Renal Flashcards
1
Q
What are the three effects of Angiotensin II?
A
- systemic vasoconstriction
- constriction of efferent arteriole
- Increased aldosterone synthesis
2
Q
Concentration of tubular fluid in proximal tubule
A
isotonic with plasma (300 mosm/L)
3
Q
Concentration of tubular fluid in descending loop of henle
A
Increasing (water permeable)
400-1200mOsm/L
4
Q
Concentration of tubular fluid in ascending loop of henle
A
Decreasing (salt permeable)
1200-200mOsm/L
5
Q
Lowest osmolality site in nephron, assuming low ADH
A
Distal convoluted tubule. Impermeable, so fluid stays hypotonic with increased reabsorption of solutes
6
Q
When does ARPKD present?
A
At birth. In contrast, dominant form comes years later.
7
Q
Urea acts on which segment of the collecting duct?
A
medullary segement to increase urea and water reabsorption
8
Q
When does the pronephros degenerate?
A
4 weeks
9
Q
Mesonephros
A
Functions as kidney for the first trimester
10
Q
Metanephros appears wheN?
A
5th week of gestation. It becomes the permanent kidney
11
Q
Ureteric bud comes from
A
caudal end of mesonephros
12
Q
Ureteric bud gives rise to:
A
ureter, pelvises, calyces, collecting ducts
13
Q
what interaction needed to form normal kidney
A
ureteric bud pokes the metanephric tissue
–induces metanephric tissue to format glomerulus to distal tubule
14
Q
most common site of obstruction in fetus
A
ureteropelvic junction
15
Q
Potter’s syndrome
A
Oligohydramnios–>
limb deformities
facial deformities
pulmonary hypoplasia
16
Q
Causes of Potter’s
A
ARPKD
posterior urethral valves
bilateral renal agenesis
IF YOU CAN”T PEE in utero, you get potters
17
Q
Horseshoe kidney assoc’d with
A
Turner syndrome
18
Q
Nonfunctional kidney with cysts and connective tissue in utero. What caused this?
A
abnormal interaction btw ureteric bud and metanephros
19
Q
Describe path of blood into the kidney
A
renal artery segmental artery interlobal artery arcuate artery interlobular artery
20
Q
Which kidney do you harvest for donation?
A
Left kidney=it has a longer renal vein
21
Q
ureters pass over/under the ductus deferens/uterine artery?
A
under
22
Q
60-40-20 rule
A
60% weight is TBW
40% ICF
20% ECF
23
Q
measure plasma volume
A
radiolabeled albumin
24
Q
measure extracellular volume
A
inulin
25
what gives negative charge in GFR?
heparan sulfate
26
clearance eq:
C=UV/P
U=urine concenctration
V=urine flow rate
P=plasma concentration
27
how to calc GFR
clearance of inulin or creatinine
28
When is creatinine clearance not accurate for GFR?
When GFR is very low. will have higher concentration of creatinine in urine
29
Calculation for effective renal plasma flow (ERPF)
clearance of PAH
PAH=filtered AND secreted into the proximal tubule. all that enters the kidney is excreted
30
RBF=
RPF/(1-Hct)
--ERPF underestimates true RPF by 10%
31
Filtered load=
GFR*plasma concentration
32
NSAIDs
constrict afferent arteriole
33
ACE-I
dilate efferent arteriole
34
prostaglandins
dilate afferent arteriole
35
angiotensin II
constricts efferent arteriole
36
increased plasma protein
decrease GFR
| decrease FF
37
constriction of ureter
decrease GFR
| decrease FF
38
Hartnup's disease
deficiency of tryptophan(neutral amino acid) transporter in proximal tubule. neutral AA excreted in urine.
results in pellagra
39
blood glucose level when glucosuria starts? max saturation?
160 mg/DL
| 350mg/DL
40
which part of nephron generates ammonia?
Prox tubule
41
PTH and ATII on prox tubule
PTH: inhibits Na/Phosphate cotransport
ATII: stimulates Na/H exchange=contraction alkalosis. Holding onto sodium at expense of alkalosis
42
What % Na absorbed at each nephron segment?
