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Nephrology Flashcards

1
Q

Board answer for BP management

A

Ambulatory blood pressure monitoring

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2
Q

How to dose HCTZ

A

Keep it at 25 mg. You don’t get a significant antihypertensive effect beyond this but do get a significant increase in side effects.

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3
Q

When to start bicarb in CKD and why

A
  • Serum bicarb chronically below 22

- Alkali therapy can delay progression of CKD

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4
Q

Treatment of minimal change glomerulopathy

A

High dose prednisone (1-2 mk/kg per day for 8 to 12 weeks, then taper)

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5
Q

what is standard treatment of nephrotic syndrome

A
  • ACE or ARB
  • Diuretics for edema
  • Statin
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6
Q

Term for renal disorder that can develop from MGUS

A

monoclonal gammopathy of renal significance (MGRS)

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7
Q

Labs for MGRS (monoclonal gammopathy of undetermined significance)

A

nephrotic and subnephrotic proteinuria, hematuria, elevated creatinine

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8
Q

Treatment of IgA nephropathy

A

ACE or ARB (this inhibits protein production and slows disease progression)

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9
Q

Lab features of polydypsia

A
  • very low urine osmolality (less than 100)

- low urine sodium

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10
Q

serum sodium with diabetes insipidus

A

Typically normal but can be elevated in patients who do not have access to water

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11
Q

How to prevent calcium oxalate kidney stones in patients with chronic diarrhea

A

Potassium citrate (urine citrate is reduced because diarrhea causes a metabolic acidosis. Also, calcium binds to fat as opposed to oxalate with chronic pancreatitis due to fat malabsorption which leaves oxalate free to be absorbed and excreted in the urine)

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12
Q

Med that will also reduce progression of kidney disease and CV events in patients with CKD from DM2

A

SGLT2

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13
Q

Treatment of rhabdo induced AKI

A

Aggressive fluid resuscitation with NS to goal UOP 200-300 mL/h

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14
Q

How to reduce incidence of contrast-induced nephropathy

A

Normal saline

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15
Q

Presentation of milk alkali syndrome + cause

A
  • Ingestion of large amounts of calcium

- hypercalcemia + metabolic alkalosis + AKI

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16
Q

Treatment of ethylene glycol toxicity

A

IV hydration
Fomepizole
Hemodialysis (need to dialyze toxin)

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17
Q

Presentation of ethylene glycol toxicty

A

CNS depression
Anion gap acidosis
Increased osmolal gap
Kidney failure

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18
Q

Evaluation of membranous glomerulopathy

A

Age and sex appropriate cancer screening

Hep B and C, lupus and syphilis testing

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19
Q

Anticoagulation for membranous glomerulopathy

A

Is higher risk, particularly when albumin is below 2.8 but there is no conscenus and guidelines generally recommend monitoring rather than anticoagulation

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20
Q

How to test for diabetes insipidus + how it works

A

Water deprivation test (response to exogenous ADH supports diagnosis of central DI, whereas lack of response is seen in nephrogenic DI)

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21
Q

Why heparin can cause hyperkalemia

A

Hypoaldosteronism

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22
Q

clinical outcomes of peritoneal vs. hemodialysis

A

Comparable

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23
Q

Important complication of peritoneal dialysis

A

Peritonitis

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24
Q

Treatment of stage 2 hypertension

A

Combination therapy with antihypertensives of different classes

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25
Q

Stage 2 HTN definition

A

BP greater than 140 over 90

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26
Q

More efficacious antihypertensives in AA patients

A

Thiazide diuretics or CCBs

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27
Q

Renal disease typically caused by multiple myeloma

A

Cast nephropathy

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28
Q

Clinical features of ANCA-associated glomerulonephritis

A

Vasculitic prodrome (malaise, arthralgia, myalgia, skin findings) + hematuria + proteinuria

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29
Q

Biopsy of RPGN

A

Pauci-immune staining
Linear staining
Granular staining

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30
Q

Cause of pyroglutamic acidosis

A
  • Happens in people taking therapeutic doses of acetaminophen chronically in setting of critical illness, poor nutrition, chronic liver or kidney disease
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31
Q

Presentation of pyroglutamic acidosis

A

Mental status changes + gap acidosis

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32
Q

Presentation of D-lactic acidosis

A

Gap acidosis + neuro dysfunction (confusion, slurred speech, ataxia) + patient with short-bowel syndrome

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33
Q

Labs for D-lactic acidosis

A

NORMAL serum lactic (not measured by conventional lab assays)

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34
Q

Pathophys of D-lactic acidosis

A

Patients with short-bowel syndrome following jejunoileal bypass or small bowel resection –> excess carbohydrates reach the colon and are metabolized to d-lactate

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35
Q

Presentation of salicylate toxicity

A

Respiratory alkalosis OR both respiratory alkalosis + gap acidosis

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36
Q

Propylene glycol toxicity presentation

A

gap acidosis + AKI

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37
Q

Gap acidosis differential

A 
M - Methanol
U - Uremia
D - DKA
P - Paraldehyde
I - Iron, INH
L - Lactic acidosis
E - ethanol, ethylene glycol
S - salicylate/aspirin
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38
Q

what are the ANCA associated glomerulonephritidis?

