CKD (Specht) Flashcards

1
Q

CKD definitions

A
  • Any chronic change in kidney disease
    • structure
    • function
  • CKD is
    • permanent
    • progressive

*can’t recover, but can compensate for a period of time

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2
Q

CKD DX

A
  • Dysfunction
    • GFR
    • electrolytes
    • acid base
    • hormones
    • biomarkers
  • Damage / dz
    • appearance
    • biomarkers
    • pathology
  • Secondary / compensatory change
    • renal: inc PTH
    • Hypertension
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3
Q

Common lab values

A
  • Serum biochem
    • BUN, Cr
    • Phos, K+, TCO2, Alb
    • tCa / iCa++, Na+, Cl-
  • Urinalysis
    • USG, Protein, Sediment
  • CBC
    • Hct, other
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4
Q

GFR estimation

A
  • Creatinine, BUN, SDMA follow similar curve
    • normal GFR: flat curve, then steep line
  • Suggest use of stricter limits on acceptable creatinine levels
  • SDMA
    • better for animals with lack of muscle mass, or muscle wasting
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5
Q

Other informations

A
  • Blood pressure
  • urine protein to creatinine (UPC)
  • Imaging (AXR, AUS)
  • Urine culture
  • other
    • specific infectious dz
    • PTH/iCa++
    • Aspirates/biopsies
    • Others
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6
Q

Underlying dz

A
  • > 50% cases are idiopathic
    • age-related, accumulation of injuries
  • Specific causes
    • toxicity
    • infection
    • cancer
    • obstruction
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7
Q

CKD vs Pre-renal azotemia vs AKI

A
  • Pre-renal azotemia
    • sig dehydration/hypovolemia
    • low cardiac output
  • AKI
    • very important to recognize
      • diagnostic, prognostic and therapeutic differences
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8
Q

IRIS staging

A
  • based on creatinine
  • subcategories
    • proteinuria
    • blood pressure
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9
Q

Why use IRIS staging

A
  • Consistent records
  • Client communication
    • ‘expert’ support for your recommendations
  • Earlier recognition and response to CKD….?
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10
Q

IRIS staging

Key points

A
  • patient must be at a stable point in disease
    • > 2-3 weeks
  • Helps with communication and studies
  • Basis for published treatment recommendations
    • evidence regarding appropriate treatments
  • Be careful making prognostic statements
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11
Q

CKD General Management strategies

A
  • no cure
  • look for/treat underlying dz
  • discontinue nephrotoxic meds
  • pay attention to dose and frequency of medications that are eliminated by kidneys
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12
Q

CKD: specific management strategies

A
  • Therapy should be tailored to specific patients
  • secondary problems
    • Hyperphosphatemia
    • Systemic hypertension
    • Proteinuria
    • hypo/hyper kalemia
    • metabolic acidosis
    • anemia
    • nausea, vomiting
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13
Q

Diet/nutrition

A
  • renal diets (good evidence of significant survival)
    • reduced phospohorus (protein)
    • omega-3 FA
    • vitamins
  • Recommend for stage 2 dz or higher
  • Calories are important, don’t force feed
    • mirtazapine: apppetite stimulant
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14
Q

Fluids

A
  • almost universal recommendation to maintain normal volume and hydration
    • support GFR and uremic toxin clearance
    • Prevent clinical signs
    • minimize progression
  • For uremic crisis - IV fluids
    • Replacement + maintenance + losses
  • For stable CRF
    • fresh drinking water avail
    • serial measurements of body weight
    • extra fluids PRN SQ or E-tube

*not extra but enough fluids to keep up with losses

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15
Q

Control of serum phosphorus conc

A
  • Minimize progression
  • prevent tissue mineralization
  • avoid secondary hyperparathyroidism
  • variable recommendations
    • target value
    • method
      • renal diet
      • fluid support
      • phosphate binders
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16
Q

