CKD Flashcards
The different ways to name CKD
CRI = chronic renal insufficiency
Progressive kidney disease
Nephropathy
CKD definition
Abnormalities of kidney structure or function, present for > 3 months, with implications for health
Markers of kidney disease
1 or more of the following:
Albuminuria
Urine sediment abnormalities (casts)
Electrolyte and other abnormalities d/t tubular disorders
Abnormalities detected by histology (biopsy)
Structural abnormalities detected by imaging (polycystic kidney disease)
Hx of kidney transplant
CKD GFR
< 60
CKD susceptibility factors
Older age Decreased kidney mass Low birth weight FH of CKD US ethnic minority status Low income or education
CKD initiation factors
DM
HTN
Glomerulonephritis
What is the main structural marker for kidney damage?
Proteinuria
Albumin excretion rate (AER) classifications
Normal-Mildly increased: < 30
Moderately increased: 30-300
Severely increased: > 300
Protein Excretion Rate (PER) classifications
Normal-Mildly increased: < 150
Moderately increased: 150-500
Severely increased: > 50
Albumin-to-Creatinine Ratio (ACR) classifications
Normal-Mildly increased: < 30
Moderately increased: 30-300
Severely increased: > 300
Protein-to-Creatinine Ratio (PCR) classifications
Normal-Mildly increased: < 150
Moderately increased: 150-500
Severely increased: > 500
Protein reagent strip classifications
Normal-Mildly increased: negative to trace
Moderately increased: Trace to +
Severely increased: + to greater
Ways to assess renal disease
Proteinuria SCr (BMP) GFR BP Sx CBC Urinalysis Imaging Cystatin C
What assessments must be screened annually for high risk patients?
SCr GFR BP Sx CBC Urinalysis
Cystatin C
Low molecular weight protein
Freely filtered by glomerulus
Completely reabsorbed by tubules then catabolized
Not affected by age, gender, race or muscle mass
CKD G1
GFR >/= 90
“Normal or high”
No sx
CKD G2
GFR 60 - 89
“Mildly decreased”
No sx
CKD G3
G3a: GFR 45-59 "Mild-moderately decreased" G3b: GFR 30-44 "Moderately-severely decreased" Both sx: generally asx; HTN, anemia
CKD G4
GFR 15-29
“Severely decreased”
Sx: Nocturia, fatigue, cold intolerance, anorexia, hyperphosphatemia, hypocalcemia, metabolic acidosis
CKD G5
GFR < 15 (or dialysis)
“Kidney failure”
Sx: Malaise, lack of energy, pruritus, N/V, myoclonus, asterixis, seizures
Albuminuria A1
AER/ACR < 30
“Normal-Mildly increased”
Albuminuria A2
AER/ACR 30-300
“Moderately increased”
Albuminuria A3
AER/ACR > 300
“Severely increased”
Progression of CKD
Small fluctuations in GFR are common
Requires multiple SCr and eGFR measurements over time
Defined as 1 or more of the following:
-Decline in GFR category with a 25% or greater drop in eGFR from baseline
-Sustained decline in eGFR of more than 5
Desired outcomes of renal disease
Reverse or delay progression of renal injury
Reduce incidence of stage 5 CKD
Specifically for stage 5 on HD
Nutritional management of renal disease
Dietary protein restriction Sodium restriction Smoking cessation Exercise Wt loss
Dietary protein restriction in renal disease
0.8 g/kg/d
Only for patients with GFR < 30 (G4 and G5)
Sodium restriction in renal disease
< 2 g/d
Exercise in renal disease
30 minutes for 5 times a week
Weight loss in renal disease
BMI between 20-25
Pharmacologic therapy
Glycemic control
HTN
Glycemic goals in renal disease
A1c: 7.0%
Pre-prandial: 70-130
Post-prandial: < 180
HTN goals in renal disease
= 140/90 (DM or non-DM w/ACR < 30)
= 130/80 (DM or non-DM w/ACR > 30)
HTN DOC in renal dz
ACR > 30: ACE/ARB
DM w/ACR > 30: ACE/ARB
Any pt w/ACR < 30: diuretic
Smoking cessation in renal dz
May limit progression of dz
Complications of CKD
Fluid and electrolyte disturbances Metabolic acidosis Anemia Decreased calcium and Mineral and Bone Disorder Renal osteodystrophy
Treatment of sodium and fluid balance in renal disease
No-added salt diet
Fluid restriction (reserve for dialysis pts between sessions)
Diuretics (Loop +/- thiazide)
Sodium and fluid balance goal
Serum Na between 135-145 w/o volume overload or depletion
Sodium and fluid balance in CKD
