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Renal Flashcards

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.

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2
Q

The metanephric mesenchyme gives rise to what?

A

Glomerulus through distal convoluted tubule

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3
Q

What is the most common site of unilateral obstruction (hydronephrosis) in the fetus?

A

Ureteropelvic junction

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4
Q

What is the most common site of bilateral obstruction (hydronephrosis) in the fetus?

A

Posterior urethral valves

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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).

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6
Q

Horseshoe kidney is associated with what syndrome?

A

Turner

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7
Q

What is the most common congenital kidney anomaly?

A

Horseshoe kidney

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8
Q

An abnormal interaction between the metanephric mesenchyme and ureteric bud leads to what?

A

Multicystic dysplastic kidney; Non-inherited, usually unilateral –> asymptomatic

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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

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10
Q

How is renal clearance calculated?

A

Cx = UxV/Px

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11
Q

What substance is used to calculate GFR?

A

Inulin

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12
Q

What substance is used to calculate Effective renal plasma flow?

A

PAH

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13
Q

How is renal blood flow calculated?

A

RBF = RPF/(1-HCT)

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14
Q

How is filtration fraction calculated?

A

FF = GFR/RPF

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15
Q

What is a normal FF?

A

20%

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16
Q

How is filtered load (mg/min) calculated?

A

FL = GFR (mL/min) x plasma concentration (mg/mL)

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17
Q

Angiotensin II preferentially constricts what in the kidney?

A

Efferent arteriole

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18
Q

What effect would decreased plasma protein concentration have on the GFR?

A

Increased GFR

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19
Q

What effect would increased plasma protein concentration have on the GFR?

A

Decreased GFR

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20
Q

At what threshold does glucosuria begin?

A

~200mg/dL

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21
Q

Where in the nephron is NH3 secreted?

A

Proximal convoluted tubule

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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

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23
Q

What is Angiotensin II’s effect on the nephron?

A

Stimulates Na/H exchange to increase Na water and bicarb reabsorption

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24
Q

Where exactly do loop diuretics act?

A

Na/K/2Cl cotransporter in the thick ascending loop of Henle

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25
Q

Where exactly do thiazides act?

A

Inhibit the Na/Cl cotransporter in the distal convoluted tubule

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26
Q

Where exactly does aldosterone act on the nephron?

A

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

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27
Q

Where exactly do amiloride and triamterene act?

A

Block Na channel on collecting tubule

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28
Q

What are ADH’s actions on the nephron?

A

Inserts more aquaporin channels on luminal side of collecting tubule

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29
Q

What is the pathophysiology of Fanconi syndrome?

A

Reabsorptive defect in proximal convoluted tubule

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30
Q

What is the pathophysiology of Bartter syndrome?

A

(Autosomal recessive) Reabsorptive defect in the thick ascending loop of Henle

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31
Q

What is the pathophysiology of Gitelman syndrome?

A

(Autosomal recessive) Reabsorptive defect of NaCl in distal convoluted tubule

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32
Q

What is the pathophysiology of Liddle syndrome?

A

(Autosomal dominant) Higher Na reabsorption in distal and collecting tubules

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33
Q

What is the treatment of Liddle syndrome?

A

Amiloride

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34
Q

Describe the RAAS system

A

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.

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35
Q

What is the purpose of the juxtaglomerular apparatus?

A

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.

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36
Q

How do NSAIDs harm the kidney?

A

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.

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37
Q

How does ANP act on the kidney?

A

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!

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38
Q

Does acidosis cause hyper or hypokalemia?

A

Hyperkalemia

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39
Q

Does alkalosis cause hyper or hypokalemia?

A

Hypokalemia

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40
Q

What are the clinical findings of low serum Na?

A

Nausea, malaise, stupor, coma

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41
Q

What are the clinical findings of high serum Na?

A

Irritability, stupor, coma

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42
Q

What are the clinical findings of low serum K?

A

U waves on ECG, flattened T waves, arrhythmias, muscle weakness

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43
Q

What are the clinical findings of high serum K?

A

Wide QRS and peaked T waves on ECG, arrhythmias, muscle weakness

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44
Q

What are the clinical findings of low serum Ca?

A

Tetany, seizures, QT prolongation

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45
Q

What are the clinical findings of high serum Ca?

A

Renal stones, bone pain, abdominal pain, anxiety, altered mental status, but no necessarily calciuria; “Stones, bones, groans, psychiatric overtones”

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46
Q

What are the clinical findings of low serum Mg?

A

Tetany, torsades de pointes

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47
Q

What are the clinical findings of high serum Mg?

