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Nephrology Board Review Pearls > Nephrology Pearls of Wisdom > Flashcards

Nephrology Pearls of Wisdom Flashcards

1
Q

tuberous sclerosis genetics

A

AD

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2
Q

medication class that slows tumor growth in tuberous sclerosis

A

mTOR inhibitors

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3
Q

what are the mTOR inhibitors?

A
  • sirolimus (aka rapamycin)
  • everolimus
  • temsirolimus
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4
Q

renal manifestation of tuberous sclerosis

A
  • renal angiomyolipomas

- RCC (very rare)

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5
Q

Fabry disease genetics

A

XL

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6
Q

Fabry disease mutation

A

GLA mutation

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7
Q

skin manifestation seen in Fabry disease

A

angiokeratomas

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8
Q

enzyme defect causing Fabry disease

A

a-galactosidase A

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9
Q

finding seen on EM in Fabry disease

A

Zebra bodies

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10
Q

Zebra bodies can also be seen on patients taking what medication?

A

hydroxychloroquine

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11
Q

treatment for Fabry disease

A

ERT (enzyme replacement therapy)

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12
Q

MCD age distribution

A

children and elderly (bimodal distribution)

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13
Q

what should be ruled out in patients with MCD?

A
  • NSAID use
  • lymphoma
  • lithium use
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14
Q

if AIN and AKI think of

A

NSAID use

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15
Q

rate of relapse in MCD

A

50%

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16
Q

what other renal manifestation is also commonly seen in patients with MCD?

A

ATN

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17
Q

ADPKD1 compared to ADPKD2

A

occurs earlier and more ESRD

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18
Q

PKD1, which chromosome?

A

16

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19
Q

PKD2, which chromosome?

A

4

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20
Q

polycystin proteins affect what?

A

cilium

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21
Q

extrarenal manifestations of ADPKD

A
  • brain aneurysms
  • diverticula
  • abdominal wall hernias
  • MVP
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22
Q

preferred bp medication for PKD

A

ACEI

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23
Q

PKD medication to slow cyst growth

A

vaptans

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24
Q

West African Sub-Saharan gene that protects against trypanosomes

A

APOL1

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25
Q

2 variants of APOL1

A

G1 and G2

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26
Q

2 high-risk alleles of APOL1 increase risk of

A
  • HIV nephropathy
  • sickle cell nephropathy
  • ESRD from FSGS
  • hypertensive nephrosclerosis
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27
Q

2 high-risk alleles of APOL1 increase what in ESRD patients?

A

survival

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28
Q

what % of African Americans carry 2 high risk alleles

A

14%

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29
Q

MCC of AIN

A

abx, namely B-lactams and sulfa-based antibiotics

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30
Q

AIN from abx have what w/i infiltrate?

A

eosinophils

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31
Q

AIN from NSAIDs does NOT have what?

A

eosinophils

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32
Q

what improves short- and long-term outcome if administered early in AIN?

A

steroids

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33
Q

rash is seen in AIN when caused by

A

abx

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34
Q

in AIN, which medication class do you NOT see rash?

A

PPIs

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35
Q

aside from AIN, other manifestations seen in IgG4-related disease

A
  • pancreatitis
  • retroperitoneal fibrosis
  • masses in other organs
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36
Q

aside from AIN, other manifestations seen in sarcoidosis

A
  • hypercalcemia

- hypercalciuria

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37
Q

monoclonal gammopathy of renal significance (MGRS)

  • AL amyloidosis
  • is usually what type?
A

lambda

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38
Q

monoclonal gammopathy of renal significance (MGRS)

  • AL amyloidosis
  • what size fibrils?
A

10 nm

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39
Q

monoclonal gammopathy of renal significance (MGRS)

  • light-chain deposition disease (LCDD)
  • is usually what type?
A

kappa > lambda

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40
Q

monoclonal gammopathy of renal significance (MGRS)

  • light-chain deposition disease (LCDD)
  • staining?
A

tubular light chain staining

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41
Q

monoclonal gammopathy of renal significance (MGRS)

  • light-chain deposition disease (LCDD)
  • appearance on biopsy?
A

nodular, looks like diabetic KW disease

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42
Q

monoclonal gammopathy of renal significance (MGRS)

  • cast nephropathy
  • usually what type?
A

kappa = lambda

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43
Q

monoclonal gammopathy of renal significance (MGRS)

  • cast nephropathy
  • what’s seen on LM?
A

fractured casts

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44
Q

monoclonal gammopathy of renal significance (MGRS) can present w/?

A

Fanconi syndrome (proximal tubulopathy)

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45
Q

in monoclonal gammopathy of renal significance (MGRS), urine dipstick doesn’t detect what?

A

light chains (Bence Jones proteins)

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46
Q

serum [Na+] ~

A

(TBNa+ + TBK+)/TBW

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47
Q
  • hyponatremia
  • hypotonic
  • hypERvolemic
  • urine Na+ < 20 mmol/L
A
  • heart failure

- liver failure

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48
Q
  • hyponatremia
  • hypotonic
  • hypERvolemic
  • urine Na+ > 20 mmol/L
A
  • renal failure
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49
Q
  • hyponatremia
  • hypotonic
  • EUvolemic
  • urine Na+ > 20 mmol/L
  • urine Osm > 100
A
  • SIADH
  • adrenal insufficiency
  • hypothyroidism
  • stress
  • drug use
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50
Q
  • hyponatremia
  • hypotonic
  • EUvolemic
  • urine Na+ > 20 mmol/L
  • urine Osm < 100
A
  • primary polydipsia

- low solute intake

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51
Q
  • hyponatremia
  • hypotonic
  • EUvolemic
  • urine Na+ > 20 mmol/L
  • variable urine Osm
A

reset osmostat

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52
Q
  • hyponatremia
  • hypotonic
  • hypovolemia
  • urine Na+ > 20 mmol/L
A
  • salt wasting nephropathy
  • hypoaldosteronism
  • active diuretic use
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53
Q
  • hyponatremia
  • hypotonic
  • hypovolemia
  • urine Na+ < 20 mmol/L
A
  • extrarenal sodium loss (GI)

- remote diuretic use

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54
Q
  • hyponatremia

- hypertonic

A
  • hyperglycemia

- mannitol

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55
Q
  • hyponatremia

- normo-osmolar

A
  • hyperlipidemia

- HLD can be 2/2 lipoprotein X a/w cholestatic or obstructive jaundice

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56
Q

presentation of D-lactic acidosis

A
  • AMS

- ataxia

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57
Q

lactic acid level in D-lactic acidosis

A

normal, because they only measure L-lactate

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58
Q

cause for D-lactic acidosis

A

colonic bacteria exposed to glucose, usually from blind loop

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59
Q

tx for D-lactic acidosis

A

complex carbohydrate diet and antibiotics

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60
Q

vbg vs abg

  • pH in vbg compared to abg
  • pCO2 in vbg compared to abg
  • HCO3 in vbg compared to abg
  • pO2 in vbg compared to abg
A
  • lower by 0.04
  • higher by 4
  • higher by 1
  • lower
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61
Q

MCC of serum osmolal gap

A

ethanol

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62
Q

osmolal gap and AG in isopropyl alcohol

A
  • increased osmolal gap

- NO AG (unless shock develops leading to lactic acidosis)

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63
Q

in ICU patient w/ AG consider what possible cause

A

propylene glycol from iv gtts

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64
Q

in ER patient w/ AG consider what possible causes

A
  • salicylate
  • EG
  • methanol
  • metformin intoxication
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65
Q

sglt2 inhibitor w/ AG, think of

A

euglycemic DKA

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66
Q

what elements are mismeasured as Cl-?

