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
2
Q
BP cuff measurements
A
width 40% of arm circumference
length 80-100% of arm circumference
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
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
5
Q
Who should be screened for renovascular HTN
A
2 or more of the following:
- Sudden onset or worsening HTN, age>55 or <30
- Abdominal bruit
- HTN resistant to 3 drugs
- Creatnine increase of >30% on ACEi or ARB
- Other atherosclerotic vascular diseases, Particularily in smokers or DLP
- Recurrent pulmonary edema associated with HTN surges
6
Q
What is the screening test for Renovascular hypertension (4 possible)
A
Doppler
Captopril renogram
MRA
CTA
7
Q
Who should be worked up for FMD related Renal artery stenosis
A
- Asymmetric kidneys (>1.5 cm difference)
- Abdominal bruit with no atherosclerotic risk factors
- Confirmed FMD in another vascular bed
- Family Hx of FMD
8
Q
How do you work up FMD
A
CTA or MRA
When confirmed, screen vasculature from head to pelvis with CTA or MRA
9
Q
What are the SPRINT inclusion criteria
A
SBP > 130, age >50 and 1 or more of:
- Clinical or subclinical CVD
- CKD: eGFR 20-59, proteinuria <1g/day – non diabetics
- 10 year CV risk > 15%
- Age > 75
10
Q
What are the SPRINT exclusion criteria
A
- DM
- Previous stroke
- GFR <20
- Proteinuria > 1g/day
- PKD
- Contraindications:
- Non-adherence
- Standing SBP<110
- secondary HTN
- Can’t measure BP accurately
- life-limiting illness
11
Q
What are the non-pharmacological interventions used in HTN
A
- Exercise: 30-60 min. Moderate intensity, dynamic, 4-7 days per week
- Weight: BMI 18.5-24.9 Waist circumference <102(M) <88 (F)
- Alcohol: Abstain OR reduce to <2drinks per day (prevention) and if >6 drinks a day, reducing to <2 can reduce BP
- Diet: DASH diet, Increase K intake if not high risk for hyperkalemia
- Salt: <5g/day Na
- Stress reduction: inc CBT and relaxation techniques
- Smoking cessation
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)
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
14
Q
Indications to CONSIDER stenting in RAS
A
- Uncontrolled HTN resistant to maximally tolerated pharmacotherapy
- Progressive renal function decline
- Acute pulmonary edema
15
Q
Firstline antihypertensives for isolated systolic hypertension
A
- Thiazide
- Long acting DHP-CCB
- ARB
16
Q
Firstline antihypertensive for diastolic hypertension
A
- Thiazide
- BB if <60
- ACE/ARB
- Long acting DHP-CCB
17
Q
Firstline antihypertensives for LVH
A
- Thiazide
- ACE/ARB
- Long-acting DHP-CCB
*Do not use vasodilators
**Avoid BB
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
19
Q
Firstline antihypertensive in CAD
A
- ACE/ARB
Then can add CCB or BB
ACE + CCB over ACE+thiazide
20
Q
Firstline antihypertensive in stable CAD
A
BB or CCB
21
Q
Firstline antihypertensive in recent MI
A
BB+ACE
22
Q
Firstline antihypertensive in EF<40%
A
ACE + BB
ARB in intolerante to ACE
Hydralazine + ISDN if can’t use ACE/ARB
23
Q
Second-line antihypertensive in EF<40%
A
MRA
24
Q
Treatment of anti-GBM
A
- Pulse steroids (6 months)
- Cyclophosphamide (2-3 months)
- PLEX (until titers no-longer detectible, usually 14 exchanges)
25
What vasculitidies are associated with Anti-MPO and anti-PR3 antibodies
26
What are the clinical features of ANCA associated vasculitides?