A

Diminished DTRs, lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia

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48
Q

What are the clinical findings of low serum phosphate?

A

Bone loss, osteomalacia

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49
Q

What are the clinical findings of high serum phosphate?

A

Renal stones, metastatic calcifications, hypocalcemia

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50
Q

What is the Henderson-Hasselbalch equation?

A

pH = 6.1 + log([HCO3-]/0.03PCO2)

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51
Q

When do you use Winter’s formula?

A

To calculate predicted respiratory compensation for a simple metabolic acidosis. If measured PCO2 differs significantly, a mixed acid-base disorder is most likely.

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52
Q

What is Winter’s formula?

A

PCO2 = 1.5[HCO3-]+8 +/-2

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53
Q

How is anion gap calculated?

A

Anion gap = Na - (Cl + HCO3)

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54
Q

What are the causes of an increased anion gap metabolic acidosis?

A

“MUDPILES” : Methanol, Uremia, DKA, Propylene glycol, Iron tablets, INH, Lactic acidosis, Ethylene glycol, Salicylates, cyanide, toluene

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55
Q

What are the causes of a normal anion gap metabolic acidosis?

A

“HARD-ASS” : Hyperalimentation, Addison disease, Renal tubular acidosis, Diarrhea, Acetazolamide, Spironolactone, Saline infusion

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56
Q

What is a normal anion gap?

A

8-12 mEq/L

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57
Q

What do RBC casts indicate?

A

Glomerulonephritis, ischemia, or malignant hypertension

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58
Q

What do fatty casts indicate?

A

Nephrotic syndrome

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59
Q

What do granular “muddy brown” casts indicate?

A

Acute tubular necrosis

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60
Q

What do waxy casts indicate?

A

Advanced renal disease/chronic renal failure

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61
Q

What do hyaline casts indicate?

A

Nonspecific, can be normal finding, often seen in concentrated urine samples

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62
Q

A “focal” glomerular disorder refers to what?

A
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63
Q

How do kidney stones present?

A

Unilateral flank pain, colicky pain radiating to groin, and hematuria

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64
Q

What is the most common type of kidney stone?

A

Calcium

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65
Q

What is the shape of a calcium oxalate stone?

A

Octahedron

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66
Q

What is the shape of a calcium phosphate stone?

A

Elongated, wedge-shaped, rosettes

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67
Q

Calcium oxalate stones precipitate at what pH?

A

Low pH

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68
Q

Calcium phosphate stones precipitate at what pH?

A

High pH

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69
Q

Crohn disease is associated with which type of kidney stone?

A

Calcium oxalate

70
Q

Ammonium magnesium phosphate (AMP) stones precipitate at what pH?

71
Q

Uric acid stones precipitate at what pH?

72
Q

Cystine stones precipitate at what pH?

73
Q

What is the shape of ammonium magnesium phosphate (AMP) stones?

A

“Coffin lid”

74
Q

AMP kidney stones are caused by infection with which types of bugs?

A

Urease positive bugs (Proteus, Staph, Klebsiella), due to alkalinization of urine

75
Q

What kind of calculus does an AMP stone produce?

76
Q

What is the shape of uric acid stones?

A

Rhomboid or rosettes

77
Q

What are the risk factors for a uric acid stone?

A

Low urine volume, hot arid climates, and acidic pH

78
Q

What is the treatment of calcium stones?

A

Thiazides (Ca-sparing) and citrate

79
Q

What is the treatment of AMP stones?

A

Eradicate underlying infection and surgical removal of calculus

80
Q

What is the treatment of uric acid stones?

A

Alkalinization of urine and hydration

81
Q

What is the shape of cystine stones?

82
Q

Cystine kidney stones are usually seen in what kind of patient?

A

Children, secondary to cystinuria. Staghorn calculi.

83
Q

What is the treatment of cystine stones?

A

Alkalinization of urine and hydration

84
Q

Which nephrotic syndrome is associated with HIV infection?

85
Q

What is the most common nephrotic syndrome in children?

A

Minimal change disease

86
Q

Which nephrotic syndrome may be triggered by recent infection, immunization, or immune stimulus?

A

Minimal change disease

87
Q

Which nephrotic syndrome is associated with Hodgkin lymphoma?

A

Minimal change disease

88
Q

What is the pathophysiology of MCD?

A

Cytokine damage leading to effacement of foot processes.

89
Q

What is the treatment and response to treatment of MCD?

A

Excellent response to corticosteroids

90
Q

Which nephrotic syndrome is associated with sickle cells disease?

