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USMLE STEP 1 > Renal > Flashcards

Renal Flashcards

1
Q 
ACE Inhibitors 
Names
Uses
Toxicity
Contraindications
A

Captopril, Enalapril, Lisinopril
CHF, HTN, Diabetes, Renal Disease
Cough, Angioedema, Teratogen, Cr Increase, Hypotension, HyperK
Do not use in Renal Artery Stenosis

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2
Q

How are ATII Receptor Blockers Different from ACEI?

A

Do not cause cough or angioedema because they do not affect inhibit Bradykinin degradation

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3
Q

How do diuretics affect urine NaCl

A

Increased. Serum NaCl may decrease

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4
Q

How do diuretics change urine [K]?

A

All diuretics increase urine K except for KSD.

Serum K may decrease

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5
Q

Which Diuretics cause Acidosis?

A

CAI (decreased bicarb reabsorption) and KSD (hyperK –> H leaving cells)

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6
Q

Which diuretics cause alkalemia?

A

Loop and Thiazide
Decreased Vol –> ATII –> Na/H exchanger –> bicarb reabsorption (contraction alkalosis)
Decreased K –> H entering cells
Decreased K –> H (instead of K) exchanged for Na in CT

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7
Q 
K Sparring Diuretics
Names
Use
MoA
Tox
A

Spironolactone, Eplerenone, Amiloride, Triamterene
Increased Ald, Decreased K, CHF
S –/ Ald R, T and A –/ Na Channels
Increased K –> Arrhythmias, S –> gynecomastia + anti androgen

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8
Q

Which diuretics affect urine Ca?

A

Urine Ca increases with LD and decreases with Thiazide

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9
Q

Thiazide Diuretics
Uses
MoA
Toxicity

A

–/ NaCl reabsorption in DT
HTN, CHF, Increased Ca in Urine, Nephrogenic Diabetes Insipidus
Hyper Glucose, Lipids, Uric Acid, Ca
(HICC the GLUC)

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10
Q

Ethacrynic Acid

A

Like Furosemade for people allergic to Sulfur

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11
Q 
Loop Diuretics
Name
Use
Inhibited by
MoA (2)
Tox
A

Furosemide
–/ NaK2Cl pump, –> PGE –> AA dilation
Inhibited by NSAIDs
Edema (CHF, cirrhosis, Nephrotic Syndrome, Pul Edema), HTN, Hypercalcemia
Ototoxic, HypoK, Mg and Ca, Dehydration, Alergy, Alkalosis, Interstitial Nephritis, Gout

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12
Q

CAI
Names
Use
Tox

A 
Acetazolamide
Glaucoma, Make Urine Basic, Alkalosis, Altitude Sickness, Pseudotumor Cerebri
Met Acidosis (with increased Cl), Paresthesia, NH3 toxicity, Sulfa allergy
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13
Q 
Mannitol
Uses
MoA
Tox
Contras
A

Shock, OD, ICP, IOP
Osmotic Diuretic
Pul Edema, Dehydration
Contraindicated in CHF, anuria

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14
Q

Urea transport in the Kidney

A

PT: reabsorbed, Descending LoH: secreted, CD: Reabsorbed or stays in lumen depending on ADH

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15
Q

ADH and Urea

A

ADH –> UT1 in medullary collecting to increase Urea reabsorption which adds to corticopappillary osmotic gradient

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16
Q

Where is Vit D made in the Kidney?

What stimulates its production?

A

PT

PTH –> 1 alpha hydroxylase (which converts 25 vit D to 1, 25 vit D)

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17
Q

How does Vit D promote bone mineralization?

A

Vit D –> Osteoblasts –> alkaline phasphatase

AP hydrolyzes Pyrophasphate and other inhibitors of Ca-PO4 crystallization.

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18
Q

Functions of Vit D

A

GI reabsorption of Ca and PO4
Bone mineralization
Maintains serum [Ca]
–> monocytes to become osteoclasts

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19
Q

Drugs associated with Hematuria

A

Anticoagulants (warfarin and heparin)

Cyclophasphamide –> hemorrhagic cystitis and increased risk for transitional cell carcinoma

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20
Q

Tests for Protienuria

A

Dipstick for albumin

SSA (sulfosalicylic acid) for albumin and globins

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21
Q

Urea and GFR

A

Increased GFR –> Decreased Urea reabsorption

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22
Q

Functional Proteinuria

A

Not associated with rena disease

fever, exercise, CHF, Orthostatic

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23
Q

Overflow Proteinuria

A

LMW proteinuria

Multiple Myeloma, Hemoglobinuria, Myoglobinuria

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24
Q

Tubular Proteinuria

A

Defect in PT reabsorbing LMW proteins
Hg or Pb poisoning
Fanconi Syndrome
Hartnup Disease

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25
Q

When would BUN Decrease?

A

Increased Volume
Decreased Urea Synthesis
Decreased Protein intake

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26
Q

BUN/Cr > 15

A

Prerenal azotemia

Early postrenal azotemia

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27
Q

Bilateral Renal Agenesis
What does it lead to?
What are the signs of this?