1. Constitutional symptoms
2. Arthralgias and rash
3. sinusitis, asthma, pulmonary hemorrhage
4. Nephritis
5. Mononeuritis multiplex
27
How are ANCA vasculitides treated
_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
28
What immune complex vasculitis comes with low C3 and normal C4
Post-strep/infectious GN
29
Symptoms of Post-strep/ infecitous GN
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)
30
In the presence of low C3 and normal C4, what is required to increase the likelihood of a diagnosis of post-strep/infectious GN
+ASOT
+anti-DNAse B
\*No biopsy unless considering other GN or course varies from usual trajectory
31
How is post-strep GN treated
Supportive care only
treat infection if present
resolves in 3-4 weeks
32
What immune complex vasculitis comes with _normal C3_ and _low C4?_
MPGN
33
Name the ethiologies of MPGN
1. **HCV**
2. **Cryoglobulinemia**
3. infections
4. complement dysregulation
5. monoclonal gammopathies
6. Autoimmune diseases
7. TMA/HUS
34
How does MPGN usually manifest
Nephritic syndrome
35
What immune complex vasculitis presents with _low C3_ and _low C4_ (most common)
SLE
36
How do you diagnose MPGN
Biopsy
37
How is MPGN managed
By treating the underlying cause?
\*If idiopathic then can consider immunosupression
38
How does SLE nephritis presents
An nephritic syndrome
39
How do you diagnose SLE nephritis
Renal Bx
elevated DsDNA suggestive
40
How is class III and IV lupus nephritis treated
Induction with steroids, cyclophosphamide or MMF
41
How is class V SLE nephritis treated
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
42
What immune complex vasculitis presents with normal C3 and C4
IgA nephropathy
43
What conditions are associated with IgA nephropathy
1. Caeliac disease
2. HIV
3. Cirrhosis
44
How does IgA nephropathy present
\*\*Various presentations\*\*
* Microscopic hematuria
* gross hematuria
* proteinuria
* RPGN or nephrotic syndrome
Flares with any infection
HSP: systemic IgA vasculitis with arthritis, purpura, GI symptoms
45
How is IgA nephropathy diagnosed
Renal biopsy if it will change management
46
How is IgA nephropathy treated
* 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
47
What are the different categories of proteinuria
48
What are the causes of nephrotic syndrome
1. FSGS
2. Minimal change
3. Membranous nephropathy
4. others
1. Amyloid
2. MGRS
3. DM
49
What are the secoondary causes of Minimal change disease
1. Heme cancers (**HL** and leukemia)
2. Drugs (**NSAIDS**, **COX2i**, Li)
3. Allergy (bee stings)
4. Infectious (rare, includes Tb)
50
What are the secondary causes of FSGS
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
What are the secondary causes of membranous nephropathy
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
What blood tests are associated with membranous nephropathy
Anti-PLA2R
THSD7A
53
What cancer screening should be done in patients with membranous nephropathy
Based on patient caracteristics (age based + pretest probability)
54
How is nephrotic syndrome managed
* 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
Which patients with nephrotic syndrome should be anticoagulated
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
What are the 3 causes of AIN
1. Drugs (#1!)
2. Infections
3. Systemic illnesses (S's: Sarcoid, sjogren, IgG4 disease)
57
How does AIN present
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
What drugs most commonly cause AIN
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
How is AIN treated
Removal of offending agent
Bx if severe renal failure/HD
Consider glucocorticoids empirically in select cases (still should get Bx)
60
What are the cutoffs for the KDigo criteria for CKD and proteinuria
61
When should Statins be started in CKD and what LDL levels should be targetted?
* 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
What are the CKD targets for the following biochem tests:
* K
* HCO3
* PO4
* Ca
* PTH
* Hb
* Tsat
* ferritin
* 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
How is hypocalcemia managed in CKD
Calcitriol (1.25 Vitamin D)
64
How is anemia managed in CKD patients
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
Which foods are rich in potassium
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
Which foods are high in phosphate?
1. Dairy
1. **Cheese**
2. milk
2. Protein
1. Shellfish
2. liver
3. **deli meats**
67
How is hyperphosphatemia managed in CKD
Phosphate binders
First line are calcium containing due to cost
Should "look into" getting patients on non calcium containing phosphate binders
68
How is a PTH \> 9x ULN managed
1. IF Ca and PO4 are not high: Give calcitriol
2. OTHERWISE: Cinecalcet
3. Surgical parathyroidectomy in select patients
69
How is osteoporosis/CKD-MBD managed
* 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
Name symptoms of uremia
* 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
Describe the staging of diabetic nephropathy
72
What is recomended for screening of diabetic nephropathy
Screen T1DM 5 years after Diagnosis and T2DM at the time of diagnosis.