A

GPA + MPA

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39
Q

Management of abdominal compartment syndrome

A

Abdominal compartment decompression

Correction of positive fluid balance

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40
Q

Definition of abdominal compartment syndrome

A

Sustained intra-abdominal pressure greater than 20 + at least one organ dysfunction

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41
Q

Settings in which abdominal compartment syndrome occurs

A

Abdominal surgery
Large volume fluid resuscitation
Multiple transfusions

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42
Q

Presentation of abdominal compartment syndrome

A

Distended abdomen
Ascites
Sodium-avid AKI (increased pressure compresses the renal parenchyma and vasculature, causing decrease in GFR)

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43
Q

AIN clinical features

A

Hematuria + pyuria + white cell casts

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44
Q

Age cutoff for working up hematuria

A

Age greater than 35 (should also prompt urology referral even if self-limited)

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45
Q

Appearance of erythrocyte casts and specificity

A
  • cylindrical or tubular structure + agrunular spherocytes

- Specific for hematuria of glomerular origin

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46
Q

RF’ of vancomycin nephrotoxicity

A

CKD + supra therapeutic troughs + concomitant diuretic use

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47
Q

Microscopy findings with ATN

A

Numerous renal tubular epithelial cells + granular casts

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48
Q

Features of AIN

A

Classic triad = fever + rash + eosinophilia (but only 30% of patients have this)
*UA with hematuria + pyuria + casts

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49
Q

Features of contrast-induced nephropathy

A

Occurs within 48 hours of exposure to contrast

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50
Q

Treatment of acute symptomatic hyponatremia

A

A 100-mL bolus of 3% saline w/ goal increase in sodium of 2-3
- Can be repeated 1-2x until symptoms resolve

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51
Q

Why MDMA causes hyponatremia

A

SIADH + stimulates thirst receptors

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52
Q

Goal sodium correction in hyponatremia

A

Less than 10 in 24 hr period (remember, if the patient isn’t symptomatic you have plenty of time to correct sodium)

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53
Q

Management of ACS in a patient with CKD

A

Immediate cath (mortality is far higher with cardiovascular disease than with CKD)

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54
Q

Renal clinical features of sarcoidosis

A

Nephrocalcinosis from hypercalcemia and hypercalciuria

55
Q

Extrapulmonary organ involvement with sarcoid

A

Skin
arthralgia
eyes

56
Q

Physiology of hyponatremia in pregnancy

A

Plasma volume increases with water retention greater than sodium retention so mild hyponatremia is common in pregnancy

57
Q

management in dyslipidemia in CKD

A

All adults over 50 with a GFR less than 60 but not on dialysis, should be on a statin

58
Q

Image type to diagnose nephrolithiasis

A

NONCON helical abdominal CT

59
Q

Benign causes of increased serum creatinine

A

Increased muscle mass
Creatine supplements
(creatinine is derived from the metabolism of creatinine produced by muscle)

60
Q

Management of recurrent kidney stones

A

24 hour urine studies
IF citrate normal –> Thiazide diuretic (will decrease calcium excretion into urine, reducing hypercalciuruia and calcium oxalate stone formation)
IF citrate low –> start potassium citrate

61
Q

Management of membranous glomerulopathy

A

Observe for 6-12 months while on nephrotic syndrome meds (ACEi, statin, diuretic) to allow time for possible spontaneous remission before initiating immunosuppression (30% have spontaneous remission)

62
Q

First line immunosuppressive therapy for membranous glomerulopathy

A

Alternating months of steroids and cyclophosphamide

63
Q

Management of renal artery stenosis

A

Medical management (ACE inhibitor + treat CV risk factors statin because it is due to atherosclerosis)

64
Q

term for kidney injury from contrast

A

Contrast-induced nephropathy

65
Q

how to reduce incidence of contrast induced nephropathy when cath’ing patient with CKD

A

IV isotonic fluid before and after cath

66
Q

Type 1 RTA clinical features + pathophys

A
  • Defect in urine acidification in the distal nephron

- NAGMA (can’t secrete hydrogen ions0 + basic urine (pH 7) + hypokalemia + increased calcium phosphate kidney stones

67
Q

Clinical features of kidney injury caused by NSAIDS

A

Interstitial nephritis (proteinuria)