A

Causes Potter Syndrome
Extremity deformities, Facial deformities, Pulmonary hypoplasia
Incompatible with life

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28
Q

If the renal artery is narrowed, what is the kidney’s response?

A

JG apparatus releases Renin and undergoes hypertrophy and hyperplasia (in order to secrete more renin)

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29
Q

What makes up the JG apparatus?

A

JG cells = modified smooth muscle cells of AA and EA
Macula Densa = tall, narrow cells in DT
The MD responds to [Cl] (via NaK2Cl pump) and transmits this information to JG cells which respond by secreting Renin

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30
Q

Path of K reabsorption in the Kidney

A

2/3 reabsorbed in PT
20% in LoH
Secreted in CD unless in a low K state –> Intercalated cells reabsorb K (K/H exchanger)

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31
Q

Factors that Increase K secretion in CD

A

High K diet, Aldosterone, Alkalosis (K/H exchanger), Diuretics (except KSD)

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32
Q

Renal angiomyolipomas
What are they?
How are they diagnosed?
What are they associated with?

A

Benign tumor made of blood vessels, SM, and fat
Diagnosed with abdominal CT because of low density of fat
Associated with Tuberous Sclerosis

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33
Q

What kind of Hypersensitivity Rxn is PSGN?
Describe the PathoPhys?
Describe appearance in Immunofluorescence and EM?

A

Type III: Immune Complex Mediated
After GAS infection, IC formed against bacterial antigens cross react w/ GMB and deposit in subepithelial portion of the glomerulus.
Lumpy Bumpy on IF and electron dense humps on EM

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34
Q

Horseshoe Kidney cannot ascend because it is trapped behind …

A

IMA

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35
Q

List 3 factors that increase PT Na Reabsorption

A

Increased Luminal Flow
ATII (decreased cAMP)
NE (via PKC)

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36
Q

List 2 factors that decrease PT Na Reabsorption

A

DA

PTH (increased cAMP)

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37
Q

When does the Pronephros form and degenerate?

A

Week 4

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38
Q

When does the Mesonephros function as the kidney?

A

1st Trimester

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39
Q

When does metanephros first appear?

Until when does nephrogenesis continue?

A

Week 5

Nephrogenesis continues through week 32-36

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40
Q

Fate of Mesonephros

A

Male: Mesonephros –> Wolffian duct –> ductus deferens and epididymis
Female: –> Gartners ducts

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41
Q

Kidney derived from Ureteric Bud

Fully canalized by week..

A

Collecting Duct, Calyces, Pelivs, Ureter

Fully canalized by week 10

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42
Q

Metanephric mesoderm gives rise to…

A

Glomerulus through collecting tubule

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43
Q

Last part of kidney to canalize?

A

Ureteropelvic junction

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44
Q

What is the most common site of obstruction and cause of hydronephrosis in the fetus?

A

Ureteropelvic Junction

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45
Q

Causes of Potter’s Syndrome?

A

ARPKD, Posterior Urethral Valves, Bilateral Renal Agenesis

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46
Q

Horseshoe kidney associated with…

A

Turners Syndrome

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47
Q 
Multicystic Dysplastic Kidney
Due to...
Leads to...
Kidney consists of...
Uni or Bi?
Symptoms?
Diagnosed by...
A

Due to abnormal interaction bet ureteric bud and metanephric mesenchyme
Leads to non functional kidney
Kidney consists of cysts and connective tissue
Unilateral
Asymptomatic
Diagnosed by prenatal US

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48
Q

Which Kidney is taken from a living donor? Why?

A

Left because of longer renal vein

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49
Q

Ureter re uterine artery and ductus deferens?

A

Ureter goes Under uterine artery and ductus deferens

water under the bridge

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50
Q

% of total body weight that is water? extracellular? plasma? interstitial?

A

60% water –> 2/3 intracellular, 1/3 extracellular

1/4 plasma, 3/4 interstitial

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51
Q

What substance measures plasma Vol?

A

radiolabeled albumin

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52
Q

What substance measures extracellular vol?

A

Inulin

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53
Q

Osmolarity of the body?

A

290 mOs/L

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54
Q

Glomerular filtration barrier composed of:

A 
Fenestrated capillaries (size)
Fused BM with heparin sulfate (neg charge barrier)
Podocyte foot processes (epithelium)
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55
Q

In Nephrotic Syndrome, what happens to the charge barrier in the Glomerulus?

A

Lost

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56
Q

Clearance formula

A

C = UV/P

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57
Q

C

A

Reabsorption

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58
Q

C>GFR

A

Secretion

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59
Q

Using Cr to estimate GFR

A

Slight overestimation because Cr is secreted

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60
Q

Normal GFR

A

100ml/min

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61
Q

Calculating GFR (2 formulas)

A

C inulin, C creatinine, or K[(Pgc-Pbs)-(Pigc-Pibs)]

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62
Q

What substance is used to measure ERPF? Why?

