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Therapeutics II > Exam 2 (AKI, CKD) > Flashcards

Exam 2 (AKI, CKD) Flashcards

1
Q

Criteria for CKD

A

If either of the following is present for >3 months
-Markers of kidney damage (one or more)
Albuminuria, urine sediment, electrolyte or other
disorders, H/O transplant, other
-Decreased GFR (<60mL/min)

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2
Q

What is the easiest way to know if a patient has CKD?

A

By monitoring decreased GFR using MDRD.

Can also assess protein in urine because that typically doesnt happen in AKI

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3
Q

Stages of CKD

A 
1- Normal, GFR>90mL/min
2-Mildly decreased, GFR 60-89
3- Mild to moderate decrease, GFR 45-59
    Moderate to severely decreased, GFR 30-44
4- Severe decreased GFR, GFR 15-29
5- Kidney Failure, GFR <15 or dialysis
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4
Q

What are the common causes of ESRD?

A

Diabetes and HTN are the main causes

Can also be because of glomerulonephritis

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5
Q

CKD susceptibility risk factors

A

Diabetes, HTN, Older age (>55), family history, racial or ethnic minority

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6
Q

Progression factors of CKD

A 
higher levels of proteinuria
Higher BP
Poor glycemic control
Smoking
Hyperlipidemia
Drugs
Obesity
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7
Q

CKD complications

A

CVD
Anemia
Altered bone and mineral metabolism

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8
Q

Pathophysiology of CKD

A

Loss of nephron mass-damage due to one or more of the progression factors
Glomerular capillary HTN- mediated by AT II
Proteinuria- Both a marker of damage and can lead to further damage as proteins are toxic to tubular cells

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9
Q

If a patient had a recent infection, symptoms with urination, a skin rash, or arthritis, what might be the potential problem?

A

Post-step glomerulonephritis
UTI
Lupus

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10
Q

If a patient has chronic disease such as CHF, cirrhosis, diabetes, HTN, what might be the potential problem?

A

Prerenal CKD or CKD

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11
Q

If a patient has a family history, what might be the potential problem?

A

Polycystic kidney disease

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12
Q

What lab values should you measure for CKD patients?

A

Estimated GFR (at least annually)
BP
Urine examination (at least annually)
-Albumin:Cr ratio (UACR) in early morning urine
sample(Albuminuria if >30)
-Examination for casts, sediment, etc.
Imaging studies

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13
Q

What is progression of CKD defined as?

A

A drop in GFR more than 5mL/min/year

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14
Q

What are common CKD complications?

A

Anemia, HTN, Vit D deficiency, acidosis, hyperphosphatemia, hyperparathyroidism

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15
Q

What are interventions of CKD that can delay progression?

A

ACE-Is, ARBs, BP control, blood glucose control

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16
Q

How do ACE-Is and ARBs delay the progression of CKD?

A

They lower systemic blood pressure, thus lowering glomerular capillary blood pressure and protein filtration rate. They also reduce AT II mediated cell proliferation and fibrosis.
This is accomplished in very low doses.

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17
Q

What is the evidence of ACE-Is and ARBs in delaying progression of CKD?

A

Should be used if UAE >30mg/day with diabetes

Should be used in all CKD pts with UAE >300mg/day

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18
Q

Patiromer (Veltassa)

A

Non-absorbed cation exchange polymer (K+ binder, exchanges for Na)
Used in patients with chronic hyperkalemia associated with ACE/ARB use
8.4g QD- Space out from other oral medications by 3 hours
May cause constipation or diarrhea

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19
Q

Sodium Zirconium Cyclosilicate (Lokelma)

A

Used in patients with chronic hyperkalemia associated with ACE/ARB use.
Use this or Patiromer (Not both)
10mg TID- space out from other medications by at least 2 hours
May cause edema

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20
Q

What do we do if Cr increases more than expected when a patient is on an ACE or an ARB?

A

If increased 30-50%, reduce dose
If increased >50%, D/C
This is a dose related effect

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21
Q

Can ACE and ARBs be used together?

A

No
Too high of a risk for hypotension, hyperkalemia, and decrease in kidney function.
This combination could cause an AKI on top of a patients CKD.

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22
Q

ACE-Is and Aldosterone blockers in CKD

A

Avoid combination except in CHF patients because of the high risk of hyperkalemia

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23
Q

Diuretics in CKD

A

Generally necessary in most CKD patients to help control fluid volume and BP
Most CKD patients have hypernatremia so diuretics reduce the Na levels.
Diuretics work synergistically with ACEe/ARBs by activating RAAS and promoting fluid retention

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24
Q

When do you use which diuretic in CKD

A

Thiazides if CrCl >30ml/min
Loops for CrCl <30ml/min
Cautious use of K-sparing diuretics especially if pt is on an ACE/ARB or has CrCl <30ml/min
Overdoing diuresis can lead to decreased GFR

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25
Q

What electrolytes do you monitor for with diuretic use?

A 
Hypokalemia- loop and thiazide
Hyperkalemia- K sparing
Hypomagnesemia- Loop
Hypocalcemia-Loop
Hypercalcemia- Thiazide
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26
Q

What are additional antihypertensive options for CKD?

A 
Beta-blockers- Not helpful or harmful in CKD but proven CVD benefits. Must counsel patient if diabetic. Do not use or  adjust dosage of atenolol (renally cleared)
Non-DHP CCBs (Verapamil, Dilt)- reduces proteinuria
Avoid DHPs (nifedipine, Amlodipine) unless out of options and avoid aliskiren because of hyperkalemia.
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27
Q

What constitutes uremia?

A

Having baseline symptoms chronically

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28
Q

Nutrition considerations for CKD

A

Eat low K and Phos foods
Keep salt intake <2g/day
Low sugar, low carb, normal BMI

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29
Q

What is the general approach of HTN and CKD?

A

Goal is to prevent ESRD and CVD
Most patients will be on 2 or more antihypertensives
Monitor BP and level of proteinuria
Side effects are more likely in CKD pts

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30
Q

What did the SPRINT trial teach us?

A

CKD is worsened if BP gets too low.

Because of this trial we now have a goal BB for CKD+HTN pts <130/80 (ACC guidelines)

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31
Q

If urine albumin is >300 in a HTN/CKD pt, what do you do?

A

Maximize ACE-Is when protein is in urine.
Give ACE-Is across the board if protein in urine.
May have to use additional HTN medications if blood pressure is not <130/80

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32
Q

Hemoglobin A1C

A

Measures long-term diabetes control.
Keeping A1c <7% slows the development of complications
Macrovascular complications-CAD, stroke
Microvascular complications- Nephropathy, retinopathy, neuropathy

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33
Q

Medications in diabetes

A

Insulin- renally cleared (be cautious with dosing)
Oral agents:
sulfonylureas- cleared by kidney (Glipizide is only one w/o active metabolites so it is preffered)
Metformin- if drug and metabolites accumulate it causes lactic acidosis

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34
Q

Diabetic nephropathy

A

Generally occurs with 10 years of poorly controlled diabetes.
Has persistent albuminuria
20-40% of diabetic patients develop CKD

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35
Q

Pathophysiology of diabetic nephropathy

A 
Mesangial cell hypertrophy (reduced GFR)
Advanced glycation end products (leads to sclerosis and fibrosis of glomerulus)
Oxidative stress
Damaged glomerular filtration barrier
Tubulointerstitial injury
RAAS
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36
Q

Screening of diabetic nephropathy

A

Urine albumin excretion tested annually
If >30, repeat 2 more times within 3-6 months
Positive test if 2/3rds are positive
SCr annually (calculate GFR)

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37
Q

Treatment of diabetic nephropathy

A

Intensive glucose control to slow progression of albuminuria (A1C <7%)
Control BP <130/80 with ACE
Control albuminuria- ACE or ARB
Smoking cessation
Protein restriction (0.6-0.8g/kg/day)
DM alone is not an indication for ACE/ARB, must also have CKD

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38
Q

Tight glucose control in CKD

A

Blood sugar goals
Pre-prandial 80-140mg/dL
Post-prandial <180mg/dL
A1C goal <7%

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39
Q

GLP-1 agonists and SGLT2 inhibitors in CKD

A

Both classes reduce CV events

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40
Q

Incidence of CVD in CKD patients

A

> 50% of dialysis pts have coronary calcifications
CHF is the leading CV condition you will see (HTN+volume overload)
40% increase of stroke
Pts should be on high-intensity statin and ASA

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41
Q

Cardiac monitoring for CKD

A

BNP
-BNP is not accurate when GFR <60mL/min
Troponins
-Not accurate when GFR <60mL/min

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42
Q

What is the significance of proteinuria?