91
Q

Which nephrotic syndrome is associated with heroin abuse?

92
Q

What kind of proteins are lost in urine in MCD?

A

Albumin only

93
Q

What imaging is needed to visualize the damage of MCD?

A

EM (normal LM and IF)

94
Q

Which nephrotic syndrome is associated with massive obesity, IF tx, and chronic kidney disease due to congenital absence or surgical removal?

95
Q

What is the most common nephrotic syndrome in African Americans and Hispanics?

96
Q

What is the most common cause of nephrotic syndrome in Caucasian adults?

A

Membranous nephropathy

97
Q

What is the most common nephrotic syndrome in patients with SLE?

A

Membranous nephropathy

98
Q

Which nephrotic syndrome presents with “tram-track appearance?”

A

Type I membranoproliferative glomerulonephritis

99
Q

How does amyloidosis of the kidney look under LM?

A

Congo red stain shows apple-green birefringence under polarized light

100
Q

Where exactly does amyloid deposit within the kidney?

101
Q

Antibodies to phospholipase A2 Rs will cause what kidney disease?

A

Membranous nephropathy

102
Q

How does membranous nephropathy look on EM?

A

“Spike and dome” appearance with subepithelial deposits

103
Q

How does membranous nephropathy look on LM?

A

Diffuse capillary and GBM thickening

104
Q

How does membranous nephropathy look on IF?

A

Granular as a result of immune complex deposition

105
Q

Which glomerulonephritis syndromes are a nephritic syndrome that can also present with nephrotic syndrome?

A

MPGN and DPGN

106
Q

Which glomerulonephritis syndromes are associated with HBV and HCV?

A

Membranous nephropathy and MPGN Type I

107
Q

Which glomerulonephritis syndrome is associated with C3 nephritic factor (antibody)

A

MPGN Type II

108
Q

What is the pathophysiology of diabetic glomerulonephropathy?

A

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
Q

In membranous nephropathy, where on the glomerulus do immune complexes deposit?

A

Between foot processes and basement membrane

110
Q

In MPGN Type I, where on the glomerulus do immune complexes deposit?

A

Between basement membrane and endothelial cells

111
Q

In MPGN Type II, where on the glomerulus do immune complexes deposit?

A

Within basement membrane

112
Q

Kimmelstiel-Wilson nodules are seen in which nephrotic syndrome?

A

Diabetic glomerulonephropathy

113
Q

What are the hallmarks of nephrotic syndrome?

A

Proteinuria (> 3.5 g/day), hyperlipidemia, fatty casts, edema, thromboembolism risk, and infection risk

114
Q

What are the hallmarks of nephritic syndrome?

A

Hematuria, RBC casts, azotemia, oliguria, HTN, proteinuria (

115
Q

What is seen on EM with acute poststreptococcal glomerulonephritis?

A

Subepithelial humps (immune complexes)

116
Q

Adults with poststreptococcal glomerulonephritis may progress to what?

A

Rapidly progressive (crescentic) glomerulonephritis

117
Q

The crescents of RPGN are composed of what?

A

Fibrin and macrophages - inflammatory debris

118
Q

If linear IF is present in RPGN, what disease should be suspected?

A

Goodpasture syndrome

119
Q

What is the renal consequence of Wegener’s syndrome?

120
Q

What is the renal consequence of microscopic polyangiitis?

121
Q

What is seen on EM with diffuse proliferative glomerulonephritis (DPGN)?

A

Subendothelial and sometimes intramembranous IgG-based ICs often with C3 deposition (granular)

122
Q

What is the most common cause of nephropathy worldwide?

A

IgA nephropathy aka Berger disease

123
Q

What is Alport syndrome?

A

Mutation in type IV collagen which leads to splitting of glomerular basement membrane. Presents with isolated hematuria.

124
Q

How does EM of IgA nephropathy look?

A

Mesangial IC deposits

125
Q

Renal cell carcinoma originates from which cells?

A

Proximal tubule cells (polygonal clear cells)

126
Q

What are risk factors of renal cell carcinoma?

A

Smoking and obesity (just like everything else…)

127
Q

How does renal cell carcinoma spread?

A

Hematogenously - invades renal vein then IVC, mets to lung and bone

128
Q

How is renal cell carcinoma staged?

129
Q

Renal angiomyolipomas are frequently seen with which disease?

A

Tuberous sclerosis

130
Q

Renal cells carcinomas are associated with gene deletion on which chromosome?

131
Q

Renal oncocytoma is a benign tumor of what cell type?