A

PAH because it is filtered and actively secreted. All PAH that goes in goes out

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63
Q

ERPF calculation

A

C pah

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64
Q

RBF calculation

A

RPF/(1-Hct)

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65
Q

By how much is ERPF different from RPF

A

ERPF underestimates RPF by ~10%

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66
Q

Filtration Fraction

A

GFR/RPF

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67
Q

Filtered Load

A

GFR x Px

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68
Q

How do NSAIDs affect RPF, GFR and FF?

A

NSAIDs –/ Prostaglandins (which normally dilate AA)

NSAIDs –> Decreased RPF and GFR –> no change in FF

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69
Q

How do ACEI affect RPF, GFR, and FF

A

ACEI –/ ATII (which normally constricts EA)

ACEI –> Increased RPF, Decreased GFR –> Decreased FF

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70
Q

How does AA constriction affect RPF, GFR, and FF?

A

RPF: Decreases
GFR: Decreases
FF: NC

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71
Q

How does EA constriction affect RPF, GFR, and FF?

A

RPF: Decreases
GFR: Increases
FF: Increases

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72
Q

How does increased plasma [protein] affect RPF, GFR, and FF?

A

RPF: NC
GFR: Decreases
FF: Decreases

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73
Q

How does decreased plasma [protein] affect RPF, GFR, and FF?

A

RPF: NC
GFR: Increases
FF: Increases

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74
Q

How does Constriction of the Ureter affect RPF, GFR, and FF?

A

RPF: NC
GFR: Decreases
FF: Decreases

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75
Q

Excretion rate?

A

V x U

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76
Q

Net Reabsorption Calculation

A

Filtered - excreted

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77
Q

Net Secretion Calculation?

A

Excreted - Filtered

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78
Q

At what [Glucose] does Glucosuria begin

A

160mg/dL

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79
Q

Tm of Glucose

A

350mg/dL

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80
Q

Normal Pregnancy can alter reabsorption of certain solutes in the PT. Which ones?

A

Can reduce reabsorption of Glucose and AA

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81
Q

Hartnups Disease
Cause
Results in…

A

Deficiency of neutral AA (Tryptophan) transporter in PT

Leads to Pellagra

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82
Q

What is secreted by the PT? Why?

A

NH3 as a buffer for secreted H+

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83
Q

PTH on PT

MoA

A

Inhibits Na/PO4 cotransporter –> PO4 excretion. Will also decrease Na reabsorption in PT
–> cAMP and IP3

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84
Q

ATII on PT
MoA
What can it lead to?

A

ATII –> Na/H exchanger –> increased Na, H2O and Bicarb reabsorption
ATIIR –/ cAMP, ATiiR –> IP3
Can lead to contraction alkalosis

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85
Q

PTH on DT

A

PTH –> Na/Ca exchanger in basal membrane –> Increased Ca Reabsorption

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86
Q

Receptor for ADH

Type of cell responsive to ADH?

A

V2 receptor on Principal Cells

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87
Q

[Inulin] along PT

A

Increases in Concentration by not Amount because of water reabsorption

88
Q

Cl reabsorption in PT

What proteins reabsorb Cl

A

Occurs at a slower rate than Na reabsorption in the proximal 1/3 and then matches Na distally –> [Cl] increases then plateaus
Reabsorbed by Cl/Base exchanger

89
Q

What stimulates Renin release?

A

Decrease in BP, Decreased Na(Cl) delivery to DT, Increased Sympathetic tone (β1 Receptors)

90
Q

What does ACE do?

A

Converts AT1 to AT2

Degrades Bradykinin

91
Q

Main Functions of ATII

A
  • -> AT1 receptor –> Vascular SM constriction
  • -> EF constriction
  • -> Adrenal Cortex –> Aldosterone
  • -> Post Pituitary –> ADH
  • -> PT –> Na/H exchanger
  • -> DT –> Na/Cl cotransporter
  • -> Hypothalamus –> Thirst
92
Q

ATII and Baroreceptors

A

ATII affects baroreceptors function to limit reflex bradycardia which would normally accompany its pressor effects

93
Q 
ANP
Released by...
In response to...
MoA
How does it affect Na?
Net Effect:
A

Released by atria in response to increased volume
ANP –> cGMP –> vascular smooth muscle relaxation –> increased GFR –> decreased renin release
Increased GFR –> Increased Na filtration (w/o compensatory Na reabsorption distally)
Net effect is Na and volume loss

94
Q

ADH primarily regulates:
Will also respond to:
Which one takes precedence?

A

ADH primarily regulates: Osm
Will also respond to: Vol
Which one takes precedence –> vol

95
Q

Aldosterone primarily regulates:

A

Volume

96
Q

How do Beta Blockers affect RAA System?

A

BB –/ Beta1R in JGA

Thereby BB –/ Renin release

97
Q

Where is Erythropoietin made?

What stimulates its production?

