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RCPSC > Nephrology > Flashcards

Nephrology Flashcards

1
Q

What are the BP thresholds for diagnosing hypertension with the various BP measurement methods

A

AOBP: 135/85, 130/80 in DM
Non-AOBP: 140/90, 130/80 in DM
24hrs ambulatory: 135/85 daytime, 130/80 (24hrs)
Home BP: 135/85

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2
Q

BP cuff measurements

A

width 40% of arm circumference
length 80-100% of arm circumference

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3
Q

What are the thresholds to diagnose HTN in non-diabetics when no ambulatory BP measurements are available

A

Visit 2: >140/80 WITH macrovascular disease, CKD, T2DM
Visit 3: Mean BP >160/100
Visit 5: Mean BP > 140/90

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4
Q

What investigations should be done at diagnosis for hypertension

A

LBC, Fasting glucose and/or A1C, lipid profile, UA
ACR if diabetic, renal disease, or proteinuria on UA
ECG if suspicion for LVH, systolic or diastolic dysfunction, or CAD

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5
Q

Who should be screened for renovascular HTN

A

2 or more of the following:

  1. Sudden onset or worsening HTN, age>55 or <30
  2. Abdominal bruit
  3. HTN resistant to 3 drugs
  4. Creatnine increase of >30% on ACEi or ARB
  5. Other atherosclerotic vascular diseases, Particularily in smokers or DLP
  6. Recurrent pulmonary edema associated with HTN surges
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6
Q

What is the screening test for Renovascular hypertension (4 possible)

A

Doppler
Captopril renogram
MRA
CTA

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7
Q

Who should be worked up for FMD related Renal artery stenosis

A
  1. Asymmetric kidneys (>1.5 cm difference)
  2. Abdominal bruit with no atherosclerotic risk factors
  3. Confirmed FMD in another vascular bed
  4. Family Hx of FMD
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8
Q

How do you work up FMD

A

CTA or MRA
When confirmed, screen vasculature from head to pelvis with CTA or MRA

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9
Q

What are the SPRINT inclusion criteria

A

SBP > 130, age >50 and 1 or more of:

  1. Clinical or subclinical CVD
  2. CKD: eGFR 20-59, proteinuria <1g/day – non diabetics
  3. 10 year CV risk > 15%
  4. Age > 75
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10
Q

What are the SPRINT exclusion criteria

A
  1. DM
  2. Previous stroke
  3. GFR <20
  4. Proteinuria > 1g/day
  5. PKD
  6. Contraindications:
    - Non-adherence
    - Standing SBP<110
    - secondary HTN
    - Can’t measure BP accurately
    - life-limiting illness
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11
Q

What are the non-pharmacological interventions used in HTN

A
  1. Exercise: 30-60 min. Moderate intensity, dynamic, 4-7 days per week
  2. Weight: BMI 18.5-24.9 Waist circumference <102(M) <88 (F)
  3. Alcohol: Abstain OR reduce to <2drinks per day (prevention) and if >6 drinks a day, reducing to <2 can reduce BP
  4. Diet: DASH diet, Increase K intake if not high risk for hyperkalemia
  5. Salt: <5g/day Na
  6. Stress reduction: inc CBT and relaxation techniques
  7. Smoking cessation
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12
Q

What are the BP treatment targets

A

SPRINT: SBP<120
DM: <130/80
Low risk: <140/90
For CKD patients, individualize. If PKD target <110*

(HTN Canada)

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13
Q

What are the 1st and 2nd line BP med options in diabetes?