Decreased ability to concentrate or dilute urine
Decreased total renal Na excretion = Increased body fluid = Volume overload
Monitoring of Sodium and fluid balance in CKD
BP
Volume status
Serum electrolytes
Potassium homeostasis in CKD
Regulated by renal excretion, shifting in and out of cell, GI excretion
G4 - G5 = body can no longer adapt to decreased renal excretion of K = hyperkalemia
Potassium goals in CKD
Prevent hyperkalemia and adverse consequences
G2-G3s: K in normal range (3.5 - 5.0)
G4 - G5: K between 4.5-6
Potassium acute treatment
same as AKI (calcium gluconate, insulin plus glucose, albuterol)
Chronic potassium treatment in CKD
Dietary restrictions Prevent constipation Eliminate medications likely to cause hyperkalemia Sodium polystyrene sulfonate Patiromer
Sodium polystyrene sulfonate
MOA: exchanges Na for K w/in large intestines
SE: constipation, hypernatremia, interstitial necrosis
Safety alert: Do not take any medications for 6 hours before/after
Patiromer
MOA: exchanges Ca for K within the colon = decreased free K in colon = decreased serum levels
Administer w/food
SE: constipation, hypomagnesemia, N/D, ab discomfort, flatulence
Safety alert: Do not take any medications for 6 hours before/after
Comments: Primary use is in patients with CKD receiving at least one RAAS inhibitor medication
Metabolic acidosis
pH < 7.35
pCO2 < 35
HCO3 < 24
Metabolic acidosis presentation
Fatigue
Decreased exercise tolerance
Hyperkalemia
Metabolic acidosis pathophysiology
Decreased ammonia synthesis =
Decreased urinary buffer =
Decreased net H+ excretion =
Decreased pH
Metabolic acidosis goal
Normalize pH
Maintain serum HCO3 within normal range (22-28)
Prevent complications of severe acidosis (bone dz, decreased cardiac contractility)
Asx metabolic acidosis treatment
Patients with mild acidosis generally do not need emergent treatment
Severe metabolic acidosis
pH < 7.2
Serum HCO3 < 15
When to treat metabolic acidosis
Serum HCO3 < 22
Metabolic acidosis alkalinizing agents
Sodium bicarbonate
Sodium citrate/citric acid
Potassium citrate/citric acid
Citric acid/sodium citrate/potassium citrate
Anemia of CKD
Hgb < 13 in males
Hgb < 12 in females
Anemia of CKD contributing factors
Decreased EPO production Uremic toxins decrease RBC lifespan Iron deficiency Blood loss from HD and lab testing Poor nutrition (decreased folic acid and B vitamins) Severe mineral and bone disorder
Anemia of CKD patient evaluation
RBC indices
Absolute reticulocyte count
Iron indices
Folic acid and vitamin B12
Anemia of CKD goals
Increased oxygenation
Improve QOL
Prevent complications
Target Hgb: = 11.5 (KDIGO); = 11 (manuf./FDA)
Anemia of CKD treatment
Iron supplementation
Initiate when TSAT = 30% and ferritin = 500
Oral iron supplements
10% absorbed in duodenum and upper jejunum
Decreased absorption with food
Convenient for patients without IV access
Oral iron supplement formulations
Ferrous sulfate (20%) Ferrous sulfate, exsiccated (30%) Ferrous fumarate (33%) Ferrous gluconate (12%) Iron polysaccharide complex (100%) Heme iron polypeptide (100%)
Oral iron supplementation adverse effects
GI: N, constipation, abdominal cramping
Oral iron supplementation drug interactions
Vitamin C
FQs
PPIs/H2RAs
Tetracyclines
IV iron supplementation formulations
Iron dextran
Sodium ferric gluconate
Iron sucrose
Ferumoxytol
IV iron supplementation ADR
Anaphylaxis (Iron dextran) -BBW -Test dose required Infusion rxns: hypotension, arthralgias, myalgias, fever, flushing, HA Risk of iron overload
Erythropoietin stimulating agents MOA
Same biologic activity as endogenous erythropoietin
When to initiate Erythropoietin stimulating agents
CKD ND: Hgb < 10
CKD 5D: Hgb: 9-10 to avoid falling below 9
When to interrupt or reduce ESA dose
Hgb approaching/exceeding 11
ESA BBW
Increased risk of death, MI and stroke
ESA drugs
Epoetin alfa
Darbepoetin
Peginesatide
Epoetin alfa SE
HTN Arthralfia Muscle spasm Pyrexia Dizziness
Darbepoetin SE
HTN Dyspnea Peripheral edema Cough Procedural hypotension
Which ESA(s) were/was removed from the market?