A

EPO released by interstitial cells in the peritubular capillary bed in response to hypoxia

98
Q

Prostaglandins and the kidney?

A

Paracrine secretion vasodilates the AA to Increase GFR

99
Q

PTH
Released in response to:
Leads to:

A

Released in response to Decreased Ca, Increased PO4, or Decreased VitD
Leads to Increased Ca reabsorption (DT), Decreased PO4 reabsorption (PT), and Increased VitD production

100
Q

What stimulates Aldosterone production?

A 
Decreased Vol (ATII)
Increased K
101
Q

What ions does Aldosterone affect?

A

Increased reabsorption of Na

Increased secretion of K and H

102
Q

What shifts K out of cells (HyperK)?

A

DO Insulin LAB

Digitalis, HyperOsmolarity, Insulin deficiency, Lysis of cells, Acidosis, Beta Antagonists

103
Q

What shifts K into cells (HypoK)?

A

“Insulin shifts K into cells”

Hypo-osmolarity, Insulin, Alkalosis, Beta agonists

104
Q

Low [Na] presents with:

A

Nausea, Malaise, Stupor, Coma

105
Q

High [Na] presents as

A

Irritability, stupor, coma

106
Q

Low [K] presents as

A

U wave, Flat T wave, Arrhythmias, muscle weakness

107
Q

High [K] presents as

A

Wide QRS and peaked T waves, Arrhythmias, muscle weakness

108
Q

Low [Ca] presents as

A

Tetany, seizures

109
Q

High [Ca] presents as

A

Stones (renal stones), Bones (pain), Groans (abdominal pain), Psychiatric overtones (anxiety, altered mental status), but not necessarily calcinuria

110
Q

Low [Mg] presents as

A

Tetany, arrhythmias

111
Q

High [Mg] presents as

A

“Lazy DR. Better Hike/Cram Ca”

Lethargy, decreased deep tendon reflexes, bradycardia, hypotension, cardiac arrest, hypocalcemia

112
Q

Low [PO4] presents as

A

Bone loss, osteomalacia

113
Q

High [PO4] presents as

A

Renal stones, metastatic calcifications, hypocalcemia

114
Q

Metabolic Acidosis: pH, PCO2, [HCO3], Compensatory response?

A

Low pH, Low PCO2, Low [HCO3], Immediate hyperventilation

115
Q

Metabolic Alkalosis: pH, PCO2, [HCO3], Compensatory response?

A

High pH, High PCO2, High [HCO3], Immediate hypoventilation

116
Q

Respiratory Acidosis: pH, PCO2, [HCO3], Compensatory response?

A

Low pH, High PCO2, High [HCO3], Delayed increase in bicarb reabsorption

117
Q

Respiratory Alkalosis: pH, PCO2, [HCO3], Compensatory response?

A

High pH, Low PCO2, Low [HCO3], Decreased renal bicarb reabsorption

118
Q

Kidney Henderson-Hasselbalch Equation for Kidney

A

pH = 6.1 + log ([HCO3]/.(.03 x PCO2))

119
Q

How does one predict the compensation for a simple Met Acidosis? What if actual PCO2 is different from predicted?

A

Winters Formula: PCO2 = (1.5 x [Bicarb]) + 8) +/- 2

If not as predicted: Mixed acid/base disorder

120
Q

Anion Gap Calculation

Normal Anion Gap?

A

Na - (Cl + HCO3)

Normally 8-12 mEq/L

121
Q

Causes of Resp Acidosis?

A

Hypoventilation due to Obstruction, Disease, Opioids or Sedatives, Muscle weakness

122
Q

Causes of Anion Gap Met Acidosis

A 
MUDPILES
Methanol (formic acid), Uremia, Diabetic ketoacidosis, Propylene glycol, Iron tablets or INH, Lactic acidosis, Ethylene glycol (Oxalic Acid), Salicylates (late)
123
Q

Causes of Non Anion Gap Met Acidosis

A

HARD ASS

Hyperalimentation, Addisons Disease, Renal Tubular Acidosis, Diarrhea, Acetazolamide, Spironolactone, Saline infusion

124
Q

Causes of Resp Alkalosis?

A

Hyperventilation (i.e. altitude sickness)

Salicylates (early)

125
Q

Causes of Met Alkalosis?

A

Loop Diuretics, Vomiting, Antaacids, Hyperaldosteronism

126
Q 
Type 1 Renal Tubular Acidosis
Location of defect
Defect
Urine pH
Associated with
Increased risk for
A

Defect in DT ability to excrete H
Urine pH > 5.5
Associated with HypoK
Increased risk for CaPO4 kidney stones because of increased urine pH and bone resorption

127
Q 
Type 2 Renal Tubular Acidosis
Defect in
Defect
Seen in what disease?
Urine pH
Associated with
Increased risk for
A 
Defect in PT HCO3 reabsorption
Seen in Fanconi Syndrome
Urine pH < 5.5
Associated with hypoK
Increased risk for hypophosphatemic rickets
128
Q

Mechanism of Type 4 Renal Tubular Acidosis

A

Low Aldosterone or lack of response to aldosterone –> hyperK –> impaired ammoniagenesis in PT –> PT loses buffering capacity –> urine pH decreases

129
Q

What do Casts in Urine indicate?

