10a: Renal Flashcards
1
Q
Embryology: the (X) functions as the interim kidney in developing embryo for the first (Y) weeks
A
X = mesonephros Y = 12 (first trimester)
2
Q
The ureteric bud arises from (X) and eventually gives rise to which part(s) of kidney?
A
X = caudal end of mesonephric duct
Ureter, pelvises, calyces, collecting ducts
3
Q
Woman taking (X) drugs puts baby at risk for Potter sequences. What are the symptoms/findings?
A
X = ACEi/ARB (causes oligohydramnios, since A-II required for kidney development)
“POTTER” =
- Pulmonary hypoplasia (cause of death)
- Oligohydramnios
- Twisted face (low-set ears, retrognathia, flat nose)
- Twisted skin
- Extremity defects (club feet)
- Renal failure in utero
4
Q
Patient with Duplex Collecting system is at high risk for:
A
UTIs (strongly associated with vesicoureteral reflux and ureteral obstruction)
Note: Duplex collecting system means two ureters for one kidney
5
Q
Which amino acid is provided by amniotic fluid and helps in fetal lung development?
A
Proline
6
Q
List the components of the glomerular filtration barrier, starting from inside Bowman capsule
A
- Podocytes (epithelial layer)
- Glomerular BM
- Fenestrated capillary endothelium
7
Q
T/F: The mesangial cells of the kidney are located in Bowman capsule
A
False - located near afferent/efferent arterioles in glomerulus
8
Q
Ureters pass (over/under) which key vessels in males/females?
A
Under (“water under the bridge”)
F: uterine artery
M: vas deferens
9
Q
Plasma volume, part of (ECF/ICF) can be measured by which method?
A
ECF (25% of it)
Radiolabeling albumin
10
Q
ECF volume can be measured by which method?
A
Radiolabeling mannitol or inulin
11
Q
Glomerular filtration barrier is selective based on size and charge of molecules. Which parts of barrier are responsible for these?
A
Size: slit diaphragm (podocyte feet with basement membrane) and fenestrated capillary endothelium
Charge: negatively-charged glycoproteins on all three layers (prevent neg-charged molecules from entering)
12
Q
Renal clearance equation:
A
(Ux)*(V)/(Px)
13
Q
T/F: Oncotic pressure of glomerular capillary normally equals zero
A
False - oncotic pressure of Bowman space normally zero
14
Q
Best estimate of GFR is (X). (Y) is also used, but tends to (over/under)-estimate the value
A
X = inulin clearance
Y = creatinine clearance;
Over-estimates (moderately secreted by tubules)
15
Q
A reduction of GFR by half will (increase/decrease) serum Cr by which factor?
A
Increase; 2x
16
Q
Renal (plasma/blood) flow can be estimated using (X) clearance
A
Plasma flow (RPF) X = PAH (para-aminohippuric acid)
Note: Renal blood flow can be calculated via RPF/(1-Hct)
17
Q
Filtration fraction equation:
A
GFR/RPF (normally about 20%)
18
Q
Filtered load equation:
A
GFR*Px
19
Q
Prostaglandins (dilate/constrict) (X) arteriole in kidney and Angiotensin II (dilates/constricts) (Y) arteriole. Which of these affects filtration fraction?
A
Dilate;
X = afferent
Constricts
Y = efferent
Angiotensin II (increases FF since increases GFR, decreases RPF)
20
Q
How does dehydration affect filtration fraction in kidney?
A
Decrease (decrease in GFR, but even greater decrease in RPF)
21
Q
After certain point, efferent arteriole constriction will actually decrease (GFR/FF).
A
GFR (flow-mediated increase in glomerular cap oncotic P)
Note: FF will ALWAYS be increased with efferent arteriole constriction due to greater decrease in RPF
22
Q
Glucosuria in normal adult will begin at plasma conc of (X). And at transport rate of (Y) mg/min, all transporters are fully saturated
A
X = 200 mg/dL Y = 375
23
Q
In metabolic (acidosis/alkalosis), renal ammoniagenesis is stimulated. (X) is metabolized to eventually form ammonium and (Y).