1. Prox tubule=65-80%
2. L of H=10-20
3. DCT=5-10%
4. 3-5%
43
Thick loop of henle
Na/K/2Cl resorption
- -paracellular resorption of Mg2+ and Ca2+
- -dilution of urine as it passes
44
What allows paracellular resorption in thick ascending limb?
potassium backleak.
45
DCT transporter
Na/Cl apical cotransporter
| --urine becomes hypotonic
46
PTH effect on DCT
Stimulates Ca/Na Xchange on basolateral surface increasing Ca resorption
47
Thiazide mechanism
Blocks Na/Cl apical cotransporter
| -->indirectly blocks Na/Ca2+ exchanger
48
Mechanism of amiloride/triamterene
Blocks ENaC channel in principal cell of CT
49
[Tubular Fluid]/[Plasma] ratio
If >1, solute is reabsorbed less quickly than water
| If <1, solute reabsorbed more quickly than water
50
very high TF/P
PAH/creatinine/inulin
51
moderate TF/P
urea/Cl
52
TF/P=1
K/Na
53
TF/P <1
phosphorus
| bicarb
54
TF/P <<1
amino acids and glucose (virtually completely reabsorbed
55
Tx: hypovolemic hyponatremia
NS
56
tx: hypervolemic hyponatremia
Salt and fluid restriction, furosemide
57
Euvolemic hyponatremia
free water restriction (NOT hypertonic saline--otherwise will fluid overload them)
58
SIADH hyponatremia
do NOT give normal saline! will excrete sodium and retain water. Give convaptan and water restrict
59
when should you give hypertonic saline?
hyponatremia with NEURO deficits or seizures
60
Six effects of angiotensin II
1. Vascular smooth muscle
2. constricts efferent arteriole
3. aldosterone
4. ADH
5. Increased prox tubule Na/H
6. Stimulates hypothalamus
61
ADH regulates
osmolarity (except in extreme low blood volume)
62
Aldo regulates
blood volume
63
How do beta blockers decrease BP?
inhibiting B1 receptors on the JGA
64
How much K is reabsorbed along the nephron?
65% PCT
30% ascending L of H
5-100% at DCT
65
How does ANP work?
Increases Na filtration and GFR at PCT with no compensatory Na resorption distally.
-->Na and H2O loss
66
PTH effect on kidney
Increased Ca resorption (DCT)
Decreased PO4 resorption (PCT)
Increased activation of vitamin D
67
Causee of hyperkalemia
```
digitalis
hyperosmolarity
insulin deficiency
cell lysis
acidosis
Beta adrenergic antagonist
```
68
Hyponatremia Sx
nausea, malaise
| stupor coma
69
hypernatremia sx
irritability
| stupor coma
70
hypokalemia sx
arrhythmias, muscle weakness
71
-U wave on ECG, flattened T waves
hypokalemia
72
hypocalcemia sx
tetany and seizures
| --decreases threshold potential
73
Hypomagnesia
tetany and arrhythmias
74
hypermagnesia
```
cardiac arrest
hypocalcemia
decreased DTRs
bradycardia
hypotension
```
75
hypophosphatemia
osteomalacia
76
Hyperphosphatemia
renal stones
metastatic calcifications
hypocalcemia
77
How to tell if there is a mixed disorder (acid base)?