A

Renal (vs. Bladder) origin

130
Q

RBC Casts Indicate

A

Glomerulonephritis, Ischemia, MalHTN

131
Q

WBC Casts indicate

A

Tubulointerstitial inflammation, acute pyelonephritis, transplant rejection

132
Q

Fatty Casts
Appearance
Indication

A

Oval Fat Bodies

Indicate Nephrotic Syndrome

133
Q

Granular (Muddy Brown) Casts Indicate

A

ATN

134
Q

Waxy Casts indicate

A

Advanced renal disease, Chronic renal failure

135
Q

Hyaline casts indicate

A

Non-specific. Can be a normal finding

136
Q

Causes of hematuria without casts

A

Bladder Cancer or Kidney Stones

137
Q

Causes of pyuria without casts

A

Acute Cystitis

138
Q

Definition of Focal Glomerular Disorder

A

<50% glomeruli involved

139
Q

Definition of Diffuse Glomerular Disorder

A

> 50% glomeruli involved

140
Q

Definition of Proliferative Glomerular Disorder

A

Hypercellular glomeruli

141
Q

Definition of Membranous Glomerular Disorder

A

Thickening of glomerular BM

142
Q

Definition of Primary Glomerular Disorder

A

Only glomeruli involved

143
Q

Definition of Secondary Glomerular Disorder

A

Glomeruli + other organ involved

144
Q

Names of Nephritic Syndromes

A

“PARIS”
PSGN, RPGN, Berger’s IgA Glomerulonephrtopathy, Alport Syndrome
(DPGN and MPGN can also be nephrotic)
(SLE can also cause a nephritic syndrome)
“PIG ARMS” includes Goodpastures and MPGN

145
Q

Names of Nephrotic Syndromes

A

“F. SAM M.D.”
Focal Segmenting Glomerulosclerosis, Amyloidosis, SLE, Membranous Nephropathy, Minimal Change Disease, Diabetic Glomerulonephropathy
(DPGN and MPGN can also be nephritic)

146
Q

Presentation of Nephrotic Syndrome
Casts
Associated with
Increased risk for

A

“Protein LEACHs out”
Proteinuria > 3.5 g/day, ↑Lipids, Edema, hypoAlbuminia, ↑Cholesterol, HTN (Na retention)
Fatty Casts
Associated with Thromboembolism (hypercoagulable state due to ATIII loss)
Increased risk for infection (from loss of gamma Igs)

147
Q 
FSGS
LM
EM
Rate
Associated with diseases? drug use? lifestyle? medicines?
A

LM: segmental sclerosis and hyalinosis
EM: effacement of foot processes
Most common nephrotic syndrome in adults
Associated with HIV, Heroin, Obesity, Interferon treatment, Chronic kidney disease (due to congenital absence or removal)

148
Q 
Membranous Nephropathy
Mechanism
LM
EM
IF
What diseases present this way?
Rate
Caused by
A 
"MP"
Subepithelial IC deposition 
LM: Diffuse capillary and BM thickening 
EM: "Spike and Dome" with subepithelial deposits
IF: Granular (IgG and C3)
SLE's presentation
2nd most common Nephrotic in adults
Causes: idiopathic, drugs, infections, SLE, tumors
149
Q 
Minimal Change Disease
Pathogenesis
LM
EM
Describe the Proteinuria 
Triggered by
Most common in
Treatment
A

T Cell Cytokines
LM: normal
EM: foot process effacement
Selective loss of albumin, not globins, because of BM polyanion loss
Triggered by recent infection or immune stimulus
Most common in children
Responds to corticosteroids

150
Q

Amyloidosis
LM
Associated with…

A

LM: congo red stain shows apple-green birefringence under polarized light
Associated with chronic conditions like Multiple Myeloma, TB, and RA

151
Q 
MPGN Type I
Mechanism
IF
Appearance
Associated with
A

Subendothelial IC deposits
IF: Granular
Tram-Track appearance due to BM splitting caused by mesangial ingrowth
HBV, HCV

152
Q

MPGN Type II
Mechanism
Appearance
Associated with

A

Intramembranous IC deposits
AutoAb –/ degradation of C3 convertase which leads to low levels of C3
“Dense deposits”
Associated with C3 nephritic factor

153
Q

Diabetic Glomerulonephropathy

Mechanism

A

Nonenzymatic Glycosylation of BM –> ↑ permeability to proteins + ↑ thickness
NEG of EA –> hyaline arteriolosclerosis –> ↑GFR –> hyperfiltration –> damage to mesangial cells –> mesagnial expansion
Osmotic damage to glomerular capillary endothelial cells (Glucose –> sorbitol which is osmotically active and leads to swelling and cellular damage)

154
Q

ATII receptor MoA

A

ATIIR –> IP3

ATIIR –/ cAMP

155
Q

In Nephrotic Syndrome, what is the glomerular injury due to?

