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CKD Flashcards

1
Q

What is the evidence for lipid therapy in non-dialysis CKD patients?

In dialysis patients?

A
  1. CKD-ND:
    1. Secondary prevention: yes
    2. Primary prevention: if other CVD risk factors (eg. DM, HTN, smoking, etc.) (or if 10-yr predicted risk of major CVD >7.5-10%)
    3. SHARP trial: LDL-lowering therapy with simvastatin and ezetimibe reduced atherosclerotic events in CKD pt’s (mainly ischemic stroke and arterial revasc procedures)
  2. CKD-D:
    1. No evidence. 4D and AURORA trials showed NO cardiovasc benefit in dialysis patients.SHARP trial showed benefit in combination of nondialysis + dialysis but not in dialysis subgroup (though not powered for this).
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2
Q

DM meds and GFR cut-off

A
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3
Q

What did the SHARP trial show?

A

LDL-lowering therapy with simvastatin and ezetimibe reduced atherosclerotic events in CKD-ND pt’s (mainly ischemic stroke and arterial revasc procedures)

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4
Q

What did the 4D and AURORA trials show?

A

4D and AURORA trials showed NO cardiovasc benefit in dialysis patients.SHARP trial showed benefit in combination of nondialysis + dialysis but not in dialysis subgroup (though not powered for this).

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5
Q

Indications for parathyroidectomy

A
  • Refractory hypercalcemia and hyperphosphatemia
  • Symptoms - bone pain, severe pruritus, myopathy
    • If PTH <800, consider bone biopsy to r/o adynamic bone disease b/c that will worsen post-parathyroidectomy
  • Calciphylaxis
  • Fractures
  • Pre-transplant
  • PTH >1000 refractory to medical therapy, even if asymptomatic (may reduce morality, CV risk, fracture risk)
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6
Q

Dialysis Hb target per CSN?

A

100-110

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7
Q

Anemia targets for Fe sat, ferritin?

A

Fe sats >=30%

Ferritin >500

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8
Q

ESA hyporesponsiveness causes

A
  1. Fe deficiency
  2. Infection
  3. Inflammation
  4. HyperPTH
  5. Pure red cell aplasia (old ESAs)
  6. Hemolysis – blood loss
  7. Aluminum toxicity
  8. Underdialysis
  9. ACEi
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9
Q

Types of phosphate binders, pros and cons

A
  • Calcium based – effective and cheap, may be associated with vascular calcification, hypercalcemia, adynamic bone disease
  • Non-calcium based – can be used in hypercalcemia, expensive, reduce cholesterol, lowers LDL (sevelamer)
  • Iron – effective, iron load, may cause acid base abnormalities
  • Aluminum – effective, risk of deposition in bone resulting in anemia
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10
Q

4 situations where MDRD formula may not be accurate

A
  • Non-caucasian
  • Higher renal function levels (GFR > 60)
  • Muscular individuals
  • Children < 18y , and elderly
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11
Q

Disadvantages of MDRD

A
  1. Doesn’t account for muscle mass
  2. Doesn’t account for tubular secretion of creatinine
  3. Not reliable in non-steady state conditions
  4. Not reliable at extremes of age
  5. MDRD not as accurate as ckd-epi if gfr>60
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12
Q

3 endogenous factors that decrease vascular calcification

A

Fetuin A

Matrix GLA protein

Pyrophosphate

Osteoprotegrin

Klotho

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13
Q

Poor prognostic markers of diabetic nephropathy

A
  1. HTN/poor BP control
  2. High degree of proteinuria
  3. Poor glycemic control
  4. Race - African American, First Nations
  5. Obesity
  6. Smoking
  7. Age
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14
Q

4 classes of anti-proteinuric meds

A
  1. ACE/ARB
  2. SGLT2
  3. MRAs
  4. Non-dihydropirodine CCB
  5. Direct renin inhibitors - Aliskiren
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15
Q

What are three changes that occur in the parathyroid glands that occur during the decrease in GFR from 60 to 15 ml/min?

A
  • PTH gland hypertrophy
  • Downregulation of CaSR expression on parathyroid gland
  • Downregulation of Vitamin D receptor on parathyroid gland
  • Downregulation of Klotho-FGFR1 receptor complex on parathyoid gland
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16
Q

Side effects of cinacalcet

A

N/V/Abdo pain

Hypocalcemia

Hyperphosphatemia in pre-dialysis CKD (lower PTH in intact renal function leads to decreased renal wasting of phos)

Hypotension

Adynamic bone disease if excessive PTH suppression

17
Q

Long-term complications of acquired cystic kidney disease in HD patient?

A
  1. Malignant transformation, RCC (dialysis patients may be at increased risk)
  2. Cyst rupture and hemorrhage
  3. Cyst infection/abscess
  4. Erythrocytosis
18
Q

Cardiovascular benefits of treating anemia with EPO?

Other benefits?

A
  • LVH regression
  • Decreased exercised-induced myocardial ischemia
  • Improved cardiac output (anemia causes high cardiac output and HF)

Other benefits:

  • Improved symptoms
  • Improved QoL
  • Decreased transfusion requirements
  • Improved cognitive function
19
Q

Benefits for treating acidosis in CKD?

A

Decrease progression of CKD

Decrease bone buffering / improve bone health

Improve nutritional status (acidosis increase muscle breakdown)

20
Q

4 non-immune causes for progression of CKD

A
  1. Intraglomerular hypertension and glomerular hypertrophy
  2. Proteinuria
  3. Tubulointerstitial fibrosis
  4. Metabolic acidosis
  5. Smoking
  6. Dyslipidemia 4 (weak)
  7. Hyperuricemia
  8. Hyperphosphatemia
  9. HTN
21
Q

Contraindications to ACE

A

Angioedema

Pregnancy

AKI

22
Q

Consequences of hyperphosphatemia in HD patients

A
  1. Secondary hyperparathyroidism and metabolic bone disease (Increased bone turnover causes osteitic fibrosa cystica)
  2. Vascular and metastatic calcification and calciphylaxis (if associated with elevated calcium)
  3. Associated with increased mortality in dialysis patients
  4. Pruritis
23
Q

Post-op orders post-parathyroidectomy

A
  1. q6h labs - Ca, iCa, phos, Mg, Na, K
  2. Calcium carbonate 1200 mg TID in between meals
  3. Calcitriol 0.5 mcg po bid
  4. If iCa <1 or symptomatic hypocalcemia:
    1. 1-2 amps Ca gluconate IV
    2. Calcium glulconate 10% 100 mL in 1L NS (=900 mg elemental Ca, 1mg/mL), start at 50 mL/hr
  5. Increase dialysate Ca prn
  6. Replace phos and Mg as needed
  7. Expect hyperkalemia POD 1+2 (rebound), dialyze prn

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