative glomerulonephritis

140
Q

Most common cause of nephrotic syndrome in children

A

Minimal change disease (lipoid nephrosis)

mostly primary and is triggered by recent infection, immunization, immune stimulus. –> excellent response to steroids

light microscopy - normal
Immunofluorescence - negative
Electron microscopy - effacement of podocyte foot processes

141
Q

Most common cause of nephrotic syndrome in AF and Hispanics

A

Focal segmental glomerulosclerosis (nephropathy)

primary or secondary

primary has inconsistent response to steroids and make progress to chronic kidney disease

light microscopy- Segmental sclerosis and hyalinosis

Immunofluorescence- often negative but may be + for nonspecific focal deposits of IgM, C3, C1

Electron microscopy - effacement of foot processes similar to minimal change disease

142
Q

Membranous nephropathy/ membranous glomerulonephritis

A

can be primary or secondary

primary has poor response to steroids and can progress to CKD

Light microscopy- diffuse capillary and GBM thickening
Immunofluorescence- granular due to IC deposition
Electron microscopy- spike and dome” appearance of subepithelial deposits

143
Q

Most common organ to be affected by amyloidosis

A

Kidney!

light microscopy - congo red stain shows apple green birefringence under polarized light due to amyloid deposition in the mesangium

Nephropathy

144
Q

Most common cause of end stage renal disease in the united states

A

Diabetic glomerulonephropathy

Hyperglycemia –> nonenzymatic glycation of tissue proteins –> mesangial expansion

GBM thickening and increased permeability

Hyperfiltration due to glomerular HTN and increased GFR –> glomerular hypertrophy and glomerular scarring (glomerulosclerosis) leading to further progression of nephropathy

Light microscopy- Mesengial expansion, GBM thickening, eosinophilic nodular glomerulosclerosis (kimmelstiel-wilson lesions)

145
Q

Acute poststreptococcal glomerulonephritis

A

seen in children 2-4 weeks after a group A strep infection of pharynx or skin.

resolves in children
Adults can get renal insufficiency

sx: peripheral, periorbital edema, cola colored urine, HTN. + strep titers/serologies, decrease complement levels (C3) due to consumption

LM: glomeruli enlarged and hypercellular
IF: starry sky granular appearance. Lumpy bumpy. Due to IgG, IgM, C3 deposition along GBM and mesangium
EM: subepithelial immune complex humps

146
Q

Acute poststreptococcal glomerulonephritis is what type of hypersensitivity reaction

A

type III

147
Q

This nephritis results in a crescent moon shape on light microscopy

A

rapidly progressive (crescentic) glomerulonephritis

cresent consists of fibrin and plasma proteins with glomerular parietal cells, monocytes, and macrophages

148
Q

What conditions can result in rapidly progressive glomerulonephritis

A

1) good pastures
2) Granulomatosis with polyangitis (wegners)
3) Microscopic polyangitis

149
Q

This nephritic syndrome is mostly due to SLE

A

Diffuse proliferative glomerulonephritis

Light microscopy: wire looping of capillaries
IF: granular
EM: subendothelial and sometimes intramembranous IgG based ICs often with C3 deposition

150
Q

IgA nephropathy (Berger disease)

A

episodic hematuria that occurs concurrently with resp or GI tract infections (IgA is secreted by mucosal linings)

Renal pathology of IgA vasculitis or HSP

LM: mesengial proliferation
IF: IgA based IC deposits in mesangium
EM: mesengial IC deposition

151
Q

Alport syndrome is due to a mutation in

A

type IV collagen

152
Q

Alport syndrome

A

mutation in type IV collagen results in thining and splitting of glomerular basement membrane

153
Q

Triad of eye problems, glomerulonephritis, sensorineural deafness

A

cant see, cant pee, cant hear a bee

Alport syndrome

EM: basket weave

154
Q

Type I membranoproliferative glomerulonephritis may be secondary to _____ or _____ infection

A

hep B or hep C

155
Q

Type II membranoproliferative glomerulonephritis is associated with _____ nephritic factor

A

C3

IgG antibody that stabilizes C3 convertase which results in persistent complement activation –> drop in C3 levels

intramembranous deposits also called dense deposit disease

156
Q

Type I and II membranoproliferative glomerulonephritis have this appearance on H&E and PAS stains

A

mesangial ingrowth –> GBM splitting –> tram track appearance on H&E and PAS stains

