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Steph ASN BRCU Review > ASN QBank Pearls - Potassium, Acid Base, Tubulointerstitial Disorders, and Nephrolithiasis > Flashcards

ASN QBank Pearls - Potassium, Acid Base, Tubulointerstitial Disorders, and Nephrolithiasis Flashcards

1
Q
  • low PRA (plasma renin activity)
  • high PAC (plasma aldosterone concentration)
  • aldosterone synthesis independent of renin levels
A

primary aldosteronism

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2
Q
  • low PRA
  • high PAC
  • high urine free cortisol/cortisone ratio
  • high ACTH
  • AD
  • cortisol-producing zona fasciculata defect d/t promoter fusion causing ACTH dependent activation of aldosterone synthase on cortisol precursors
A

glucocorticoid-remediable aldosteronism

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3
Q
  • low PRA
  • high PAC
  • mass > 5 cm
A

adrenal Ca

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4
Q
  • high PRA
  • high PAC
  • atherosclerosis
  • hypoxia-induced
A

renovascular HTN

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5
Q
  • high PRA
  • high PAC
  • unregulated synthesis
A

renin-secreting tumor

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6
Q
  • low/normal PRA
  • low/normal PAC
  • high cortisol
  • high urine free cortisol/cortisone ratio
  • excess cortisol production
A

Cushing disease

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7
Q
  • low/normal PRA
  • low/normal PAC
  • high cortisol
  • high urine free cortisol/cortisone ratio
  • mutation of 11-BHSD2
A

syndrome of apparent mineralocorticoid excess (SAME)

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8
Q

syndrome of apparent mineralocorticoid excess (SAME) causes

A
  • can be inherited 

  • can be acquired;
  • black European licorice (glycyrrhizic acid)
  • itraconazole
  • ectopic ACTH
  • grapefruit
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9
Q
  • low/normal PRA
  • low/normal PAC
  • low/normal cortisol
  • low/normal urine free cortisol/cortisone ratio
  • hypokalemia
  • AD
  • ENaC gain of function mutation
A

Liddle syndrome

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10
Q
  • low/normal PRA
  • low/normal PAC
  • low/normal cortisol
  • low/normal urine free cortisol/cortisone ratio
  • worse w/ pregnancy and spironolactone
A

mineralocorticoid receptor gain of function mutation (Geller’s syndrome)

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11
Q
  • young female with HTN and hypokalemia
  • family h/o early onset HTN and hemorrhagic stroke
  • urinary K+ wasting
  • increased urinary excretion of aldosterone and 18-OH cortisol during salt loading
A

glucocorticoid remediable aldosteronism

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12
Q

treatment of glucocorticoid remediable aldosteronism

A

spironolactone and dexamethasone

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13
Q
  • severe HTN with metabolic alkalosis and hypokalemia

- young women during the second and third trimester of pregnancy

A

mineralocorticoid corticoid receptor mutation (Geller’s syndrome)

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14
Q

MR 810 mutation is activated by what medication, thereby worsening hypertension and hypokalemia

A

spironolactone

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15
Q

treatment of mineralocorticoid corticoid receptor mutation (Geller’s syndrome)

A
  • often requires delivery

- subsequent management includes avoidance of spironolactone

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16
Q

hyperemic optic disks and putamen swelling are suggestive of

A

methanol intoxication

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17
Q

changes in mentation as a result of methanol are present w/i the first 6-24 hours but can be the only abnormality for as long as 72-96 hours if patients have also ingested, what?

A

ethanol (competes for ADH)

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18
Q

methanol metabolite

A

formic acid

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19
Q
  • changes in mentation
  • HAGMA
  • large osmolal gap
  • less likely to have cerebral edema
A

ethylene glycol toxicity

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20
Q
  • ketoacidosis (typically after patient stops drinking)

- usually small osmolal gap

A

ethanol toxicity

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21
Q

solvent used for lorazepam, diazepam, and phenobarbital

A

propylene glycol

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22
Q
  • large osmolal gap
  • HAGMA
  • AKI
  • can progress to multisystem organ failure, if severe
  • usually a/w dosages above the recommended range of 0.1 mg/kg/hr and/or renal impairment
A

propylene glycol toxicity

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23
Q
  • HTN at young age
  • CVA at young age
  • low aldosterone level
  • hypokalemia
  • metabolic alkalosis
A

Liddle’s syndrome

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24
Q
  • hypokalemia

- normo- or hypotension

A

Bartter’s or Gitelman’s syndromes

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25
Q
  • hyperkalemia
  • HTN
  • metabolic acidosis
A

Gordon’s syndrome (pseudohypoaldosteronism type 2)

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26
Q
  • if metabolic acidosis, compensation should be what?- - calculation
A
  • respiratory alkalosis

- ∆CO2 = ∆HCO3 x 1.2

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27
Q
  • if metabolic alkalosis, compensation should be what?

