Renal Flashcards
(172 cards)
1
Q
The ureteric bud is derived from what? What does it give rise to?
A
Derived from caudal end of mesonephric duct. Gives rise to ureter, pelvises, calyces, and collecting ducts.
2
Q
The metanephric mesenchyme gives rise to what?
A
Glomerulus through distal convoluted tubule
3
Q
What is the most common site of unilateral obstruction (hydronephrosis) in the fetus?
A
Ureteropelvic junction
4
Q
What is the most common site of bilateral obstruction (hydronephrosis) in the fetus?
A
Posterior urethral valves
5
Q
Describe Potter syndrome
A
Due to ARPKD, posterior urethral valves, or bilateral renal agenesis. Oligohydramnios leads to compression of the fetus (limb deformities, low-set ears, pulmonary hypoplasia).
6
Q
Horseshoe kidney is associated with what syndrome?
A
Turner
7
Q
What is the most common congenital kidney anomaly?
A
Horseshoe kidney
8
Q
An abnormal interaction between the metanephric mesenchyme and ureteric bud leads to what?
A
Multicystic dysplastic kidney; Non-inherited, usually unilateral –> asymptomatic
9
Q
What is the macula densa?
A
Closely packed specialized cells lining wall of thick ascending limb at transition to distal convoluted tubule; sensitive to NaCl concentration
10
Q
How is renal clearance calculated?
A
Cx = UxV/Px
11
Q
What substance is used to calculate GFR?
A
Inulin
12
Q
What substance is used to calculate Effective renal plasma flow?
A
PAH
13
Q
How is renal blood flow calculated?
A
RBF = RPF/(1-HCT)
14
Q
How is filtration fraction calculated?
A
FF = GFR/RPF
15
Q
What is a normal FF?
A
20%
16
Q
How is filtered load (mg/min) calculated?
A
FL = GFR (mL/min) x plasma concentration (mg/mL)
17
Q
Angiotensin II preferentially constricts what in the kidney?
A
Efferent arteriole
18
Q
What effect would decreased plasma protein concentration have on the GFR?
A
Increased GFR
19
Q
What effect would increased plasma protein concentration have on the GFR?
A
Decreased GFR
20
Q
At what threshold does glucosuria begin?
A
~200mg/dL
21
Q
Where in the nephron is NH3 secreted?
A
Proximal convoluted tubule
22
Q
What is PTH’s effect on the nephron?
A
Inhibits Na/Phosphate cotransporter in the proximal convoluted tubule which leads to phosphate excretion
23
Q
What is Angiotensin II’s effect on the nephron?
A
Stimulates Na/H exchange to increase Na water and bicarb reabsorption
24
Q
Where exactly do loop diuretics act?
A
Na/K/2Cl cotransporter in the thick ascending loop of Henle
25
Where exactly do thiazides act?
Inhibit the Na/Cl cotransporter in the distal convoluted tubule
26
Where exactly does aldosterone act on the nephron?
Acts on mineralocorticoid receptor to insert more Na channels on luminal side of collecting tubule - this leads to more reabsorption of Na in exchange for secreting K and H
27
Where exactly do amiloride and triamterene act?
Block Na channel on collecting tubule
28
What are ADH's actions on the nephron?
Inserts more aquaporin channels on luminal side of collecting tubule
29
What is the pathophysiology of Fanconi syndrome?
Reabsorptive defect in proximal convoluted tubule
30
What is the pathophysiology of Bartter syndrome?
(Autosomal recessive) Reabsorptive defect in the thick ascending loop of Henle
31
What is the pathophysiology of Gitelman syndrome?
(Autosomal recessive) Reabsorptive defect of NaCl in distal convoluted tubule
32
What is the pathophysiology of Liddle syndrome?
(Autosomal dominant) Higher Na reabsorption in distal and collecting tubules
33
What is the treatment of Liddle syndrome?
Amiloride
34
Describe the RAAS system
Angiotensinogen is produced by the liver. Renin is secreted by the juxtaglomerular cells in response to low BP, low Na delivery (macula densa), and high beta1 sympathetic tone. Renin converts angiotensinogen to angiotensin I. ACE secreted by lungs and kidneys convert AT I to AT II.
35
What is the purpose of the juxtaglomerular apparatus?
Consists of JG cells and macula densa. JG cells secrete renin in response to low renal blood pressure, low NaCl delivery to distal tubule, and beta1 sympathetic tone.
36
How do NSAIDs harm the kidney?
NSAIDS block renal-protective PG synthesis. PG works by vasodilating the afferent arterioles to increase RBF. Blocking this would decrease GFR, which may lead to acute renal failure.