A
  • bromide

- iodide

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67
Q

high unmeasured cation

A

lithium

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68
Q

high unmeasured cation in MM

A

gammaglobulins (severe hypergammaglobulinemia)

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69
Q

elements that are unmeasured cations

A
  • Ca++

- Mg++

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70
Q

mechanism of PPI causing hypomagnesemia

A

decreased intestinal Mg absorption

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71
Q

urine FeMg in PPI use

A

low

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72
Q

hypomagnesemia causes

A
  • hypoparathyroidism –> hypocalcemia

- K+ wasting

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73
Q

medications that cause renal wasting of hypomagnesemia

A
  • aminoglycosides
  • cisplatin
  • cetuximab
  • loop diuretics
  • thiazide diuretics (except amiloride)
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74
Q

syndrome that leads to hypomagnesemia

A

Gitelman syndrome

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75
Q

causes of Fanconi syndrome

A
  • tenofovir (+/- nephrogenic DI)
  • ifosfamide (+/- nephrogenic DI)
  • cisplatin
  • MM
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76
Q

adults need w/u for what when Fanconi syndrome is diagnosed?

A

paraproteinemia

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77
Q

what do you see on labs w/ Fanconi syndrome?

A
  • renal K+, PO4, and urate wasting

- aminoaciduria

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78
Q

what other renal abnormality can be seen w/ Fanconi syndrome?

A

proximal, type 2, RTA

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79
Q

magnesium in Fanconi syndrome

A

normal

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80
Q

HAGMA in elderly woman

A

5-oxoproline (pyroglutamic acid) d/t acetaminophen use

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81
Q

HAGMA from sglt2 inhibitor

A

severe ketoacidosis w/ euglycemia

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82
Q

HAGMA from metformin

A

D lactic acidosis

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83
Q

HAGMA from linezolid

A

lactic acidosis

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84
Q

HAGMA from diethylene glycol

A
  • brake fluid

- cranial nerve abnormalities

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85
Q

hypomagnesemia causes

  • UMg < 20
  • FeMg < 2.5
A
  • PPI

- diarrhea

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86
Q

hypomagnesemia

  • UMg > 20
  • FeMg > 2.5
  • what do you check next?
A

check 24-hour urine Ca++

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87
Q

hypomagnesemia causes

  • UMg > 20
  • FeMg > 2.5
  • if 24-hour urine Ca++ < 150
A
  • thiazide diuretics

- Gitelman syndrome

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88
Q

hypomagnesemia causes

  • UMg > 20
  • FeMg > 2.5
  • if 24-hour urine Ca++ > 250
A
  • loop diuretics
  • Bartter syndrome
  • cisplatin
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89
Q

hypokalemia causes

  • low/normal volume state
  • low bicarbonate
A
  • diarrhea
  • laxative use
  • toluene
  • RTA
  • NAGMA
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90
Q

hypokalemia causes

  • low/normal volume state
  • low magnesium
A
  • familial hypomagnesemia
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91
Q

hypokalemia causes

  • low/normal volume state
  • urine Cl- low
A
  • vomiting
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92
Q

hypokalemia causes

  • low/normal volume state
  • urine Cl- high
  • urine Ca++ LOW
A
  • thiazide diuretics

- Gitelman syndrome

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93
Q

hypokalemia causes

  • low/normal volume state
  • urine Cl- high
  • urine Ca++ HIGH
A
  • loop diuretics

- Bartter syndrome

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94
Q

hypokalemia causes

  • high volume state
  • LOW renin and LOW aldosterone
A
  • Liddle syndrome
  • apparent mineralocorticoid excess (AME)
  • licorice
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95
Q

hypokalemia causes

  • high volume state
  • LOW renin and HIGH aldosterone
A
  • primary hyperaldosteronism
  • Cushing
  • glucocorticoid remediable aldosteronism (GRA)
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96
Q

hypokalemia causes

  • high volume state
  • HIGH renin and HIGH aldosterone
A
  • malignant HTN
  • renal artery stenosis (RAS)
  • renin secreting tumor
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97
Q

tolvaptan for hyponatremia

A
  • start only in hospital
  • do NOT fluid restrict
  • avoid in liver disease
  • need HIGHER doses in CHF
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98
Q

tolvaptan effect in ADPKD

A
  • slows cyst growth

- slows GFR loss

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99
Q

tolvaptan dose in ADPKD

A

2-4 times that for hyponatremia

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100
Q

adverse effects from hypophosphatemia

A
  • rhabdomyolysis
  • respiratory failure
  • heart failure
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101
Q

pseudohypophosphatemia cause

A
  • when labs drawn from catheter w/ heparin
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102
Q

distal, type 1, RTA

- what disease should you think of?

A

Sjogren

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103
Q

distal, type 1, RTA

- urine pH

A

> 5.5 (inappropriately high)

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104
Q

distal, type 1, RTA

- urine AG

A

POSITIVE

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105
Q

distal, type 1, RTA

- kidney stone type

A

CaPO4 stones

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106
Q

distal, type 1, RTA

- treatment

A

NaHCO3 1 meq/kg/day po

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107
Q

incomplete distal, type 1, RTA is seen in what cystic kidney disease?

A

medullary sponge kidney

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108
Q

what should be treated first in distal, type 1, RTA?

