Renal - Shepler Flashcards
Acute Kidney Disease Definition
- short term
- one minute you’re good, the next, you’re not
CKD
Chronic Kidney Disease
Defined as abnormalities of kidney structures, present for >3 months with implications for health
Classified based on cause, GFR and albuminuria category
ESRD
End Stage Renal Disease
KDOQI
Kidney Disease Outcomes Quality Initiative
KDIGO
Kidney Disease Improving Global Outcomes
Incidence and Prevalence
- 678,383 patients with ESRD as of December 31, 2014
- 2,000,000 patients with ESRD estimated by 2030
- 120,688 new cases of ESRD in 2014
Major Causes of CKD
- Diabetes mellitus
- HTN
- glomerulonephritis (inflammation of kidney filters)
Prognosis of CKD
G1 = Normal or high (Best)
G2 = Mildly decreased
G3a = Mildly to modreately decreased
G3b = Moderately to severely decreased
G4 = Severely decreased
G5 = Kidney failure (Worst)
Glomerular filtration rate that indicates kidney failure
<15 ml/min/1.73m^2
Estimating the kidney function (Creatinine Clearance)
Cockroft and Gault formula, most commonly used in practice
*accurate for pts with stable kidney function
Good predictor of GFR and easy to use
Cockroft and Gault formula tends to _________ renal function
overestimate
Cockroft and Gault Equation
Men: CrCl = (140-age)IBW / (Scr x 72);
Women: CrCl x 0.85
CrCl measured in
ml/min
IBW measured in
kg
Scr measured in
mg/dL
SUN (serum nitrogen concentration) measured in
mg/dL
Alb measured in
gm/dL
Adjusted Body Weight (AjBW)
If pt is 130% of their IBW use AjBW = IBW + 0.4 (ABW - IBW)
ABW = Actual body weight
EGFR used to
stage disease
CrCl used to
dose drugs
Uremia Definition
Accumulation of waste molecules in the blood that are normally removed by the kidneys
Clinicians monitor the BUN to assess S/Sx
One possible effect on the body = Uremic frost = Crystals form = itchy
Fluid Retention
Pts develop edema (pitting and/or pulmonary) and BP increases
Fluid Restrict pts with retention?
Not normally necessary if Na is controlled. Large amounts of free water should be avoided
Fluid retention: Diuretics
-Used to treat volume overload and HTN in pts with renal insufficiency (those making some urine)
Fluid Retention: Loop Diuretic Treatment Option
- all loops similar to one another, therefore a poor response to one will be a poor response to all
- loops are REALLY good for fluid control
Fluid retention drug considerations
- thiazides are ineffective when CrCl < 30ml/min
- loops will work when CrCl < 30ml/min
- furosemide bioavailability (10 - 100%) is usually about 50% — oral dose may be twice the IV dose
- avoid potassium sparing diuretics
- as renal function declines and loop diuretic dose is maximized, thiazide can be added to overcome the diuretic resistance
***DIURETICS ONLY WORK IF THE KIDNEY IS WORKING
Furosemide sporadic bioavailability
-oral bioavailability = 10 - 100
***might need to titrate
Ethacrynic Acid Note
- risk of INCREASED ototoxicity
- still used, just an old drug
Complications associated with CKD + ESRD
- uremia
- fluid retention
- electrolyte imbalances
- mineral and bone imbalances (CKD-MBD)
—maybe more
Na Electrolyte Imbalances
No need to severely Na restrict pts beyond a no salt added diet UNLESS NEEDED FOR HYPERTENSION OR EDEMA (So <2g Na/day or <5g NaCl per day)
- use saline containing IV solutions with caution
- make outpatients aware of hidden high Na content foods (hot dogs, canned soups)
K goal for pre-dialysis K concentration
4.5 - 5.5 mEq/L
might seem high BUT these patients are resistant to effects of hyperkalemia
K Electrolyte Imbalance
Restrict to 3gm/day
K Electrolyte Imbalances
- avoid high potassium foods (tomatoes, dried fruits, salt substitutes, fresh fruits)
- treatment for hyperkalemia
3 parameters impacting PTH gland
- Increased phos
- Decreased Ca
- Decreased Vit D
- ALL INCREASE PTH
Long term impact of increased Ca
- Ca in blood
- pulls Ca out of blood
- bone fractures in vertebrae
- painful
Different types of parathyroidism
- Primary = tumor on gland
- Secondary = hyperparathyroidism (nothing is really wrong, affected by many things)
Hyperphosphatemia
- problem for nearly all ESRD pts
- nearly all pts receive phosphate binders
- agents bind dietary phosphate which is ingested in food. the chelate is eliminated in feces
Difference between phosphate and phosphorus
- phosphate = describes dietary intake
- phosphorus = the portion of phosphate that is measured in the blood
phosphate binders are
GIVEN WITH MEALS
Key points of calcium and phosphorus ish
- hyperphos is an issue
- decreased vitamin is an issue
- hypo Ca is an issue. Must consider Ca, phos, vit D and the intact PTH
Phosphate Binder Examples (Calcium containing)
- Ca carbonate (TUMs)
- Ca acetate (PhosLo
Calcium carbonate (TUMs)
- 40% elemental Ca
- Dose = TID w/ meals
- SE = constipation
- DO NOT EXCEED 1500mg/day of elemental Ca
- cheap!