Peginesatide
Which ESA(s) require adequate iron?
Epoetin alfa and Darbepoetin
ESA dose adjustment
Dose increases: once every 4 weeks
-If hgb has not increased by > 1 after 4 weeks = increase by 25%
Dose reductions: Can be more frequent
-With rapid hgb rise (> 1 in any 2wk period) = reduce by 25%
Use lowest dose possible
ESA monitoring
Monitor Hgb at least weekly until stable then monthly
Mineral and Bone Disorder and Renal Osteodystrophy aka
Secondary hyperparathyroidism
Renal osteodystrophy classifications
Osteomalacia
Osteitis fibrosa cystica
Adynamic bone disease
Osteomalacia definition
Softening of bones (defective mineralization)
Osteitis fibrose cystica definition
Replacement of bone with fibrous tissue (high bone turnover)
Adynamic bone disease definition
Decreased bone formation without a mineralization defect
MBD and ROD goals
Prevent MBD and ROS and associated consequences
Maintain Ca, PO4, iPTH levels
Corrected calcium equation
Observed Ca + 0.8 x (4 - albumin level)
Corrected calcium levels
Normal: 8.5 - 10.8
CKD 3: “Normal”
CKD 4: “Normal”
CKD 5: 8.4 - 9.5
Phosphorous levels
Normal: 2.7 - 4.6
CKD 3: “Normal”
CKD 4: “Normal”
CKD 5: 3.5 - 5.5
Ca x P levels
All: < 55
Intact PTH (iPTH) levels
Normal: 10 - 60
CKD 3: 35 - 70
CKD 4: 70 - 110
CKD 5: 150 - 300
Evaluation of a patient for MBD and ROD
Serum Ca Serum PO4 Vitamin D BMD PTH
MBD and ROD non-pharm treatment
Dietary PO4 restriction
Parathyroidectomy (last line)
Major treatment failure with dietary PO4 restriction
Non-compliance
What foods contain PO4
Meat Dairy Nuts Dried beans Colas Peanut butter Beer
MBD and ROD pharm treatment
Phosphate binding agents
Vitamin D
Calcimimetics
Phosphate binding agents pathophysiology
Bind dietary phosphorous in the GI tract = form insoluble salts = excreted in feces
Phosphate binding agents
Calcium carbonate Calcium acetate Sevelamer Lanthanum Sucroferric oxyhydroxide Aluminum-containing agents Magnesium-containing agents
How must phosphate binding agents be taken?
With meals
Calcium carbonate SE
Constipation
N/V/D
Increased Ca
Calcium acetate SE
Constipation
N/V/D
Increased calcium
Sevelamer SE
Pruritus
N/V/D
Lanthanum SE
N/V/D
Sucroferric oxyhydroxide SE
Dark colored feces
N/D
What % of ca is calcium carbonate
40% elemental
What % of ca is calcium acetate
25% elemental
1st line phosphate binding agents
Calcium carbonate and Calcium acetate
*Except when vascular or soft-tissue calcifications are present
Calcium carbonate and Calcium acetate comments
Can increase aluminum absorption
Calcium carbonate and Calcium acetate DDI
Iron
Zinc
FQs
Sevelamer comments
Do not crush or chew tablets
Does not affect serum Ca
Initial dose based on serum PO4 level
Which phosphate binding agents can be used with calcifications?