Phosphate binders

A
  • Aluminum based: tastes yucky
    • Effective, inexpensive
    • toxicity
      • subtle neuro to seizures
    • complexed with
      • hydroxide, oxide, carbonate
  • Calcium based
    • a little more expensive
    • may help minimize secondary inc PTH
    • toxicity
      • hypercalcemia: inc risk of mineralization
    • complexed with
      • acetate, citrate, carbonate
  • Others
    • sevelamer
    • lanthanum
    • epakatin

*may be synergistic

17
Q

Control of hypertension

A
  • important to control
  • difficulties
    • ‘white coat effect’
    • where / how to measure
  • monitor and treat with hypertensive agents if
    • dogs repeatedly > 160-170
    • cats repeatedly > 170
    • evidence of end-organ damage
18
Q

Control hypertension dogs

stepwise

A
  • Na restriction
  • ACEi at standard doses
  • Double dose of ACEi
  • ACEi& CCB
  • ACEi, CCB and hydralazine

*small inc in Cr is ok trade-off

19
Q

Control hypertension cats

stepwise

A
  • Na restriction
  • CCB at standard doses
  • Inc CCB dosing
  • CCB and ACEi

*ensuing small inc in Cr is ok trade-off

20
Q

Control of proteinuria

A
  • Increasing awareness and detection of proteinuria
  • Goals
    • minimize progression, improve survival
  • strong evidence for effectiveness
  • to monitor effectively requires UPC (urine protein:Cr ratio)
  • Recomendations
    • monitor UPC
    • investigate further and treat if
      • UPC > 0.5-1.0
    • Typically use ACEi
      • Enalapril
      • benzapril
21
Q

Acid-base balance

A
  • Often overlooked
  • threshold values
    • pH < 7.25
    • HCO3- = 16
  • target values
    • pH >/= 7.3
    • HCO3- >/= 17
  • Usually use K+ citrate unless hyperkalemic
  • IRIS stage 2+ => dogs >/= 18; cats >/= 16

Total CO2 can approx bicarb measurement

22
Q

Serum potassium conc

A
  • inc or dec potassium potentially detrimental
  • recommendations
    • supplement when
      • hypokalemic (with or without clinical signs)
      • repeatedly in the low end of dose range
    • if acidotic, Specht uses K+ citrate
    • if not acidotic, Specht uses K+ gluconate
23
Q

Acid blockers

(GI issues)

A
  • used to minimize gastric hyperacidity
  • evidence is anecdotal
    • gastrin metabolized and excreted by kidneys
  • recommendation
    • PPI (or H2 blockers)
      • when clinical signs, lab evidence of bleeding
      • in most cases of CRF with Creatinine > 3 mg/dL
24
Q

Hematocrit

anemia

A
  • anemia
    • predominantly due to dec EPO sensitivity
    • GI loss, dec RBC life span, vit def, iron def
  • Recommendations
    • try to get reticulocyte count
      • to prove it is non-regenerative
    • if non-regenerative with normal morph and Hct < 20%
      • consider darbopoeitin (1 vial is 100$ weekly admin)
          • iron
        • +/- B12

* There is a human erythropoeitin that may induce a reactivity to animals own cells making them transfusion dependent

25
Q

Calcitriol

A
  • Goal: normalization of PTH levels
  • Good evidence for positive effect
    • definite reduction in PTH for both dogs and cats
  • Controls secondary renal hyperparathyroidism
  • Requires exceptionally close and frequent monitoring
    • PTH, iCa++, Phosphorus
  • potential hazards / complications
    • dose response variability
    • hypercalcemia
    • mineralization
      • phosphorus must be , 6.0 mg/dL before starting
26
Q

Azodyl

A
  • Probiotic: ‘enteral dialysis’
  • little evidence that reduction in BUN and some Cr affects GFR
  • Specht doesn’t really use yet
27
Q

Mainstays of CKD treatment

A
  1. Diet
  2. Maintain hydration
  3. Limit protein
  4. Blood pressure control
28
Q

Conclusions

A
  • Lots of treatment options, many with limited evidence regarding effectiveness
  • Treatment should be individualized
  • CKD is dynamic, requires intense monitoring and management