A
  • hypokalemia

- giving bicarb first will further lower K+ can lead to respiratory failure

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109
Q

hypophosphatemia causes

  • LOW UPhos
  • < 100 mg/day
  • FePO4 < 5%
A

cellular shifts

  • refeeding syndrome
  • treatment of DKA
  • hyperventilation

GI loss

  • alcoholism
  • chronic diarrhea
  • milk-alkali (calcium-alkali) syndrome (Ca2+ binding to PO4- in GIT)
# sudden drop in PTH
- s/p parathyroidectomy (hungry bone syndrome)
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110
Q

hypophosphatemia causes

  • HIGH UPhos
  • > 100 mg/day
  • FePO4 > 5%
  • serum Ca++ LOW
A
  • vitamin D deficiency
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111
Q

hypophosphatemia causes

  • HIGH UPhos
  • > 100 mg/day
  • FePO4 > 5%
  • serum Ca++ HIGH
A

PHPT

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112
Q

hypophosphatemia causes

  • HIGH UPhos
  • > 100 mg/day
  • FePO4 > 5%
  • serum Ca++ NORMAL
  • FGF-23-MEDIATED
A
  • XLH
  • ADHR
  • ARHR
  • TIO
  • FD
  • linear sebaceous nevus syndrome
  • postrenal transplantation hypophosphatemia
  • iron polymaltose infusions
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113
Q

hypophosphatemia causes

  • HIGH UPhos
  • > 100 mg/day
  • FePO4 > 5%
  • serum Ca++ NORMAL
  • NON-FGF-23-mediated
A
  • diuretics
  • drug-induced
  • Fanconi syndrome
  • genetic causes
  • hyperparathyroidism
  • HHRH (hereditary hypophosphatemic rickets with hypercalciuria; NPT2c)
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114
Q
  • XLH name

- associated gene

A
  • XL hypophosphatemia

- PHEX

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115
Q
  • ADHR name

- associated gene

A
  • AD hypophosphatemic rickets

- FGF-23

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116
Q
  • ARHR name

- associated gene

A
  • AR hypophosphatemic rickets

- DMP1, ENPP1

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117
Q

TIO name

A

tumor-induced osteomalacia

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118
Q

FD name

A

fibrous dysplasia

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119
Q
  • HHRH name

- associated gene

A
  • hereditary hypophosphatemic rickets w/ hypercalciuria

- NPT2c

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120
Q

GENETIC causes of hypophosphatemia

  • HIGH UPhos
  • > 100 mg/day
  • FePO4 > 5%
  • serum Ca++ NORMAL
  • NON-FGF-23-mediated
A
  • HHRH (hereditary hypophosphatemic rickets with hypercalciuria; NPT2c)
  • Dent’s disease
  • cystinosis
  • NaPi2a mutations
  • others
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121
Q

DRUG-INDUCED hypophosphatemia

  • HIGH UPhos
  • > 100 mg/day
  • FePO4 > 5%
  • serum Ca++ NORMAL
  • NON-FGF-23-mediated
A
  • adefovir
  • aminoglycosides
  • cisplatin
  • ifosfamide
  • imatinib
  • streptozocin
  • tenofovir
  • tetracyclines
  • toluene

Andrew And Carol, If I’m Supposed To, Ten Tents

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122
Q

Alport’s disease genetics

A
  • XL

- young men

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123
Q

Alport disease mutation

A

alpha 5 chain of type 4 collagen

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124
Q

clinical manifestations of Alport disease

A
  • renal disease
  • deafness
  • anterior lenticonus
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125
Q

clinical manifestations in WOMEN w/ Alport disease

A
  • hematuria ONLY

- rarely CKD

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126
Q

can be seen in Alport disease patients POST-renal transplant

A

crescentic anti-GBM GN, but NO pulmonary hemorrhage

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127
Q

EM findings in crescentic anti-GBM GN in Alport disease

A

basement membrane looks layered

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128
Q

TBMD genetics

A
  • AD

- family history w/o ESRD or deafness

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129
Q

TBMD clinical manifestations

A
  • microscopic hematuria
  • usually minimal proteinuria
  • usually clinically benign
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130
Q

hypocomplementemic GNs

- SLE

A
  • classical pathway

- usually BOTH C3 and C4

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131
Q

hypocomplementemic GNs

- cryoglobulinemia

A
  • classical pathway
  • VERY LOW C4; can be undetectable
  • sometimes low C3
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132
Q

hypocomplementemic GNs

- postinfectious GN

A
  • alternate pathway

- C3 ONLY

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133
Q

hypocomplementemic GNs

- MPGN

A
  • alternate pathway
  • C3 ONLY
  • especially in C3 nephropathy
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134
Q

hypocomplementemic GNs can also be seen in what instances?

A
  • chronic infection
  • subacute bacterial endocarditis
  • HCV
  • AED
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135
Q

hypocomplementemic GNs

- C3 GN

A
  • C3 ONLY
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136
Q

hypocomplementemic GNs

- DDD

A
  • C3 ONLY
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137
Q

primary membranous GN lab and histological finding

A

PLA2R Ab in serum and on biopsy stain

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138
Q

primary membranous GN is a/w what Ab?

A

IgG4

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139
Q

membranous GN w/ “full-house” IF

A

think of SLE

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140
Q 
lupus nephritis
- class 1
A

minimal mesangial LN

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141
Q

lupus nephritis

  • class 1
  • LM findings
A

normal

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142
Q

lupus nephritis

  • class 1
  • IF findings
A

mesangial immune deposits

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143
Q

lupus nephritis

  • class 1
  • clinical manifestations
A

mild proteinuria

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144
Q 
lupus nephritis
- class 2
A

mesangial proliferative LN

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145
Q

lupus nephritis

  • class 2
  • LM findings
A
  • mesangial hypercellularity
  • mesangial matrix expansion
  • mesangial immune deposits
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146
Q

lupus nephritis

  • class 2
  • IF and EM findings
A
  • mesangial immune deposits

- few subepithelial or subendothelial immune deposits

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147
Q

lupus nephritis

  • class 2
  • clinical manifestations
A
  • mild renal disease such as hematuria or proteinuria

- usually no specific treatment needed

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148
Q 
lupus nephritis
- class 3 A
A

active lesions

- focal proliferative LN

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149
Q 
lupus nephritis
- class 3 A/C
A

active and chronic lesions

- focal proliferative and sclerosing LN

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150
Q 
lupus nephritis
- class 3 C
A

chronic inactive lesions

- focal sclerosing LN

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151
Q

lupus nephritis

  • class 3
  • LM findings
A
  • active or inactive, focal, segmental, or global GN

- < 50% of all glomeruli

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152
Q

lupus nephritis

  • class 3
  • IF and EM findings
A

subendothelial and mesangial immune deposits

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153
Q

lupus nephritis

  • class 3
  • clinical manifestations
A
  • mild to moderate renal disease
  • hematuria
  • moderate proteinuria
  • worsening renal function in significant minority
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154
Q 
lupus nephritis
- class 4-S (A)
A

active lesions

- diffuse segmental proliferative LN

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155
Q 
lupus nephritis
- class 4-G (A)
A

active lesions

- diffuse global proliferative LN

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156
Q 
lupus nephritis
- class 4-S (A/C)
A

active and chronic lesions

- diffuse segmental proliferative and sclerosing LN

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157
Q 
lupus nephritis
- class 4-G (A/C)
A

active and chronic lesions

- diffuse global proliferative and sclerosing LN

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158
Q 
lupus nephritis
- class 4-S (C)
A

chronic inactive lesions w/ scars

- diffuse segmental sclerosing LN

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159
Q 
lupus nephritis
- class 4-G (C)
A

