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Flashcards in Renal Deck (216):
1

ACE Inhibitors
Names
Uses
Toxicity
Contraindications

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

2

How are ATII Receptor Blockers Different from ACEI?

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

3

How do diuretics affect urine NaCl

Increased. Serum NaCl may decrease

4

How do diuretics change urine [K]?

All diuretics increase urine K except for KSD.
Serum K may decrease

5

Which Diuretics cause Acidosis?

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

6

Which diuretics cause alkalemia?

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

7

K Sparring Diuretics
Names
Use
MoA
Tox

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

8

Which diuretics affect urine Ca?

Urine Ca increases with LD and decreases with Thiazide

9

Thiazide Diuretics
Uses
MoA
Toxicity

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

10

Ethacrynic Acid

Like Furosemade for people allergic to Sulfur

11

Loop Diuretics
Name
Use
Inhibited by
MoA (2)
Tox

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

12

CAI
Names
Use
Tox

Acetazolamide
Glaucoma, Make Urine Basic, Alkalosis, Altitude Sickness, Pseudotumor Cerebri
Met Acidosis (with increased Cl), Paresthesia, NH3 toxicity, Sulfa allergy

13

Mannitol
Uses
MoA
Tox
Contras

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

14

Urea transport in the Kidney

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

15

ADH and Urea

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

16

Where is Vit D made in the Kidney?
What stimulates its production?

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

17

How does Vit D promote bone mineralization?

Vit D --> Osteoblasts --> alkaline phasphatase
AP hydrolyzes Pyrophasphate and other inhibitors of Ca-PO4 crystallization.

18

Functions of Vit D

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

19

Drugs associated with Hematuria

Anticoagulants (warfarin and heparin)
Cyclophasphamide --> hemorrhagic cystitis and increased risk for transitional cell carcinoma

20

Tests for Protienuria

Dipstick for albumin
SSA (sulfosalicylic acid) for albumin and globins

21

Urea and GFR

Increased GFR --> Decreased Urea reabsorption

22

Functional Proteinuria

Not associated with rena disease
fever, exercise, CHF, Orthostatic

23

Overflow Proteinuria

LMW proteinuria
Multiple Myeloma, Hemoglobinuria, Myoglobinuria

24

Tubular Proteinuria

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

25

When would BUN Decrease?

Increased Volume
Decreased Urea Synthesis
Decreased Protein intake

26

BUN/Cr > 15

Prerenal azotemia
Early postrenal azotemia

27

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

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

28

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

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

29

What makes up the JG apparatus?

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

30

Path of K reabsorption in the Kidney

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

31

Factors that Increase K secretion in CD

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

32

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

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

33

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

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

34

Horseshoe Kidney cannot ascend because it is trapped behind ...

IMA

35

List 3 factors that increase PT Na Reabsorption

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

36

List 2 factors that decrease PT Na Reabsorption

DA
PTH (increased cAMP)

37

When does the Pronephros form and degenerate?

Week 4

38

When does the Mesonephros function as the kidney?

1st Trimester

39

When does metanephros first appear?
Until when does nephrogenesis continue?

Week 5
Nephrogenesis continues through week 32-36

40

Fate of Mesonephros

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

41

Kidney derived from Ureteric Bud
Fully canalized by week..

Collecting Duct, Calyces, Pelivs, Ureter
Fully canalized by week 10

42

Metanephric mesoderm gives rise to...

Glomerulus through collecting tubule

43

Last part of kidney to canalize?

Ureteropelvic junction

44

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

Ureteropelvic Junction

45

Causes of Potter's Syndrome?

ARPKD, Posterior Urethral Valves, Bilateral Renal Agenesis

46

Horseshoe kidney associated with...

Turners Syndrome

47

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

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

48

Which Kidney is taken from a living donor? Why?

Left because of longer renal vein

49

Ureter re uterine artery and ductus deferens?

Ureter goes Under uterine artery and ductus deferens
(water under the bridge)

50

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

60% water --> 2/3 intracellular, 1/3 extracellular
1/4 plasma, 3/4 interstitial

51

What substance measures plasma Vol?

radiolabeled albumin

52

What substance measures extracellular vol?