A

Results from injury to glomerular filtration (marker of kidney disease)
Marker of systemic injury (increased CV risk)

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43
Q

Dyslipidemia in CKD

A

All CKD patients >50 should receive a high-dose intensity statin
Avoid statins in dialysis patients
The increased risk of proteinuria with statins is dose related so rosuvastatin must be limited to 10mg/day in stages 4 and 5

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44
Q

What did the SHARP trial teach us?

A

Do not give statins in dialysis pts

Eze/simv combo did not reduce events

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45
Q

Polycystic kidney disease (PKD)

A

Genetic autoimmune disorder
Causes fluid filled cysts on both kidneys which cause a dramatic increase in size
2 forms- autosomal dominant and recessive (infants)

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46
Q

Symptoms of PKD

A 
HTN
Family history
heart problems or strokes
kidney stones
constant or intermittent pain in back or side
hematuria
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47
Q

Treatment of PKD

A

Manage pain
Treat infections
Treat HTN- goal <130/80
Prepare for ESRD (dialysis or transplant)

Tolvaptan has some data that shows that it may slow the increase in renal volume and decline in renal function

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48
Q

What are the methods of urine analysis?

A

Random (no warning or prep)
Clean catch, midstream (1st half discarded, second half collected and evaluated)
Bladder catherization- avoid if possible
Suprapubic needle aspiration- Needle directly into bladder to catch urine
24 hr urine collection- cumbersome and inaccurate

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49
Q

What are the definitions of polyuria, oliguria, and anuria?

A

Polyuria-excess urine production
Oliguria- Urine production <500mL/24 hours
Anuria- Urine production <50mL/24 horus

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50
Q

What do the following odors of urine mean? Sweet or fruity, foul, strong

A

Sweet or fruity- Glucose, ketones
Foul- infection
Strong- dehydration, foods

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51
Q

What drugs change the color of urine?

A

Nitrofurantoin- brown
Amitriptyline- Green/blue
Phenazopyridine- orange
Rifampin- Red

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52
Q

What is the purpose of the urinalysis?

A 
To reveal diseases that may go unnoticed. 
Glomerulonephritis
Hypertensive nephropathy
Renal failure
Infection
Diabetes
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53
Q

Why do hypertensive patients get a urinalysis every year?

A

Because it takes 1/2 of the nephrons to be damaged in order to affect the creatinine.

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54
Q

How do infections affect the urine pH?

A

They increase it (more basic)

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55
Q

Specific gravity of urine

A

Normal range (1.002-1.035)
Measures urine density
Ability of the kidney to concentrate urine
High specific gravity=Dehydrated patient=Hypovolemia
High specific gravity=kidney stones

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56
Q

Protein in urine

A 
Normal is negative or trace 
Primarily albumin
Protein is filtered at the glomerulus and reabsorbed in the proximal tubule. If there is protein in the urine, there has been tubular damage. 
Microalbuminuria- 30-300mg/day
Macroalbuminuria- >300mg/day
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57
Q

Glucose in urine

A

Normal is negative

Usually correlates with blood glucose >180mg/dl, because it “spills” into the urine.

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58
Q

Ketones in urine

A

Normal is negative
Spilled into the urine when the body cannot utilize glucose or lack of glucose intake.
Find in patients with life-threatening hyperglycemia (diabetic ketocacidosis)
Blood glucose 800-1000mgdL or starvation

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59
Q

Bilirubin in urine

A

Normal is negative

If present, a marker of liver disease

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60
Q

Blood in urine

A

Normal is negative
Called hematuria
Correlates clinically with an injury to the kidney (UTI, traumatic sample, injury, stones)
Can also be caused by mygoglobinuria from rhabdomyolysis

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61
Q

Nitrites in urine

A

Normal is negative
Bacteria in the urine is converted into nitrates, which then get converted into nitrites.
Presence of nitrites in urine signals the presence of gram negative organisms in the urine.
A negative result does not rule out a UTI, but a positive result indicates a UTI

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62
Q

Leukocyte esterase in urine

A

Normal is negative
Positive test detects the presence of lysed white blood cells in urine.
Indicates infection

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63
Q

Red blood cells in urine sediment

A 
Normal 0-2/hpf
Hematuria
A marker of:
Glomerular disease
Tumors that affect urinary tract
Kidney trauma
Renal infarcts
Infections
Traumatic catheterizations
Renal stones
Nephrotoxins
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64
Q

White blood cells in urine sediment

A

Normal 0.-3/hpf
Termed pyuria
Marker of infection, glomerulonephritis, interstitial nephritis, inflammation, or rejection of transplant

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65
Q

Squamous epithelial cells in urine sediment

A

If present, likely contaminated with skin flora

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66
Q

Bacteria and yeast in urine sediment

A

Should not be present, if present look at nitrates, WBCs, etc.
Correlates clinically with s/s of a UTI
Can be caused by asymptomatic bacteruria, chronically catheterized patients, pregnancy, or be a contaminated specimen.
Culture and Sensitivity (C&S) is next step
Significant bacteruria >100,000 CFU of one organism needs to be addressed
Repeat if only yeast because contamination likely occurred.

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67
Q

Casts in urine sediment

A

Means any nephrons have been damaged
Collection of protein, cells, and debris
Formed in distal tubule and collecting duct
Important marker of kidney damage

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68
Q

Types of casts

A

Hyaline- most common, marker of kidney disease
Red cells- hematuria, glomerulonephritis (GN)
Granular- significant renal disease, “muddy brown”, ATN or GN
Epithelial- interstitial nephritis, ATN
Waxy- degenerated granular casts, marker of significant CKD

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69
Q

Crystals in urine sediment

A

Formed by precipitation of urine salts subjected to changes in pH or concentration
Calcium- kidney stones
Urate- hyperuricemia
Both could indicate post-renal obstruction
Some drugs (sulfonamides) may crystallize in the urine so you have to take with water.

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70
Q

UA markers of renal disease

A

Protein, blood/hematuria, casts (hyaline or granular)

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71
Q

UA markers of infection

A

Nitrites (gram neg), leukocyte esterase, pyuria/WBC, bacteria if above are found and symptomatic

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72
Q

What does mucous in UA indicate?

A

Contaminated specimen

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73
Q

Azotemia

A

Accumulation of nitrogenous wastes in blood (increased BUN)

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74
Q

Uremia

A

Constellation of symptoms associated with azotemia

Uremic symptoms drive treatment recommendations

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75
Q

Oliguria

A

Urine output <500ml/day

Signal high risk of morbidity and mortality

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76
Q

Anuria

A

Urine output <50ml/day

Signal high risk of morbidity and mortality

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77
Q

Nonoliguria

A

Urine output >500ml/day

Urine output is normal, but patient has AKI

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78
Q

What is the KDIGO definition of AKI?

A

Rapid (hours to days) deterioration of renal function.
This can be shown by:
-Increase in creatinine of >/=0.3mg/dl in <48 hours
OR
-Increase in creatinine to >/=1.5 times baseline which is presumed to have occurred in the prior 7 days
OR (less commonly used)
-Urine output <0.5mg/kg/hr for 6 hours. The urine output is more immediately affected by AKI than SCr.

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79
Q

What might future definitions of AKI include?

A

Tubular injury and kidney stress biomarkers

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80
Q

What is the difference between AKI and CKD?

A

AKI- abrupt onset, often reversible if treated early
CKD- the end result of irreparable damage to the kidneys. Develops slowly over the course of years. Technically defined as greater than 3 months of chronically decreased GFR. You have to lose 1/2 of your nephrons before CKD occurs.

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81
Q

Epidemiology of AKI

A

2-20% of hospitalized patients
(20-60%) ICU patients
Associated with significant morbidity and mortality
Mortality of 15-40% if acquired in hospital-prevention is key!

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82
Q

Why do so many ICU patients develop an AKI?

A

The body adapts to serious illness by bringing blood to the brain and heart.
Some patients in ICU are given pressors (Norepinephrine) to increase BP and they cause AKIs because they are very nephrotoxic. Sacrifice kidneys to save the patient.

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83
Q

What constitutes the syndrome of AKI?

A

Accumulation of nitrogenous waste products (Increased BUN and Cr)
Increased SCr
Derangement of extracellular fluid balance
Acid-base disturbance
Electrolyte and mineral disorders (hyperkalemia and hyperphosphatemia)

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84
Q

What are the symptoms of AKI?