pCO2 and HCO3 move in opposite directions
OR
pCO2 predicted is very different
78
predicted pCO2=
(1.5 HCO3 + 8) +/-2
79
Henderson-Hasselbach
pH=6.1+log [HCO3]/(0.03*pCO2)
80
When do you check anion gap
metabolic acidosis present
81
Eq for anion gap
Na-Cl-HCO3
| --Over 12 is abnormal
82
Increase anion gap metabolic acidosis
```
Methanol
Uremia
Diabetic ketoacidosis
Propylene glycol
Iron/INH
Lactic acidosis
Ethylene glycol
Salicylic acid
```
83
Causes of normal anion gap acidosis
```
Hyperalimentation
Addison's disease
Renal tubular acidosis
Diarrhea
Acetazolamide
Spironolactone
Saline infusion
```
84
Causes of primary metabolic alkalosis
loop diuretics
vomiting
antacid use
hyperaldosteronism
85
Type 1 RTA
CT cannot excrete H+
86
Type 2 RTA
Cannot resorb bicarb
87
Type 4 RTA
lack of aldosterone effect
88
RTA: pt with urine pH > 5.5 and is hypokalemic
Type 1
89
RTA: Pt has a urine pH < 5.5 and is hypokalemic
Type 2 RTA
90
RTA: hyperkalemic patient with low urine pH and low BP
Type 4 RTA
91
Increased urine pH puts you at risk for
calcium phosphate stones
92
Type 2 RTA associated with
Fanconi's syndrome
93
WBC caste:
tubulointerstitial inflammation
acute pyelonephritis
transplant rejection
94
fatty casts or oval fat bodies
nephrotic syndrome
95
granular muddy brown casts
acute tubular necrosis
96
Waxy casts
advanced renal disease
97
Hyaline casts
normal
98
Nephrotic syndromes
```
Minimal change disease
Membranous nephropathy
Focal segmental glomerulosclerosis
Amyloidosis
Diabetic glomerulonephropathy
```
99
Nephritic syndromes
Acute poststreptococcal GN
Rapidly progressive GN
Berger's IgA GN
Alport
100
Combined Nephritic and Nephrotic syndromes
Diffuse proliferative GN
| Membranous GN
101
Sx of nephrotic syndrome
proteinuria
hyperlipidemia
fatty casts
edema
102
Why are pts with nephrotic syndrome at risk for thromboembolism and infection?
AT III is lost in urine
| Loss of IgG
103
Most common cause of nephrotic syndrome in adults
FSGS
104
LM: segmental sclerosis and hylinosis
EM: effacement of foot proceses
FSGS
105
LM: GBM thickening
EM: spike and dome with subepithelial deposits
IF: granular
membranous
106
causes of FSGS
HIV, kidney disease, heroin, obesity, interferon
107
causes of membranous
SLE< drugs, infection
108
LM: normal
EM: foot process effacement
minimal change
109
Tx of minimal change
corticosteroids
110
cause of minimal change
loss of polyanion in GBM causing ONLY albumin loss
111
LM: congo red stain with apple-green birefirencence
amyloidosis.
assoc'd with multiple myeloma, TB, RA
112
Subendothelial deposits with tram track appearance
| IF: granular
type I MPGN
113
LM: Intramembranous dense deposits
MPGN
114
Type I MPGN associated with
HBV, HCV
115
Type II MPGN associated with
C3 nephritic factor
116
nephritic sx:
azotemia
oliguria
hypertension
proteinuria <3.5 g/day
117
LM: lumpy bumpy glomeruli
EM: subepithelial immune complexes
IF: granular C3, IgG, IgM
acute post strep GN. occurs a few weeks after infection
118
LM: crescent shape made of fibrin and C3b proteins
rapidly progressive GN
119
causes of rapidly progressive GN
1. goodpasture's syndrome
2. Wegener's granulomatosis
3. Microscopic polyangiitis
120
LM: wire looping of capillaries
EM: subendothelial IgG with C3
IF: granular
Diffuse proliferative glomerulonephritis
121
LM: mesangial proliferation
EM: mesangial IC deposits
IF: IgA deposits in mesangium
Berger's disease. occurs a few days after infection
122
Split basement membrane with GN, deafness, and eye problems
Alport syndrome
123
What's mutate in alport syndrome?
type IV collagen.
124
alport inheritance
X linked
125
Which kidney stones can you NOT see on an Xray?