157
Q

Most common kidney stone presentation

A

calcium oxalate stone in patient with hypercalciuria and normocalcemia

158
Q

Calcium oxalate

A

hypocitraturia, low pH, radioopaque on xray and CT, shaped like an envelope or dumbbell

can result from ethylene glycol (antifreeze), vitamin c abuse, malabsorption

treat with thiazides, citrate, low sodium diet

159
Q

Calcium phosphate

A

increased pH, radioopaque on xray and CT, wedge shaped prism

tx with low sodium diet and thiazides

160
Q

Ammonium magnesium phosphate (struvite)

A

increased pH, radiopaque on xray and CT, coffin lid appearance

Usually due to urease + bugs that hydrolyze urea to ammonia –> urea alkalinization

forms staghorn calculi

tx: eradication of underlying infection, surgical removal of stone

161
Q

Uric acid

A

decreased pH, radiolUcent on xray, minimally visible on MRI, rhomboid or rosettes

hyperuricemia. Often seen in diseases with increased cell turnover

treat with alkalinization of urine, allopurinol

162
Q

cystine

A

decreased pH, radioopaque on xray and CT, hexagonal

cystine reabsorbing PCT transporter loses function, causes cystinuria

results in COLA - cysteine, Ornithine, lysine, arginine poor reabsorption

staghorn calculi

+ sodium nitroprusside test

treat with low sodium diet, alkalinization of urine, chelating agents if refractor

163
Q

serum _____ becomes elevated if obstruction is bilateral or if patient has obstructed solitary kidney

A

creatinine

164
Q

Most common primary renal maligancy. Most common in men 50-70 yo. Increased incidence with smoking and obesity

A

Renal cell carcinoma (RCC=3 letters= chromosome 3 gene deletion)

polygonal clear cells that accumulate lipids and carbs. Often golder yellow due to increased lipid content

originate from the PCT __> invades renal vein (may develop varicocele if left sided) __ IVC –> hematogenous spread –> metastasis to lung

pt can also present with hematuria and polycythemia

rarely curative

165
Q

Benign epithelial cell tumor arising from collecting ducts and results in a well circumscribed mass with central scar. Patient has painless hematuria and large eosinophilic cells with abundant mitochondria without perinuclear clearing

A

Renal oncocytoma

166
Q

Most common renal malignancy of early childhood between 2-4 yo

A

Nephroblastoma (wilms tumor)

167
Q

Nephroblastoma (wilms tumor)

A

presents with large palpable unilateral flank mass and or hematuria. Contains embryonic glomerular structures

168
Q

Nephroblastoma (wilms tumor) results from what kind of mutation

A

LOF mutations of tumor suppressor genes WT1 and WT2 on chromosome 11

169
Q

Denys drash syndrome

A
  • Wilms tumor
  • Diffuse mesangial sclerosis (Early onset nephrotic syndrome)
  • Dysgenesis of gonads (male pseudohermaphroditism), WT1 mutation
170
Q

WAGR complex

A

wilms tumor
Aniridia (absence of iris)
Genitourinary malformation
Mental retardation/intellectual disability (WT1 deletion)

171
Q

Beckwith-wiedemann syndrome

A

wilms tumor, macroglossia, organomegaly, hemihyperplasia (WT2 mutation)

172
Q

Transitional cell carcinoma

A

urothelial carcinoma

most common tumor of urinary tract system

painless hematuria without casts

risk: Phenacetin, Smoking, Aniline dyes, and cyclophosphamide

173
Q

Squamous cell carcinoma of the bladder

A

chronic irritation of urinary bladder can result in squamous metaplasia –> dysplasia and squamous cell carcinoma

risk: schistosoma haematobium infection, chronic cystitis, smoking, chronic nephrolithiasis.

present with painless hematuria

174
Q

Patient leaks with urge to void immediately due to overactive bladder (detrusor instability)

A

related to UTI

urgency incontinence

175
Q

Overflow incontinence

A

imcomplete emptying (detrusor underactivity or outlet obstruction) –> leak with overfilling

176
Q

What is the most common cause of UTI? what are the other causes?