- calculation

A
  • respiratory acidosis

- ∆CO2 = ∆HCO3 x 0.6

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28
Q
  • ACUTE respiratory acidosis, compensation should be what?

- calculation

A
  • metabolic alkalosis

- ∆HCO3 = ∆CO2 x 0.1

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29
Q
  • CHRONIC respiratory acidosis, compensation should be what?

- calculation

A
  • metabolic alkalosis

- ∆HCO3 = ∆CO2 x 0.3

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30
Q
  • ACUTE respiratory alkalosis, compensation should be what?

- calculation

A
  • metabolic acidosis

- ∆HCO3 = ∆CO2 x 0.2

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31
Q
  • CHRONIC respiratory alkalosis, compensation should be what?
  • calculation
A
  • metabolic acidosis

- ∆HCO3 = ∆CO2 x 0.5

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32
Q

Winter’s formula

A

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

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33
Q
  • large osmolal gap
  • normal anion gap (unless hypotension leads to lactic acidosis)
  • ketonemia
  • ketonuria
A

isopropyl alcohol toxicity

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34
Q

major metabolite of isopropyl alcohol

A

acetone

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35
Q

reason for ketonemia and ketonuria in isopropyl alcohol toxicity

A

major metabolites of isopropyl alcohol is acetone

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36
Q

when is hemodialysis indicated in isopropyl alcohol toxicity

A
  • severe coma
  • hypotension, or
  • serum isopropanol levels > 200 mg/dL
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37
Q

what is NOT indicated for isopropyl alcohol toxicity?

A
  • ADH inhibition with fomepizole or ethanol
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38
Q
  • weight loss drug

- hyperoxaluria

A

orlistat

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39
Q

heavy metal a/w battery plant

A

cadmium

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40
Q

heavy metals a/w foundry

A

beryllium and lead

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41
Q
  • heavy metal
  • bone disease
  • stones
  • HTN
  • CKD (chronic tubulointerstitial nephritis with non-nephritic proteinuria and a bland urine sediment)
A

cadmium

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42
Q
  • gout
  • HTN
  • CKD (chronic tubulointerstitial nephritis with non-nephritic proteinuria and a bland urine sediment)
A

lead toxicity

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43
Q

Chinese herb may have this and it is nephrotoxic and leads to CKD (chronic interstitial nephritis)

A

aristolochic acid

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44
Q

patients exposed to this have a lifelong risk of transitional cell carcinoma especially after transplantation, where it may occur in > 30%

A

aristolochic acid

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45
Q

what is recommended to be considered prior to transplant in patients with aristolochic acid nephropathy

A

bilateral nephrectomy

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46
Q
  • recently described rejection episode requiring an increase in immunosuppression
  • hemorrhagic cystitis
  • allograft dysfunction
A

BK viremia

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47
Q

fruit a/w oxalate nephropathy, especially in patients with pre-existing CKD

A

star fruit

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48
Q

ephedra adverse effects

A
  • HTN

- stones

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49
Q
  • normal UA
  • normal renal function
  • hypokalemia
  • metabolic alkalosis
  • HTN
  • what syndrome does this patient have?
  • what is the cause?
A
  • apparent mineralocorticoid excess syndrome (AMES)

- glycyrrhizic acid from herbal products

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50
Q

noni juice can cause

A

hyperkalemia

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51
Q
  • nephrotic range proteinuria 2/2 MCD

