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
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
3
Q
How do diuretics affect urine NaCl
A
Increased. Serum NaCl may decrease
4
Q
How do diuretics change urine [K]?
A
All diuretics increase urine K except for KSD.
Serum K may decrease
5
Q
Which Diuretics cause Acidosis?
A
CAI (decreased bicarb reabsorption) and KSD (hyperK –> H leaving cells)
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
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
8
Q
Which diuretics affect urine Ca?
A
Urine Ca increases with LD and decreases with Thiazide
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)
10
Q
Ethacrynic Acid
A
Like Furosemade for people allergic to Sulfur
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
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
13
Q
Mannitol Uses MoA Tox Contras
A
Shock, OD, ICP, IOP
Osmotic Diuretic
Pul Edema, Dehydration
Contraindicated in CHF, anuria
14
Q
Urea transport in the Kidney
A
PT: reabsorbed, Descending LoH: secreted, CD: Reabsorbed or stays in lumen depending on ADH
15
Q
ADH and Urea
A
ADH –> UT1 in medullary collecting to increase Urea reabsorption which adds to corticopappillary osmotic gradient
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)
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.
18
Q
Functions of Vit D
A
GI reabsorption of Ca and PO4
Bone mineralization
Maintains serum [Ca]
–> monocytes to become osteoclasts
19
Q
Drugs associated with Hematuria
A
Anticoagulants (warfarin and heparin)
Cyclophasphamide –> hemorrhagic cystitis and increased risk for transitional cell carcinoma
20
Q
Tests for Protienuria
A
Dipstick for albumin
SSA (sulfosalicylic acid) for albumin and globins
21
Q
Urea and GFR
A
Increased GFR –> Decreased Urea reabsorption
22
Q
Functional Proteinuria
A
Not associated with rena disease
fever, exercise, CHF, Orthostatic
23
Q
Overflow Proteinuria
A
LMW proteinuria
Multiple Myeloma, Hemoglobinuria, Myoglobinuria
24
Q
Tubular Proteinuria
A
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