A

E coli is most common overall
Staph sapro (sexually active)
Klebsiella
Proteus mirabilis (urine has ammonia scent)

177
Q

UTI lab findings

A

+ leukocyte esterase
+ nitrites (indicated gram -)
Sterile pyuria and - urine cultures suggest urethritis by N gonorrhoeae or chlamydia trachomatis

178
Q

Acute pyelonephritis

A

neutrophils infiltrate renal interstitium

affect cortex with sparing of glomeruli/vessels

WBC in urine ( +/- WBC cast)

CT shows striated parenchymal enhancement

179
Q

Chronic pyelonephritis

A

due to recurrent acute pyelonephritis

coarse asymmetric corticomedullary scarring , blunted calyx

Tubules contain eosinophilic casts resembling thyroid tissue (thyroidization of kidney)

180
Q

Xanthogranulomatous pyelonephritis

A

seen with chronic pyelonephritis

grossly orange nodules that can mimic tumor nodules; characterized by widespread kidney damage due to granulomatous tissue containing foamy macrophages

associated with proteus infection

181
Q

Acute kidney injury -abrupt decline in renal function as measured by increase of _____ and ____

A

creatinine and BUN

or by oliguria/anuria

182
Q

Prerenal azotemia

A

due to decreased RBF –> decreased GFR

Na/H20 and urea retained by kidney in an attempt to conserve volume

this increases BUN/creatinine ratio (urea is reabsorbed, creatinine is not) and decrease FEna

higher urine osmolality compared to intrinsic renal and postrenal injury

183
Q

Intrinsic renal failure

A

due to acute tubular necrosis : patchy necrosis –> debris obstructing tubule and fluid backflow across necrotic tubule –> decrease GFR

Urine has epithelial/granular casts

Urea reabsorption is impaired

decrease BUN/creatinine ratio and increase FE sodium

184
Q

Postrenal azotemia

A

due to outflow obstruction. develops only with bilateral obstruction or in a solitary kidney

185
Q

Chronic renal failure

A

usualyl due to HTN, DM, congenital anomalies

186
Q

Hypocalcemia, hyperphosphatemia, and failure of vitamin D hydroxylation associated with chronic renal disease and leads to

A

Secondary hyperparathyroidism

High serum PO4 can bing Ca and result in tissue deposits. This causes a drop in Ca

Decrease 1,25 OH2D3 results in decreased intestinal Ca absorption

results in subperiosteal thinning of bones

187
Q

Acute interstitial nephritis (tubulointerstitial nephritis)

A

Acute interstitial renal inflammation

pyuria (classically eosinophils) and azotemia occuring after administration of drugs that act as haptens, inducing hypersensitivity

Pee (diuretics)
Pain free (NSAIDs)
Penicillins and cephalosporins
Proton pump inhibitors
rifamPIN
188
Q

Most common cause of acute kidney injury in hospitalized patients

A

Acute tubular necrosis

189
Q

Acute tubular necrosis

A

can be fatal during the oliguric phase

increases FE sodium

granular “muddy brown” casts

can also be caused by ischemic - secondary to decreased renal blood flow which results in death of tubular cells that may slough into tubular lumen

Can also be caused by nephrotoxic due to secondary injury resulting from toxic substances

proximaly tubules are especially susceptible to nephrotoxic injury

190
Q

Acute tubular necrosis stages

A

1) inciting event
2) maintenance phase -oliguric. Risk of hyperkalemia, metabolic acidosis, uremia
3) recovery phase-polyuric, BUN and serum creatinine fall, risk of hypokalemia and renal wasting of other electrolytes minerals

191
Q

Vasospasms + DIC can result in generalized cortical infarction of both kidneys

A

Diffuse cortical necrosis

associated with obstetric catastrophes and septic shock

192
Q

Renal papillary necrosis

A

sloughing of necrotic renal papillae –> gross hematuria and proteinuria

may be triggered by recent injection or immune stimulus

associated with sickle cell disease or trait, acute pyelonephritis, NSAIDs, diabetes mellitus

193
Q

Numourous cysts in cortex and medulla. The kidneys are enlarged B/L. Eventually leads to destruction of parenchyma and progressive renal failure

A

autosomal dominant polycystic kidney disease

194
Q

Cystic dilation of colelcting ducts that presents in infancy.

A

Autosomal revessive polycystic kidney disease

associated with congenital hepatic fibrosis

significant oliguric renal failure in utero can lead to potter sequence.

195
Q

Inherited disease causing tubulointerstitial fibrosis and progressive renal insufficiency with inability to concentrate urine

A

Autosomal dominant tubulointerstitial kidney disease

or medullary cystic kidney disease

medullary cysts usually not visualized and there are smaller kidneys on ultrasound

poor prognosis

196
Q

mutation in PKD1 on chromosome 16 is common in what renal cyst disorder

A

Autosomal dominant polycystic kidney disease

also PKD2 on chromosome 4

associated with berry aneurysms, mitral valve prolapse, benign hepatic cysts, diverticulosis

197
Q

Ureter is immediately anterior to

A

internal iliac artery

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