A
Acidosis
X = glutamine (to glutamate and then to alpha-KG and then to glucose + CO2)
Y = HCO3 (combines with CO2 and reabsorbed into blood)
24
Q
Posterior fracture of L 12th rib: which structure likely injured?
A
L kidney
25
Ureter courses (anterior/posterior) to gonadal vessels and then anterior to (X) key vessel in the true pelvis
Posterior
| X = internal iliac a
26
T/F: PCT absorbs the majority of water, regardless of hydration status
True (60%)
27
Which key hormones work on the proximal tubule?
1. A-II: increases Na/H exchange to increase Na, H2O and HCO3 reabsorption
2. PTH: inhibits Na/PO4 co-transport (increases PO4 excretion)
28
(X) portion of tubule is the concentrating segment. And (Y) is the diluting segment.
```
X = thin descending loop of Henle (permeable to water, not solutes)
Y = thick ascending loop of Henle (permeable to solutes, not water)
```
29
Thick ascending loop of Henle: which ions are reabsorbed by transporter?
Na/K/Cl2 co-transporter
30
Describe the mechanism behind paracellular transport of (X) ions in (Y) segment of kidney tubules
```
X = Mg, Ca
Y = Thick ascending limb
```
K back-leak into lumen gives it positive potential, inducing paracellular reabsorption of Mg, Ca into interstitium
31
Which key ions are being reabsorbed in DCT of kidney?
Na/Cl (cotransporter); Ca (channel)
32
Which key hormones work on the distal convoluted tubule?
1. PTH: upregulates basolateral Na/Ca antiporter to increase Ca reabsorption (decreasing Ca conc in tubule cell induces more Ca absorption from lumen via apical channel)
2. A-II (increase Na reabsorption)
3. ANP (decrease Na reabsorption)
33
T/F: Aldosterone binds to Collecting tubule transporters to upregulate Na absorption at the expense of H and K.
False - binds to mineralocorticoid receptors and upregulates gene expression/protein synthesis of the transporters
34
Alpha-intercalated cell: H (enters/exits) lumen while (X) (enters/exits).
Enters (secreted from alpha-intercalated cell)
X = K exits (reabsorbed into cell)
H/K ATPase; ammonium is generated in lumen
35
(X) cells in Collecting duct of nephron are responsible for reabsorbing Na from lumen via (Y) channel
```
X = Principal
Y = ENaC (apical membrane)
```
36
Child presents with hypertension, hypokalemia, and metabolic alkalosis, so you check (X) levels and find they are undetectable. If this is a receptor issue, what's the likely Dx? Rx?
X = aldosterone
Liddle syndrome (hyperactive ENaC); Amiloride
37
Fanconi syndrome: main defect is...
Decreased reabsorption of AA, glucose, HCO3, PO4 in PCT (resulting in Type II renal tubule acidosis)
38
(X) syndrome is reabsorptive defect in thick ascending loop of Henle, affecting (Y) transporter.
```
X = Bartter (AR inheritance)
Y = Na/K/Cl2 (presents similarly to chronic loop diuretic use)
```
39
(X) syndrome is reabsorptive defect in DCT, affecting (Y) transporter.
```
X = Gitelman (AR inheritance)
Y = Na/Cl co-transporter (similar to using chronic thiazide diuretics)
```
40
Which metabolic abnormalities would you expect to see in Bartter syndrome?
Decreased Na/K/Cl2 transport in TAL
Hypokalemia, metabolic alkalosis, Hypocalcemia (hypercalciuria)
41
Which metabolic abnormalities would you expect to see in Gitelman syndrome?
Decreased Na/Cl co-transport in DCT
Hypokalemia, metabolic alkalosis, Hypercalcemia (hypocalciuria), HypoMg-emia
42
Syndrome of apparent mineralocorticoid excess: what's the main defect?
Deficiency of 11-beta-hydroxysteroid dehydrogenase (typically converts cortisol to cortisone, the latter of which is inactive on mineralocorticoid receptors)
43
Syndrome of apparent mineralocorticoid excess: what are the main symptoms?