A

Cytokines damage podocytes causing them to fuse and destroy - charge of GBM

156
Q

Which diabetes causes Diabetic Glomerulonephropathy?

A

Both. 1 (40%) > 2 (20%)

157
Q

Diabetic Glomerulonephropathy

LM

A

LM: Mesangial expansion, BM thickening, eosinophilic nodular glomerulosclerosis (Kimmelstiel-Wilson Lesion)

158
Q

Nephritic Syndrome
What kind of process?
What is it mediated by?

A

Inflammatory Process mediated by neutrophils

159
Q

Nephritic Syndrome Presentation

A 
"PR  HOZ"
Proteinuria (<3.5g/day)
RBC casts
Hematuria, HTN (due to salt retention)
Oliguria
aZotemia
160
Q

PSGN
Presentation
Treatment

A

“Throat, Bloat, Coke”
Child w/ previous infection (GAS), peripheral + periorbital edema, HTN, and dark urine
Resolves Spontaneously

161
Q

PSGN
LM
EM
IF

A

LM: Glomeruli enlarged and hypercellular. Neutrophils, “lumpy bumpy”
EM: Subepithelial IC humps
IF: Granular appearance due to IgG, IgM and C3 deposition along BM and mesangium

162
Q

RPGN (crescentic)
LM
IF
What are in the crescents?

A

LM + IF: crescent moon shape

Crescents = fibrin + plasma proteins (C3) with glomerular parietal cells, monocytes, and macs

163
Q

RPGN prognosis

A

Poor (days to weeks)

164
Q

Diseases that result in RPGN

Markers for them?

A

Goodpasture’s (hematuria + hemoptysis), Wegener’s (cANCA), Microscopic polyangiitis (pANCA)

165
Q

How Goodpasture’s –> RPGN
What kind of Rxn?
Mechanism

A

Type II Hypersensitivity Rxn

Abs to GBM + alveolar BM

166
Q

Goodpasture’s IF

A

Linear pattern

167
Q 
DPGN
Mechanism 
What diseases cause it?
LM
EM
IF
A 
Subendothelial IC mediated
SLE + MPGN cause it
LM: wire looping of capillaries
EM: subendothelial and sometimes intramembranous IgG-based IC often with C3 deposition
IF: granular
168
Q

Most common cause of death in SLE

A

DPGN

169
Q

Which diseases can cause concurrent nephrotic and nephritic syndromes?

A

SLE and MPGN

170
Q 
Berger's Disease (IgA Nephropathy)
Related to what other disease?
LM
EM
IF
A 
"AM" Think Mesangium
Related to Henoch-Schonlein Purpura
LM: mesangial proliferation
EM: mesangial IC deposits 
IF: IgA based IC deposits in mesangium
171
Q

When does Berger’s disease often presents/flares?

A

Often presents/flares with URI or acute gastroenteritis

172
Q 
Henoch-Schonlein Purpura 
Kind of vasculitis?
Most common vasculitis in...
Classic Presentation
Disease Mediated by
Associated with
Age of lesions?
A 
Small vessels
Most common vasculitis in children
"NAPA"
Child following URI with Nephropathy, Abdominal pain (melena), Purpura, Arthralgia 
Mediated by IgA complex deposition
Associated with IgA nephropathy
Multiple lesions of same age
173
Q 
Wegener's Granulomatosis (Granulomatosis with Polyangiitis)
Kind of vasculitis?
Presentation
Histo
Blood
CXR
Treatment
A 
Small vessels 
Upper Respiratory Tract: Perforated nasal septum, sinusitis, otitis media, mastoiditis
Lower RT: Hemoptysis, Cough, Dyspnea
Renal: Hematuria, RBC Casts
Focal Necrotizing vasculitis + Necrotizing granulomas in the lung and upper airway + Necrotizing glomerulonephritis
c-ANCA
Large Nodular Densities 
Cyclophosphamide and corticosteroids
174
Q

Alport Syndrome
Mechanism
Genetics
Presentation

A

“Imagine the V in IV splitting the BM”
Mutation in IV collagen –> split basement membrane
X linked
Glomerulonephritis, deafness, eye problems

175
Q

Treat and prevent Kidney Stones with

A

Fluid intake

176
Q

Ca Kidney Stones
Frequency
Precipitates at what pH
XR

A

80%
CaPO4 –> ↑pH
CaOxalate –> ↓pH
Radiopaque

177
Q

Oxalate crystals can result from

A

Ethylene glycol or VitC abuse

178
Q

Treatment for recurrent kidney stones

A

Thiazide and citrate

179
Q

Most common kidney stone presentation Re: Kind of Kidney stone, Urine, and Blood?

A

CaOxalate stone in pt with hypercalcinuria and normocalcemia

180
Q

Ammonium MgPhosphate Kidney Stones (struvite)
Frequency
Precipitates at pH
XR

A

15%
Precipitates at ↑pH
Radiopaque

181
Q

Ammonium MgPhasphate Kidney Stones
Caused by
Mechanism
What can they form?