- problem = has calcium, some will go into blood
Calcium acetate (PhosLo)
- 25% elemental Ca
- BID - TID with meals
- DO NOT EXCEED 1500 MG DAILY
- Phoslo 667 mg = 169 mg elemental calcium
- when given at the same elemental dose, calcium acetate will bind twice as much phosphate compared to calcium carbonate
- Ca acetate produces fewer hypercalcemia events
Non-calcium containing phosphate binders
- sevelamer carbonate (Renvela)
- lathanum carbonate (Fosrenol)
- sucroferric oxyhydroxide (Velphoro)
- Auryxia (ferric citrate)
- Aluminum hydroxide (amphojel)
- Magnesium carbonate (Mag-Carb)
- Nicotinic acid and nicotinamide
Sevelamer (Renvela)
- AE: GI upset, N/V, diarrhea
- ***decreased LDL by 15 - 30%
- always take with food
- not absorbed. low risk of systemic toxicity
- decrease uric acid serum concentrations –> good for gout
Lanthanum carbonate (Fosrenol)
- ***dosed daily with meals
- may titrate this drug
- eliminated in the feces
- no long term accumulation
- SE: mainly GI
- efficacy at diff pHs
- **pH 3 = 97.5% phos bound
- **pH 5 = 97.1 % phos bound
- **pH 7 = 66.6% phos bound
Sucroferric oxyhydroxide (Velphoro)
- minimal effect on iron stores
- SE = may cause DARKENED stools due to iron content
Auryxia (ferric citrate)
- for CKD pts on dialysis
- each tablet has 1g ferric citrate
- may cause DISCOLORED feces
- DOES impact iron levels
- increases ferritin
- increases TSAT
Aluminum hydroxide (Amphojel)
- old
- only use short term, if at all (< 4wks) — why? Al is eliminated by kidney, could build up. SE = ALUMINUM TOXICITY
Magnesium carbonate (Mag-Carb)
-dosed with meals
Dietary Restrictions of Phosphorus
-800-1000 mg/day if:
- **Phos >4.6 mg/dL (CKD stage 3 and 4)
- **Phos >5.5 mg/dL (CKD stage 5)
- **Phos > target range for stage 3,4 or 5
Foods that contain high phosphorus
- meat
- nuts
- dairy
- dried beans
- colas
- bear
If someone has kidney disease they should _____ using NSAIDs
STOP
Hyperphosphatemia and the kidney’s inability to activate vitamin D lead to
a decrease in Ca serum concentrations. Triggers the Parathyroid gland to secrete more PTH to increase the Ca mobilization from the bone
Vitamin D (ergocalciferol) and active vitamin D sterols (calcitriol and paricalcitol and doxercalciferol) are used to treat
SHFP. They increase vitamin D concentrations and decrease PTH concentrations through negative feedback mechanism
25-hydroxyvitamin D [25(OH)D] and 1,25(OH)2D3
25-hydroxyvitamin D [25(OH)D] is converted by the kidney to 1,25(OH)2D3. CKD stage 3 and 4 patients usually have enough kidney function left to run this conversion on their own. Stage 5 ESRD patients often do not and require the already active (converted) forms of vitamin D.