Inulin

53

Osmolarity of the body?

290 mOs/L

54

Glomerular filtration barrier composed of:

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

55

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

Lost

56

Clearance formula

C = UV/P

57

C

Reabsorption

58

C>GFR

Secretion

59

Using Cr to estimate GFR

Slight overestimation because Cr is secreted

60

Normal GFR

100ml/min

61

Calculating GFR (2 formulas)

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

62

What substance is used to measure ERPF? Why?

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

63

ERPF calculation

C pah

64

RBF calculation

RPF/(1-Hct)

65

By how much is ERPF different from RPF

ERPF underestimates RPF by ~10%

66

Filtration Fraction

GFR/RPF

67

Filtered Load

GFR x Px

68

How do NSAIDs affect RPF, GFR and FF?

NSAIDs --/ Prostaglandins (which normally dilate AA)
NSAIDs --> Decreased RPF and GFR --> no change in FF

69

How do ACEI affect RPF, GFR, and FF

ACEI --/ ATII (which normally constricts EA)
ACEI --> Increased RPF, Decreased GFR --> Decreased FF

70

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

RPF: Decreases
GFR: Decreases
FF: NC

71

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

RPF: Decreases
GFR: Increases
FF: Increases

72

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

RPF: NC
GFR: Decreases
FF: Decreases

73

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

RPF: NC
GFR: Increases
FF: Increases

74

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

RPF: NC
GFR: Decreases
FF: Decreases

75

Excretion rate?

V x U

76

Net Reabsorption Calculation

Filtered - excreted

77

Net Secretion Calculation?

Excreted - Filtered

78

At what [Glucose] does Glucosuria begin

160mg/dL

79

Tm of Glucose

350mg/dL

80

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

Can reduce reabsorption of Glucose and AA

81

Hartnups Disease
Cause
Results in...

Deficiency of neutral AA (Tryptophan) transporter in PT
Leads to Pellagra

82

What is secreted by the PT? Why?

NH3 as a buffer for secreted H+

83

PTH on PT
MoA

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

84

ATII on PT
MoA
What can it lead to?

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

85

PTH on DT

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

86

Receptor for ADH
Type of cell responsive to ADH?

V2 receptor on Principal Cells

87

[Inulin] along PT

Increases in Concentration by not Amount because of water reabsorption

88

Cl reabsorption in PT
What proteins reabsorb Cl

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

What stimulates Renin release?

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

90

What does ACE do?

Converts AT1 to AT2
Degrades Bradykinin

91

Main Functions of ATII

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

92

ATII and Baroreceptors

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

93

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

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

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

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

95

Aldosterone primarily regulates:

Volume

96

How do Beta Blockers affect RAA System?

BB --/ Beta1R in JGA
Thereby BB --/ Renin release

97

Where is Erythropoietin made?
What stimulates its production?

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

98

Prostaglandins and the kidney?

Paracrine secretion vasodilates the AA to Increase GFR

99

PTH
Released in response to:
Leads to:

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

What stimulates Aldosterone production?

Decreased Vol (ATII)
Increased K

101

What ions does Aldosterone affect?

Increased reabsorption of Na
Increased secretion of K and H

102

What shifts K out of cells (HyperK)?

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

103

What shifts K into cells (HypoK)?

"Insulin shifts K into cells"
Hypo-osmolarity, Insulin, Alkalosis, Beta agonists

104

Low [Na] presents with:

Nausea, Malaise, Stupor, Coma

105

High [Na] presents as

Irritability, stupor, coma

106

Low [K] presents as

U wave, Flat T wave, Arrhythmias, muscle weakness

107

High [K] presents as

Wide QRS and peaked T waves, Arrhythmias, muscle weakness

108

Low [Ca] presents as

Tetany, seizures

109

High [Ca] presents as

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

110

Low [Mg] presents as

Tetany, arrhythmias

111

High [Mg] presents as

"Lazy DR. Better Hike/Cram Ca"
Lethargy, decreased deep tendon reflexes, bradycardia, hypotension, cardiac arrest, hypocalcemia

112

Low [PO4] presents as

Bone loss, osteomalacia

113

High [PO4] presents as

Renal stones, metastatic calcifications, hypocalcemia

114

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

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

115

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

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

116

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

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

117

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

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

118

Kidney Henderson-Hasselbalch Equation for Kidney

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

119

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

Winters Formula: PCO2 = (1.5 x [Bicarb]) + 8) +/- 2
If not as predicted: Mixed acid/base disorder

120

Anion Gap Calculation
Normal Anion Gap?