A

Caused by infection with urease+ bugs (proteus mirabilis, Staph, Klebsiella)
The bugs hydrolyze urea to ammonia and this alkalizes urine
Can form staghorn calculi that can be a nidus for UTIs

182
Q

Uric Acid Kidney Stones
Frequency
Precipitates at pH
XR

A

5%
Precipitates at ↓pH
RadiolUcent

183
Q 
Uric Acid Kidney Stones
Visible on
Associated with
Often seen in what kind of diseases?
Treatment
A

Visible on CT and US but not XR
Associated with hyperuricemia (gout)
Often seen in diseases with high cellular turnover (leukemia)
Treat w/ alkalinization of urine

184
Q 
Cystine Kidney Stones
Frequency
Precipitates at pH
XR
Usually Secondary to
Appearance of stone
Treatment
A 
1%
Precipitates at ↓pH
Radiopaque
Secondary to cystinuria
Hexagonal crystals
Treat w/ alkalinization of urine
185
Q 
Hydronephrosis 
What happens?
Can be caused by
Leads to
May result in
A

Backup of urine into the kidney
Caused by urinary tract obstruction or vesicoureteral reflux
Leads to dilation of renal pelvis and calyces
Results in parenchymal thinning

186
Q

ATN
Frequency?
Reversible?
When does death most frequently occur?

A

Most common cause of intrinsic renal failure
Self reversible in some cases but can be fatal if untreated
Death most often occurs during oliguric phase

187
Q

ATN

What causes it?

A 
Renal ischemia (from shock, sepsis)
Crush injury (myogloniburia)
Drugs, toxins
188
Q

Acute Tubular Necrosis Stages

A

Initiation: Ischemic injury. Usually unnoticed
Maintenance
Recovery:

189
Q 
ATN Maintenance Stage
Urinating/Quality of urine
Edema?
GFR?
Electrolytes (K and Na) 
pH
Casts 
Duration
A 
Oliguria. Low Urine Osm.
Fluid overload (edema)
Increased Cr/BUN, 
Increased K. High Na excretion.  
Anion Gap Met Acidosis (because of retention of H and anions). 
Muddy Brown Casts. 
Last 1-3 days
190
Q

ATN Recovery Stage
Urinating/Quality of urine
Electrolytes

A

Diuresis, Hypotonic urine, Low K, Mg, PO4, and Ca

191
Q 
Renal Papillary Necrosis 
What is happening?
Urine?
Triggered by
Associated with
A

Sloughing of renal papillae
Gross hematuria and proteinuria
May be triggered by a recent infection or immune stimulus
Associated with DM, Acute Pyelonephritis, Chronic Phenacetin Use (acetaminophen)
Sickle Cell Anemia

192
Q

Acute Renal Failure (Acute Kidney Injury)

Definition

A

Abrupt decline in renal function with ↑ Cr and ↑ BUN over several days

193
Q

Prerenal azotemia
Result of
BUN/Cr ratio

A

↓RBF –> ↓GFR

BUN/Cr ↑

194
Q 
Intrarenal azotemia
Generally due to
Less commonly due to
Mechanism
Casts
BUN/Cr
A

Generally due to ATN or ischemia/toxins
Less commonly due to acute glomerulonephritis
Necrosis –> debris obstructing tubule –> fluid back flow –> ↓GFR
Epithelial/granular casts
BUN/Cr ↓

195
Q

Post Renal azotemia
What causes obstruction?
Develops only when obstruction is?

A

Due to outflow obstruction (stones, BPH, neoplasia, congenital abnormalities)
Develops only with bilateral obstruction

196
Q 
Prerenal Azotemia
Urine Osm (mOsm/kg)
Urine Na (mEq/L)
FENa
BUN/Cr
A

Urine Osm (mOsm/kg) > 500
Urine Na (mEq/L) < 20
FENa < 1%
BUN/Cr > 20

197
Q 
Intrarenal Azotemia
Urine Osm (mOsm/kg)
Urine Na (mEq/L)
FENa
BUN/Cr
A

Urine Osm (mOsm/kg) < 350
Urine Na (mEq/L) > 40
FENa > 2%
BUN/Cr < 15

198
Q 
Postrenal Azotemia 
Urine Osm (mOsm/kg)
Urine Na (mEq/L)
FENa
BUN/Cr
A

Urine Osm (mOsm/kg) < 350
Urine Na (mEq/L) > 40
FENa > 2%
BUN/Cr > 15

199
Q 
Consequences of Renal Failure
Na/Water
K
pH
Urea
Blood
Bones
Lipids
Growth
A 
Na/Water retention --> CHF, Pul Edema, HTN)
HyperK
Met Acidosis
Uremia
Anemia (low EPO)
Renal Osteodystrophy
Dyslipidemia (↑ Tris)
Growth retardation and developmental delay (children)
200
Q