Vitamin D synthesis overview
7-dehydrocholesterol in skin
–> sun exposure
–> cholecalciferol (D3)
–> 25 hydroxylase in liver
–> 25-hydroxyvitamin D
–>1-alpha-hydroxylase in kidney
–> 1,25-dihydrovitamin D (active)
–> binding to vitamin D receptors
–> biological actions
Vitamin D (D2 and D3 require activation) Drugs
Ergocalciferol (calciferol) and Cholecalciferol are both for stage 3 and 4 patients (pts still have some kidney function left)
Ergocalciferol is D_
D2
Cholecalciferol is D_
D3
Activated vitamin D compounds are for
CKD stage 5 and some CKD stage 3 and 4 patients
Activated vitamin D Examples
- Calcitriol (Rocaltrol and Calcijex)
- Paricalcitol (Zemplar)
- Doxercalciferol (Hectorol)
Calcitriol (Rocaltrol and Calcijex)
-approved for use in pediatrics
***carries greatest risk of hypercalcemia
-cheap
Paricalcitol (Zemplar)
- 30% reduction in the PTH
- Approved for pediatrics
- most favorable ADE profile
- less calcemic activity compared to calcitriol
- $$$
Doxercalciferol (Hectorol)
- $$$
- prohormone that becomes activated in the LIVER but if someone has liver failure (or maybe an alcoholic) –> the drug wont work
- > /= 30% reduction in PTH
- higher incidence of hyperphosphatemia (but still rare)
- lower incidence of hypercalcemia compared to calcitriol
Calcium homeostasis and secondary hyperparathyroidism (1 class of drugs)
Cinacalcet (Sensipar) - Oral
Etelcalcetide (Parsabiv) - IV
Cinacalcet is a type
II calcimimetic agent
mimics the action of calcium but does so by binding to the cacium sensing receptor (CaR) and inducing a conformational change to the receptor, triggering the parathyroid gland to decrease PTH secretion.
Etelcalcetide (Parsabiv) is (-)
Contraindicated in hypocalcemia. If Ca is <7.5 mg/dL, withhold cinacalcet/etelcalcetide until Ca is = or > 8 mg/dL.
Anemia 4 key points
Nearly all ESRD patients will develop anemia by one or more of the following mechanisms.
- Decreased production of erythropoietin
- Uremia causes a decreased life span of red blood cells
- Vitamin losses during dialysis – folate, B12, B6
- Dialysis – loss of blood through dialyzer (hemolysis)
Anemia S/Sx
- HA
- fatigue
- dizziness
- decreased cognition
Anemia treatment goals
i. reverse signs and symptoms of tissue oxygen deprivation and left ventricular hypertrophy
ii. increase exercise tolerance and capacity
iii. optimize survival
iv. increase or quality of life
Hemoglobin is _____ stable than a hematocrit
MORE
Hb is the best assessment parameter for anemia due to its increased stability over the hematocrit (Hct).
Anemia monitoring standards
i. Hemoglobin (Hb)
Hb is the best assessment parameter for anemia due to its increased stability over the hematocrit (Hct).
ii. Hb vs. Hct
iii. KDIGO guidelines recommend monitoring Hb annually in CKD 3, twice/year in CKD 4-5ND, and every 3 months in CKD 5D as a means to screen for anemia.
If patients have existing anemia, then monitor Hb for CKD 3- 5ND every 3 months and CKD 5D monthly.
iv. Diagnosis of anemia and further workup should be initiated when:
Hb < 12g/dL in females
Hb <13g/dL in males
v. What is the goal Hb? This depends on if you are using an ESA – see below.
Diagnosis of anemia in men vs women
what is normal
- Hb < 12g/dL in females (normal = 14g/dL)
- Hb <13g/dL in males (normal = 15.5 g/dL)
Anemia treatment comparisons
- Ferritin = storage form of Fe (warehouse)
- TSAT = Transferring saturation (delivery truck of Fe)
Define erythropoiesis
the generation of new red blood cells requires iron.
KDIGO suggests that
iron supplementation if TSAT <30% and serum ferritin is <500 ng/mL.
Monitor TSAT and ferritin
every 3 months. There is no longer a specific range for targeting TSAT and ferritin. KDIGO further recommends that iron should not be given if TSAT
>30% and/or ferritin is >500 ng/mL.
Oral Iron
Will not likely be sufficient for correcting and maintaining iron stores for hemodialysis patients
May be used for CKD patients or peritoneal dialysis patients
Drug products include ferrous salts (sulfate, gluconate, and fumerate); various other products are available as well.
***Dose = 200 mg of elemental iron per day at least! Heme iron
-SE: stomach upset (hurts to absorb). Best absorbed in an acidic environment
What to consider when giving iron?
- food increases stomach pH
- Enteric coating interferes with absorption
- pts on meds increase pH
Heme iron
Greater absorption, different absorption site –> not subject to 200 mg/day rule
Heme iron examples
- Proferrin ES
- Proferrin Forte
IV route ______ route for CKD 5D patients
PREFERRED
IV Iron Agents
- Iron Dextran (infed, dexferrum)
- Sodium ferric gluconate (Ferrlicit)
- Iron Sucrose (Venofer)
- Ferric carboxymaltose (Injectafer)
- Ferumoxytol (Feraheme)
Iron sucrose
indication for patients not yet on dialysis
Feraheme
interferes with magnetic resonance(MR) imaging for up to 3 months after the second injection. MR imaging should be completed prior to starting ferumoxytol.