chronic inactive lesions w/ scars

- diffuse global sclerosing LN

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160
Q

lupus nephritis

  • class 4
  • LM findings
A
  • active or inactive, segmental or global GN > 50% glomeruli
  • diffuse segmental (class 4-S) when 50% glomeruli have SEGMENTAL lesions
  • global (class 4-G) when 50% have GLOBAL lesions
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161
Q

lupus nephritis

  • class 4
  • IF and EM findings
A

subendothelial immune deposits

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162
Q

lupus nephritis

  • class 4
  • clinical manifestations
A
  • HTN
  • edema
  • active urinary sediment
  • worsening renal function
  • nephrotic range proteinuria
  • active extrarenal SLE in many patients
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163
Q 
lupus nephritis
- class 5
A

membranous LN

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164
Q

lupus nephritis

  • class 5
  • LM findings
A
  • diffuse GBM thickening w/o inflammatory infiltrate
  • subepithelial deposits and BM spikes on silver and trichrome stains
  • may occur in combination w/ class 2 or 4
  • may show advanced sclerosis
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165
Q

lupus nephritis

  • class 5
  • IF and EM findings
A
  • subepithelial and intramembranous immune deposits

- subendothelial deposits present ONLY when proliferative component present

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166
Q

lupus nephritis

  • class 5
  • clinical manifestations
A
  • nephrotic syndrome

- usually w/o manifestations of active SLE

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167
Q 
lupus nephritis
- class 6
A

advanced sclerosis LN

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168
Q

lupus nephritis

  • class 6
  • LM findings
A
  • advanced glomerular sclerosis = 90% of glomeruli
  • severe IFTA
  • manifestations of irreversible renal injury
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169
Q

lupus nephritis

  • class 6
  • clinical manifestations
A
  • significant CKD or ESRD in most cases

- unlikely to respond to medical therapy

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170
Q

if PLA2R negative, think of

A
  • cancer
  • SLE
  • medications
  • viral infections
  • syphilis
  • parasites
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171
Q

membranous GN treatment

A
  • RAAS blockade x 6 months
  • if NO response;
  • steroids w/ CYA,
  • steroids w/ tacrolimus,
  • steroids alternating w/ chlorambucil (Ponticelli protocol),
  • steroids alternating w/ CP (Ponticelli protocol),
    OR
  • rituximab
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172
Q

anti-GBM disease age distribution

A
  • bimodal

- young men and elderly

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173
Q
  • anti-GBM Abs can be seen in what disease?

- how does it affect prognosis?

A
  • ANCA vasculitis

- worsens prognosis

174
Q

anti-GBM disease, if anuric

A

rarely recovers

175
Q

does anti-GBM recur in patients or transplant?

A

usually no

176
Q

anti-GBM a/w

A
  • smoking

- hydrocarbon exposure

177
Q

HIVAN is typically what on histology?

A

collapsing FSGS

178
Q

HIVAN RUS

A

large kidneys

179
Q

HIVAN clinical manifestations

A
  • no HTN

- little to no edema

180
Q

HIVAN pathology

A
  • microcysts

- tubular reticular inclusions (TRIs)

181
Q

common in HIVAN

A

immune complex disease lesions

182
Q

increased risk of HIVAN in patients w/ what?

A

APOL-1 high-risk alleles

183
Q

IgA nephropathy pathogenesis

A

abnormal polymeric IgA, missing galactose on side chain (glycosylation)

184
Q

IgA nephropathy epidemiology

A
  • Asians
  • Hispanics
  • rare in African Americans
185
Q

IgA nephropathy commonly seen in

A

liver disease, but usually not clinically important

186
Q

IgA nephropathy in transplant

A

high recurrence?

187
Q

IgA dominant PIGN seen w/?

A
  • Staphylococcus aureus infections, especially in DM

- bad prognosis

188
Q

scleroderma renal crisis clinical manifestations

A
  • malignant HTN
  • TMA
  • MAHA (microangiopathic hemolytic anemia)
  • AKI
189
Q

scleroderma renal crisis more common w/

A

severe skin involvement

190
Q

scleroderma renal crisis lifesaving treatment

A

RAAS blockade

191
Q

scleroderma renal crisis can be caused by

A

steroids

192
Q

sickle cell nephropathy renal manifestations

A

microscopic hematuria to papillary necrosis

193
Q

urine in sickle cell nephropathy

A

isosthenuria early in disease

194
Q

RTA in sickle cell nephropathy

A

type 4 RTA

195
Q

can cause proteinuria and ESRD in sickle cell disease patients

A

FSGS

196
Q

hematuria in SCT

A

can be microscopic or gross hematuria

197
Q

what cancer can be seen in SCT?

A

rarely, medullary cell Ca (aggressive)

198
Q

primary FSGS acts like

A

MCD

199
Q

if FSGS is steroid non-responsive think of

A

podocin mutation

200
Q

FSGS variant w/ best steroid response

A

tip lesion

201
Q

more common in secondary FSGS

A

perihilar lesions

202
Q

causes of FSGS

A
  • primary (idiopathic)
  • secondary;
  • familial/genetic
  • virus-associated
  • drug-induced
  • adaptive
203
Q

collapsing FSGS a/w

A
  • HIV-1
  • parvovirus B19
  • pamidronate
204
Q

TMA results from

A
  • alternate complement pathway abnormalities

- factor H, factor 1, C3, factor B, thrombomodulin

205
Q

TMA can p/w

A
  • AKI
  • HTN
  • MAHA
206
Q

recurrence rate of TMA in transplant patients

A

high

207
Q

causes of NAGMA

A
  • GI (diarrhea)
  • renal (RTAs)
  • hyperkalemia
  • aldosterone deficiency
208
Q

causes of NAGMA w/ POSITIVE urine anion gap

A
  • distal, type 1, RTA
  • proximal, type 2, RTA, prior to reaching steady state
  • toluene
209
Q

causes of NAGMA w/ NEGATIVE urine anion gap

A
  • diarrhea

- proximal, type 2, RTA, at steady state

210
Q

causes of HAGMA

  • high acid input
  • ingestion
A
  • EtOH
  • methanol
  • ethylene glycol
  • ASA
211
Q

causes of HAGMA

  • high acid input
  • production
A
  • shock
  • lactic acidosis
  • ketoacidosis
  • starvation
  • DM
  • EtOH
212
Q

causes of HAGMA

- low acid input

A
  • AKI

- CKD

213
Q

NAGMA HARDUP

A
  • Hyperalimentation/HCl
  • Acetazolamide
  • RTA
  • Diarrhea
  • Ureteroenteric fistula (ileal conduit)
  • Post-hypOcapnic state
214
Q