Similar to hyperaldosteronism (hypertension, hypokalemia, metabolic alkalosis) but low aldosterone levels since cortisol is activating the mineralocorticoid receptors
44
Patient eating (X), which is present in licorice, can acquire which syndrome?
X = glycyrrhetinic acid
Syndrome of apparent mineralocorticoid excess
45
Syndrome of apparent mineralocorticoid excess: Rx?
Corticosteroids (to decrease endogenous cortisol production)
46
List the solutes absorbed more quickly than water in the PCT
Glucose, AA, HCO3
47
Along the proximal tubule, tubular inulin (increases/decreases/doesn't change) in concentration. And in total amount?
Increases in concentration, but not amount (due to H2O reabsorption)
48
In early PCT, Cl reabsorption occurs at (faster/slower/same) rate as Na
Slower (then matches Na reabsorption rate more distally)
49
Angiotensin II has effects on which parts of brain?
1. Post pit (increase ADH secretion)
| 2. Hypothalamus (increase thirst)
50
ANP and BNP have which effect on GFR?
Increase (dilate afferent, constrict efferent; promote natiuresis)
51
List the components of the Juxtaglomerular apparatus
1. Mesangial cells
2. JG cells = modified smooth muscle (of afferent arteriole)
3. Macula densa = NaCl sensor (of DCT)
52
Where is 1-alpha hydroxylase found in kidney?
PCT cells
53
(X) chatecholamine is secreted by (Y) tubular cells in kidney and works to promote:
```
X = DA
Y = PCT
```
Natriuresis (at low doses; vasodilator that increases RBF)
54
(X) (increases/decreases) urea permeability in collecting duct
X = ADH
| Increases
55
(Acidosis/alkalosis), (hyper/hypo)-osmolarity, and (X) adrenergic (agonists/antagonists) shift K out of cells.
Acidosis; hyperosmolarity
| X = beta antagonists (decrease Na/K ATPase)
56
Which key drugs shift potassium out of cells (causing hyperkalemia)?
1. Digoxin
2. BB
3. Succinylcholine
57
Which electrolyte abnormality causes U waves on EKG?
Hypokalemia
58
Muscle weakness is primarily a feature of which electrolyte abnormality?
Low or high K
59
Hypercalcemia symptoms
"Stones, bones, groans, thrones, pysch overtones"
1. Renal stones
2. Bone pain
3. Abdominal pain
4. Increased urinary frequency
5. Anxiety, altered mental status
60
Which electrolyte disturbance can cause Torsades?
Hypomagnesemia
| Hypocalcemia can cause prolonged QT
61
Osteomalacia/rickets primarily due to which electrolyte disturbance?
Low PO4
62
Gap metabolic acidosis differential
MUDPILES
1. MeOH
2. Uremia
3. DKA
4. Propylene glycol (antifreeze)
5. Isoniazid or Iron tablets
6. Lactic acidosis
7. Ethylene glycol (antifreeze)
8. Salicylates (late)
63
Non-gap metabolic acidosis differential
HARDASS
1. Hyperalimentation (artificial nutrient supply)
2. Addison's
3. Renal tubular acidosis
4. Diarrhea
5. Acetazolamide
6. Spironolactone
7. Saline infusion
64
Chronic COPD patient will likely have which acid/base abnormality?
Respiratory acidosis due to hypercapnia (with compensatory increase in serum HCO3 and near-normal pH)
65
Measuring (X) urine levels helps differentiate between etiologies of metabolic alkalosis. Give examples.