37
How does ANP act on the kidney?
ANP is secreted in response to increased atrial pressures. Causes an increase in GFR and Na filtration with no compensatory Na reabsorption in distal nephron. Na loss and volume loss!
38
Does acidosis cause hyper or hypokalemia?
Hyperkalemia
39
Does alkalosis cause hyper or hypokalemia?
Hypokalemia
40
What are the clinical findings of low serum Na?
Nausea, malaise, stupor, coma
41
What are the clinical findings of high serum Na?
Irritability, stupor, coma
42
What are the clinical findings of low serum K?
U waves on ECG, flattened T waves, arrhythmias, muscle weakness
43
What are the clinical findings of high serum K?
Wide QRS and peaked T waves on ECG, arrhythmias, muscle weakness
44
What are the clinical findings of low serum Ca?
Tetany, seizures, QT prolongation
45
What are the clinical findings of high serum Ca?
Renal stones, bone pain, abdominal pain, anxiety, altered mental status, but no necessarily calciuria; "Stones, bones, groans, psychiatric overtones"
46
What are the clinical findings of low serum Mg?
Tetany, torsades de pointes
47
What are the clinical findings of high serum Mg?
Diminished DTRs, lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia
48
What are the clinical findings of low serum phosphate?
Bone loss, osteomalacia
49
What are the clinical findings of high serum phosphate?
Renal stones, metastatic calcifications, hypocalcemia
50
What is the Henderson-Hasselbalch equation?
pH = 6.1 + log([HCO3-]/0.03PCO2)
51
When do you use Winter's formula?
To calculate predicted respiratory compensation for a simple metabolic acidosis. If measured PCO2 differs significantly, a mixed acid-base disorder is most likely.
52
What is Winter's formula?
PCO2 = 1.5[HCO3-]+8 +/-2
53
How is anion gap calculated?
Anion gap = Na - (Cl + HCO3)
54
What are the causes of an increased anion gap metabolic acidosis?
"MUDPILES" : Methanol, Uremia, DKA, Propylene glycol, Iron tablets, INH, Lactic acidosis, Ethylene glycol, Salicylates, cyanide, toluene
55
What are the causes of a normal anion gap metabolic acidosis?
"HARD-ASS" : Hyperalimentation, Addison disease, Renal tubular acidosis, Diarrhea, Acetazolamide, Spironolactone, Saline infusion
56
What is a normal anion gap?
8-12 mEq/L
57
What do RBC casts indicate?
Glomerulonephritis, ischemia, or malignant hypertension
58
What do fatty casts indicate?
Nephrotic syndrome
59
What do granular "muddy brown" casts indicate?
Acute tubular necrosis
60
What do waxy casts indicate?
Advanced renal disease/chronic renal failure
61
What do hyaline casts indicate?
Nonspecific, can be normal finding, often seen in concentrated urine samples
62
A "focal" glomerular disorder refers to what?
63
How do kidney stones present?
Unilateral flank pain, colicky pain radiating to groin, and hematuria
64
What is the most common type of kidney stone?
Calcium
65
What is the shape of a calcium oxalate stone?
Octahedron
66
What is the shape of a calcium phosphate stone?
Elongated, wedge-shaped, rosettes
67
Calcium oxalate stones precipitate at what pH?
Low pH
68
Calcium phosphate stones precipitate at what pH?
High pH
69
Crohn disease is associated with which type of kidney stone?
Calcium oxalate
70
Ammonium magnesium phosphate (AMP) stones precipitate at what pH?
High pH
71
Uric acid stones precipitate at what pH?
Low pH
72
Cystine stones precipitate at what pH?
Low pH
73
What is the shape of ammonium magnesium phosphate (AMP) stones?
"Coffin lid"
74
AMP kidney stones are caused by infection with which types of bugs?
Urease positive bugs (Proteus, Staph, Klebsiella), due to alkalinization of urine
75
What kind of calculus does an AMP stone produce?
Staghorn
76
What is the shape of uric acid stones?
Rhomboid or rosettes
77
What are the risk factors for a uric acid stone?
Low urine volume, hot arid climates, and acidic pH
78
What is the treatment of calcium stones?
Thiazides (Ca-sparing) and citrate
79
What is the treatment of AMP stones?
Eradicate underlying infection and surgical removal of calculus
80
What is the treatment of uric acid stones?
Alkalinization of urine and hydration
81
What is the shape of cystine stones?
Hexogonal
82
Cystine kidney stones are usually seen in what kind of patient?
Children, secondary to cystinuria. Staghorn calculi.
83
What is the treatment of cystine stones?
Alkalinization of urine and hydration
84
Which nephrotic syndrome is associated with HIV infection?