HAGMA GOLDMARK

A
  • Glycols
  • Oxoproline (pyroglutamic acid)
  • L-lactate
  • D-lactate
  • Methanol
  • Aspirin
  • Renal failure
  • Ketones
215
Q

mortality in HD decreased in

A
  • blacks
  • larger BMI
  • longer tx time
216
Q

mortality in HD increased in

A
  • hyperphosphatemia

- hypoalbuminemia

217
Q

mortality in HD a/w

A
  • low K+ baths

- higher UF rates

218
Q

mortality in HD a/w what conditions

A
  • restless leg syndrome
  • sleep d/o’s
  • pruritus
  • ESA resistance
219
Q

clinical manifestations of lead nephropathy

A
  • HTN
  • gout
  • CKD
  • AKI w/ acute Pb intoxication
220
Q

lead nephropathy histopathology

A

chronic tubulointerstitial nephritis

221
Q

causes of lead nephropathy

A
  • battery factory work

- moonshine consumption

222
Q

diagnose lead toxicity

A

EDTA test

223
Q

lead exposure a/w

A

CKD

224
Q

lithium nephropathy clinical manifestations

A
  • nephrogenic DI
  • CKD in chronic exposure
  • ATN in acute toxicity
225
Q

may prevent toxicity w/ chronic lithium use

A

amiloride

226
Q

a/w lithium nephropathy

A
  • distal, type 1, RTA
  • MCD
  • drug-induced FSGS (rare)
227
Q

treatment of acute lithium overdose

A
  • dialyze (beware of rebound, HD x 4 hours, CRRT as adjuvant)
228
Q

IgG4-related disease histopathology

A

AIN w/ “storiform” (swirly) pattern

229
Q

IgG4-related disease clinical manifestations

A
  • kidney mass
  • AI pancreatitis +/- pancreatic mass
  • retroperitoneal fibrosis
  • aortitis
230
Q

IgG4-related disease serum IgG4 level

A

high

231
Q

IgG4-related disease treatment

A
  • steroids, long course

- high relapse rate

232
Q

mechanism of hypercalcemia in sarcoidosis

A

granulomatous production of 1-25 vitamin D (1-hydroxylation)

233
Q

most common renal manifestation of sarcoidosis

A

hypercalciuria

234
Q

if tubulointerstitial nephritis and UVEITIS think

A

TINU (tubulointerstitial nephritis and uveitis)

235
Q

histopathology of sarcoidosis

A

renal granulomas, but not always

236
Q

test which may help in diagnosis of idiopathic AIN

A

ACE level

237
Q

sarcoidosis treatment

A
  • steroids acutely

- methotrexate, MMF, or azathioprine chronically

238
Q

clinical manifestations in pregnancy

A
  • cardiac output increases
  • plasma volume increases
  • GFR increases
239
Q

serum Cr in pregnancy

A

should be low

240
Q

physiology of low bp in pregnancy

A

SVR decreases more than CO increases

241
Q

acid base in pregnancy

A

respiratory alkalosis (d/t progesterone) w/ compensatory NAGMA

242
Q

hyponatremia in pregnancy is d/t?

A

reset osmostat

243
Q

treatment for primary hyperoxaluria

A

OLT

244
Q

secondary (enteric) hyperoxaluria seen in

A

intestinal bypass (bariatric surgeries)

245
Q

secondary (enteric) hyperoxaluria can cause

A
  • CaOxalate stones
  • CKD
  • ESRD
246
Q

other causes of secondary (enteric) hyperoxaluria

A
  • excessive vitamin C
  • cashews
  • starfruit (carambola) juice
  • Orlistat
247
Q

secondary (enteric) hyperoxaluria treatment

A
  • oral calcium to bind ingested oxalate and prevent absorption
  • low-oxalate diet
248
Q

metabolic alkalosis

  • urine Cl- < 15 mmol/l
  • chloride RESPONSIVE
A
  • GI loss

- renal loss

249
Q

metabolic alkalosis

  • urine Cl- < 15 mmol/l
  • chloride RESPONSIVE
  • causes of GI loss
A
  • gastric fluid losses
  • Cl- losing diarrhea
  • laxative abuse
250
Q

metabolic alkalosis

  • urine Cl- < 15 mmol/l
  • chloride RESPONSIVE
  • causes of renal loss
A
  • diuretic use
  • severe hypokalemia
  • post-hypercapnic alkalosis
251
Q

treatment of chloride RESPONSIVE metabolic alkalosis

A
  • volume expansion (NaCl)

- K+ replacement (KCl)

252
Q

metabolic alkalosis

  • urine Cl- > 20 mmol/l
  • chloride RESISTANT
  • causes
A
  • mineralocorticoid excess
  • ACTIVE diuretic use
  • Bartter syndrome
  • Gitelman syndrome
  • Cushing syndrome
  • hypokalemia
253
Q

treatment of chloride RESISTANT metabolic alkalosis

A
  • treat cause

- NaCl INeffective

254
Q

medications that cause CaPO4 stones

A
  • topiramate
  • zonisamide
  • acetazolamide
255
Q

cause of indinavir stones

A

indinavir

256
Q

cause of atazanavir stones

A

atazanavir

257
Q

medications that cause CaOxalate stones

A
  • Orlistat

- vitamin C

258
Q

laxative abuse causes what kind of stones

A

ammonium acid urate stones

259
Q

cause of sulfa stones

A

sulfa medications

260
Q

Gitelman syndrome is like taking which diuretic

A

thiazide diuretics

261
Q

Bartter syndrome is like taking which diuretic

A

loop diuretics

262
Q

Gitelman syndrome abnormal transporter

A

NaCl cotransporter

263
Q

Bartter syndrome abnormal transporter

A

NaK2Cl cotransporter

264
Q

Bartter age group

A

childhood

265
Q

Gitelman age group

A

adulthood

266
Q

Bartter genetics

A

AR

267
Q

Gitelman genetics

A

AR

268
Q

Bartter and Gitelman both require what to be ruled out first?

A

diuretic abuse

269
Q

Gitelman is a/w

A
  • hypomagnesemia (renal Mg2+ wasting)

- hypocalciuria

270
Q

Bartter is a/w

A

hypERcalciuria

271
Q

Bartter and Gitelman treatment

A

amiloride or spironolactone

272
Q

other treatment for Bartter and why

A
  • NSAIDs

- PGs elevated in Bartter

273
Q

AA amyloidosis histopathology

A
  • Congo red stain positive
  • no light chain restriction
  • amyloid A protein positive
274
Q

AA amyloidosis seen in

A
  • chronic skin infection; IVDA skin poppers
  • chonic OM
  • TB
275
Q

AA amyloidosis seen in which conditions

A
  • chronic inflammatory diseases
  • Crohn’s disease
  • RA
  • familial Mediterranean fever (FMF); renal amyloidosis
276
Q

AA amyloidosis can be seen in which hereditary condition?

A

hereditary fibrinogen A

277
Q

what conditions and medications should you think of in proximal RTA?

A
  • MM
  • amyloidosis
  • Fanconi syndrome
  • tenofovir
  • ifosfamide
  • cisplatin
278
Q

K+ level in proximal RTA

A

low

279
Q

what treatment should initially be avoided in proximal RTA as to not worsen hypokalemia?