68
Q

Type 2 RTA clinical features + cause

A
  • Proximal tubular defect in reclaiming bicarb

- NAGMA + hypokalemia + glycosuria + proteinuria + phosphate wasting

69
Q

How to differentiate NAGMA

A

Calculate urine anion gap

70
Q

Management of alcoholic ketoacidosis

A 
Thiamine first (to decrease risk of precipitating Wernicke's)
D5NS
71
Q

management of edema in nephrotic syndrome

A

Low salt diet + loop diuretic

72
Q

Other causes of secondary FSGS

A

Premature birth

Solitary kidney

73
Q

Risk of VTE in membranous glomerulopathy correlates to…

A

Degree of hypoalbuminemia (albumin less than 2.8)

74
Q

patients with membranous glomerulopathy are at increased risk of…

A
  • gout (true of all CKD patients due to reduced uric acid secretion)
  • malignancy
75
Q

Management of HTN in CKD patient

A

ACE or ARB

76
Q

Preeclampsia clinical features

A

New-onset hypertension + proteinuria + new onset end-organ damage (liver, kidney, pulmonary edema, HA or visual symptoms, or thrombocytopenia)

77
Q

HELLP syndrome clinical features

A

Hemolysis
Elevated liver enzymes
Low platelets

78
Q

Fabry disease clinical features

A

Episodic pain + burning sensation in hands and feet + decreased perspiration + angiokeratomas

79
Q

Management of cardio renal syndrome

A

Loop diuretics

80
Q

Features of cardio renal syndrome

A
  • Elevated BUN-creatinine ratio

- Diuretic resistant heart failure (failure to improve CHF symptoms despite increasing diuretic requirement)

81
Q

When do you need to dialyze CHF patients with cardio renal syndrome

A

Severe volume overload refractory to medical management

82
Q

Goals of anemia management in CKD

A

Target transferrin saturation greater than 30% + ferritin level greater than 500

83
Q

workup for renovascular hypertension + caveat

A

Kidney US with doppler (no studies have shown a benefit from percutaneous intervention so should be reserved for people with strong indications such as FMD)

84
Q

Metabolic alkalosis workup

A

Differentiate saline responsive from saline unresponsive
Urine chloride
- low = vomiting, NG suction, diuretic use (GI losses so reabsorbing chloride)
- high = saline-resistant due to mineralocorticoid excess (Cushing syndrome + primary aldosteronism)

85
Q

IgG4 related disease clinical features

A

Renal disease + autoimmune pancreatitis + allergic rhinitis + submandibular gland swelling

86
Q

IgG4 related disease lab features

A

Elevated ANA
Low serum complement
Elevated serum IgG + IgE
Peripheral eosinophilia

87
Q

What are the calcineurin inhibitors

A

Tacrolimus

Cyclosporine

88
Q

Hypermagnesemia treatment

A

Stop magnesium containing medications
NS bolus’s (increase secretion of mag) + furosemide
IV calcium (calcium counteracts neuromuscular effects of magnesium)

89
Q

What you’re looking for with urine microscopy for ATN

A

Granular casts and/or renal epithelial cells

90
Q

What is masked hypertension

A

BP that is normal in the office but elevated in the ambulatory setting

91
Q

How to differentiate chronic HTN from gestational HTN

A

Chronic HTN = HTN recognized before 20 weeks gestation
*In normal pregnancy BP declines during the first trimester, decreases further in 2nd trimester, and rises slowly thereafter. Thus, HTN in the first trimester suggests that it predates the pregnancy. Gestational HTN manifests later and resolves within 12 weeks of delivery.

92
Q

Management of BP in pregnant women

A

Goal 160/105

*avoid over treatment and associated fetal risk

93
Q

Anti-phospholipase A2 receptor antibodies are associated with…

A

Membranous glomerulopathy

94
Q

Management of suspected white coat hypertension

A

Ambulatory blood pressure monitoring

95
Q

Type IV RTA clinical features

A

Hyperkalemia + NAGMA + impaired urine acidification (positive urine anion gap) + pH <5.5

96
Q

When does hyperkalemia manifest with CKD

A

Usually stage 4 or worse – GFR <40-45

97
Q

Management of lupus patient developing kidney disease

A

Kidney biopsy (guides treatment and to determine class of lupus nephritis. there are multiple classes of lupus nephritis – focal or diffuse proliferative lupus nephritis, lupus membranous nephropathy)

98
Q

Blood pressure management in advanced CKD

A

loop diuretics (thiazides become less effective. useful for hyperkalemia and metabolic acidosis. sodium retention and impaired natriuresis lead to volume expansion and increased BP)

99
Q

Most appropriate venous access for a patient with advanced CKD

A 
NO PICCS (they can cause vein trauma and venous stenosis). need to protect upper extremity veins.
*Tunneled IJ central line
100
Q

initial management of HTN in diabetics

A

Start ACE/ARB (don’t want for trial of lifestyle modification)

101
Q

Medications that reduce proximal tubule secretion of creatinine (causing benign elevation in creatinine/no effect on GFR) + management

A

Bactrim
Dolutegravir/Bictegravir
Cimetidine
*recheck creatinine in 1 week

102
Q

Kidney stones caused by topamax

A

Calcium phosphate (carbonic anhydrase inhibitor so causes a decrease in urinary citrate excretion and formation of alkaline urine)

103
Q

Most common type of kidney stone

A

calcium oxalate

104
Q

tubulontersitial nephritis on UA

A

Pyuria + proteinuria + hemautira

105
Q

high serum potassium without ECG changes, think..