Low molecular weight vs. high molecular weight iron
Low molecular weight = Infed
High molecular weight = Dexferrum
***BOTH ARE DEXTRAN
Pts with high MW iron had
higher rate of anaphylaxis
Erythropoiesis Stimulating Agents (ESAs) used
used after all other correctable causes of anemia have been addressed
When suggested to use ESAs?
When not on dialysis yet
CKD 3-5ND Hb < 10 g/dL; Hb falling at a rapid rate; needed to avoid blood transfusion
CKD 5D Start when Hb is between 9 and 10 g/dL
ESA improves quality of life but
increases risk of cerebral vascular events
HARD cut-off of ESA at
11.5 g/dL
Recombinant human erythropoietin (rHuEPO, epoetin alfa, Epogen, Procrit, EPO)
stimulates erythroid progenitor cells
Epogen was the _____ drug
FIRST
Recombinant human erythropoietin has an ___ preferred route
SC!
Darbepoetin alfa (Aranesp)
samed concept as recombinant human erythropoietin
***dosed ONCE per week IV or SC
Methoxy polyethylene Glycol
- extended half-life
- dosed once every two weeks
ESA adverse effects (Epogen, Aranesp, and Mircera)
Pure Red Cell Aplasia PRCA: antibodies develop to erythropoietin; DC drug permanently
HTN: Most common, increase in BP by 23% in patients
Causes of ES therapy failure
***Lack of vitamins or iron
Aluminum toxicity Active bleed
Drug induced bone marrow suppression
Acute inflammation or infection
Acid Base Disorders: ESRD pts cannot
excrete H+ ions and develop metabolic acidosis.
Acid Base treatment usually starts when
bicarb is <20 mEq/L
Treatment options
a) Dialysis – increase bicarbonate in dialysate (usually always corrects the problem in dialysis patients)
b) Shohl’s solution – contains 1 mEq sodium and 1 mEq bicarbonate (as sodium citrate) per ml of solution.
c) sodium bicarbonate tablets 325mg and 650mg strengths
1 gram of sodium bicarbonate contains 11.9 mEq of sodium and 11.9 mEq of bicarbonate.
d) Dose(mEq) = Vd bicarb(0.5 L/kg) x wt(kg) x (24mEq/L – HCO3),
administer over several days
Most common treatment option of acid base disorders
Sodium bicarbonate tablets
Nutrition for acid base disorders
- Protein and energy requirements (ESRD vs CKD) ***Protein: 0.8 g/kg/day if GFR < 30 ml/min
CKD 3,4
- 2 g/kg/day if have ESRD
- Water soluble vitamin replacement Nephrocaps,
- B + C for dialysis patients (Potential intervention to put pts on this)
Nephron FA
Uremic bleeding is a _____ complication of chronic kidney disease pts
common
mechanism is not fully understood. due partially to impaired binding of von willebrand factor to platelet membrane glycoprotein receptors
Signs of uremic bleeding
purpura, ecchymoses, epistaxis, and bleeding from hemodialysis access sites.
Treatment of uremic bleeding
a) red cell transfusions
b) cryoprecipitate (fraction of blood containing factor VIII, fibrinogen, fibronectin)
c) DDAVP
d) conjugated estrogens
Single most important cause of ESRD worldwide
DKD - diabetic kidney disease
DKD mechanism of action
excess glucose in the blood enters the glomerular cells and through multiple biochemical mechanisms alters the ability of the glomerulus to filter waste products from the blood appropriately.
Microalbuminuria
a) one of the best predictors of DKD; also a risk factor for heart attack and stroke
b) ACR value between 30-300 mg/g = microalbuminuria
c) 2-3 consecutive ACRs in this range is “persistent” microalbuminuria
d) all diabetic patients should have an ACR annual spot urine check for microalbuminuria
e) Target HbA1c approximately 7%
***Treatment of DKD
a) SGLT2 inhibitors and metformin - control blood glucose (if eGFR >30)
b) HgbA1c <6.5 – 8.0% in non-dialysis dependent CKD
c) lifestyle modifications – weight loss
e) protein requirements CKD stage 1-4 = 0.8 g/kg/day
f) antihypertensives – ACE inhibitors and ARBs because they decrease proteinuria in addition to their blood pressure lowering effects.
g) hypertensive DKD CKD patients may require multiple drug combinations. ACE I and ARB combination therapy may increase hyperkalemia and acute kidney injury. NEJM 2013;369:20