A 
Decreased urine output (70%)
Edema (especially lower extremity)
Mental status change (uremia) 
Heart failure
N/V (uremia)
Pruritus (uremia)
Symptoms that correlate with any associated electrolyte disorders
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85
Q

What constitutes uremia?

A 
Renal failure
Mental status changes (lethargy, confusion)
Muscle weakness
Anorexia
Dysgeusia (metallic taste)
Pericarditis (can cause fatal arrhythmias)
Neuropathy
N/V
Pruritis
Dyspnea
Pulmonary edema
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86
Q

What are the types of AKI?

A

Prerenal, intrarenal, postrenal

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87
Q

What are the types of intrarenal AKI?

A

Vascular, glomerular, tubular, interstitial

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88
Q

Prerenal azotemia

A

Caused by decreased blood flow to the kidney. This causes decreased filtration of toxins and increased SCr and BUN (azotemia)
The integrity of renal tissue is preserved initially so it may be reversible! It causes ischemic damage if not corrected.

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89
Q

Which patients are most likely to have prerenal azotemia?

A

Patients with dehydration and hypotension

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90
Q

What factors increase the susceptibility to renal hypoperfusion?

A
  • Structural changes in arteries (old age >75)
  • Chronic HTN or acute hypotension
  • CKD
  • Reduction in vasodilatory prostaglandins
  • Failure to vasoconstrict the efferent arterioles (ACE/ARB)
  • Renal artery stenosis
  • Intravascular volume depletion (dehydration, CHF, liver disease)
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91
Q

Why are elderly patients (>75) more susceptible to renal hypoperfusion?

A

Elderly people have decreased renal blood flow and their SCr may not increase because they have lower muscle mass.

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92
Q

Which medications cause an impaired compensatory mechanism?

A

NSAIDs- suppress afferent arteriole vasodilation that body would desire to increase renal blood flow
ACE/ARBs- suppress the efferent vasoconstriction that body would desire to maintain adequate perfusion pressure inside the glomerulus

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93
Q

Signs/Symptoms of hypovolemia

A 
Decreased blood pressure
Increased HR
Orthostasis
Pallor, dry mucous membranes
BUN:SCr ratio increased
FENa
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94
Q

Main categories of prerenal AKI

A 
decreased circulatory volume (hypovolemia)
diminished cardiac output (HF)
hypotension
impaired compensatory regulation
Systemic/renal vasoconstriction
Renovascular obstruction
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95
Q

What causes decreased circulatory volume, and thus a prerenal AKI?

A 
Dehydrated patient
Renal losses- diuretics, diabetes
Skin losses- sweating, burns
Third spacing due to hypoalbuminuria- cirrhosis 
Hemorrhage
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96
Q

plasma BUN:Cr ratio

A

Normal ratio is 20:1
In pre-renal AKI- >20 usually. Rises faster than usual due to more reabsorption
If BUN and SCr are elevated, but the ratio is still close to 20, then this is indicative or a chronic renal disorder.

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97
Q

FENa

A

Fractional excretion of sodium
FENa=(Urine Na+plasma Cr)/(Plasma Na+ Urine Cr) x 100
FENa <1%= prerenal AKI ( body is trying to preserve Na in the face of volume depletion)
FENa>2%= acute tubular necrosis (body cannot preserve Na because tubules are damaged)

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98
Q

What kind of medication will elevate urine sodium and make FENa calculation innacurate?

A

Loop diuretics (furosemide)

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99
Q

Risk factors for ACE/ARB induced AKI

A

Reduced renal blood flow- CHF, bilateral renal artery stenosis
Volume depletion- dehydration, excessive diuresis

Hold ACE/ARBs if patient is volume depleted!

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100
Q

What should you do if SCr rises with ACE/ARB?

A

It is expected to rise up to 30%
It should stabilize, but if it doesn’t D/C medicine and correct underlying condition (rehydration)
Consider captopril if you still want an ACE but are unsure of renal effects. It has a very short 1/2 life.

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101
Q

Effects of ACEI-s on the kidneys

A

Protects the kidney by decreased pressure inside the glomerulus

  • Reduces damage to glomerulus and reduces protein spillage in urine
  • This is why ACE-is are drugs of choice for diabetics and those with hypertensive kidney disease

May decrease renal function by decreasing pressure inside glomerulus
-Decreases filtration of creatinine which raises SCr levels

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102
Q

Effects of NSAIDs on the kidneys

A

Inhibition of cyclo-oxygenase leads to vasoconstriction of afferent arterioles
This reduces GFR
This sets up patients who are already at risk of reduced GFR to go into renal failure- elderly, CHF, hypotensive, dehydration

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103
Q

What are the causes of systemic/ renal vasoconstriction that can cause a prerenal AKI?

A

pressors- vasopressors
General anesthesia
Afferent vasoconstriction- sepsis, cyclosporine, tacrolimus, radiocontrast dyes

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104
Q

Why do NSAIDs increase the risk of AKI?

A

afferent vasoconstriction

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105
Q

What is hepatorenal syndrome?

A

It is found in patients with liver failure because liver failure causes renal failure
Portal HTN causes ascites and renal vasoconstriction

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106
Q

Cyclosporine/Tacrolimus

A

Afferent constrictors
Used to prevent rejection of implanted organs
Can have acute and chronic toxicity
Renal function improves rapidly following dose reduction.
Prevention- closely monitor levels, use CCBs to manage HTN (dilate afferent arterioles)

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107
Q

Intrarenal AKI- vascular

A

Clot in renal artery
Can be caused by thromboembolic disease, angioplasty, severe CHF, AFIB, etc.)
Bilateral 15-30% of time
Symptoms- flank pain, tenderness
Tx- anticoagulant medications if unilateral, surgery if bilateral

Could also be caused by high cholesterol

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108
Q

Renal artery stenosis

A

Correlates with poor cardiac health
Consider RAS when there is an abrupt onset of HTN in a young pt or there is refractory HTN
Avoid ACE/ARB
Treat surgically via angioplasty

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109
Q

Acute tubular necrosis (ATN)

A

Intrarenal tubular AKI
Slow to resolve
Prolonged prerenal azotemia of any cause
Ischemic- due to lack of blood flow and O2 supply (sepsis, surgery)
Nephrotoxic- endogenous (body is creating)
Myoglobin, myeloma, uric acid

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110
Q

What exogenous nephrotoxins can cause ATN?

A 
Aminoglycosides
Amphotericin B
Cisplatin and carboplatin
Cyclosporine, tacrolimus
Intratubular drug precipitation
Rhabdo (statins, cocaine)
Iodinated contract dyes
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111
Q

What do you typically see on a UA with ATN?

A

Granular casts (Muddy brown)

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112
Q

Aminoglycosides

A

Cause ATN by proximal tubule cell damage
Examples: gentamycin, tobramycin, amikacin
These abx are used in life-threatening situations and the tx plans are very individualized.
Generally see ATN after 5-10 days (SCr will rise)

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113
Q

What are the risk factors for aminoglycoside toxicity?

A

Large cumulative doses and multiple daily doses
Use of furosemide or other loops in conjunction
Pre-existing renal disease, elderly, sepsis, dehydration

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114
Q

Aminoglycoside considerations

A

Monitor SCr daily and d/c if it rises quickly
Consider inhaled formulation if resp infection
Recovery from ATN takes about 3 weeks, but some nephrons never recover

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115
Q

Amphotericin B

A

Broad spectrum antifungal agent that is used when nothing else is available
Causes ATN in the proximal and distal tubules
Afferent vasoconstriction and ischemic injury
If you have to run it- run it slowly over 24 hours because the amount of exposure is reduced.

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116
Q

Amphotericin B considerations

A

Use liposomal formulation if you can (costly)
Associated with substantial losses in Mg and K
Prevention- avoid cumulative exposure, avoid nephrotoxins, hydrate

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117
Q

Cisplatin and Carboplatin

A

ATN (proximal)
Elevations in SCr generally appear 10-12 days after initiation of therapy and recover by day 21
Prevent toxicity- reduce dose/frequency, use carboplatin over cisplatin, pre-hydrate with NS, Amifostine to help direct drugs to cancer cells

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118
Q

Intratubular precipitation

A

Tumor lysis syndrome- elevated uric acid levels often due to chemotherapy
Intratubular drug precipitations- sulfonamides, methotrexate, acyclovir, triamterene (take with H2O)
Rhabdo- statins, cocaine

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119
Q

Instrinsic AKI rhabodomyolysis

A

Mech- myoglobin from muscle breakdown precipitates in the tubules and obstructs them
Causes- trauma, toxins/drugs (statins), seizures, infections
Treatment- hydration and urine alkalization with sodium bicarb, Maintain UOP at 300ml/hr
You will be able to tell if the urine is clear of myoglobin by color (myoglobin makes urine red, purple, or dark brown)

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120
Q

Acute interstitial nephritis (AIN)

A

Allergic hypersensitivity response
fever, rash, eosinophilia are common
UA- may have eosinophils, hematuria, pyuria, and arthralgia

Can occur one day to several weeks after exposure

Often caused by drugs

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121
Q

Drugs that commonly cause AIN

A 
Allopurinol
Quinolones (cipro)
Furosemide (and other loops)
NSAIDs
Penicillin
Phenytoin
Sulfa drugs
Thiazides
PPIs

Usually reversible if caught on time!