A

1st line:
IF CV disease. or risk factors, CKD/microalbuminuria:
Use ACEi or ARB
if not:
ACEi, ARB, DHP CCB, thiazide

2nd line (with 1st line ace): 
DHP-CCB

Possibly consider SGLT2

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14
Q

Indications to CONSIDER stenting in RAS

A
  1. Uncontrolled HTN resistant to maximally tolerated pharmacotherapy
  2. Progressive renal function decline
  3. Acute pulmonary edema
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15
Q

Firstline antihypertensives for isolated systolic hypertension

A
  1. Thiazide
  2. Long acting DHP-CCB
  3. ARB
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16
Q

Firstline antihypertensive for diastolic hypertension

A
  1. Thiazide
  2. BB if <60
  3. ACE/ARB
  4. Long acting DHP-CCB
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17
Q

Firstline antihypertensives for LVH

A
  1. Thiazide
  2. ACE/ARB
  3. Long-acting DHP-CCB

*Do not use vasodilators
**Avoid BB

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18
Q

Firstiline antihypertensive for non-diabetic with CKD and proteinuria

A

ACE/ARB

*Additive Tx: Thiazide
**If vol overload, can use Lasix instead of ACE

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19
Q

Firstline antihypertensive in CAD

A
  1. ACE/ARB

Then can add CCB or BB
ACE + CCB over ACE+thiazide

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20
Q

Firstline antihypertensive in stable CAD

A

BB or CCB

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21
Q

Firstline antihypertensive in recent MI

A

BB+ACE

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22
Q

Firstline antihypertensive in EF<40%

A

ACE + BB
ARB in intolerante to ACE
Hydralazine + ISDN if can’t use ACE/ARB

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23
Q

Second-line antihypertensive in EF<40%

A

MRA

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24
Q

Treatment of anti-GBM

A
  1. Pulse steroids (6 months)
  2. Cyclophosphamide (2-3 months)
  3. PLEX (until titers no-longer detectible, usually 14 exchanges)
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25
Q

What vasculitidies are associated with Anti-MPO and anti-PR3 antibodies

A
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26
Q

What are the clinical features of ANCA associated vasculitides?

A
  1. Constitutional symptoms
  2. Arthralgias and rash
  3. sinusitis, asthma, pulmonary hemorrhage
  4. Nephritis
  5. Mononeuritis multiplex
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27
Q

How are ANCA vasculitides treated

A

Induction:

  • Cyclophosphamide preferred if RPGN, Cr>354
  • Rituximab preferend if:
    • Premenopausal women
    • Men interested in preserving fertility
    • Frail older adults
    • Relapsed disease
    • As per ACR: anytime there is no RPGN

Maintenance:

  • Azathioprine OR continue Rituximab
  • Taper glucocorticoids
  • No maintenance if HD dependant patient x3 months with no extra-renal manifestations

When to use PLEX

  • Anti-GBM positive (“double positive”)
  • Consider if Cr>500
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28
Q

What immune complex vasculitis comes with low C3 and normal C4

A

Post-strep/infectious GN

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29
Q

Symptoms of Post-strep/ infecitous GN

A
  1. Starts 2-3 weeks post strep-throat, strep-cellulitis, chronic abcess, endocarditis etc…
  2. Presentation varies from microscopic hematuria to proliferative GN (red brown urine, proteinura, edema, HTN, AKI)
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30
Q

In the presence of low C3 and normal C4, what is required to increase the likelihood of a diagnosis of post-strep/infectious GN

A

+ASOT

+anti-DNAse B

*No biopsy unless considering other GN or course varies from usual trajectory

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31
Q

How is post-strep GN treated

A

Supportive care only

treat infection if present

resolves in 3-4 weeks

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32
Q

What immune complex vasculitis comes with normal C3 and low C4?

A

MPGN

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33
Q

Name the ethiologies of MPGN

A
  1. HCV
  2. Cryoglobulinemia
  3. infections
  4. complement dysregulation
  5. monoclonal gammopathies
  6. Autoimmune diseases
  7. TMA/HUS
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34
Q

How does MPGN usually manifest

A

Nephritic syndrome

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35
Q

What immune complex vasculitis presents with low C3 and low C4 (most common)

A

SLE

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36
Q

How do you diagnose MPGN

A

Biopsy

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37
Q

How is MPGN managed

A

By treating the underlying cause?