Na - (Cl + HCO3)
Normally 8-12 mEq/L

121

Causes of Resp Acidosis?

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

122

Causes of Anion Gap Met Acidosis

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

123

Causes of Non Anion Gap Met Acidosis

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

124

Causes of Resp Alkalosis?

Hyperventilation (i.e. altitude sickness)
Salicylates (early)

125

Causes of Met Alkalosis?

Loop Diuretics, Vomiting, Antaacids, Hyperaldosteronism

126

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

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

Type 2 Renal Tubular Acidosis
Defect in
Defect
Seen in what disease?
Urine pH
Associated with
Increased risk for

Defect in PT HCO3 reabsorption
Seen in Fanconi Syndrome
Urine pH < 5.5
Associated with hypoK
Increased risk for hypophosphatemic rickets

128

Mechanism of Type 4 Renal Tubular Acidosis

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

129

What do Casts in Urine indicate?

Renal (vs. Bladder) origin

130

RBC Casts Indicate

Glomerulonephritis, Ischemia, MalHTN

131

WBC Casts indicate

Tubulointerstitial inflammation, acute pyelonephritis, transplant rejection

132

Fatty Casts
Appearance
Indication

Oval Fat Bodies
Indicate Nephrotic Syndrome

133

Granular (Muddy Brown) Casts Indicate

ATN

134

Waxy Casts indicate

Advanced renal disease, Chronic renal failure

135

Hyaline casts indicate

Non-specific. Can be a normal finding

136

Causes of hematuria without casts

Bladder Cancer or Kidney Stones

137

Causes of pyuria without casts

Acute Cystitis

138

Definition of Focal Glomerular Disorder

<50% glomeruli involved

139

Definition of Diffuse Glomerular Disorder

>50% glomeruli involved

140

Definition of Proliferative Glomerular Disorder

Hypercellular glomeruli

141

Definition of Membranous Glomerular Disorder

Thickening of glomerular BM

142

Definition of Primary Glomerular Disorder

Only glomeruli involved

143

Definition of Secondary Glomerular Disorder

Glomeruli + other organ involved

144

Names of Nephritic Syndromes

"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

Names of Nephrotic Syndromes

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

146

Presentation of Nephrotic Syndrome
Casts
Associated with
Increased risk for

"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

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

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

Membranous Nephropathy
Mechanism
LM
EM
IF
What diseases present this way?
Rate
Caused by

"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

Minimal Change Disease
Pathogenesis
LM
EM
Describe the Proteinuria
Triggered by
Most common in
Treatment

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

Amyloidosis
LM
Associated with...

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

151

MPGN Type I
Mechanism
IF
Appearance
Associated with

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

152

MPGN Type II
Mechanism
Appearance
Associated with

Intramembranous IC deposits
AutoAb --/ degradation of C3 convertase which leads to low levels of C3
"Dense deposits"
Associated with C3 nephritic factor

153

Diabetic Glomerulonephropathy
Mechanism

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

ATII receptor MoA

ATIIR --> IP3
ATIIR --/ cAMP

155

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

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

156

Which diabetes causes Diabetic Glomerulonephropathy?

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

157

Diabetic Glomerulonephropathy
LM

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

158

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

Inflammatory Process mediated by neutrophils

159

Nephritic Syndrome Presentation

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

160

PSGN
Presentation
Treatment

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

161

PSGN
LM
EM
IF

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

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

LM + IF: crescent moon shape
Crescents = fibrin + plasma proteins (C3) with glomerular parietal cells, monocytes, and macs

163

RPGN prognosis

Poor (days to weeks)

164

Diseases that result in RPGN
Markers for them?