X = Cl
1. Loops (increased urine Cl)
2. Vomiting (decreased urine Cl)
3. Hyperaldosteronism (high BP and high urine Cl)
66
Renal tubular acidosis with low urine pH
Type 4 (hyperkalemic RTA) and early on in Type 2 (PCT RTA)
67
Heparin can cause Type (X) RTA
X = 4 (via inhibiting zona glomerulosa and thus aldosterone production)
68
Amphotericin B toxicity can cause Type (X) RTA
X = 1 (at DCT)
69
Multiple myeloma can cause Type (X) RTA
X = 2 (PCT; Fanconi)
70
Waxy renal casts seen in:
ESRD/chronic renal failure
71
Hyaline renal casts seen in:
Normal finding (concentrated urine sample)
72
Classic bladder cancer Sx
Gross hematuria (gradually reddening urine)
73
Nephritic syndrome is due to (X) disruption whereas nephrotic is due to (Y) disruption
```
X = GBM (inflammatory process)
Y = podocyte (massive proteinuria)
```
74
Post-strep glomerulonephritis EM findings
Sub-epithelial electron-dense bumps (immune complex)
75
"Granular" appearance of glomerulus on immunofluorescence signifies which pathogenesis?
Immune complex (IgG, IgM, C3 deposition)
76
Renal nephritic/nephrotic syndrome: LM shows mesangial proliferation and EM shows mesangial immune complex deposits. Dx?
IgA nephropathy (most common glomerulonephritis)
77
Nephritic presentation of SLE is (X). And nephrotic presentation is (Y).
```
X = Diffuse proliferative glomerulonephritis (common cause of death in SLE)
Y = Membranous nephropathy
```
78
"Tram tracking" on PAS/H&E stain of glomeruli
Membranoproliferative glomerulonephritis (due to mesangial ingrowth splitting GBM)
79
Glomerulonephritis, sensorineural deafness, and retinopathy/lens dislocation
Alport syndrome (mutation in type IV collagen leads to thinning/splitting of basement membrane)
"Can't see, can't pee, can't hear a bee"
80
Glomeruli on EM have "basket weave" appearance
Alport syndrome (glomerulonephritis)
81
"Wire-looping" capillaries on LM of glomeruli
Diffuse proliferative GN (like SLE)
"Wire Loopus"
82
Nephritic syndrome associated with Hep (B/C) infection
B or C
Membranoproliferative GN (Type I)
83
Nephritic syndrome associated with C3 nephritic factor activating complement system
Membranoproliferative GN (Type II) aka Dense deposit disease
84
(Nephritic/nephrotic) syndrome are accompanied by (increase/decrease) in serum lipid levels. Why?
Nephrotic; increase (hyperlipidemia)
Liver senses low serum proteins and so pumps up protein (including lipoproteins) synthesis
85
(Nephritic/nephrotic) syndrome are accompanied by (hyper/hypo)-coagulability. Why?
Nephrotic
| Hypercoagulability (increased anti-thrombin III loss in urine)
86
(Nephritic/nephrotic) syndrome are accompanied by increased risk of infection. Why?
Nephrotic
Increased loss of Ig in urine
87
(X) disease: selective loss of albumin in urine
X = minimal change disease (due to podocyte effacement and decreased anionic properties of BM)
Most common nephrotic syndrome in children
88
Minimal change disease Rx
Corticosteroids (excellent response)
89
FSGS can be distinguished from minimal change disease via which ways?
1. Non-selective proteinuria (not just albuminuria)
| 2. Non-responsive to corticosteroids
90
Most common cause of nephrotic syndrome in AA and Hispanics
FSGS
91
Nephrotic syndrome(s) associated with Hepatitis B or C infection
FSGS, Membranous nephropathy
92
GBM and mesangial changes in diabetic glomerulonephropathy is the result of which process?
Non-enzymatic glycosylation (increases GBM thickness/permeability; hyaline arteriosclerosis of efferent arterioles causes mesangial expansion)
93
"Spike and dome" appearance with subepithelial deposits: (X) nephropathy
X = membranous (granular due to immune complex deposition)
94
Most common cause of nephrotic syndrome in Caucasian adults
Membranous nephropathy
95
Primary Membranous nephropathy MOA:
Ab against phosphlipase A2 receptor (abundant on podocytes)
96
Secondary Membranous nephropathy causes
SLE, solid tumors (lung, colon), drugs (NSAIDs, gold, penicillamine), infections (HBV, HCV)
97
Nephrotic syndrome(s) associated with HIV and sickle cell disease
FSGS
98
Most common kidney stones are (X) stones with which electrolyte abnormality?