Uric acid stones
126
octahedron kidney stones
calcium oxalate
127
which stones precipitate at a high pH?
struvite
| calcium phosphate
128
Most common kidney stone presentation
calcium oxalate stone in a pt with hypercalciuria and normalcalcemia
129
Treatment for calcium stones
thiazides and citrate
130
Causes of oxalate stones
ethylene glycol and vitamin C overdose
131
staghorn calculi
struvite stones (ammonium magnesium phosphate)
132
Tx for calcium stones
thiazides and citrate
133
Cause of struvite stones
urease positive bugs:
1. proteus
2. staph
3. klebsiella
134
hexagonal crystals
cysteinuria
135
coffin lid stones
struvite
136
rhombus red brown stones
uric acid
137
renal cell carcinoma histology
clear limid filled cells
138
RCC associated with a gene deletion on
chromosome 3
139
RCC produces
EPO
ACTH
PTHrP
140
PPresentation of RCC
hematuria
flank mass
polycythemia
141
Tx: RCC
Resection. Resistant to conventional chemo and radiation
142
WWilm's tumor (nephroblastoma) histology
embryonic glomerular structures. Child 2-4 has flank mass and hematuria
143
Wilm's tumor deltion
WT1 tumor suppressor on chromosome 11
144
WAGR complex
wilm's
aniridia
genitourinary malformation
mental retardation
145
biopsy of kidney: papillary growth lined by transitional epithelium with mild nuclear atypia
transitional cell carcinoma
146
Transitional cell carcinoma associated with
```
PeeSAC
phenacetin
Smoking
aniline dyes
cyclophosphamide
```
147
ppainless hematuria suggests
bladderr canceer
148
Where can transitional cell carcinoma occur?
calyces, pelvis, ureters, bladder
149
acute pyelonephritis affects which part of kidneys?
Cortex. glomeruli and vessels are spared
150
Cause of chronic pyelonephritis
vesicoureteral reflux or chronic kidney stones. Normal person shouldn't get recurrent UTIs-->chronic pyelonephritis
151
WWhich parts affected in chronic pyelonephritis?
Corticomedullary scarring with blunted calyces. Tubules have eosinophilic casts
152
HIstology of chronic pyelonephritis
Lymphocytic invasion with fibrosis
153
presentation of drug induced interstitial nephritis
eosinophilic pyuria
| azotemia
154
How long after drug will drug TIN happenn?
After 1-2 weeks..
Can be months with NSAIDs
155
Which drugs cause TIN (allergic reaction to drug)
penicillin
diuretics
sulfonamides
rifampin
156
Diffuse cortical necrosis caused by
Vasospasm and DIC. Associated with obstetric catastrophes and septic shock
157
maintenance phase of acute tubular necrosis
oliguric for 1-3 weeks. Risk of hyperkalemia
158
Recovery phase of acute tubular necrosis
polyuric. Risk of hypokalemiia
159
Causes of toxic ATN
```
Aminoglycosides
heavy metals
myglobinuria
ethylene glycol-->oxalate crystals
radiocontrast dye
urate
```
160
Renal papillary necrosis caused by
diabetes
acute pyelonephritis
chronic phenacetin (acetaminophen)
sickle cell
161
Difference in handling of BUN vs creatinine
BUN is reabsorbed
| Creatinine is NOT reabsorbed
162
Acute renal failure: prerenal azotemia
BUN: Cr is increased >20
| -urea retained by kidney to conserve volume
163
Intrinnsic renal failure
BUN: Cr ratio decreased <15
- caused by ATN/ischemia/toxins/crescentic GN
- granular casts
- Tubules filled with debris
- decreased BUN reabsorption
164
PPostrenal azotemia
BUN: Cr >15
| -Caused by outflow obstruction (bilateral)
165
Urine osm: >500
| Urine Na < 1%
prerenal
166
Urine osm: 40
| FeNa >2%
Intrinsic or post-renal. Differentiate these by looking at the BUN: Cr ratio
167
Consequences of renal failure
```
Fluid/sodium retention (CHF)
hyperkalemia
metabolic acidosis
anemia
increased triglycerides
```
168
Side effect of increased BUN and Cr
```
Nausea
asterixis
pericarditis
encephalopathy
platelet dysfunction
```
169
Renal osteodystrophy
Failure of vitamin D hydroxylation
hypocalcemia
hyperphosphatemiia
-->2ndary hyper PTH
170
WWHy does hyperphosphatemia worsen renal osteodystrophy?