A

bicarbonate

280
Q

proximal RTA is benign, except in

A

children - stunts growth

281
Q

urine pH in proximal RTA once steady state is reached

A

< 5.5 (appropriately low to maintain homeostasis)

282
Q

treatment for proximal RTA

A

10-15 meq/kg/day bicarb and K+ citrate

283
Q

fibromuscular dysplasia epidemiology

A
  • usually young women

- rare in blacks

284
Q

what is icodextrin, and what is it metabolized into?

A
  • glucose polymer

- metabolized to maltose

285
Q

how does UF occur w/ icodextrin?

A

from colloid oncotic osmotic pressure

286
Q

can occur in up to 10% of patients on icodextrin

A

rash

287
Q

what is a rare complication of icodextrin?

A

sterile peritonitis

288
Q

icodextrin can be useful in what situation?

A

type 1 UF failure for high solute transporters

289
Q

through what pores does UF occur w/ icodextrin use?

A

medium sized, 4-6 nm, interendothelial cell pores

290
Q

recirculation in HD equation

A

% = P-A/P-V x 100

  • P = peripheral blood urea concentration
  • A = PRE-dialyzer arterial access
  • V = POST-dialyzer venous access
291
Q

what are the 2 systemic causes that can lead to a decreased Kt/V?

A
  • access recirculation

- cardiopulmonary recirculation, especially at lower CO

292
Q

cardiopulmonary recirculation in HD can occur w/?

A

CVC

293
Q

MCC of recirculation in AVF or AVG

A

outflow stenosis

294
Q

Kt/V not affected by

A
  • pre-dialysis BUN
  • diet compliance
  • frequency of HD
295
Q

how is Kt/V achieved?

A

diffusive clearance AND convective clearance from UF removal

296
Q

Kt/V increased by what factors?

A
  • increase in BFR
  • increase in DFR
  • time on HD
  • mass transfer of dialyzer (size)
297
Q

Kt/V treatment goal which ONLY applies to 3x/week HD

A

1.2

298
Q

Kt/V decreased by what factors?

A
  • access recirculation

- dialyzer fiber clotting

299
Q

often preceded by a period of type 1 (high effective peritoneal surface area) UF failure

A

encapsulating peritoneal sclerosis

300
Q

can present early w/ bloody PD fluid

A

encapsulating peritoneal sclerosis

301
Q

can present later w/ peritoneal calcification or intestinal obstruction w/ complete cocooning of peritoneal membrane

A

encapsulating peritoneal sclerosis

302
Q

treatment for encapsulating peritoneal sclerosis

A
  • switch to HD and start steroids
  • tamoxifen if diagnosed early
  • surgery for bowel obstruction
303
Q

can occur in PD patients even after transplant

A

encapsulating peritoneal sclerosis

304
Q

complication of PD a/w high mortality rate

A

encapsulating peritoneal sclerosis

305
Q

calcific uremic arteriolopathy (calciphylaxis) usually occurs in what tissue type?

A

fatty tissues

306
Q

calcific uremic arteriolopathy (calciphylaxis) sex distribution

A

women > men

307
Q

calcific uremic arteriolopathy (calciphylaxis) signs/symptoms

A
  • painful
  • very tender
  • indurated nodules
  • subcutaneous plaques that eventually become necrotic
308
Q

calcific uremic arteriolopathy (calciphylaxis) diagnosis

A
  • bone scan which shows soft tissue calcium deposition

- biopsy should be avoided d/t poor healing

309
Q

risk factors for calcific uremic arteriolopathy (calciphylaxis)

A
  • warfarin
  • corticosteroids
  • vitamin D analogs
  • possibly severe hyperparathyroidism
310
Q

calcific uremic arteriolopathy (calciphylaxis) treatment

A
  • remove risk factors
  • sodium thiosulfate (12.5-25 g IV) after HD
  • hyperbaric O2 may help wound healing
311
Q

least common cause of all infectious peritonitis

A

fungal peritonitis (3-6%)

312
Q

major risk factor for fungal peritonitis

A

antibiotic use to treat bacterial peritonitis

313
Q

fungal peritonitis can be avoided during treatment of bacterial peritonitis by doing what?

A

antifungal ppx

314
Q

fungal peritonitis treatment

A
  • prolonged antifungal tx

- prompt PD catheter removal

315
Q

fungal peritonitis is more common after what?

A

gram negative peritonitis

316
Q

fungal peritonitis commonly results in

A

PD dropout and switch to HD

317
Q

decrease in Kt/V in a new start HD patient is usually d/t what?

A

loss of residual renal function (RRF) over time

318
Q

what can slow down loss of residual renal function (RRF) in PD patients?

A

ACEI

319
Q

should be used for V in PD patients

A

ideal body weight

320
Q

not affected by PET transport group types

A

Kt/V

321
Q

survival in PD patients is related to what?

A

renal-Kt/V&raquo_space; PD Kt/V (RRF enhances survival)

322
Q

polyuria definition

A

UOP > 3 L/24 hours

323
Q

polyuria

  • > 1000 mOsm/day
  • osmotic diuresis
  • causes
A
  • glucose
  • mannitol
  • urea
  • resolving ATN
  • diuretics
  • propylene glycol
324
Q

polyuria

  • < 800 mOsm/day
  • water diuresis
  • next step
A

water deprivation test

325
Q

polyuria

  • < 800 mOsm/day
  • water diuresis
  • Na+ > 140 meq/l
  • water deprivation test shows NO change in UOsm
A

give DDAVP

326
Q

polyuria

  • < 800 mOsm/day
  • water diuresis
  • Na+ > 140 meq/l
  • water deprivation test shows NO change in UOsm
  • if INCREASE in UOsm after DDAVP
A

central DI

327
Q

polyuria

  • < 800 mOsm/day
  • water diuresis
  • Na+ > 140 meq/l
  • water deprivation test shows NO change in UOsm
  • if still NO CHANGE in UOsm after DDAVP
A

nephrogenic DI

328
Q

polyuria

  • < 800 mOsm/day
  • water diuresis
  • Na+ LESS THAN 140 meq/l
  • water deprivation test shows INCREASE in UOsm
A

primary polydipsia

329
Q

PD noninfectious complications

A
  • pleural effusions, right > left
  • chylous ascites
  • ventral hernias
  • transient green effluent s/p cholecystectomy
  • bloody effluent in premenopausal women w/ menses or ovarian cyst rupture
330
Q

transplant medication adverse effects;

- cyclosporine

A
  • HTN
  • hyperkalemia
  • HLD
  • renal dysfunction
  • gingival hyperplasia
  • hirsutism
331
Q

transplant medication drug-drug interactions;

- cyclosporine

A
  • diltiazem
  • verapamil
  • increases CSA level
332
Q

transplant medication adverse effects;

- tacrolimus

A
  • HTN (Na+ retention)
  • hyperkalemia
  • tremor
  • renal dysfunction
  • hyperglycemia
  • alopecia
333
Q

transplant medication drug-drug interactions;

- tacrolimus

A
  • diltiazem
  • verapamil
  • increases FK level
334
Q

transplant medication adverse effects;

- sirolimus

A
  • proteinuria
  • HLD
  • cytopenia
  • slow wound healing
  • pulmonary infiltrates
335
Q

transplant medication adverse effects;

- mycophenolate

A
  • GI upset
  • myelosuppression
  • hepatotoxic
  • teratogenic
336
Q

transplant medication adverse effects;

- azathioprine

A
  • skin cancer
  • myelosuppression w/ allopurinol or febuxostat use d/t decreased xanthine oxidase
  • myelosuppression in patients w/ TMPT (thiopurine S-methyltransferase) deficiency
337
Q

AMR often occurs when?