X = Ca oxalate
Hypercalciuria despite NORMOcalcemia (maybe due to dehydration or increased Ca gut reabsorption followed by immediate secretion)
99
How do citrate levels affect (X) kidney stone formation?
X = Ca
Normally bind Ca (and prevent its precipitation) in tubules; in acidemia, citrate reabsorption increased to bind H+ (increase risk Ca kidney stone formation)
100
Diarrhea increases risk of (X) kidney stone formation
X = Ca and uric acid
(Diarrhea causes met acidosis, increasing citrate reabsorption; also met acidosis will increase urinary H secretion, acidifying urine and predisposing to Urate stone formation)
101
High protein diet increases risk of (X) kidney stone formation
X = Ca
| Causes met acidosis due to protein breakdown, increasing citrate reabsorption
102
Ca kidney stones can form as a result of vitamin (X) deficiency
X = C (due to low citrate levels)
103
T/F: Low Ca intake will decrease chance of Ca stone formation
False - low Ca intake means more free oxalate to be absorbed in gut and thus excreted in urine (Ca oxalate stone formation risk)
104
Most common kidney stones seen in children
Ca- phosphate
105
Hereditary disorder in (X) leads to impaired reabsorption of which amino acids, thus disposing child to (Y) kidney stones
X = PCT transporter
For Cystine, Ornithine, Arg, Lys ("COAL")
Y = cystine
106
Na-cyanide and nitropruside added to urine turns it red-purple. What is this a test for?
Cystinuria
107
Renal cell carcinoma: gross and histo appearance.
Most commonly "clear cell carcinoma"
Gross: golden-yellow (high lipid content)
Histo: Polygonal clear cells (filled with accumulated lipids/CHO)
108
Renal cell carcinoma: originates from (X) cells and most often spreads via (blood/lymph) to which organs?
X = PCT
Blood (renal vein if on left, then IVC)
Lung and bone
109
T/F: Renal cell carcinoma is resistant to chemo and radiation
True
110
Renal cell tumor arising from collecting ducts
Renal oncocytoma (very rare; benign, well-circumscribed with central scar)
111
Child born with mental retardation and Aniridia (absent iris) likely has which tumor?
Wilms/Nephroblastoma (WT1 deletion; WAGR complex)
112
Wilms tumor arises from which cells?
Metanephric blastema (hence name nephroblastoma)
113
Wilms tumor, early nephrotic syndrome, and male pseudohermaphroditism triad
Denys-Drash (WT1 mutation)
114
Wilms tumor, macroglossia, organomegaly
Beckwith-Wiedemann (WT2 mutation)
115
"Overactive bladder" aka detrusor hyperactivity is (X) incontinence
X = urge (leakage with urge to void immediately)
116
"Underactive bladder" aka detrusor hypoactivity is one cause of (X) incontinence. What's another cause?
X = overflow (incomplete voiding and leaks with overfilling)
Outlet obstruction (ex: BPH)
117
Patient with Multiple Sclerosis presents with incontinence. What is the most likely etiology?
Urge (micturition control centers are compromised)
118
"Thyroidization" of kidney refers to:
Eosinophilic casts that form due to chronic pyelonephritis (resemble thyroid tissue)
119
Consequences of renal failure:
"MAD HUNGER"
1. Metabolic Acidosis
2. Dyslipidemia
3. Hyperkalemia
4. Uremia (high BUN)
5. Na/H2O retention (edema, HF, HT)
6. Growth retardation/developmental delay
7. EPO failure (anemia)
8. Renal osteodystrophy (subperiosteal thinning)
120
T/F: Glomeruli are spared in acute interstitial nephritis
True
121
Which metabolic abnormalities are seen in maintenance phase of acute tubular necrosis?
Hyperkalemia, metabolic acidosis (H+ and anion retention), uremia; also oliguria leading to V overload
122
Which metabolic abnormalities are seen in recovery phase of acute tubular necrosis?
Hypokalemia