- minimal evidence of eosinophilia, rash, or fever

A

NSAIDs

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52
Q

lead is a cation that affects what part of the nephron

A

organic cation transport (OCT) system in the proximal tubule

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53
Q

cadmium affects what part of the nephron

A

proximal tubule

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54
Q

gold causes

A

nephrotic syndrome from membranous disease

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55
Q

platinum causes

A

ATN through both apoptosis and necrosis, especially in the proximal tubule

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56
Q

calcium oxalate stone risk factors

A
  • hypercalciuria
  • increased salt intake
  • hypocitraturia
  • high sulfate and low urine
  • bariatric surgery (enteric hyperoxaluria)
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57
Q

major base in urine

58
Q

best marker for dietary acid intake

A

sulfate excretion

59
Q

single most important pathogenic factor in uric acid stone formation

A

low urine pH

60
Q

ethylene glycol metabolites

A

glycolaldehyde, which is then oxidized to glycolic acid

61
Q

ethanol metabolites

A

acetaldehyde then acetic acid, and acetyl-CoA

62
Q

risk factors for cysteine stone formation

A
  • low UOP
  • low urine pH
  • high dietary protein intake (lower risk factor)
63
Q

treatment for cystinuria

A
  • oral α-mercaptopropionylglycine 


- genetic counseling of the family

64
Q

what are the finding of allergic interstitial nephritis?

  • kidney size
  • skin rash
  • eosinophilia
  • nephrotic syndrome
  • kidney biopsy results
A
  • large
  • present
  • present
  • absent
  • interstitial T cells
65
Q

classic presentation of a penicillin- or antibiotic-induced interstitial nephritis

A

triad

  • fever
  • rash
  • eosinophilia
66
Q

allergic interstitial nephritis hypersensitivity type

67
Q

which syndromes are associated with granulomatous interstitial nephritis?

A
  • tubulointerstitial nephritis and uveitis (TINU) 

  • sarcoidosis
  • granulomatosis w/ polyangiitis
  • Crohn’s disease
68
Q

what test indicates the presence of AIN and not ATN?

A

positive gallium scan

69
Q

initiation of what medication for a diagnosis of AIN, leads to accelerated recovery of renal function and an improved long-term renal function? and in what time period should they be given?

A

steroids, w/i 2 weeks

70
Q

complete recovery of renal function occurs in what percentage of AIN cases, with the remaining cases developing CKD?

71
Q

what stain on kidney biopsy indicates the presence of collagen, and therefore, a positive stain will be indicative of a patient with interstitial fibrosis and CKD?

A

trichrome stain

72
Q

Hansel stain is interpreted as positive once urine eosinophils represent what percentage of urine WBCs?

73
Q

what are some of the many other causes of urine eosinophils other than AIN?

A
  • ATN
  • cystitis
  • prostatitis, and
  • atheroembolic disease (AED)
74
Q
  • refractory hypokalemia
  • metabolic alkalosis, and
  • hyperglycemia
A

increased ACTH production leading to increased cortisol

75
Q

Cushing disease source of excess cortisol

A

pituitary gland (makes ACTH)

76
Q

Cushing syndrome source of excess cortisol

A

adrenal gland (makes cortisol)

77
Q

treatment of increased ACTH production by lung cancer (more common w/ SCLC)

A
  • treat tumor
  • steroid synthesis inhibitors (ketoconazole, metyrapone, and octreotide), and
  • MR and ENaC blockers
78
Q

thyroid disease may cause hypokalemia (associated with a K+ cell shift), but not metabolic alkalosis

A

thyrotoxicosis

79
Q

renal adverse effects of ifosfamide

A
  • Fanconi syndrome
  • proximal phosphate wasting
  • AKI, and
  • nephrogenic DI
80
Q

timeline of ifosfamide renal tubular dysfunction

A

can develop months after completing chemotherapy

81
Q

tumor-produced FGF-23 will lead to

A

phosphate wasting and hypophosphatemia

82
Q

what electrolyte disturbances develop in the setting of obstructive uropathy

A

hyperkalemia w/ metabolic acidosis

83
Q

topiramate does what in the kidneys?

A

inhibits carbonic anhydrase

84
Q

topiramate is a/w

A

proximal RTA (and distal RTA), and calcium phosphate stones

85
Q

atazanavir is a/w

A

urinary crystals and nephrolithiasis

86
Q

triamterene is a/w

A

urinary crystals, but NOT stones

87
Q

oslistat is a/w

A

enteric hyperoxaluria and calcium oxalate crystals

88
Q

most likely cause of urinary stones

A

atazanavir

89
Q

why does atazanavir cause urinary stones?

A

poor solubility in urine

90
Q

atazanavir is most soluble in what urine pH?

A

acidic urine, pH < 4.5

91
Q

acyclovir is a/w

A

urinary crystals but has NOT been a/w nephrolithiasis

92
Q

which medications do NOT form urinary crystals?