Tissue calcifications occur within tissues-->calcium phosphate instead of being excreted
171
Why do pts with ADPKD get hypertension?
Increased renin production
172
ADPKD associated with
berry aneurysms
mitral valve prolapse
benign hepatic cysts
173
AARPKD
presents in infant, often as potter's syndrome
174
AARPKD associated with
congenital hepatic fibrosis. After birth, will have HTN, portal HTN, progressive renal insufficiency
175
Medullary cystic disease
tubulointerstitial fibrosis and renal insufficiency-->cannot concentrate urine.
Inherited with shrunken kidneys seen on ultrasound
176
where does mannitol affect the nephron?
The thin descending limb
177
where does acetazolamide work its effect?
Proximal tubule
178
mmannitol indications
Drug overdose
| elevated ICP
179
Mannitol toxicity
pulmonary edema
180
when is mannitol contraindicated
CHF and anuria
181
iindications acetazolamide
urinary alkalization
altitude sickness
glaucoma
metabolic alkalosis
182
acetazolamide toxicity
metabolic acidosis
NH3 tox
sulfa allergy
183
calcium wasting diuretic
loop diuretics
184
furosemide indications
CHF, cirrhosis, nephrotic syndrome, pulmonary edema (too much fluid)
hypertension, hypercalcemia
185
Toxicity of loops
```
ototoxicity
hypokalemia
dehydration
allergy (sulfa)
nephritis
Gout
```
186
Ethacrynic acid
Non sulfonamide loop diuretic. Virtually the same, can also cause gout
187
indications for hCTZ
HTN CHF
hypercalciuria
nephrogenic diabetes insipidus
188
Name the K sparing diuretics
Spironolactone
Triamterene
Amiloride
189
Mehcanism: spironolactone and eplerenone
Competitive aldosterone antagonists.
190
mmechanism triamterene and amiloride
Block ENaC at cortical collecting duct
191
IIndications for spironolactone
hyperaldosteronism
K depletion
CHF
192
side effects of spironolactone
Hyperkalemia
| Antiandrogenic effects--man boobs
193
WWhich diuretics cause acidemia?
carbonic anhydrase inhibitors--decrease HCO3 reabsorption
aldosterone--blocks K/H secretion. Also, hyperkalemia increases H leak from cells
194
Which diuretics cause alkalemia?
loop and thiazide diuretics
- -Contractiion alkalosis
- -hypokalemia worsens alkalosis
195
Urine calcium increases with
loops
196
Why are ARBs better than ACE-Is?
they don't increase bradykinin
| -->no cough or angioedema. ACE is still able to break down bradykinin
197
What do ACEI do to GFR?
Decrease GFR, b/c efferent arterioles are opened
198
Why is ACE good for CHF?
prevents remodeling
199
ACE-I toxicity
```
Cough
angioedema
Teratogen
decrease GFR
Hyperkalemia
hypotension
```
200
When are ACE inhibitors contraindicated?
bilateral renal artery stenosis
201
dysplastic kidney--how is it inherited?
Not inherited. COngenital malformation of renal parenchyma characterized by cysts and abnormal tissue, especially CARTILAGE. NOT BILATERAL LIKE ADPKD
202
baby with portal htn
ARPKD
203
berry aneurysm
ADPKD. cysts in the liver, kidney, and brain.
204
mitral valve prolapse
ADPKD association
205
how is medullary cystic kidney disease inherited?
autosomal dominant with SHRUNKEN kidneys
206
IF Fena is <1% this tells you
tubular function is intact=can resorb sodium. this happens in prerenal ATN
207
why is BUN:cr <15 in intrarenal renal failure
epithelial cells are not working, cannot resorb BUN, so it is excreted through the kidneys
208
Why is BUN:Cr>20 in pre-renal failure?