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122
Q

Chronic interstitial nephritis

A

Often caused by NSAIDs, lithium, cyclosporine/tacrolimus

Delayed, irreversible damage

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123
Q

Contrast-Induced nephropathy (CIN)

A

AKI occurring w/in 48 hours of exposure to IV contrast

Generally find hyaline and granular casts on UA

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124
Q

Risk factors for CIN

A 
Pre-existing renal disease
HTN
CHF
pre-procedural hypovolemia
Nephrotoxic agents
Intra-procedural hypotension
Age >75
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125
Q

Metformin and CIN

A

Metformin itself is not nephrotoxic, but it has a metabolite that is cleared by the kidneys leading to lactic acidosis
D/C metformin prior to procedure and for 48 hours after

126
Q

Prevention of CIN

A

Remove renal toxins
hydration- volume supplementation with NS 3-12 hrs before procedure (min 300-500ml)
choice and quality of contrasts (target low-osmolar and iso-osmolar dyes)
end-organ protection (statins?)
monitor
Maintain adequate BP

127
Q

N-acetyl cysteine (NAC)

A

Cyto-protective agent against oxidative injury (free radical scavenger)
Vasodilator
NAC 600mg BID the day before and of contrast surgery
Best data in angioplasty

128
Q

Statins and CIN

A

Give prophylaxis dose of statin prior to contrast

129
Q

Post-procedure monitoring for contrast surgery

A

SCr for 48 hours
BP
No metformin or nephrotoxins
UOP- 150ml/hr for 6 hours

130
Q

What type of kidney injury can piperacillin/tazobactam cause?

A

AIN

131
Q

Glomerulonephrophathy

A

5% of AKI
Can cause acute and/or chronic kidney failure
Nephritic- 1-3.5g/24 hours of proteinuria
Nephrotic- >3.5g/24 hours of proteinuria

132
Q

Types of glomerulonephropathy

A 
Can be either:
diffuse- all glomeruli
focal-some not all
segmental- part of individual glomerulus
proliferative- overgrowth 
membranous- thickening of GBM
sclerotic
133
Q

Pathophysiology of glomerulonephropathy

A

Antibodies made to antigens in the glomerulus become trapped in glomerulus, leading to capillary damage
May progress to ESRD

134
Q

Nephritic syndrome

A

Inflammatory syndrome that leads to glomerular capillary rupture- can be triggered by infection or autoimmune disorder
Abrupt onset of azotemia, oliguria, hematuria
RBC casts and granular casts are present

135
Q

Nephrotic syndrome

A

Proteinuria >3.5g/day
Marked edema and hypoalbuminuria
-Kidney has loss of oncotic pressure and increased reabsorption of Na due to resistance to ANP
Hyperlipidemia
Hypercoaguable state (increased platelet aggregation)

Tx- limit fluid and Na intake, loop diuretics

136
Q

Treatment of glomerulonephritis

A

Immunosuppressants- corticosteroids, cytotoxic agents (cyclophosphamide, chlorambucil, azathioprine, methotrexate)
-Cyclosporine, mycofenolate mofetil
Plasmapheresis

137
Q

Glomerulopathies

A

Usually found in children, usually accompanied by AIN
For adults, you see with NSAID use
Abrupt nephrotic-range proteinuria, hypoalbuminemia, hyperlipidemia

138
Q

Types of glomerulopathy

A

focal segmental- leads to ESRD
membranous- idiopathic
IgA mediated- most common, steroids + tight BP control for tx
rapidly progressive- steroids+cytotoxic agents
post-streptococcal- most common in children, often dont know you have
lupus nephritis-steroids+immunosuppressants together

139
Q

postrenal obstruction AKI

A 
Stones- cause anuria
bladder obstruction
neurogenic bladder
crystallization of drugs
Drugs that cause urinary retention (anticholinergics, antihistamines, phenazothiazines, narcotics)
140
Q

General workup of an AKI pt

A

Find cause of AKI
UA
labwork

141
Q

Management of AKI

A 
Treat depending on etiology
Hypovolemia- fluid resuscitation (NS)
Hypotension- vasopressors, stop HTN meds
AIN or ATN due to drugs- d/c and hydrate
Treat infections
Correct acid-base disturbances  (metabolic acidosis- sodium bicarb)
Correct electrolyte disturbances
142
Q

Indications for dialysis

A 
A- acidosis
E- electrolytes (hyperkalemia)
I- intoxications
O- overload, fluid
U- uremia
143
Q

Hemoglobin

A

Most important for determining anemia
-oxygen carrying molecule
Men: 13-17.5g/dL
Women: 12-16g/dL

144
Q

Hematocrit

A

Volume of RBCs per unit of blood volume
Men: 42-53%
Women: 36-46%

145
Q

Mean Corpuscular Volume (MCV)

A

Average volume of each RBC

Normal range 80-100

146
Q

Anemia classifications

A 
Large RBC's= macrocytic= High MCV
       -folic acid and vitamin B12 deficiency
Normal RBC=normocytic 
        -anemia of chronic disease 
Small RBC=microcytic=low MCV
         -iron deficiency anemia
147
Q

Erythropoietin

A

Hormone that initiates and stimulates the production of RBCs
It is the prime regulator of RBC production
Produced by the kidneys

148
Q

ESAs

A

Erythropoietin stimulating agents

Darbepoetin, epoetin

149
Q

Hypoxia- inducible factor (HIF)

A

Gene product that is found in the cells that produce erythropoietin

  • Recognize oxygen availability
  • Drugs can target this factor and make it stimulate erythropoietin production and iron absorption and transport.
150
Q

Hepcidin

A

Central regulator of iron homeostasis
Synthesized in hepatocytes
-Inhibits intestinal iron uptake
-High iron levels stimulate production of hepcidin.
-Hepcidin is reduced in iron deficiency anemia

Cleared by kidneys so levels are elevated in CKD patients.

151
Q

Pathophysiology of anemia in CKD

A

Decreased erythropoietin production (stages 4 and 5)
Blood loss from testing
Reduced life span of RBCs due to uremia
Iron, folate, or B12 deficiency
Increased risk of bleeding due to platelet dysfunction

152
Q

Consequences of anemia with CKD

A

Reduced oxygen delivery to tissues
Compensated by increased cardiac output
LVH
Cardiac and renal damage

153
Q

How often should hemoglobin be monitored with CKD?

A

W/O anemia- 2 times a year, every 3 months if on dialysis

W/ anemia- Every 3 months, monthly if on dialysis

154
Q

Iron indices

A

Transferrin saturation (Tsat)-

 - carrier protein for iron
 - indicator of iron immediately available to the bone marrow to incorporate into Hgb
 - can be affected by nutrition status 
 - Normal is 20-50%

Serum Ferritin-
-indirect measure of storage iron
-Artificially elevated during infection or inflammation
Normal 12-200ng/ml (most >100)

155
Q

General approaches to iron therapy

A

Iron is required as a building block for Hgb synthesis

Goal is to minimize blood transfusions, decrease need for/dose of ESA, and relieve symptoms

156
Q

Iron targets

A

If CKD w/ anemia +/- ESA
Dialysis- IV iron
Non-dialysis- PO (1-3 months) or IV

-If ferritin <500 and/or TSAT <30%
Do not administer iron to intentionally keep the iron goals

157
Q

Oral iron

A

Difficult to use for replacement therapy, better for management
Ferrous sulfate, ferrous gluconate, Slow Fe, ferrous fumarate, Niferex

158
Q

Why is oral iron inadequate?