Sevelamer
Lanthanum comments
Chewable tablets
Primary use - Stage 5
Sucroferric oxyhydroxide comments
Only for patients on HD
Chewable
Contains 500mg elemental iron
Sucroferric oxyhydroxide DDI
Avoid w/vitamin D analogs and levothyroxine
Aluminum-containing agents
3rd line - increased risk of toxicity
Limit to 4 weeks
SE: bone disease, anemia, encephalopathy
Magnesium-containing agents
Not generally recommended
SE: severe diarrhea, abdominal cramps, hypermagnesemia, hyperkalemia
When to initiate vitamin D therapy?
< 30
Vitamin D precursors
Ergocalciferol
Cholecalciferol
Active Vitamin D
Calcitriol
Vitamin D analogs
Paricalcitol
Doxercalciferol
Vitamin D precursor MOA
Metabolized to active form of vitamin D then same MOA
Calcitriol and Paricalcitol MOA
Binds to and activates Vitamin D receptor in kidney, parathyroid gland, intestine and bone
Doxercalciferol MOA
Metabolized to active form of vitamin D then same MOA
Ergocalciferol SE
GI upset
Hypercalcemia
Hyperphosphotemia
Cholecalciferol SE
Lipid abnormalities
Hypervitaminosis D
Calcitriol SE
GI upset
Hypercalcemia
Hyperphosphotemia
Paricalcitol SE
GI upset
Edema
HTN
Doxercalciferol SE
Edema
HA
N/V
Which vitamin D is primarily used for vitamin D deficiency or insufficiency
Ergocalciferol
Which vitamin D is primarily used for prevention
Cholecalciferol
Which vitamin D’s come in both PO and IV form?
Calcitriol
Paricalcitol
Doxercalciferol
When do patients receive calcitriol IV?
Stage 5
Calcimimetics
Cinacalcet
Etelcalcetide
When are calcimimetics used?
Dialysis
Calcimimetic MOA
Works on calcium-sensing receptor of parathyroid gland
Mimics extracellular ionized calcium = decreased PTH = decreased serum calcium
Cinacalcet SE
GI upset
Hypocalcemia
Myalgia
Etelcalcetide SE
Hypocalcemia
Worsening HF
GI bleeding
How many drugs are needed for HTN in renal disease?
Most will need >/= 3
Other complications of CKD
Nutrition status Hyperlipidemia Uremic bleeding Gastrointestinal disorders Immune function Pruritus Neurologic abnormalities Endocrine disorders
Protein-energy malnutrition causes
Anorexia
Altered taste sensation
Unpalatable food (PO4 and Na restrictions)
Protein-energy malnutrition treatment
Replace B and C vitamins and folic acid in dialysis patients
When to treat hyperlipidemia in CKD?
Treat if have other risk factors
KDIGO lipid guidelines
“Fire and Forget” strategy
Non-dialysis and non-transplant patients only
Only recommend - statin or statin/ezetimibe combo
Uremic bleeding contributing factors
D/t platelet abnormalities (decreased platelet aggregation and adhesiveness)
Heparin administered with dialysis
Other anticoagulants/antiplatelet agents for other indications
Uremic bleeding treatment
Cryoprecipitate (has factor VII and fibrinogen which helps decrease bleeding time)
Fresh frozen plasma (FFP)
Desmopressin
GI disorders SE
Anorexia
Hiccups
Metallic taste in mouth
Immune function causes
Uremic toxins may alter cell-mediated immunity
HD patients at increased risk with vascular access (exposure to infectious sources)
Pruritus contributing factors
Inadequate dialysis, dry skin, CKD-MBD, increased histamine levels
Pruritus treatment
Sufficient dialysis
Oral antihistamines
Topical steroids
Neurologic abnormalities causes
Uremic encephalopathy
Peripheral neuropathy
Uremic encephalopathy
Changes in consciousness, thinking, memory, speech, movement, emotion
Less common in earlier initiation of dialysis in stage 5
Peripheral neuropathy treatment
TCAs
Gabapentin
Endocrine disorders
Hypothyroidism
Hypothalamus disorders
Glucose management issues
Hypothyroidism labs
Decreased T4 but TSH usually norma
Decreased T4 to T3 conversion
Replace thyroid hormone if TSH elevated
Hypothalamus disorder presentation
Hypothermia - 1 degree less than normal
Hyperglycemia cause
Peripheral insulin resistance
Hypoglycemia cause
Decreased renal insulin degradation