*If idiopathic then can consider immunosupression

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38
Q

How does SLE nephritis presents

A

An nephritic syndrome

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39
Q

How do you diagnose SLE nephritis

A

Renal Bx

elevated DsDNA suggestive

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40
Q

How is class III and IV lupus nephritis treated

A

Induction with steroids, cyclophosphamide or MMF

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41
Q

How is class V SLE nephritis treated

A

ACE/ARB for proteinuria

BP control

Statin

Hydroxychloroquine for all

*If progressive renal dysfunction:

  • Renal U/S, rule out renal vein thrombus.
  • Consider Repeat renal Bx (?concurrent class III/IV)
  • ? additional immunosuppression
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42
Q

What immune complex vasculitis presents with normal C3 and C4

A

IgA nephropathy

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43
Q

What conditions are associated with IgA nephropathy

A
  1. Caeliac disease
  2. HIV
  3. Cirrhosis
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44
Q

How does IgA nephropathy present

A

**Various presentations**

  • Microscopic hematuria
  • gross hematuria
  • proteinuria
  • RPGN or nephrotic syndrome

Flares with any infection

HSP: systemic IgA vasculitis with arthritis, purpura, GI symptoms

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45
Q

How is IgA nephropathy diagnosed

A

Renal biopsy if it will change management

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46
Q

How is IgA nephropathy treated

A
  • ACE/ARB if proteinuria >0.5g/day. Aim for <0.5-1g per day
  • Adequate BP control
  • *NEW KDIGO* Consider 6 mo steroids if high risk progressive CKD
    • Refractory proteinuria (>0.75-1 despite optimal medical therapy)

*Fish oil not in guidelines

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47
Q

What are the different categories of proteinuria

A
48
Q

What are the causes of nephrotic syndrome

A
  1. FSGS
  2. Minimal change
  3. Membranous nephropathy
  4. others
    1. Amyloid
    2. MGRS
    3. DM
49
Q

What are the secoondary causes of Minimal change disease

A
  1. Heme cancers (HL and leukemia)
  2. Drugs (NSAIDS, COX2i, Li)
  3. Allergy (bee stings)
  4. Infectious (rare, includes Tb)
50
Q

What are the secondary causes of FSGS

A
  1. Infectious
    1. HIV
    2. Parvo B19
    3. EBV
  2. Drugs
    1. Heroin
    2. Pamidronate
    3. Anabolic steroids
  3. Hyperfiltration
    1. Obesity
    2. Single kidney
    3. Reflux nephropathy
51
Q

What are the secondary causes of membranous nephropathy

A
  1. SLE
  2. Cancer
    1. Solid malignancies>heme malignancies (CLL)
  3. Infections
    1. HBV
    2. HCV
    3. Syphilis
    4. HIV
  4. Drugs
    1. NSAIDS
    2. Anti-TNF
    3. Gold
    4. Penicillamine
  5. Sarcoidosis
52
Q

What blood tests are associated with membranous nephropathy

A

Anti-PLA2R

THSD7A

53
Q

What cancer screening should be done in patients with membranous nephropathy

A

Based on patient caracteristics (age based + pretest probability)

54
Q

How is nephrotic syndrome managed

A
  • General care
    • Edema: Na restriction + loop diuretics
    • Hypercholesterolemia: Statins, healthy heart diet
    • Proteinuria: ACE, BP control
    • Thrombosis: consider full does anticoagulation with warfarin in primary diseases
  • Definitive management
    • Immunosupression in many cases
    • Treat underlying cause if secondary
  • Pearls
    • SMOKING CESSATION FOR ALL
    • Dietary Na<2g
    • Protein restriction if nephrotic range proteinuria
    • Target BP <120
    • Vaccinate: pneumococcal, shinrix, influenza, covid, hep b
    • Pre-immunosupression: TBST, hep serologies, HIV, strogyloides if endemic risk
    • On treatment: Contraception, gonadal protection, Bone health, TMP-SMX if high dose steroids, ritux or cyclo
55
Q