A

There is low intestinal absorption of iron even in healthy people. This occurs if ferritin >100.
Patients also have poor adherence and tolerance due to GI upset

159
Q

IV iron products

A 
Iron dextran
Iron sucrose
Sodium ferric gluconate
Ferumoxytol
Ferric pyrophosphate citrate
Ferric carboxymaltose
160
Q

IV iron dosing considerations

A

Give periodic doses when iron status is low
For continuous treatment, give smaller doses
Give larger doses to non-dialysis pts for convenience
Hold doses when TSAT >30% and ferritin >500

161
Q

Goals of ESA treatment

A

Keep Hgb no greater than 11g/dL
Reduce the need for transfusions
Decrease LVH and mortality

162
Q

Guidelines for ESA use in CKD

A

Non-dialysis- consider if Hgb <10mg/dL and patient likely to receive transfusion
-D/C when Hgb >10mg/dL
Dialysis- initiate ESA if Hgb <10mg/dL. D/C when Hgb>11

163
Q

ESA MOA

A

stimulates erythropoietin by the same mechanism as endogenous erythropoietin

164
Q

IV or SQ ESA?

A

SQ has lower bioavailability but longer 1/2 life
SQ is considered to give better response
Many dialysis pts get IV for convenience

165
Q

Precautions with ESAs

A

Increased risk of CV events (use caution in pts with H/O stroke)
Risk of tumor progression- do not use in cancer pts
Pure red cell aplasia
HTN
seizures

166
Q

Darbepoetin vs Epoetin

A

Darbepoetin has 2 additional N-linked chains and a much longer 1/2 life.
Much cheaper

167
Q

Epoetin alpha

A

Indicated for anemia secondary to CKD (both on and not on dialysis)
1/2 life of 12 h (IV) and 24h (SQ)

contraindications-
uncontrolled HTN, history of stroke

168
Q

Darbepoetin alpha

A

Indicated for anemia secondary to CKD (both on and not on dialysis)
1/2 life 21 hrs (IV) and 49 hrs (SQ)

contraindications-
uncontrolled HTN, history of stroke

169
Q

Adjusting ESA therapy

A

Goal Hgb 10-11g/dL, monitor weekly until stable and then monthly
Increase dose by 25% if:
-Hgb <10 and has not increased by 1g after 4 weeks
Increase dose no more than once/month
If inadequate response after 12 weeks use lowest dose necessary to avoid transfusions

Decrease dose by 25% if
-Hgb increases by >1g in any 2 week period

Hold if Hgb >11

170
Q

Monitoring anemia in CKD

A

Iron status evaluated every 1-3 months

Iron status has to be adequate in order to give ESA

171
Q

ESA hyporesponsiveness

A

Initial-no increase in Hgb from baseline after 1st month of ESA tx
Acquired- previously stable, now requiring 2 increases in ESA doses

172
Q

HIF stabilizing agent

A

Roxadustat oral therapy
New drug, will be approved soon
Has been shown to increase EPO levels

173
Q

Where is calcium found in the body?

A

Intracellular
Extracellular (in the blood primarily bound to protein)
Bone (99% in mineral phase, 1% available to exchange with extracellular calcium)

174
Q

What organs supply calcium to the body?

A

3 organs participate in supplying calcium to and removing from the blood.

  • small intestine-where dietary calcium absorption occurs
  • bone- reservoir of calcium. Bone reabsorption releases calcium from bone into blood.
  • Kidney- almost all of the calcium that enters the glomerulus is reabsorbed back into the blood
175
Q

Parathyroid organ effect on calcium

A

Increases blood concentration of calcium.
Normal range 10-65pg/ml
Secreted in response to low Ca, low vit D, and high phos
-Stimulates the production of the biologically active form of vitamin D in the kidney.
-Mobilizes Ca and Phos from bone
-Maximizes tubular reabsorption of calcium within the kidney and increases phosphate loss

176
Q

Vitamin D effect on calcium

A

Normal range 30-60ng/ml
-Cholesterol derivative formed in the sun after exposure to sunlight (D3)
-Dietary sources (D2 and D3)
-Converted into active form by 1-alpha-hydroxylase in the kidney.
Calcitriol is the active form of vitamin D. It is responsible for the absorption of calcium and phos in the small intestine.
-Facilitates the flux of calcium out of the bone and inhibits PTH secretion (when give as med)

177
Q

Calcitonin effect on calcium

A

Reduces blood calcium levels

  • suppresses renal tubule reabsorption of calcium (enhanced excretion)
  • inhibits bone reabsorption
178
Q

In cases of hypocalcemia, what happens to PTH, Vit D, and calcitonin?

A

PTH- secretion stimulated
Vit D- production stimulated by increase in PTH
Calcitonin- Inhibited

179
Q

In the case of hypocalcemia, what happens to the intestinal absorption of calcium?

A

It is enhanced due to Vit D

180
Q

In the case of hypocalcemia, what happens to the release of calcium and phosphate from bone?

A

It is stimulated by PTH and Vit D

181
Q

In the case of hypocalcemia, what happens to the excretion of calcium?

A

renal excretion is decreased due to enhanced reabsorption stimulated by PTH and Vit D

182
Q

In the case of hypocalcemia, what happens to the renal excretion of phosphate?

A

Increased due to PTH

183
Q

In the case of hypercalcemia, what happens to PTH, Vit D, and calcitonin?

A

PTH and Vit D are inhibited

Calcitonin secretion is stimulated

184
Q

In the case if hypercalcemia, what happens to the intestinal absorption of calcium?

A

Decreased

185
Q

In the case of hypercalcemia, what happens to the release of Ca and Phos from bone?

A

Decreased

186
Q

In the case of hypercalcemia, what happens to the renal excretion of Ca?

A

Increased

187
Q

In the case of hypercalcemia, what happens to the renal excretion of phosphate?

A

Decreased

188
Q

Normal bone turnover

A

Bone is constantly metabolically active with an annual turnover of 10% of skeleton.
PTH is constantly being turned on and off
Too high PTH=too much bone resorption= high turnover in bone=weak bone
Too low PTH= not enough turnover in bone= lower bone mass and quality= weak bone

PTH levels need to remain w/in range

189
Q

Secondary hyperparathyroidism (SHPT) and CKD

A

As kidney function decreases, two things happen

  1. ) Increased phosphate retention resulting in hyperphosphatemia. This results in hypocalcemia, stimulation of PTH, and reduced Vit D levels.
  2. ) Decreased production of calcitriol. This reduces calcium absorption by 90%.
190
Q

Hyperphosphatemia and CKD

A

Phos begins to accumulate when the GFR <30ml/min

  • Giving vitamin D to enhance calcium absorption in the small intestine also enhances phos absorption
  • Elevated PTH should enhance phos elimination renally, but as kidney function decreases this does not occur. Because PTH also releases Ca and Phos from bone, it further increases levels.
191
Q

Normal Phosphorous range

A

3.5-5.5mg/dL

192
Q

SHPT and PTH

A

Parathyroid hyperplasia occurs due to continuous production of PTH
- This makes the parathyroid gland resistant to calcium and Vit D and thus it is unable to “turn itself off”
The kidneys inability to clear PTH in cases of CKD further increases PTH levels in the body.

It is difficult to stop PTH production!

193
Q

Effect of excess PTH on the body

A

Increases rate of bone resorption which elevates serum calcium and phosphorous levels.
-There is an increased rate of bone formation so the new bone is immature and structurally weak
There is an excess of calcium-phosphorous product that leads to coronary artery calcification

194
Q

Renal Osteodystrophy

A

A condition in CKD (usually starts in stage 3) that results from SHPT, hyperphosphatemia, hypocalcemia, and Vit D deficiency

195
Q

What does renal osteodystrophy result in?

A

Skeletal conditions:

  • Osteitis fibrosa- high turnover bone disease. Occurs when PTH levels go unchecked and are very high.
  • Osteomalacia- low bone turnover caused by low calcification due to low Vit D
  • Adynamic bone disease-low bone formation caused by low levels of PTH
196
Q

Renal osteodystrophy calcifications

A

Caused by an increased calcium-phosphorous product (generally product >70). Goal is to get this product under 55!
These calcifications can occur anywhere throughout the body and are termed calciphylaxis

197
Q

Calciphylaxis

A

Severe, painful lesions that do not heal. 1 year mortality in most cases.
Calcium supplements, calcium phosphate binders, vit D and warfarin all increase risk.
Warfarin increases risk because all of the proteins that inhibit calcification are Vit K dependent.

Tx- wound care and pain management. Sodium thiosulfate prevents from occurring, control underlying issues.