A
  • emtricitabine

- tenofovir

93
Q

tenofovir renal adverse effects

A
  • proximal tubular injury w/ AKI

- Fanconi syndrome

94
Q

which medications are a/w hyperkalemia by blocking the epithelial sodium channel (ENaC) in the principal cell in the cortical collecting duct?

A
  • amiloride (K+ sparing diuretic)
  • pentamidine (PJP ppx)
  • triamterene (K+ sparing diuretic)
  • trimethoprim
95
Q

chronic linezolid treatment a/w

A

lactic acidosis (disrupts mitochondrial function)

96
Q

acetaminophen can be associated with what in alcoholics and patients w/ poor nutrition d/t underlying glutathione and deficiencies

A

oxoproline acidosis

97
Q

ketorolac is a/w

A

type 4 RTA (hyporeninemic hypoaldosteronism)

98
Q

overall prevalence of biopsy-proven acute interstitial nephritis (AIN) in biopsies obtained for any clinical indication?

99
Q

prevalence of biopsy-proven acute interstitial nephritis (AIN) in patients with AKI?

100
Q

MOST common cause of acute interstitial nephritis (AIN) in the United States?

A

medications

101
Q

MOST common cause of acute interstitial nephritis (AIN) in developing countries?

A

50% is d/t drugs and 50% is d/t infection

102
Q

which drugs are MOST commonly associated with acute interstitial nephritis (AIN)?

A

antimicrobial agents (antibiotics, antivirals, antifungals, etc)

103
Q
  • fever
  • weight loss
  • fatigue
  • on broad- spectrum antibiotics
  • diffuse rash
  • palpable adenopathy
  • severe eosinophilia
  • AKI
  • proteinuria
  • rbcs on urine
  • wbc casts
A

drug rash, eosinophilia, systemic symptoms (DRESS) syndrome with granulomatous acute interstitial nephritis 
(AIN)

104
Q

kidney biopsy diagnostic for drug rash, eosinophilia, systemic symptoms (DRESS) syndrome with granulomatous acute interstitial nephritis 
(AIN)

A

inflammatory infiltrate w/ numerous eosinophils, lymphocytes, and macrophages, as well as granuloma

105
Q

highest diagnostic utility for drug-induced acute interstitial nephritis (AIN)

A

kidney biopsy showing an inflammatory interstitial infiltrate

106
Q

what is a/w an increased likelihood that kidney function will improve following a course of steroid therapy?

A

steroids are initiated w/i 1 week of diagnosis

107
Q

are CKD and ESRD complications in patients with drug-induced AIN when the offending agent is removed?

A

yes, both CKD (up to 50%) and ESRD (> 5%) are common

108
Q
  • obese patient
  • doesn’t feel well
  • AKI
  • health store weight loss regimen
  • 2-5 wbcs
  • 1-3 rbcs
  • 1-2 waxy casts
A

aristolochic acid (AA)

109
Q

aristolochic acid (AA) has also been identified as the environmental agent underlying

A

Balkan-endemic nephropathy

110
Q
  • rapid loss of kidney function
  • shrunken kidneys
  • extensive acellular fibrosis on renal histopathology
  • often develop ESRD and uroepithelial malignancies
A

Balkan-endemic nephropathy

111
Q
  • pulmonary, eye, skin, and renal involvement

- renal biopsy findings of a cellular infiltrate and granuloma

A

sarcoidosis w/ AIN

112
Q

eye and kidney involvement w/o granuloma

A

Sjögren’s syndrome

113
Q
  • uveitis and skin involvement

- interstitial nephritis w/ granuloma

114
Q
  • malaise
  • fatigue
  • low-grade fever
  • pulmonary and renal masses
  • lymphoplasmacytic infiltrate in lung and kidney tissue
A

IgG4 disease

115
Q

IgG4 disease treatment

A

steroids, highly responsive

116
Q
  • marked plasma cell infiltrate that produces expansile destructive lesions
  • autoimmune pancreatitis
  • renal disease w/ deposits in the tubules
  • classical complement pathway is activated
  • eosinophilia
  • low-grade ANA titers
A

IgG4-related systemic disease

117
Q
  • institution/reinstitution of HAART
  • pathological inflammatory response in various organs, including kidneys
  • mononuclear infiltration of renal interstitium; essentially a form of AIN
A

immune reconstitution inflammatory syndrome (IRIS)