A

Epithelial cell

132
Q

H&E stain with large eosinophilic cells with abundant mitochondria without perinuclear clearing describes what neoplasm?

A

Renal oncocytoma

133
Q

H&E stain with polyganol clear cells filled with accumulated lipids and carbohydrates describes what neoplasm?

A

Renal cell carcinoma

134
Q

What is the most common renal malignancy of early childhood?

A

Wilms tumor (nephroblastoma)

135
Q

Wilms tumor arises from what?

A

Blastema (primitive renal tissue)

136
Q

What is the most common tumor of the urinary tract system and where does it occur?

A

Transitional cell carcinoma aka urothelial carcinoma; arises from renal calyces, renal pelvis, ureters, and bladder

137
Q

What is the #1 risk factor of transitional cell carcinoma?

A

Smoking. Again, just like everything else.

138
Q

Azo dyes are a risk factor for which malignancy?

A

Transitional cell carcinoma

139
Q

Cyclophosphamide and phenacetin are a risk factor for which malignancy?

A

Transitional cell carcinoma

140
Q

There are 2 pathways for transitional cell carcinoma: flat pathway and papillary pathway. How does the flat pathway progress?

A

High grade right away. Progresses to invasion. Associated with early p53 mutations.

141
Q

There are 2 pathways for transitional cell carcinoma: flat pathway and papillary pathway. How does the papillary pathway progress?

A

Starts low grade and progresses to high grade then invasion

142
Q

Schistosoma haematobium infection is associated with what malignancy?

A

Squamous cell carcinoma of the bladder

143
Q

Adenocarcinoma of the bladder arises from what?

A

Urachal remnant

144
Q

Sterile pyuria and negative urine cultures suggest infection with what organism?

A

Neisseria gonorrhoeae or Chlamydia trachomatis

145
Q

What part of the kidney does pyelonephritis affect?

A

Cortex; spares glomeruli

146
Q

“Thyroidization” of the kidney is seen in what disease process?

A

Chronic pyelonephritis

147
Q

Which drugs can cause drug-induced interstitial nephritis (tubulointerstitial nephritis)?

A

Diuretics, penicillins, sulfonamides, rifampin, NSAIDs

148
Q

What are the clinical findings of tubulointerstitial nephritis?

A

Anything from asymptomatic to fever, rash, hematuria, oliguria, and CVA tenderness

149
Q

What cell type is usually seen in the urine of patients with tubulointerstitial nephritis?

A

Eosinophils

150
Q

Diffuse cortical necrosis is associated with what disease processes?

A

Obstetric catastrophes and septic shock

151
Q

What happens to the GFR in acute tubular necrosis?

A

Decreased GFR due to obstruction

152
Q

What are the 3 stages of acute tubular necrosis?

A
  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
Q

Which parts of the nephron are highly susceptible to ischemic injury?

A

The proximal tubule and thick ascending limb

154
Q

What part of the nephron is highly susceptible to nephrotoxic injury?

A

Proximal tubule

155
Q

Renal papillary necrosis can be triggered by what?

A

Recent infection or immune stimulus

156
Q

What diseases is renal papillary necrosis associated with?

A

DM, acute pyelonephritis, chronic phenacetin use (acetaminophen is derivative), sickle cell anemia and trait

157
Q

What is a normal FENa?

158
Q

What is the urine osmolality in prerenal azotemia?

159
Q

What is the urine osmolality in intrinsic renal azotemia?

160
Q

What is the urine osmolality in postrenal azotemia?

161
Q

What is the FENa in prerenal azotemia?

162
Q

What is the FENa in intrinsic renal azotemia?

163
Q

What is the FENa in postrenal azotemia?

A

> 1% mild, > 2% severe

164
Q

What is the serum BUN/Cr in prerenal azotemia?

165
Q

What is the serum BUN/Cr in intrinsic renal azotemia?

166
Q

What is the serum BUN/Cr in postrenal azotemia?

A

> 15 (back pressure forces BUN back into blood),

167
Q

What are the most common causes of end-stage kidney failure?

A

DM, HTN, glomerular disease

168
Q

What does a kidney on long-term dialysis look like?

A

Shrunken with cysts, increased risk of RCC

169
Q

ADPKD is due to mutation of what?

A

PKD1 on chromosome 16 or PKD2 on chromosome 4

170
Q

What other disease manifestations is ADPKD associated with?

A

Berry aneurysms, mitral valve prolapse, benign hepatic cysts

171
Q

What is the inheritance pattern of medullary cystic disease?

172
Q

How do kidneys with medullary cystic disease look on ultrasound?

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