Which patients with nephrotic syndrome should be anticoagulated

A
  1. Albumin <20-25 AND 1 of:
    1. BMI >35
    2. Inherited thrombophilia
    3. NYHA 3-4
    4. Prolonged immobilization
    5. Proteinuria >10g/day
    6. Recent ortho/abdo surgery
  2. If high risk bleed: ASA instead
  3. DOACs not studied with this population, not ideal given low albumin
56
Q

What are the 3 causes of AIN

A
  1. Drugs (#1!)
  2. Infections
  3. Systemic illnesses (S’s: Sarcoid, sjogren, IgG4 disease)
57
Q

How does AIN present

A

Acute renal failure, sometimes with fever + rash

1 week to weeks/months after exposure to…

Hematuria, non-nephrotic range proteinuria

Pyuria and WBC casts(not always)

increased blood or urine eosinophils

58
Q

What drugs most commonly cause AIN

A
  1. Anti-inflamatories: NSAIDS, COX-2 inhibitors
  2. Anti-biotics: PNC, cephalosporins, sulfonamides, rifampin, cipro, septra
  3. Anti-gout: Allopurinol
  4. Anti-acid: PPI
  5. Anti-edema: loop diuretics, thiazides
  6. immunotherapy
59
Q

How is AIN treated

A

Removal of offending agent

Bx if severe renal failure/HD

Consider glucocorticoids empirically in select cases (still should get Bx)

60
Q

What are the cutoffs for the KDigo criteria for CKD and proteinuria

A
61
Q

When should Statins be started in CKD and what LDL levels should be targetted?

A
  • Adults aged over 50 not on HD:
    • If GFR<60 OR ACR>3, start statin
    • Target LDL<2, non-HLD<2.6 or apoB<0.8
  • HD patients
    • Don’t stop the statin if they are already on it
    • Don’t start a statin if they are not on it
62
Q

What are the CKD targets for the following biochem tests:

  • K
  • HCO3
  • PO4
  • Ca
  • PTH
  • Hb
  • Tsat
  • ferritin
A
  • K <5
  • HCO3>22
  • PO4 and Ca towards normal range
  • PTH: unknown target pre HD. Once on HD 2-9x ULN
  • Hb:95-115
  • TSat: >30%
  • Ferritin>500
63
Q

How is hypocalcemia managed in CKD

A

Calcitriol (1.25 Vitamin D)

64
Q

How is anemia managed in CKD patients

A
  1. Rule out other causes (i.e. bleeding)
  2. Iron studies, replete with monoferric, venofer or PO iron if not at target
  3. If Hb still <100: EPO target Hb no higher than 115

*Caution with EPO in patients with active Ca, previous stroke, uncontrolled BP

65
Q

Which foods are rich in potassium

A
  1. Fruits
    1. Oranges
    2. Tropical fruit (mango, papaya, pomegranate, kiwi, melons)
  2. Vegetables
    1. Avocado
    2. Tomatoes
    3. potatoes
    4. Beans
    5. Leafy green vegetables
  3. Others
    1. Nuts/seeds
    2. milk
66
Q

Which foods are high in phosphate?

A
  1. Dairy
    1. Cheese
    2. milk
  2. Protein
    1. Shellfish
    2. liver
    3. deli meats
67
Q

How is hyperphosphatemia managed in CKD

A

Phosphate binders

First line are calcium containing due to cost

Should “look into” getting patients on non calcium containing phosphate binders

68
Q

How is a PTH > 9x ULN managed

A
  1. IF Ca and PO4 are not high: Give calcitriol
  2. OTHERWISE: Cinecalcet
  3. Surgical parathyroidectomy in select patients
69
Q

How is osteoporosis/CKD-MBD managed

A
  • CKD 1-2: As per general population
  • CKD 3+:
    • PTH normal range: treat as general population
    • PTH elevated
      • Optimise BMD
      • Consider anti resorptive medications if GFR permits (usually >30 in bisphosphonates)
        • Risk of severe hypocalcemia with bisphosphonates or denosumab
70
Q