198
Q

Vascular calcifications

A

Loss of arterial elasticity-> hypertension
Development of left ventricular hypertrophy
Decreased in coronary artery perfusion
Myocardial ischemia and failure! Mortality increases with PTH>495

199
Q

Screening and goals of therapy for SHPT and CKD

A

Measure PTH, phosphorous, calcium in all CKD patients with GFR <60ml/min
BMD testing to assess fracture risk

Goals of therapy- control hyperphosphatemia, correct hypocalcemia, maintain adequate Vit D levels, consider calcimetic to directly control PTH production.

200
Q

Treatment of SHPT

A

Dietary phosphorous restriction (800-100mg/day)
Minimize exposure to aluminum (alum decreases bone mineralization)
Phosphate binders
Vit D supplementations
Calcimetics
Dialysis
Parathyroidectomy

201
Q

How do phosphate binders work?

A

Bind dietary phosphorous in the GI tract to limit absorption
Treats elevated serum phos levels
Treats elevated PTH levels even if phos is not elevated

202
Q

Phosphate binders

A

Calcium acetate (PhosLo)
-calcium carbonate is less effective
Sevelamer (non calcium non alum phos binder)
Lanthanum (non calcium non alum phos binder)
Ferric citrate (Auryxia)
Sucrogerric oxyhydroxide (Velphoro)

Generally avoid aluminum and magnesium products (antacids, antidiarrheals)

203
Q

When to use calcium phosphate binders

A

Calcium products 1st line in stage 3 and 4 CKD
-Goal phos 2.7-4.6
-Goal calcium <10.5
Stage 5 CKD- either calcium or non-calcium OK (can use together)
-D/C if calcium >9.5 or PTH <150

Be very diligent to avoid hypercalcemia!

204
Q

Non-calcium binders

A

Lanthanum, sevelamer, ferric citrate, and sucroferric oxyhydroxide
Preferred if hypercalcemia is present
Preferred in dialysis patients with severe vascular calcifications (likely reduces mortality)
Preferred if pt has low PTH
Sevelamer preferred if LDL also needs lowering
Ferric sulfate preferred if iron replacement is needed

205
Q

Vitamin D options

A 
Ergocalciferol (D2)
Cholecalciferol (D3)
Calcitriol (Active Vit D)
Doxercalciferol (liver activates)
Paracalcitriol (active)
206
Q

How to choose Vit D option

A

Ideally, give enough Vit D to suppress PTH but not cause hypercalcemia and hyperphosphatemia
-Doxercalciferol and paricalcitol produce less hypercalcemia
If not on dialysis, reserve Vit D to patients not responding to other tx
Monitor PTH, calcium, phosphate, and Ca x Ph

207
Q

When to use Vit D in CKD

A

Stage 4- initiate ergocalciferol if serum vit D levels <30 and PTH elevated
-D/C if calcium >10.2
-Add/increase dose of phosphate binder if phosphorous levels >4.6. D/C Vit D if levels persist.
-Vit D therapy still used if PTH above target range, even if Vt D >30
Stage 5 =use calcitriol, paricalcitol, or doxercalciferol if PTH >300

208
Q

Calcimimetics

A

Cinacalcet- typically stage 5 CKD

  • amplifies the effect of calcium to the parathyroid gland, reducing the secretion of PTH
  • suppresses PTH w/o causing hypercalcemia or hyperphosphatemia
  • can cause hypocalcemia

Etelcalcitide- CKD+hemodialysis

  • reduces secretion of PTH
  • more potent that cinacalcet, more hypocalcemia
209
Q

Goal treatment level of corrected calcium

A

Stage 3 and 4 CKD- Normal: 8.4-10.5

Stage 5 CKD- 8.4-9.5

210
Q

Goal treatment levels of phosphorous

A

Stage 3 and 4 CKD- 2.7-4.6

Stage 5 CKD- 3.5-5.5

211
Q

Goal treatment level of Ca x Phos (use corrected Ca)

A

Stage 3, 4, and 5 CKD- <55

212
Q

Goal treatment level of PTH

A

Stage 3 CKD- 35-70
Stage 4 CKD- 70-110
Stage 5 CKD- 150-300

213
Q

Frequency of labs for the different stages of CKD

A

Stage 3 CKD- annually
Stage 4 CKD- Q 3 months
Stage 5 CKD- Q month (except PTH- every 3 months)

214
Q

Treatment of bone disease in CKD

A

High turnover disease (high PTH)

  • CKD stage 3: PTH>70
  • CKD stage 4: PTH >110
  • CKD stage 5: PTH>300

Low turnover disease (low PTH)

  • Allow PTH to return to appropriate range for stage of CKD to increase bone turnover
  • Decrease or D/C calcium phosphate binder and/or vit D (can switch to non calcium phosphate binder)
215
Q

Elemental iron content in ferrous sulfate 325mg

A

65mg

216
Q

Elemental iron content in Slow Fe 160mg (ferrous sulfate)

A

50mg

217
Q

Elemental iron content in ferrous fumarate 300mg

A

99mg

218
Q

Elemental iron content in gluconate 325mg

A

36mg

219
Q

Elemental iron content in Niferex 50mg

A

50mg

220
Q

Elemental iron content in Niferex 150mg

A

150mg

221
Q

What is the goal for iron replacement?

A

Goal is to replace 200mg elemental iron/day

Evidence is emerging that QOD therapy may work just as well (due to hepcidin upregulation when iron is given)

222
Q

Oral iron supplements

A

Generally utilized in the early stages of CKD due to convenience. For maintenance.
Poor oral absorption (10%)
Absorption is decreased by food, acid-suppressing agents
Ascorbic acid enhances absorption

223
Q

Side effects of oral iron

A

GI: abdominal cramping, constipation, nausea

Esophagitis, esophageal ulceration

224
Q

Patient information for oral iron

A 
Iron should be taken on an empty stomach but can be taken with food if the GI side effects are intolerable
Stool discoloration (dark)
Liquid discolorations may discolor teeth
225
Q

Oral iron drug interactions

A

Acid suppressing agents reduce absorption
-H2RAs (ranitidine, famotidine)
-PPIs (omeprazole, pantoprazole, etc.)
Oral quinolones (chelation)
-Ciprofloxacin, moxifloxacin, levofloxacin
-Take quinolone 4 hours before or 8 hours after
iron product.
Oral tetracyclines (chelation)
-Doxycycline, etc.
-Give iron 4-6 hours before or 1 hour after
tetracycline product.
Calcium, aluminum, magnesium containing products
-Antacids- reduce absorption

226
Q

IV iron products

A

Iron dextran, ferric gluconate, iron sucrose, ferumoxytol, ferric pyrophosphate citrate, ferric carboxymaltose

227
Q

Iron dextran dose

A

25mg test dose with 1 hr observation then dose in ml

Give IV or IM

228
Q

Ferric gluconate dose

A

Dialysis: 125mg per dose at each dialysis session for a total of 8 sessions
IV only

229
Q

Iron sucrose dose

A

Dialysis: 100mg per dose at each dialysis session for a total of 10 sessions
Non-dialysis- 200mg per dose for a total of 5 doses in a 14 day period
IV only

230
Q

Ferumoxytol dose

A

Dialysis and non-dialysis: 510mg dose then repeat 510mg 3-8 days only
IV only

231
Q

Ferric pyrophosphate citrate dose

A

Add one amp to the dialysate solution

232
Q

Ferric carboxymaltose dose

A

750mg per dose for a total of 2 doses separated by 7 days

233
Q

Newer IV iron products

A

Ferric pyrophosphate citrate- use in hemodialysis only.
-Maintains hemoglobin w/o increasing iron stores
-Can cause HA, nausea, and hypotension but more
tolerable than most.
Ferric carboxymaltose
-Not for use in HD pts
-Causes HYPERtension, nausea, flushing

234
Q

IV iron products adverse effects

A

Allergic rxn (iron dextran-BBW)
hypotension, dizziness, dyspnea, HA, back pain, syncope, rash, pruritis, nausea
-Can increase risk of bacterial infection
-Injection site reaction
-Iron overload (hemachromatosis)

Decreasing dose and rate can decrease hypotension and flushing.

235
Q

IV iron monitoring

A

Monitor Hgb and iron indices (ferritin and transferrin concentration)

236
Q

Iron overload

A

Only happens with IV iron because hepcidin will not allow oral iron to become overloaded.
No physiologic mech for iron excretion
HD patients are at the highest risk
Can cause liver failure!

237
Q

Iron toxicity

A

Overwhelms iron binding proteins leading to free iron in blood, this leads to oxidative stress and CV disease.