Kidneys reabsorb as much fluid as possible and BUN follows
209
Why is BUN:Cr>15 in post-renal failure?
High pressure in ureters "pushes" BUN and fluid back into the body from tubular fluid
210
If pre-renal failure doesn't resolve...
becomes ischemic acute tubular necrosis. Prox tubule and medullary thick ascending limb are susceptible
211
What are consequences of ATN?
hyperkalemia with metabolic acidosis. Can't excrete potassium or organic anions (lactic acid)
212
hyperlipidemia seen in
nephrotic syndrome
213
minimal change associated with
hodgkin's lymphoma
214
most common cause of nephrotic syndrome in hispanics and A-As
FSGS
215
FSGS associated with
HIV
heroin
SCD
216
Minimal change and FSGS immunofluorexcence
None. Also poor response to tx/steroids. will progress to renal failure
217
Pt with lupus gets nephrotic syndrome
membranous nephropathy
218
Membranous nephropathy also associated with
Hep B/C
219
nephritic syndrome in lupus pt
DIffuse proliferative GN
220
granular immunofluorescence
immune complex deposition
- membranous
- membranoproliferative
221
type I membranoproliferative
subendothelial
HBV/HCV
more likely to have tram track
222
what determines if GAS can cause nephritic syndrome?
presence of M proteins
223
In adults with post-strep GN
more likely to present to crescent rapidly progressive GN
224
lupus patient with rapidly progressive glomerulonephritis
diffuse proliferative GN
225
Negative IF rapidly progressive nephritis
wegener, churg-strauss,
226
pt with rapidly progressive GN, hemoptysis, hematuria, and sinus infections
Perform cANCA--could be wegeners not goodpasteur's (classic)
227
most common cause of nephritis world wide
Berger's igA. Usually after mucosal infection, episodic.
228
churg strauss features not present in microscopic polyangiitis
Asthma
granulomatous inflammation
eosinophilia
229
tests for UTI
leukocyte esterase and nitrites
>10 WBC/hpf
culture: >100K CFU
230
sterile pyuria
chlamydia and n. gonorrhea
231
Most common pathogens for pyelonephritis
E. Coli
Klebsiella
Enterococcus
232
"thyroidization" of kidney
Chronic pyelonephritis
233
problem with staghorn calculi
can serve as a nidus for additional UTIs
234
what produces EPO
renal peritubular interstitial cells
235
why are crohn's pts more likely to make calcium oxalate stones?
Not able to absorb calcium necessary to bind oxalate
236
shrunken kidneys with cysts
Dialysis patients. Pts at increased risk for RCC
237
Triad of RCC
hematuria
palapable mass
flank pain
238
Cause of RCC
loss of VHL
- increased IGF-1
- Increased HIF=VEGF PDGF
239
wilms tumor cell
blastema
240
beckwith-Wiedemann
wilms tumor
neonatal hypoglycemia
muscular hemihypertrophy
organomegaly (tongue)
241
Serum lab levels of calcium, phoshorus, and PTH in chronic kidney disease
1. Phosphate retention
2. Low calcium from low vitamin D
3. Increased PTH
242
loop diuretics act on
thick ascending loop of henle. Decrease medullary concentration gradient
243
osmotic diuretics act on
thin descending loop
244
when do you see states of hypercalcemia and hypercalciuria?
Hyper PTH and sarcoidosis
245
Situations with hyperoxaluria
excesive intake
| low calcium diets (less calcium in gut to bind oxalate for excretion)
246
VHL deletion
chromosome 3P
247
Upper part of ureter is supplied by
The renal artery
248
Explain what happens with hypoaldosteronism to Na, K, HCO3 and Cl
Low Na
High K
acidosis=Low bicarb (H+ATP pump)
High chloride to balance out HCO3-
249
Thiazide tox
Hyperuricemia
Hypercalcemia
Hyperglycemia
Hyperlipidemia
Hypokalemia and hypotension
250
how to treat post GN glomerulonephritis
loop diuretics and vasodilators.
| --Kids recover well. Adults do not