Name symptoms of uremia

A
  • Anorexia, Weight loss, appetite loss
  • Metallic taste
  • Pericarditis
  • Peripheral neuropathy
  • Bleeding (Plt dysfunction)
  • CNS: mental status change, seizures, mood disorder
  • Amennhorea, decreased libido, erectile dysfunction
  • Nocturia, restless legs (IDA)
  • pruritus
71
Q

Describe the staging of diabetic nephropathy

A
72
Q

What is recomended for screening of diabetic nephropathy

A

Screen T1DM 5 years after Diagnosis and T2DM at the time of diagnosis.

Then yearly screening

73
Q

How should ACE and ARB be managed in DM nephropathy

A

Check Cr and K at baseline. 1-2 weeks after Rx initiation, after initiation/titration of therapy and during medical illness

74
Q

What are the non-pharmacological therapies for DM nephropathy

A

Na<2g/day

Protein 0.8 g/kg/day

Exercise 150min/week

75
Q

What is the pharmacological management of DMT2 in the context of CKD

A
76
Q

How do you differentiate acute from chronic respiratory acidosis and alkalosis

A
  • Resp acidosis:
    • Acute 10 co2 1 bic
    • Chronic 10 co2 3-4 bic
  • Resp alkalosis
    • Acute 10 co2 2 bic
    • chronic 10 co2 5 bic
77
Q

What is the AG correction for hypoalbuminemia

A

For every drop in 10 in albumin, add 2.5 to AG

78
Q

List the causes of an increased osmolar gap with or without AG increase

A
79
Q

How are type I, II and IV RTAs differentiated.Explain the differences at the following levels:

  • Location of the problem
  • HCO3 range
  • K Range
  • Urine PH
  • Other possible findings
A

Other differentiating factors:

  • Type II: hypophosphatemia, phosphaturia, glucosuria, hypouricemia
  • Type I: Stones
  • Urine pH: High in type I, low in type II
80
Q

What are the causes of secondary type I RTA

A
  • CTD (Sjogrens, RA, SLE)
  • Hypercalciuria
  • Drugs (ifosphamide, etc…)
81
Q

What causes secondary type II RTA

A
  • Fanconi’s (children)
  • Myeloma
  • Acetazolamide
  • Tenofovir
82
Q

What causes secondary type IV RTA

A
  • Drugs
    • Aldosterone antagonists
    • RAAS blockers
    • Heparin
    • calcineurin inhibitors
  • Adrenal insufficiency
  • DM​​
83
Q

How is type I RTA treated

A

Bicarb + K citrate if low K

84
Q

How is type II RTA treated

A

Bicarb + K citrate

85
Q

How is type IV RTA treated

A

Low BP: Florinef

HTN: Thiazide

86
Q

What is the formula to calculate the volume of hypertonic saline infusate to give?

A
87
Q

What medications can cause hyponatremia via innapropriate ADH secretion

A
  • TCAs
  • SSRIs
  • Carbamazepine
  • ecstasy/MDMA
  • thiazides
88
Q

Name causes of nephrogenic DI

A
  1. Lithium Hx/Use
  2. Hypercalcemia
  3. Hypokalemia
  4. Relief of post-renal obstruction
  5. Amyloidosis (rare)
  6. Hereditary/ gene mutations
89
Q

Name causes of hyperkalemia

A
  1. Increased intake
    1. Supplement
    2. Transfusions
  2. Decreased excretion
    1. Decreased tubular flow
      1. CKD
      2. Volume depletion
    2. Drugs
      1. ACE/ARB
      2. NSAIDS
      3. MRAs
    3. Hypoaldosteronism
      1. Adrenal insufficiency
      2. Type 4 RTA
  3. Shifting
    1. Cell lysis:
      1. TLS
      2. Rhabdo
      3. burns
    2. Metabolic
      1. Acidosis
      2. low insulin
    3. Hyperosmolality
      1. increased glucose
      2. Increased manitol
    4. Familial hyperkalemic periodic paralysis
  4. Facticious
    1. Fist clenching/tourniquet
    2. Hypercellular blood
    3. Hemolyzed sample
90
Q