238
Q

ESA dosing

A

Epoetin alpha: 50-100units/kg given 3 times/week (IV or SQ). Dosing same for HD and non-HD pts

Darbepoetin- Dialysis- 0.45mcg/kg IV or SQ weekly OR 0.75mcg/kg IV q 2 weeks
non-dialysis- 0.45mcg/kg IV or SQ Q4 weeks

239
Q

ESAs and Hypertension

A

Most common adverse event
ESAs expand blood volume, increase blood viscosity, and reverse hypoxic vasodilation

25-50% of patients need antihypertensive therapy

240
Q

ESAs and BBW

A

CKD

  • increases risk of CV events with a hemoglobin target >11g/dL
  • Use the lowest procrit dose sufficient to reduce need for RBC transfusions

Perisurgery (Epoetin only)
-DVT prophylaxis is recommended.
Darbepoetin does not have the same BBW, but follows same rec

241
Q

ESAs adverse reactions

A 
Hypertension
Arthralgias/HA
Muscle spasms
Dizziness
Injection site reaction
Fever
Dyspnea (darbepoetin)
242
Q

ESA administration

A
  1. ) Check expiration date
  2. ) Wash hands
  3. ) Remove cap and wipe with alcohol swab
  4. ) Remove needle cover and inject equal amount of air into vial that you are removing.
  5. ) Withdraw dose and check for and remove air bubbles in syringe
  6. ) Clean and pinch skin where injection is to occur (45 to 90 degree angle)
  7. ) Do not recap needle and expose properly
243
Q

Darbepoetin pre-filled syringe administration

A
  1. ) Wash hands
  2. ) Remove needle cover
  3. ) Follow same subcutaneous injection instructions as normal)
  4. ) Activate needle guard
  5. ) Discard in appropriate container
244
Q

ESA patient information

A

Do not shake
Protect from light
Store in refrigerator
If multi-dose vial (MDV), good for 21 days in fridge
Counsel on S/S of heart attack, stroke, and DVT/PE
Proper admin instructions

245
Q

Calcium acetate (PhosLo) 667mg tabs

A

Calcium phosphate binder

2668mg TID with meals

246
Q

Calcium acetate (PhosLo) 667mg tabs drug interactions

A 
Oral quinolones (chelation)
    -Ciprofloxacin, etc. 
    -Separate by 1-2 hours
Oral tetracyclines (chelation)
     -Doxycycline 
     - separate by 1-2 hours
247
Q

Calcium acetate (PhosLo) 667mg tabs patient counseling

A

Must take with meals
Do not take any other calcium supplements (antacids, tums)
Constipation is common

248
Q

Calcium acetate (PhosLo) 667mg tabs monitoring

A

Serum calcium, PTH, Ca x Phos product

249
Q

Sevelamer

A

Non-calcium phosphate binder
800-2400mg TID with meals
-Give dose with snacks as well
-carbonate reduces the risk of metabolic acidosis (sevelamer carbonate= Renvela)
Can be used in combination with calcium acetate
Give all other medications 1 hour before or 3 hours after

250
Q

Sevelamer AE and monitoring

A

AE- GI upset (nausea, vomiting, dyspepsia, diarrhea)

Monitoring- Phos, PTH, provides additional LDL reduction

251
Q

Lanthanum

A

Non- calcium phosphate binder
250mg-1000mg TID with meals
Have to chew tablets before swallowing!
Can be used in combo with calcium acetate
Give all other medications 2 hours before or after

AE- N/V, abdominal pain
Monitor Phos and PTH

252
Q

Auryxia (ferric citrate)

A

Non-calcium phosphate binder
Dialysis patients only
2 tabs (420mg) TID with meals
Take tetracyclines 1 hour prior and quinolones 2 hours prior
AE- may increase iron levels, darken stools, diarrhea, nausea, constipation
Monitor Phos, PTH, ferritin, TSAT

Side benefit of increasing TSAT and serum ferritin and may reduce EPO and IV dose/need

253
Q

Sucroferric oxyhydroxide (Velphoro)

A 
Non-calcium phosphate binder
500mg (1 tab) TID with meals
Chew before swallowing
No significant drug interactions
Monitor PTH, phos
AE: darkening stools, diarrhea
Dialysis only
254
Q

Vitamin D agents adverse reactions, monitoring, and drug interactions

A

AE: hypercalcemia (all cause)
N/V, edema, HA (paricalcitol, doxercalciferol)
Monitor- PTH, calcium, phosphorous, Ca x Phos
Drug interactions- Paricalcitol increased by strong 3A4 inhibitors

255
Q

Cinacalcet (Sensipar)

A

Typically used in stage 5 pts, but can be used it stage 3 and 4
30mg PO QD initially (max 180mg) with food (increases absorption)

AE: symptoms related to hypocalcemia (paresthesias, myalgias, muscle cramping, tetany, convulsions)
N/V, diarrhea

Can be used alone or in combo with Vit D and phosphate binders

256
Q

Cinacalcet (Sensipar) monitoring parameters

A

Monitor PTH, calcium (one week after initiation and any dose change, then monthly)

257
Q

Managing hypocalcemia in Cinacalcet and etelcalcitide

A

Do not start if serum calcium <8.4mg/dL
If serum calcium falls below 8.4 but greater than 7.5 or symptomatic then can consider adding or increasing dose of calcium phosphate binders or vit D
If serum calcium less than 7.5mg/dL or adding/increasing dose of calcium phosphate binders or vit D. If not possible or still symptomatic DC cinacalcet or etelcalcitide

258
Q

Etelcalcitide (Parsabic)

A

5mg IV bolus x 3 weeks at the end of dialysis
AE: symptoms related to hypocalcemia
N/V, GI bleed
No drug interactions
Monitor corrected calcium prior to initiation and 1 week after dose initiation or adjustment, then monthly
Monitor PTH prior to initiation and then 4 weeks after dose initiation or adjustment

259
Q

AKI and medication considerations

A

Use the C-G formula but understand that it is not super accurate in AKI
Use drug reference
Adjust all medication that have >30% excretion in urine
Edema is common and changes volume of distribution
Use therapeutic drug monitoring when possible!
Loading doses are often necessary when a rapid drug effect is desired
Do not does drugs based on prerenal SCr because they are often underdosed

260
Q

CKD and drug alterations

A 
Bioavailability
Distribution volume
Protein binding
Metabolic activity
Drug excretion
261
Q

Drug bioavailability (CKD drug alterations)

A

Altered in CKD by

  • changes in gastrointestinal transit time (generally does not affect extent of absorption)
  • Increased gastric pH (usually due to ammonia buildup or phosphate binder/PPI/H2RA use). This reduces the absorption of drugs that need an acidic environment.
  • Edema of the GI tract decreases absorption
  • Decreased intestinal first pass metab increases bioavailability
  • Vomiting and diarrhea (uremic symptoms many pts have)
262
Q

Drug distribution in CKD

A 
Volume of distribution is typically increased
This is due to:
-decreased protein binding
-increased tissue binding
-increased edema

Loading doses indicated in many cases

263
Q

Protein binding in CKD

A

Protein binding of many acidic drugs (warfarin, phenytoin, metolazone) and some basic drugs (diazepam) decreased
This is due to:
-changes in protein binding sites
-Uremia
-Decreased albumin
CKD pts are spilling protein in their urine so both the amount of protein available and the ability of protein to bind decreases.
This results in more “free drug” and increases drug toxicity.
Measure unbound concentrations if possible. (ex-phenytoin)

264
Q

CKD and drug metabolism

A

CKD alters other elimination pathways, notably CYP450 system.
The second phase of metabolism (conjugation rxns) are also slowed
The kidney is a site of drug metabolism and well as the liver

265
Q

Metabolites in CKD

A

Many drugs have metabolites with pharmacologic or toxic activity
Allopurinol- Oxipurinol, responsible for suppression of xanthine oxidase
Meperidine-Normeperidine, responsible for CNS stimulation and seizures
Morphine- Morphine-6-glucuronide, prolongs analgesia

266
Q

Drug excretion in CKD

A

If more than 30% of a drug is excreted unchanged in the urine, it should be renally dosed.
Dosing depends on type of kidney disease

267
Q

Dosing adjustments in CKD

A

Reduce dose

  • tends to maintain more constant drug levels
  • Lower peak, higher trough
  • Higher risk of toxicities if dosing interval is inadequate for elimination

Lengthen dosing interval

  • Lower risk of toxicity but higher risk of subtherapeutic drug concentrations
  • Better regimen for drugs with peak-related efficacy

Can do both

268
Q

Antihypertensives- Diuretics drug dosing

A

Loops preferred over thiazides with CrCl <30ml/min
Be very cautious with K sparing diuretics due to risk of hyperkalemia
Overdosing a diuretic can lead to acute renal failure, especially in CKD