A

after decreasing IS therapy

338
Q

AMR diagnosis

A
  • peritubular capillaritis
  • +C4d staining
  • +DSA
339
Q

AMR treatment

A
  • steroids
  • plasmapheresis
    AND
  • IVIG
340
Q

acute cellular (T-cell) mediated rejection pathogenesis

A

T-cell reaction to donor histocompatibility Ags

341
Q

acute cellular (T-cell) mediated rejection grading criteria

A

Banff criteria

342
Q

Banff criteria

A

grades

  • interstitium
  • tubules
  • arteries
343
Q

acute cellular (T-cell) mediated rejection treatment

A
  • steroids
  • increase IS
    and/or
  • anti-thymocyte globulin OR alemtuzumab
344
Q

immunosuppression medications mechanism of action

- belatacept

A

binds CD80 and CD86 which blocks co-stimulation of T-cells

345
Q

immunosuppression medications mechanism of action

- mTOR inhibitors (sirolimus, temsirolimus, and everolimus)

A

inhibits mammalian target of rapamycin (mTOR) kinase activity which inhibits T and B lymphocyte activation and proliferation

346
Q

immunosuppression medications mechanism of action

- basiliximab

A

IL-2 receptor blocker

347
Q

immunosuppression medications mechanism of action

- azathioprine

A

disrupts purine synthesis

348
Q

immunosuppression medications mechanism of action

- mycophenolate mofetil (MMF)

A

disrupts purine synthesis

349
Q

causes of SIADH

A
  • malignancy
  • pulmonary issues
  • CNS issues
  • nausea
  • pain
  • opiates
  • ecstasy
  • SSRIs
350
Q

should be ruled out in evaluation of SIADH

A
  • adrenal insufficiency

- hypothyroidism

351
Q

volume state in SIADH

A

euvolemic

352
Q

serum Osm in SIADH

A

hypoosmolar, < 275 mOsm/kg

353
Q

urine Osm and UNa+ in SIADH

A

> 100 mOsm/kg and > 40 mmol/l

354
Q

SIADH treatment

A
  • fluid restriction
  • oral NaCl or urea
  • 3% saline
  • V2 antagonists (not acutely)
  • demeclocycline
355
Q

distal, type 1, RTA

- K+ level

A

LOW

356
Q

distal, type 1, RTA

- bicarb level

A

NAGMA, usually < 10

357
Q

distal, type 1, RTA

- urine pH

A

> 5.5 (inappropriately HIGH)

358
Q

distal, type 1, RTA

- urine AG (INDIRECT way to measure urine NH4+)

A

POSITIVE; corresponds to LACK of urine NH4+

359
Q

distal, type 1, RTA

- causes

A
  • Sjogren
  • SLE
  • amphotericin
  • topiramate
360
Q

abused substance that mimics distal, type 1, RTA

A

toluene (found in paints, paint thinners, fingernail polish, lacquers, adhesives, and rubber)

361
Q

distal, type 1, RTA

- a/w

A
  • nephrolithiasis
  • nephrocalcinosis
  • CKD
362
Q

distal, type 1, RTA

- treatment

A

1-2 meq/kg/d of base, usually K+ citrate

363
Q

proximal, type 2, RTA

- K+ level

A

LOW

364
Q

proximal, type 2, RTA

- bicarb level

A

NAGMA, usually 12-20

365
Q

distal, type 1, RTA

- pathophysiology

A

unable to secrete NH4+

366
Q

proximal, type 2, RTA

- pathophysiology

A

decreased proximal HCO3 reabsorption (lower threshold for reabsorption)

367
Q

proximal, type 2, RTA

- urine pH once steady state is reached

A

5 (appropriately LOW)

368
Q

proximal, type 2, RTA

- urine AG (INDIRECT way to measure urine NH4+)

A

NEGATIVE; corresponds to PRESENCE of urine NH4+

369
Q

proximal, type 2, RTA

- a/w

A

Fanconi syndrome

370
Q

proximal, type 2, RTA

- effects in adults

A

benign

371
Q

proximal, type 2, RTA

- effects in children

A

stunts growth

372
Q

proximal, type 2, RTA

- treatment

A
  • 5-10 meq/kg/day of base

- potassium-sparing diuretic (amiloride, or spironolactone)

373
Q

RTA type 4 (hypoaldosteronism)

- K+ level

A

HIGH

374
Q

RTA type 4 (hypoaldosteronism)

- bicarb level

A

usually > 17

375
Q

RTA type 4 (hypoaldosteronism)

- pathophysiology

A

low aldosterone release and/or response

376
Q

RTA type 4 (hypoaldosteronism)

- urine AG

A

variable

377
Q

RTA type 4 (hypoaldosteronism)

- causes

A
  • DM
  • NSAIDs
  • cyclosporine
  • old age
378
Q

RTA type 4 (hypoaldosteronism)

- treatment

A
  • loop diuretic
  • bicarb
  • mineralocorticoid
    AND
  • K+ binding resin
379
Q

causes of osmotic nephropathy

A
  • sucrose containing IVIG
  • hydroxyethyl starch (HES)
  • dextran
380
Q

osmotic nephropathy LM on kidney biopsy

A

swollen tubular cells packed w/ numerous cytoplasmic vacuoles

381
Q

osmotic nephropathy EM on kidney biopsy

A

vacuoles with phagolysosomes containing the offending agent (sucrose, HES, etc)

382
Q

medications that decrease calcineurin inhibitor level

A
  • rifampin
  • barbiturates
  • phenytoin
  • carbamazepine
  • nafcillin
  • trimethoprim
  • imipenem
  • cephalosporins
  • St. John wort
  • INH
383
Q

medications that increase calcineurin inhibitor level

A
  • verapamil
  • diltiazem
  • ketoconazole
  • fluconazole
  • erythromycin
  • grapefruit
  • amiodarone
  • carvedilol
  • dapsone
384
Q

medications and condition that increase calcineurin inhibitor toxicity

A
  • amphotericin
  • aminoglycosides
  • NSAIDs
  • lovastatin
  • rhabdomyolysis**
385
Q