What are causes of hypokalemia

A
  1. Decreased intake
  2. Hypomagnesemia
  3. Shifting
    1. Endocrine
      1. increased insulin
      2. thyrotoxic periodic paralysis
    2. Stress
      1. Increased catecholamines
    3. Acid/base
      1. Metabolic alkalosis
    4. EtOH withdrawl
    5. Hypothermia
    6. Rx
      1. Amphetamines
      2. Antipsychotics
91
Q

How do you workup chronic hypokalemia

A

See slide 138-140

92
Q

Describe the Bosniak classification

A
  • Bosniak 1 and 2
    • Simple cysts with thin walls
    • no (1) or fine (2) calcifications
    • no (1) or thin (2) septae
    • no enhancement
  • Bosniak 2F
    • Smooth minimally thickened walls
    • May have multiple septae but smooth without contrast enhancement
    • F for follow up
  • Bosniak 3
    • One or more enhancing thick or irregular walls or septa
  • Bosniak 4
    • Like bosniak 3 but with solid enhancing nodule
93
Q

What imaging modality is used to determine the bosniak score

A

CT

Can also be commented on based on U/S

94
Q

Describe the management of renal cysts based on the bosniak score

A
  • Bosniak 1-2
    • no need to follow up
  • Bosniak 2F
    • F for follow-up
  • Bosniak 3-4
    • nephrectomy
    • surveillance or perc biopsy and possible thermal ablation if not surgical candidate
95
Q

How do you manage a solid renal mass

A
  • <1CM
    • active surveillance
  • >1 cm
    • If scan shows clear angiomyolipoma, no further workup
    • Otherwise
      1. Check for mets
      2. If life expectancy > 5 years: nephrectomy
      3. If life expectancy < 5 years or not fit for surgery: Perc biopsy, and active surveillance. Possible thermal ablation
96
Q

Name common symptoms of ADPKD

A
  1. HTN
  2. Pain (most common Sx)
    1. ​Abdo pain common in cyst rupture
  3. Hematuria (cyst rupture), proteinuria
  4. Stones – uric acid, calcium oxalate
  5. UTI – 4 weeks ABx for infected cyst !!
  6. Concentrating deficit – thirst, polydypsia, nocturia
  7. Erythrocytosis– increased EPO levels
  8. Extra-renal manifestations
    1. Liver cysts
    2. diverticuli
    3. cerebral aneurysms
    4. Pancreatic cysts
    5. Mitral valve prolapse
    6. AI
97
Q

How is ADPKD screened and diagnosed

A
  • Diagnosis done by family history and imaging
  • If known family history, do an U/S
  • if no family Hx: US, MRI, CT
  • ALL patients need a baseline total kidney volume assessment : MRI or CT
  • Follow-up imaging no more than once per year
98
Q

How is ADPKD managed

A
  1. Sodium restriction <2g/day
  2. High fluid intake
  3. If age 18-50 and GFR>60 and no significant cardiac comorbidities, target BP<110/75
  4. Tolvaptans for specific patients
99
Q

When should patients be screened for hyperaldosteronism?

A
  1. Hypertension plus one of the following
    1. Unexplained spontaneous hypokalemia (<3.5) or marked diuretic related hypokalemia (<3)
    2. HTN resistant to 3 drugs
    3. Incidental adrenal adenoma
100
Q

How do you screen for hyperaldosteronism

How is it diagnosed if the screening test is positive

A
  • Plasma aldosterone level and either plasma renin activity or plasma renin concentration
    • Do not use plasma renin concentration in patients on OCP (false positive)
    • Drugs that interfere:
      • MRA>ACE/ARB>BB,CCB
        • Hold 4 weeks prior to testing
      • alpha blockers, non-DHP CCB and hydralazine don’t interfere
  • If screening test positive do either:
    • Saline loading test
    • Captopril suppression test
    • Plasma aldosterone to renin ratio
101
Q

How is a saline loading test performed (for hyperaldosteronism)

A

Give 2L NS over 4hrs then measure plasma aldosteronism. Abnormal if over 280 pmol/l

102
Q

What is an abnormal plasma aldosterone to renin ratio

A

>1400 pmol/L/ng/ml/hr with plasma aldosterone >440

103
Q

Who should be screened for Pheochromocytoma?