269
Q

Antihypertensives- ACE/ARB drug dosing

A

> 50% risk in SCr after initiating ACE/ARB D/C med
Fosinopril is least likely to accumulate in CKD
Hyperkalemia common

270
Q

Antihypertensives- beta blockers dosing

A

Hydrophilic beta blockers (atenolol, bisoprolol, acebutolol, nadolol) are eliminated renally.
-Reduce dose by 50% if CrCl <30mL/min

Lipophilic beta blockers (metoprolol, carvedilol, labetalol, propranolol) do not need adjustment

271
Q

Misc cardiac meds dose adjustment

A

CCBs, clonidine, hydralazine, alpha blockers do not need dose adjustment
Digoxin- reduce drug by 50% if CrCl <50mL/min. Watch levels closely

272
Q

Hypoglycemic agents dose adjustment

A

Avoid metformin if CrCl <30mL/min
-cautious in patients >80, CHF, or cirrhosis

Choose glyburide over glipizide in patients with CKD

Most oral meds need renally dosed

All insulins will accumulate

273
Q

Time-dependent killing antibiotic

A

Maintaining a drug level above the minimum level needed to kill an organism
Vanc, beta lactams

274
Q

Concentration- dependent killing antibiotic

A

Try to obtain high peaks of drug to maximize killing, let that level drop to almost nothing
Quinolones, aminoglycosides

275
Q

Dosing penicillins

A

Most need to be renally dosed

Can cause seizures, thrombocytopenia

276
Q

Dosing quinolones (cipro, levaquin, avelox)

A

Avelox is the only one that does not need to be renally dosed.
Cause QTc prolongation and increased CNS manifestations

277
Q

Dosing bactrim

A

Trimethoprim interferes with the tubular secretion of creatinine so can elevated SCr
Needs to be renally dosed

278
Q

Vancomycin dosing

A

Pharmacokinetic dosing formulas needed for patients with CKD

279
Q

Nitrofurantoin dosing

A

Toxic metabolites that accumulates in renal failure
causes peripheral neuropathy
Avoid if CrCl <60mL/min

280
Q

Aminoglycosides dosing

A

Avoid in CKD patients if possible

If no other options, must carefully calculate doses and follow levels closely

281
Q

Analgesics drug dosing

A

Most opioid narcotics have metabolites that accumulate in CKD
-Meperidine
Morphine
Tramadol

Methadone and fentanyl are the safest agents

282
Q

Toxicities associated with analgesics in CKD

A 
Increased sedation
Seizures
Resp depression
Coma
Death

Be very cautious if using ER product

283
Q

Warfarin in CKD

A

Decreased protein binding is offset by increased metabolism

Uremia increases risk of bleeding due to platelet aggregation

284
Q

Dabigatran (Pradaxa) dosing

A

75mg BID if crcl 15-30ml/min (AFIB)

285
Q

Rivaroxaban (Xarelto) dosing

A 
15mg QD (stroke prevention in AFIB)
if CrCl 15-50  avoid
286
Q

Apixaban (Eliquis) dosing

A

2.5mg BID if SCr >1.5ng/dL and either >80 or <60 pounds (AFIB)
or
SCr <1.5 and both of above

287
Q

Edoxaban dosing

A

do not use if CrCl >95mL/min

30mg QD if CrCl 15-30

288
Q

Betrixaban dosing

A

80mg once then 40mg qd if CrCl 15-30

289
Q

Low molecular weight heparins and arixtra dosing

A

Do not use if CrCl <30ml/min

290
Q

Misc drugs that accumulate in CKD

A

Gabapentin-sedation
H2 blockers- CrCl must be above 50
Metoclopramide- seizures, risk of extrapyramidal symptoms
Phenergan- sedation

291
Q

What is dialysis

A

A procedure that replaces the functions of the kidney

  • removes excess fluid
  • removes water-soluble waste (primarily BUN)
  • maintenance of electrolyte homeostasis (primarily K)
292
Q

How is dialysis performed

A

Perfusing blood and a physiologic solution (dialysate) on opposite sides of a semipermeable membrane. Dialysate puts bicarb into blood.

  • Fluid and solutes move into dialysate fluid and is then discarded
  • Drugs may also be removed
293
Q

Ultrafiltration

A

Pressure of water through a membrane under a pressure gradient (hydrostatic or oncotic)

  • Primary method of removal of excess body water
  • Ultrafiltrate describes the excess fluid removed
294
Q

Diffusion

A

Movements of substances through a semi-permeable membrane across a concentration gradient
Major process involved in IHD and PD
Rate of diffusion depends on magnitude of concentration gradient, solute characteristics, membrane characteristics, and loo/fluid flow rates

295
Q

Convection

A

Movement of solutes through a membrane by the force of water. Also called solvent drag.
Particularly useful for middle-sized particles.

296
Q

Types of dialysis

A

Hemodialysis
-Intermittent hemodialysis (IHD)
Continuous renal replacement therapy (CRRT)

Peritoneal dialysis

297
Q

Intermittent hemodialysis

A

Typically 3 days/week for 3-5 hours each

Home machines exist but are rare

298
Q

Continuous renal replacement dialysis (CRRT)

A

Indicated for hospital patients in AKI that cannot tolerate intermittent HD.
Often seen in ICU pts because you can use even in low blood flow
May utilize dialysate or replacement fluids
Dialysate allows for diffusion
Replacement fluids allow ultrafiltration and convection

299
Q

Types of CRRT

A

Slow continuous ultrafiltration (SCUF)- no fluid
Continuous Veno-Venous Hemofiltration (CVVH)- replacement fluid only
Continuous Veno-Venous Hemodialysis (CVVHD)- Dialysate only
Continuous Veno-Venous Hemodiafiltration-both

300
Q

Peritoneal Dialysis

A

A process in which a patient instills sterile fluid into his/her abdomen via a surgically implanted catheter
Peritoneal membrane serves as the dialysis filter
Old fluid is drained from the abdomen prior to adding new fluid

301
Q

Hemodialysis vascular access

A
  1. ) Arteriovenous fistula
    - created surgically by joining artery and vein usually in arm or wrist
    - Vein will bulge out
  2. ) AV graft
    - synthetic, internal
  3. ) Venous catheters
    - External access directly to large veins, capped off between uses

Success Fistula> graft>catheter

302
Q

Dialysis filters

A

Housed within the dialyzer
Provides a semi permeable barrier between blood and dialysate fluid

3 types:
conventional/standard
High-efficiency- larger SA to remove water and small molecules
High-flux- most common, greater ability to remove large molecules

303
Q

2 main goals of hemodialysis

A

1.) Maintain euvolemia, goal is to return to “dry weight” after dialysis session

  1. ) Effective removal of solutes
    - primarily urea
    - also ensure electrolyte balance
304
Q

Common complications in IHD

A

Hypotension- can use midodrine prior to dialysis
Muscle cramps
Filter thrombosis- use citrate or heparin in dialysis
Infection- treat

305
Q

Medications commonly administered in dialysis

A 
Anticoagulants
Anemia management- ESAs, iron
IV Vit D
Midodrine
Catheter lock solutions
Antu-pruritics
Antibiotics
306
Q

Peritoneal Dialysis (PD)

A 
Continuous ambulatory PD (CAPD)- done manually
Automated PD (APD)- more common, generally runs while someone sleeps
Combo
307
Q

PD fluid

A

Sterile fluid designed to use osmotic pressure to remove fluids and solutes
Volume is adjusted per patient size, typically 1.5-3L

Osmotically active ingredient- Dextrose 1.5-4.25%, the higher the dextrose concentrations the more efficient removal of water

The more often the fluid is exchanged, the greater the solute clearance

308
Q

Complications of PD

A 
Mechanical problems
Hyperglycemia
Fluid overload
Chemical peritonitis
Malnutrition
Fibrin formation in dialysate
Infections
309
Q

Intraperitoneal administration of drugs

A

For a local effect- abx, heparin

For a systemic effect- may replace injections or infusions
Examples- abx, calcitriol, insulin, epoetin alfa

310
Q

Drug dosing in dialysis

A

For specific situations:
Must determine dialyzer clearance and calculate the patients estimated drug clearance.
Must add these numbers together to get total clearance.

311
Q

Drug characteristics for dialysis

A 
Lower Vd= greater clearance
Lower Mol wt= greater clearance
Lower protein binding= greater clearance
HD flow rate=faster=better clearance
Longer sessions=greater clearance

Therapeutics II (5 decks)

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