Then yearly screening
73
How should ACE and ARB be managed in DM nephropathy
Check Cr and K at baseline. 1-2 weeks after Rx initiation, after initiation/titration of therapy and during medical illness
74
What are the non-pharmacological therapies for DM nephropathy
Na\<2g/day
Protein 0.8 g/kg/day
Exercise 150min/week
75
What is the pharmacological management of DMT2 in the context of CKD
76
How do you differentiate acute from chronic respiratory acidosis and alkalosis
* 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
What is the AG correction for hypoalbuminemia
For every drop in 10 in albumin, add 2.5 to AG
78
List the causes of an increased osmolar gap with or without AG increase
79
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
Other differentiating factors:
* Type II: hypophosphatemia, phosphaturia, glucosuria, hypouricemia
* Type I: Stones
* Urine pH: High in type I, low in type II
80
What are the causes of secondary type I RTA
* CTD (**Sjogrens,** RA, SLE)
* Hypercalciuria
* Drugs (ifosphamide, etc...)
81
What causes secondary type II RTA
* Fanconi's (children)
* **Myeloma**
* Acetazolamide
* Tenofovir
82
What causes secondary type IV RTA
* Drugs
* Aldosterone antagonists
* RAAS blockers
* **Heparin**
* calcineurin inhibitors
* Adrenal insufficiency
* **DM**
83
How is type I RTA treated
Bicarb + K citrate if low K
84
How is type II RTA treated
Bicarb + K citrate
85
How is type IV RTA treated
Low BP: Florinef
HTN: Thiazide
86
What is the formula to calculate the volume of hypertonic saline infusate to give?
87
What medications can cause hyponatremia via innapropriate ADH secretion
* TCAs
* SSRIs
* **Carbamazepine**
* ecstasy/MDMA
* thiazides
88
Name causes of nephrogenic DI
1. **Lithium Hx/Use**
2. Hypercalcemia
3. Hypokalemia
4. Relief of post-renal obstruction
5. Amyloidosis (rare)
6. Hereditary/ gene mutations
89
Name causes of hyperkalemia
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
What are causes of hypokalemia
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
How do you workup chronic hypokalemia
See slide 138-140
92
Describe the Bosniak classification
* 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
What imaging modality is used to determine the bosniak score
CT
Can also be commented on based on U/S
94
Describe the management of renal cysts based on the bosniak score
* 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
How do you manage a solid renal mass
* \<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
Name common symptoms of ADPKD
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
How is ADPKD screened and diagnosed
* 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
How is ADPKD managed
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
When should patients be screened for hyperaldosteronism?
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
How do you screen for hyperaldosteronism
How is it diagnosed if the screening test is positive
* 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
How is a saline loading test performed (for hyperaldosteronism)
Give 2L NS over 4hrs then measure plasma aldosteronism. Abnormal if over 280 pmol/l
102
What is an abnormal plasma aldosterone to renin ratio
\>1400 pmol/L/ng/ml/hr with plasma aldosterone \>440
103
Who should be screened for Pheochromocytoma?
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
How do you screen for pheochromocytoma
* 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
What are the different types of kidney stones and how are they differentiated on imaging and urine pH
What diseases are associated with each
106
How are recurrent calcium oxalate stones prevented
1. Decrease Na and meat intake
2. Oxalate restriction (limit vitamin C)
3. Thiazides (if no hypercalcemia)
4. do not limit calcium intake
107
How are recurrent calcium phosphate stones prevented
1. Decrease sodium and meat intake
2. Thiazides
108
How are recurrent uric acid renal stones prevented
1. Urine alkalanization (K citrate)
2. Allopurinol
109
How are recurrent struvite stones prevented
By treating the UTI
110
How are recurrent cystine stones prevented
Urine alkalinization
111
How can contrast induced nephropathy be prevented?
Nothing effective
By convention, hold metformin, RAS blockade, diuretics NSAIDS and other nephrotoxins. Ensure euvolemia
112
How can cholesterol emboli syndrome be prevented
It can't
113
How does the timing in contrast enduced nephropathy vary from that of cholesterol emboli syndrome
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
Name the cutaneous manifestations of cholesterol emboli syndrome
Livedo reticularis
Blue toes
115
What are the most common cause of AKI in renal transplant patients
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
What are the contraindications for renal biopsy
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