A
  1. Paroxismal, unexplained, labile and/or severe sustained HTN refractory to usual therapy
  2. HTN + Symptoms of cathecolamine excess
  3. HTN triggered by beta blockers, MAO-Is, surgery, anesthesia, micturition
  4. Incidental adrenal adenoma
  5. Presence of hereditary causes
    1. V-H-L
    2. MEN 2A or 2B
    3. Neurofibromatosis type 1
104
Q

How do you screen for pheochromocytoma

A
  • 24hrs urine metanephrines and cathecolamines (with Cr to ensure proper collection)
  • can consider plasma free metanephrines and free normetanephrines
  • DO NOT DO URINARY VMA
105
Q

What are the different types of kidney stones and how are they differentiated on imaging and urine pH

What diseases are associated with each

A
106
Q

How are recurrent calcium oxalate stones prevented

A
  1. Decrease Na and meat intake
  2. Oxalate restriction (limit vitamin C)
  3. Thiazides (if no hypercalcemia)
  4. do not limit calcium intake
107
Q

How are recurrent calcium phosphate stones prevented

A
  1. Decrease sodium and meat intake
  2. Thiazides
108
Q

How are recurrent uric acid renal stones prevented

A
  1. Urine alkalanization (K citrate)
  2. Allopurinol
109
Q

How are recurrent struvite stones prevented

A

By treating the UTI

110
Q

How are recurrent cystine stones prevented

A

Urine alkalinization

111
Q

How can contrast induced nephropathy be prevented?

A

Nothing effective

By convention, hold metformin, RAS blockade, diuretics NSAIDS and other nephrotoxins. Ensure euvolemia

112
Q

How can cholesterol emboli syndrome be prevented

A

It can’t

113
Q

How does the timing in contrast enduced nephropathy vary from that of cholesterol emboli syndrome

A
  1. CIN
    1. 1-3 days post contrast load
    2. non oliguric
    3. most resolve within 1-2 weeks
  2. CES
    1. Subacute stepwise decline over weeks
    2. Early on + urine eosinophils, elevated ESR, peripheral eosinophilia, Decreased C3/C4
114
Q

Name the cutaneous manifestations of cholesterol emboli syndrome

A

Livedo reticularis

Blue toes

115
Q

What are the most common cause of AKI in renal transplant patients

A
  1. Acute rejection (***always suspect***)
    1. Varying degree of proteinuria, hematuria
    2. Bx required for diagnosis
  2. Meds (cyclosporine, tacrolimus)
    1. Reversible
    2. Bland sediment, no blood or protein
  3. Infection
    1. Bacterial-anytime, BK virus-late
    2. WBC in urine
    3. Mild proteinuria/hematuria
    4. Pain over graft if pyelo
  4. Renal artery/vein thrombosis
    1. Usually early post-op
    2. Get urgent US
  5. Hydronephrosis
  6. Recurrence of primary disease
  7. PTLD
  8. Other causes of AKI in native kidneys
116
Q

What are the contraindications for renal biopsy

A
  1. Uncontrolled severe hypertension
    1. Typically can control with BP meds
  2. Solitary kidney
  3. Hydronephrosis
  4. Active pyelonephritis
  5. Small hypoechoic kidneys
  6. Bleeding disorders
    1. HOLD ASA 5-7 days pre Bx unless fresh stents
  7. Pregnancy
  8. severe anemia or thrombocytopenia (plt <80-100)
117
Q
A

RCPSC (14 decks)

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