FSGS
85
What is the most common nephrotic syndrome in children?
Minimal change disease
86
Which nephrotic syndrome may be triggered by recent infection, immunization, or immune stimulus?
Minimal change disease
87
Which nephrotic syndrome is associated with Hodgkin lymphoma?
Minimal change disease
88
What is the pathophysiology of MCD?
Cytokine damage leading to effacement of foot processes.
89
What is the treatment and response to treatment of MCD?
Excellent response to corticosteroids
90
Which nephrotic syndrome is associated with sickle cells disease?
FSGS
91
Which nephrotic syndrome is associated with heroin abuse?
FSGS
92
What kind of proteins are lost in urine in MCD?
Albumin only
93
What imaging is needed to visualize the damage of MCD?
EM (normal LM and IF)
94
Which nephrotic syndrome is associated with massive obesity, IF tx, and chronic kidney disease due to congenital absence or surgical removal?
FSGS
95
What is the most common nephrotic syndrome in African Americans and Hispanics?
FSGS
96
What is the most common cause of nephrotic syndrome in Caucasian adults?
Membranous nephropathy
97
What is the most common nephrotic syndrome in patients with SLE?
Membranous nephropathy
98
Which nephrotic syndrome presents with "tram-track appearance?"
Type I membranoproliferative glomerulonephritis
99
How does amyloidosis of the kidney look under LM?
Congo red stain shows apple-green birefringence under polarized light
100
Where exactly does amyloid deposit within the kidney?
Mesangium
101
Antibodies to phospholipase A2 Rs will cause what kidney disease?
Membranous nephropathy
102
How does membranous nephropathy look on EM?
"Spike and dome" appearance with subepithelial deposits
103
How does membranous nephropathy look on LM?
Diffuse capillary and GBM thickening
104
How does membranous nephropathy look on IF?
Granular as a result of immune complex deposition
105
Which glomerulonephritis syndromes are a nephritic syndrome that can also present with nephrotic syndrome?
MPGN and DPGN
106
Which glomerulonephritis syndromes are associated with HBV and HCV?
Membranous nephropathy and MPGN Type I
107
Which glomerulonephritis syndrome is associated with C3 nephritic factor (antibody)
MPGN Type II
108
What is the pathophysiology of diabetic glomerulonephropathy?
Nonenzymatic glycosylation causing thickening and increased permeability of GBM. Also causes glycosylation of efferent arterioles which increases the GFR and causes mesangial expansion and sclerosis.
109
In membranous nephropathy, where on the glomerulus do immune complexes deposit?
Between foot processes and basement membrane
110
In MPGN Type I, where on the glomerulus do immune complexes deposit?
Between basement membrane and endothelial cells
111
In MPGN Type II, where on the glomerulus do immune complexes deposit?
Within basement membrane
112
Kimmelstiel-Wilson nodules are seen in which nephrotic syndrome?
Diabetic glomerulonephropathy
113
What are the hallmarks of nephrotic syndrome?
Proteinuria (> 3.5 g/day), hyperlipidemia, fatty casts, edema, thromboembolism risk, and infection risk
114
What are the hallmarks of nephritic syndrome?
Hematuria, RBC casts, azotemia, oliguria, HTN, proteinuria (
115
What is seen on EM with acute poststreptococcal glomerulonephritis?
Subepithelial humps (immune complexes)
116
Adults with poststreptococcal glomerulonephritis may progress to what?
Rapidly progressive (crescentic) glomerulonephritis
117
The crescents of RPGN are composed of what?
Fibrin and macrophages - inflammatory debris
118
If linear IF is present in RPGN, what disease should be suspected?
Goodpasture syndrome
119
What is the renal consequence of Wegener's syndrome?
RPGN
120
What is the renal consequence of microscopic polyangiitis?
RPGN
121
What is seen on EM with diffuse proliferative glomerulonephritis (DPGN)?
Subendothelial and sometimes intramembranous IgG-based ICs often with C3 deposition (granular)
122
What is the most common cause of nephropathy worldwide?
IgA nephropathy aka Berger disease
123
What is Alport syndrome?
Mutation in type IV collagen which leads to splitting of glomerular basement membrane. Presents with isolated hematuria.
124
How does EM of IgA nephropathy look?
Mesangial IC deposits
125
Renal cell carcinoma originates from which cells?
Proximal tubule cells (polygonal clear cells)
126
What are risk factors of renal cell carcinoma?
Smoking and obesity (just like everything else...)
127
How does renal cell carcinoma spread?
Hematogenously - invades renal vein then IVC, mets to lung and bone
128
How is renal cell carcinoma staged?