Liddle syndrome pathophysiology

A
  • GOF mutation

- ENaC overactivity

386
Q

apparent mineralocorticoid excess pathophysiology

A

11β-HSD2 deficiency

387
Q

glucocorticoid remediable aldosteronism pathophysiology

A
  • chimeric gene fusion (CYP11B1 and CYP11B2)
  • zona fasciculata defect
  • ACTH receptor overstimulated by cortisol
388
Q

renal artery stenosis renin/aldosterone pathophysiology

A

renal parenchymal ischemia

389
Q
  • causes of hypercalcemia
  • LOW PTH
  • normal 25-OH vitamin D
  • LOW 1,25-(OH)2 vitamin D
A
  • hyperthyroidism
  • malignancy
  • immobilization
  • Paget’s disease
  • milk alkali syndrome
390
Q

pregnancy-associated TMA

  • > 24 weeks
  • HTN, edema
  • effect of delivering fetus
A
  • preeclampsia

- improved

391
Q

pregnancy-associated TMA

  • > 27 weeks
  • liver dysfunction and coagulopathy
  • effect of delivering fetus
A
  • acute fatty liver (AFL)

- improved

392
Q

pregnancy-associated TMA

  • > 34 weeks
  • elevated LFTs (not bili), and severe MAHA
  • effect of delivering fetus
A
  • HELLP

- improved

393
Q

pregnancy-associated TMA

  • postpartum
  • renal failure
  • effect of delivering fetus
A
  • HUS

- none

394
Q

pregnancy-associated TMA

  • < 24 weeks
  • neurological symptoms
  • effect of delivering fetus
A
  • TTP

- none

395
Q

calculator for estimating likelihood of severe ADAMTS13 deficiency in adults w/ suspected TTP

A

PLASMIC score

396
Q

treatment for suspected TTP

A

plasmapheresis

397
Q

treatment for drug-induced TMA

  • quinine-containing beverage
  • IVDU
  • chemotherapy
  • CNI
A
  • d/c medication

- may be able to avoid plasmapheresis

398
Q

treatment for postpartum complement-mediated TMA

A

prompt anti-complement treatment (eculizumab)

399
Q

alternative treatment for TMA if plasmapheresis not available

A

plasma infusion until transfer to another hospital

400
Q

alternative treatment for TMA if anaphylactic reaction to plasma

A

factor VIII concentrate (contains ADAMTS13) and apheresis (plasma removal)

401
Q

alternative treatment for TMA if can’t give any blood products for religious reasons

A

intensive IS and apheresis

402
Q

how is adequate response to plasmapheresis assessed?

A

normalization of platelet count

403
Q

eculizumab is removed by

A

plasmapheresis

404
Q

what ppx must be given prior to eculizumab administration?

A
  • abx x 2 weeks before vaccine is effective

- meningococcal vaccine

405
Q

cause for primary FSGS

A
  • specific cause unknown

- ? circulating permeability factors

406
Q

cause for familial/genetic FSGS

A

mutation in podocyte genes (eg podocin, nephrin)

407
Q

causes for virus-associated FSGS

A
  • HIV-1
  • parvovirus B19
  • SM 40
  • CMV
  • EBV
408
Q

causes for drug-induced FSGS

A
  • heroin
  • interferon alfa, beta, and gamma
  • lithium
  • pamidronate
  • sirolimus
  • CNIs
  • anabolic steroids
409
Q

causes for adaptive FSGS

- conditions w/ reduced renal mass

A
  • very low birth weight
  • u/l renal agenesis
  • reflux nephropathy
  • advanced renal disease w/ reduced functioning nephrons
410
Q

causes for adaptive FSGS

- conditions w/ initially normal renal mass

A
  • HTN
  • AED
  • TMA
  • RAS
  • cyanotic congenital heart disease
  • sickle cell anemia
411
Q

the adaptive form of FSGS is mediated by adaptive structural-functional responses to glomerular hypertension caused by

A

elevated glomerular capillary pressures and flows

412
Q

initial urine pH in proximal, type 2, RTA

A

alkaline, 8

413
Q

urine NH4+ level in proximal, type 2, RTA once steady state is reached

A

HIGH

414
Q

some studies have indicated that magnesium wasting in Gitelman syndrome may be d/t down-regulation of what?

A

TRPM6 in DCT

415
Q

expected acid-base disturbance in aspirin OD

A

respiratory alkalosis w/ compensatory metabolic acidosis

416
Q

best initial test for a patient suspected of having pheochromocytoma

A

24-hour URINARY fractionated metanephrines

  • 98% sensitivity
  • 98% specificity
417
Q

best test for a patient at HIGH RISK for pheochromocytoma (high risk familial syndrome such as MEN2, or VHL syndrome)

A

plasma catecholamines

  • 96-100% sensitivity
  • only 85-89% specificity
418
Q

what treatment should a patient with pheochromocytoma receive prior to surgery?

A
  • alpha and beta blockers

- HIGH SALT diet (to mitigate volume contraction and orthostasis)

419
Q

generally, if problem on PD is inadequate solute clearance, what is the next best step?

A

increase volume in each exchange

420
Q

ACCOMPLISH trial showed combination of which antihypertensives reduced cardiovascular morbidity and mortality, and slowed CKD progression?

A

ACEI and CCB

421
Q

according to NHANES, which modifiable risk factor in patients with CKD has the highest overall survival rate compared to other modifiable risk factors?

A

smoking cessation

422
Q

renal and GU abnormalities and associated cause

- Turner’s syndrome

A

horseshoe kidney

423
Q

renal and GU abnormalities and associated cause

- epispadias

A

bladder extrophy

424
Q

renal and GU abnormalities and associated cause

  • undescended testes
  • inguinal hernias
  • CHARGE syndrome
A

hypospadias

425
Q

renal and GU abnormalities and associated cause

  • WAGR
  • aniridia
  • GU malformation
  • intellectual disability
A

Wilm’s tumor

426
Q

reabsorption (or secretion) rate formula

A

filtration rate - excretion rate

  • FR = GFR x Px
  • ER = V x Ux
  • GFR = U(inulin)/P(inulin) x V (urine flow rate)
427
Q

inulin clearance (GFR) formula

  • inulin is neither secreted NOR reabsorbed
A

U(inulin)/P(inulin) x V (urine flow rate)

428
Q

PAH clearance (ERPF) formula

  • PAH is filtered by glomeruli and actively secreted by proximal tubutes
A

CPAH = ERPF = U(PAH)/P(PAH) x V (urine excretion rate)

RBF = RPF/(1 - Hct)

429
Q

respiratory alkalosis

- for every decrease in PCO2 below 40, bicarb decreases by

A

2-3

430
Q

respiratory acidosis

- for every increase in PCO2 above 40, bicarb increases by

A

2-3

Nephrology Board Review Pearls (10 decks)

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