Uremia
Blood work
Presentation

A

↑BUN and ↑Cr

Nausea, anorexia, Pericarditis, Asterixis, Encephalopathy, Platelet dysfunction

201
Q

Renal Osteodystrophy

Pathogenesis

A

Low VitD + Kidney dysfunction –> ↓Ca and ↑PO4 –> ↑PTH –> bone resorption (subperiosteal thinning of bone)

202
Q 
Adult PKD
Gross presentation of kidney
Presentation 
Genetics w/ chromosome
Death from
Associated with
A

Multiple, large, bilateral cysts
Flank pain, hematuria, HTN, Urinary infections, Progressive renal failure
Autosomal Dominant in PKD1 or 2 on chromosome 16
Death from chronic kidney disease or HTN (↑ Renin)
Associated with Berry Aneurysm, MVP, Benign Hepatic cysts

203
Q 
AR PKD
Genetics
Associated with
Significant renal failure in utero leads to
Concerns beyond neonatal period
A

Autosomal recessive
Associated with hepatic fibrosis
In utero –> Potters
Beyond neonatal concerns –> HTN, Portal HTN, Progressive renal insufficiency

204
Q 
Medullary Cystic Disease
Genetics
What does it lead to
Inability to
Visualization?
On US
Prognosis
A 
Autosomal dominant
Leads to tubulointerstitial fibrosis and progressive renal insufficiency with inability to concentrate urine
Medullary cysts usually not visualized
US: shrunken kidney
Poor prognosis
205
Q 
Renal Cell Carcinoma
Originates from what kind of cells?
Histo
Most common in
Risk ↑ w/
Presentation
How does it spread
Metastasizes to
A

Originates from PT cells
Polygonal clear cells (accumulated lipids and Carbs)
Most common in Men 50-70
Risk ↑ w/ smoking and obesity
Hematuria, palpable mass, polycythemia, flank pain, fever, wt loss
Renal vein –> IVC
Lung and Bone

206
Q 
Renal Cell Carcinoma
Frequency
Genetics
Tumors secrete?
When is it usually detected?
Treatment
A

Most common renal cancer
Gene deletion in chromosome 3 (sporadic or von Hippel Lindau)
Paraneoplastic (EPO, ACTH, PTH)
Silent cancer because retroperitoneal. Usually detected b/c of metastases
Resection. Resistant to Chemo and Radiation

207
Q 
Wilms' Tumor (Nephroblastoma)
Frequency
Contains what kind of structures
Presentation
Genetics
Associated with what Syndrome?
A

Most common renal malignancy of early childhood (2-4)
Contains embryonic glomerular structures
Presents with huge palpable flank mass and/or hematuria
Deletion of tumor suppressor WT1 on chromosome 11
May be part of Beckwith-Wiedemann Syndrome

208
Q

Components of Beckwith-Wiedemann Syndrome

A

WARG

Wilms, Aniridia, Genitourinary malformations, Retardation

209
Q 
Transitional Cell Carcinoma 
Frequency
Can occur in
Presentation
Associated with...
A

Most common tumor of urinary tract system
Can occur in Calyces, pelvis, ureters, bladder
Painless hematuria (no casts)
“problems in the Pee SAC”
Phenacetin, Smoking, Aniline dyes, Cyclophosphamide

210
Q

Acute Pyelonephritis
Which part of kidney affected?
Presentation
Urine?

A

Affects cortex with sparing of glomeruli and vessels
Fever, CVA tenderness, nausea, vomiting
White cell casts in urine

211
Q 
Chronic Pyelonephritis
Result of
Requires 
Histo
Tubules contain
A

Result of recurrent episodes of acute pyelonephritis
Requires predisposition to infection (vesicoureteral reflux, chronic kidney stones)
Coarse, asymmetric corticomedullary scarring and blunted calyx
Tubules can contain eosinophilic casts (thyroidization of kidney)

212
Q 
Drug-Induced Interstitial Nephritis (tubulointerstital nephritis)
Presentation
Urine 
MoA
Time course and drugs
A

Azotemia, fever, rash, hematuria, CVAT. Can be asymptomatic
Pyuria (eosinophils)
Drugs act as haptens –> hypersensitivity
1-2 weeks: Diuretics, penicillin, sulfonamide, rifampin
Months: NSAIDs

213
Q

Diffuse Cortical Necrosis
What is it?
Due to
Associated with

A

Acute generalized cortical infarction of both kidneys
Combination of vasospasms and DIC
Associated with obstetric catastrophe (abruptio placentae) and Septic Shock

214
Q

Which Nephrotic/Nephritic Syndromes have Subepithelial IC deposits

A

PSGN

Membranous

215
Q

Which Nephrotic/Nephritic Syndromes have Subendothelial IC deposits

A

MPGN I

DPGN

216
Q

Charges in the Tubule of the Kidney

A

PT: -4
LoH: +7
DT: -10
CT: -50

USMLE STEP 1 (25 decks)

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