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

165

How Goodpasture's --> RPGN
What kind of Rxn?
Mechanism

Type II Hypersensitivity Rxn
Abs to GBM + alveolar BM

166

Goodpasture's IF

Linear pattern

167

DPGN
Mechanism
What diseases cause it?
LM
EM
IF

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

Most common cause of death in SLE

DPGN

169

Which diseases can cause concurrent nephrotic and nephritic syndromes?

SLE and MPGN

170

Berger's Disease (IgA Nephropathy)
Related to what other disease?
LM
EM
IF

"AM" Think Mesangium
Related to Henoch-Schonlein Purpura
LM: mesangial proliferation
EM: mesangial IC deposits
IF: IgA based IC deposits in mesangium

171

When does Berger's disease often presents/flares?

Often presents/flares with URI or acute gastroenteritis

172

Henoch-Schonlein Purpura
Kind of vasculitis?
Most common vasculitis in...
Classic Presentation
Disease Mediated by
Associated with
Age of lesions?

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

Wegener's Granulomatosis (Granulomatosis with Polyangiitis)
Kind of vasculitis?
Presentation
Histo
Blood
CXR
Treatment

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

Alport Syndrome
Mechanism
Genetics
Presentation

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

175

Treat and prevent Kidney Stones with

Fluid intake

176

Ca Kidney Stones
Frequency
Precipitates at what pH
XR

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





177

Oxalate crystals can result from

Ethylene glycol or VitC abuse

178

Treatment for recurrent kidney stones

Thiazide and citrate

179

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

CaOxalate stone in pt with hypercalcinuria and normocalcemia

180

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

15%
Precipitates at ↑pH
Radiopaque

181

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

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

Uric Acid Kidney Stones
Frequency
Precipitates at pH
XR

5%
Precipitates at ↓pH
RadiolUcent

183

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

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

Cystine Kidney Stones
Frequency
Precipitates at pH
XR
Usually Secondary to
Appearance of stone
Treatment

1%
Precipitates at ↓pH
Radiopaque
Secondary to cystinuria
Hexagonal crystals
Treat w/ alkalinization of urine

185

Hydronephrosis
What happens?
Can be caused by
Leads to
May result in

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

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

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

ATN
What causes it?

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

188

Acute Tubular Necrosis Stages

Initiation: Ischemic injury. Usually unnoticed
Maintenance
Recovery:

189

ATN Maintenance Stage
Urinating/Quality of urine
Edema?
GFR?
Electrolytes (K and Na)
pH
Casts
Duration

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

ATN Recovery Stage
Urinating/Quality of urine
Electrolytes

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

191

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

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

Acute Renal Failure (Acute Kidney Injury)
Definition

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

193

Prerenal azotemia
Result of
BUN/Cr ratio

↓RBF --> ↓GFR
BUN/Cr ↑

194

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

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

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

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

196

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

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

197

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

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

198

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

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

199

Consequences of Renal Failure
Na/Water
K
pH
Urea
Blood
Bones
Lipids
Growth

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

Uremia
Blood work
Presentation

↑BUN and ↑Cr
Nausea, anorexia, Pericarditis, Asterixis, Encephalopathy, Platelet dysfunction

201

Renal Osteodystrophy
Pathogenesis

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

202

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

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

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

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

204

Medullary Cystic Disease
Genetics
What does it lead to
Inability to
Visualization?
On US
Prognosis

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

Renal Cell Carcinoma
Originates from what kind of cells?
Histo
Most common in
Risk ↑ w/
Presentation
How does it spread
Metastasizes to

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

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

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

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

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

Components of Beckwith-Wiedemann Syndrome

WARG
Wilms, Aniridia, Genitourinary malformations, Retardation

209

Transitional Cell Carcinoma
Frequency
Can occur in
Presentation
Associated with...

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

Acute Pyelonephritis
Which part of kidney affected?
Presentation
Urine?

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

211

Chronic Pyelonephritis
Result of
Requires
Histo
Tubules contain

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

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

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

Diffuse Cortical Necrosis
What is it?
Due to
Associated with

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

214

Which Nephrotic/Nephritic Syndromes have Subepithelial IC deposits

PSGN
Membranous

215

Which Nephrotic/Nephritic Syndromes have Subendothelial IC deposits

MPGN I
DPGN

216

Charges in the Tubule of the Kidney

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