118
Q
  • Fanconi syndrome
  • AKI
  • light chain crystals in proximal tubules
A

light chain-induced acute tubular injury

119
Q

fractured, glassy casts with associated interstitial reaction/giant cell formation (engulfing casts)

A

light chain cast nephropathy associated with multiple myeloma

120
Q

renal histology demonstrates infiltration of the renal interstitium by lymphoma cells

A

acute infiltrative interstitial nephritis

121
Q

positive urine anion gap in the setting of nongap metabolic acidosis supports the diagnosis of

A

renal tubular acidosis

122
Q

urine pH is often inappropriately alkaline in the face of acidosis and is a time-honored “hallmark” of

A

DISTAL renal tubular acidosis

123
Q

with chronic metabolic acidosis, regardless of cause, what increases in response to the systemic acidosis?

A

ammoniagenesis

124
Q
  • diabetic nephropathy
  • recent decline in eGFR
  • evidence of volume overload
  • hyperkalemia, and
  • nongap metabolic acidosis
A

type 4 RTA; hyporeninemic hypoaldosteronism

125
Q
  • seen in patients of Asian or Mexican descent
  • severe pain during an acute attack d/t sudden shift of K+ from the extracellular fluid space into the intracellular compartment
  • normal total body potassium content
  • large transcellular K+ gradient leads to hyperpolarization of the cell
A

hypokalemic periodic paralysis occurring in a/w hyperthyroidism

126
Q
  • decreased total body potassium d/t renal potassium wasting
  • both intracellular and extracellular potassium are decreased
  • transcellular K+ gradient is less steep
  • cell hyperpolarization is less severe
  • less symptomatic
A
  • paint thinner abuse

- toluene-induced type 1 (distal) RTA

127
Q

toluene is metabolized to

A

hippuric acid

128
Q

nonreabsorbable anion metabolite of toluene that leads to increased distal Na+ delivery, and mild volume contraction

A

sodium salt, sodium hippurate

129
Q

explanation of normal serum K+ level w/ depleted total K+ stores in the setting of DKA

A

they are reduced d/t an osmotic diuresis, but serum levels remain normal because K+ shifts out of cells 
d/t insulin deficiency and increased osmolality

130
Q

expected uric acid level in the setting of high-dose aspirin therapy or aspirin overdose

A

low d/t increased renal excretion

131
Q

should you test European American adults with sporadic (nonfamilial) forms of FSGS for causative mutations?

132
Q
  • females with one X-linked mutation in the COL4A5 gene are carriers
  • typically develop mild disease because they possess another (normal) X chromosome
  • what renal disease?
A

Alport syndrome

133
Q

Alport syndrome mutation and location

A

COL4A5 mutation on X chromosomes

134
Q
  • single mutation in either COL4A3 or COL4A5 gene
  • hematuria
  • preserved kidney function
A

thin basement nephropathy

135
Q

progression of kidney disease strongly relates to the presence of

A

risk variants in the APOL1 with AR inheritance

136
Q

rare but a dire electrolyte abnormality of high-dose barbiturate coma therapy in order to reduce ICP in traumatic brain injury patients

A
  • hypokalemia

- and/or rebound hyperkalemia

137
Q
  • hypokalemia in absence of acidosis
  • weakness precipitated by carbohydrate load and exercise
  • low urinary K+
A

familial periodic paralysis

138
Q
  • YOUNG, usually female patients
  • very common in ASIANS
  • signs/symptoms of thyrotoxicosis
  • often have a NECK MASS
  • LOW TSH
  • high T3 or T4
A

thyrotoxic periodic paralysis

139
Q

which biochemical abnormality takes place first to maintain normal phosphorus levels the setting of progressively worsening CKD?

140
Q

What amino acid plays important role and excretion of excess acid during metabolic acidosis?

A

Glutamine via ammoniagenesis (mainly occurs in prox tubule)
1 glutamine molecule metabolized -> 2 HCO3 and 2 NH
-Bicarb is reabsorbed into bloodstream and acidic NH4 ions are excreted

141
Q

what medication worsens hyperkalemia by directly blocking potassium uptake in cells

A

beta blockers (more likely in non-cardio selective BB) ie propranolol or labetolol
MOA: block beta adrenergic receptor activation leading to decrease activity of NaK ATPase mediated intracellular translocation of K

142
Q

familial hyperaldosteronism

Steph ASN BRCU Review (11 decks)

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