TNM
129
Renal angiomyolipomas are frequently seen with which disease?
Tuberous sclerosis
130
Renal cells carcinomas are associated with gene deletion on which chromosome?
3
131
Renal oncocytoma is a benign tumor of what cell type?
Epithelial cell
132
H&E stain with large eosinophilic cells with abundant mitochondria without perinuclear clearing describes what neoplasm?
Renal oncocytoma
133
H&E stain with polyganol clear cells filled with accumulated lipids and carbohydrates describes what neoplasm?
Renal cell carcinoma
134
What is the most common renal malignancy of early childhood?
Wilms tumor (nephroblastoma)
135
Wilms tumor arises from what?
Blastema (primitive renal tissue)
136
What is the most common tumor of the urinary tract system and where does it occur?
Transitional cell carcinoma aka urothelial carcinoma; arises from renal calyces, renal pelvis, ureters, and bladder
137
What is the #1 risk factor of transitional cell carcinoma?
Smoking. Again, just like everything else.
138
Azo dyes are a risk factor for which malignancy?
Transitional cell carcinoma
139
Cyclophosphamide and phenacetin are a risk factor for which malignancy?
Transitional cell carcinoma
140
There are 2 pathways for transitional cell carcinoma: flat pathway and papillary pathway. How does the flat pathway progress?
High grade right away. Progresses to invasion. Associated with early p53 mutations.
141
There are 2 pathways for transitional cell carcinoma: flat pathway and papillary pathway. How does the papillary pathway progress?
Starts low grade and progresses to high grade then invasion
142
Schistosoma haematobium infection is associated with what malignancy?
Squamous cell carcinoma of the bladder
143
Adenocarcinoma of the bladder arises from what?
Urachal remnant
144
Sterile pyuria and negative urine cultures suggest infection with what organism?
Neisseria gonorrhoeae or Chlamydia trachomatis
145
What part of the kidney does pyelonephritis affect?
Cortex; spares glomeruli
146
"Thyroidization" of the kidney is seen in what disease process?
Chronic pyelonephritis
147
Which drugs can cause drug-induced interstitial nephritis (tubulointerstitial nephritis)?
Diuretics, penicillins, sulfonamides, rifampin, NSAIDs
148
What are the clinical findings of tubulointerstitial nephritis?
Anything from asymptomatic to fever, rash, hematuria, oliguria, and CVA tenderness
149
What cell type is usually seen in the urine of patients with tubulointerstitial nephritis?
Eosinophils
150
Diffuse cortical necrosis is associated with what disease processes?
Obstetric catastrophes and septic shock
151
What happens to the GFR in acute tubular necrosis?
Decreased GFR due to obstruction
152
What are the 3 stages of acute tubular necrosis?
1. Inciting event
2. Maintenance phase - oliguric; lasts 1-3 weeks; risk of hyperkalemia and metabolic acidosis
3. Recovery phase - polyuric; BUN and serum Cr fall; risk of hypokalemia
153
Which parts of the nephron are highly susceptible to ischemic injury?
The proximal tubule and thick ascending limb
154
What part of the nephron is highly susceptible to nephrotoxic injury?
Proximal tubule
155
Renal papillary necrosis can be triggered by what?
Recent infection or immune stimulus
156
What diseases is renal papillary necrosis associated with?
DM, acute pyelonephritis, chronic phenacetin use (acetaminophen is derivative), sickle cell anemia and trait
157
What is a normal FENa?
158
What is the urine osmolality in prerenal azotemia?
High >500
159
What is the urine osmolality in intrinsic renal azotemia?
160
What is the urine osmolality in postrenal azotemia?
161
What is the FENa in prerenal azotemia?
162
What is the FENa in intrinsic renal azotemia?
> 2%
163
What is the FENa in postrenal azotemia?
> 1% mild, > 2% severe
164
What is the serum BUN/Cr in prerenal azotemia?
> 20
165
What is the serum BUN/Cr in intrinsic renal azotemia?
166
What is the serum BUN/Cr in postrenal azotemia?
> 15 (back pressure forces BUN back into blood),
167
What are the most common causes of end-stage kidney failure?
DM, HTN, glomerular disease
168
What does a kidney on long-term dialysis look like?
Shrunken with cysts, increased risk of RCC
169
ADPKD is due to mutation of what?
PKD1 on chromosome 16 or PKD2 on chromosome 4
170
What other disease manifestations is ADPKD associated with?
Berry aneurysms, mitral valve prolapse, benign hepatic cysts
171
What is the inheritance pattern of medullary cystic disease?
Aut dom
172
How do kidneys with medullary cystic disease look on ultrasound?
Shrunken