A

pseudohyperkalemia

106
Q

Situations in which pseudohyperkalemia can occur

A

Significant leukocytosis or thrombocytosis (cell lysis can lead to K leakage)

107
Q

Goal hgb in anemia of CKD/esrd

A

10-11.5

108
Q

Goal ferritin and transferrin sat in anemia of ckd/esrd

A

transferrin saturation >30% + ferritin >500

109
Q

How to replete iron in anemia of ESRD

A

IF transferrin saturation >30 percent + patient not stage 3b or 4 → try PO iron → if no improvement, give IV iron
IF transferrin saturation <30 percent → IV iron

110
Q

Medication class inhibits erythryopoesis

A

ACEis + ARBs

111
Q

definition of allosensitization

A

exposure to an alloantigen that induces immunologic memory cells

112
Q

Organism most often responsible for infection-related glomerulonephritis

A

Staph aureus

113
Q

Phos goals in CKD4 and 5 generally

A

Lower toward reference range (not goal normal since there’s no evidence of benefit to aggressively lowering to normal range)

114
Q

Class of medications that commonly elevates blood pressure + mechanism

A

NSAIDs (increased sodium retention)

115
Q

Diseases associated with membranoproliferative glomerulonephritis

A

Hep C

116
Q

Lead nephropathy associations

A

Hyperuricemia + HTN + recurrent gout

117
Q

Nephropathy clinical features from chronic ASA or APAP

A

chronic tubulointersitial disease

118
Q

Causes of NAGMA

A

GI bicarbonate loss (diarrhea)
Renal loss of bicarbonate
Inability of kidney to excrete acid

119
Q

Explain physiology of why you calculate a urine anion gap for NAGMA

A

Normal physiologic response to acidosis is to increase urine acid excretion. Therefore, need to determine whether kidney is appropriately excreting acid or whether impaired acid excretion is the cause. You measure urine chloride as a surrogate of ammonium to determine if acid is being excreted

120
Q

Interpretation of urine anion gap

A 
negative = GI cause
positive = RTA
121
Q

Treatment of AIN

A

steroids

122
Q

D-lactic acidosis occurs in which settings

A

short-bowel syndrome (usually due to small-bowel resection or jejunoileal bypass) (excess carbohydrates reach the colon and are metabolized to D-lactate by bacteria)

123
Q

D-lactic acidosis clinical features

A

Neuro deficits (confusion, slurred speech, ataxia) + high anion gap acidosis

124
Q

Management of immunosuppressants in kidney transplant recipients planning on having a baby

A

DC mycophenolate, sirolimus, and everolimus (replace with azathioprine)
*Also should wait 1-2 years after stable allograft

125
Q

Clinical features of light chain cast nephropathy from MM

A
  • Elevated urine protein-creatinine ratio

BUT Minimal proteinuria by urine dipstick

126
Q

Most common type of kidney disease in multiple myeloma

A

Light chain cast nephropathy

127
Q

Presentation of IgA nephropathy

A

Recurrent gross hematuria occurring within days of URI or physical exercision + otherwise benign

128
Q

Other term for IgA vasculitis

A

HSP - Henoch-Schonlein purpura

129
Q

Features of IgA vasculitis

A

Abdominal pain + palpable purpura

130
Q

General approach to working up acid base disorder

A

1) Identify primary disorder
2) Determine if adequate compensatory response
3) If no adequate compensation –> mixed acid-base disorder is present

131
Q

How to determine metabolic compensation for respiratory alkalosis

A

Bicarb should be reduced by 5 mEq for each 10 decrease in PCO2 (nickel for a dime)

132
Q

Significant proteinuria with minimal proteinuria on urine dipstick suggests…

A

Bence-Jones (light chain) proteinuria (isn’t picked up by dipstick)

133
Q

When CKD patients are referred for transplant evaluation

A

eGFR <30 (need to plan ahead to find living donor or to be put on early listing if no living donor available)
- transplant is also cheaper than dialysis

134
Q

Management of hepatorenal syndrome

A
  • octreotide + midodrine or levophed
  • discontinue diuretics
  • IF albumin <2.5 → Albumin 1g/kg q8h x 3 days

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