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PHAR 255 > Kidney Disorders > Flashcards

Kidney Disorders Flashcards

1
Q

What are the main functions of the kidney?

A
  1. Excretory
  2. Endocrine (renin, prostaglandins, kinins, erythropoeitin)
  3. Metabolic (vit D activ., gluconeogenesis, insulin metabolism)
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2
Q

What are the excretory functions of the kidney?

A
  • Regulate fluid, electrolyte, and acid-base balance
  • Remove metabolic waste products & foreign chemicals from blood for urinary excretion
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3
Q

What are the components of renal excretion?

A
  • Filtration
  • Reabsorption
  • Secretion
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4
Q

What is glomerular filtration?

A

Blood is filtered by hydrostatic pressure through the capillaries that form the glomerulus into the Bowman capsule

This process results in the formation of the filtrate

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5
Q

What is the composition of filtrate?

A

Composed mainly of fluids, electrolytes, small molecules

ex. Glucose, amino acids, water, urea, creatinine

Does not include proteins and large molecules

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6
Q

What substances are reabsorbed?

A

Water and solutes including:
- NaCl, K+, HCO3-, urea, amino acids, glucose

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7
Q

What substances are secreted by the kidneys?

A

H+, K+, uric acid, certain drugs

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8
Q

What are the two secretion mechanisms?

A
  1. Active transport mechanism
  2. Diffusion across the membranes
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9
Q

What are the mechanisms of acid-base balance in the body?

A
  1. Lungs (alveolar ventilation of CO2)
  2. Kidneys (H+ excretion, bicarbonate reabsorption, phsophate and amonia buffer systems)
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10
Q

What do the kidneys do in acidosis?

A

Kidneys reabsorb all filtered bicarbonate and produces new bicarbonate

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11
Q

What doe the kidneys do in alkalosis?

A

Kidneys excrete bicarbonate to restore H+ concentration to normal

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12
Q

What are the endocrine functions of the kidney?

A
  1. Blood pressure control (renins, ADH, atrial natriuretic peptide)
  2. RBC production (erythropoeitin)
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13
Q

What is the main mechanism by which the kidneys control blood pressure?

A

Renin is released from juxtaglomerular cells in response to decreased blood pressure

Indirectly, renin leads to:
- vasoconstriction
- Na+ and water retention

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14
Q

What is the effect of the hormone, Angiotenisin II?

A

Evokes vasoconstriction of the efferent arteriole, to increase glomerular hydrostatic pressure (increased blood volume leaving circulation into the nephron tubules, which reduces overall blood volume)

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15
Q

When are prostaglandins released by the kidneys?

A

In response to decreased blood flow

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16
Q

What is the effect of prostaglandins on the kidneys?

A

Causes vasodilation of the afferent arteriole, which helps improve perfusion (increased GFR and solute excretion)

NSAIDs inhibit this mechanism, this is why they are cautioned in patients with decreased kidney function

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17
Q

What is the role of the aldosterone in kidney function?

A

Stimulate tubule reabsorption of Na+, whuch ultimately causes water retention

Indirectly also increases K+ and H+ excretion

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18
Q

What is the trigger for the release of antidiuretic hormone?

A

In respose to increased blood Na+ levels or low blood volume

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19
Q

What is the role of antidiuretic hormone in kidney function?

A

Increase water permeability of the collecting ducts, promoting water reabsorption (increased blood volume)

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20
Q

What is the trigger for the release of atrial natriuretic peptide?

A

In response to increased stretch of the heart muscle (indicative of fluid overload and is elevated in heart failure)

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21
Q

What is the role of atrial natriuretic peptide in kidney function?

A

Opposes the actions of RAAS by causing vasodilation and increased renal excretion of sodium (directly oppose action of aldosterone)

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22
Q

What is the trigger for the release of erythropoetin?

A

Produced by the kidneys in response to decreased blood oxygen levels due to conditions like anemia and hypoxia

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23
Q

What is the role of erythropoetin?

A

This hormone stimulates production of RBCs (increase O2 carrying capacity of the blood)

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24
Q

What are the metabolic functions of the kidneys?

A
  1. Metabolism of endogenous compounds
  2. Vitamin D activation
  3. Gluconeogenesis (from amino acids, minimal process)
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25
Q

What is creatinine?

A

It is a by-product of muscle metabolism that is primarily eliminated by glomerular filtration

HIgh SCr levels = low GFR, Low SCr levels = high GFR

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26
Q

What renal equation is used to classify the severity of kidney disease?

A

CKD-EPI

It is an improved version of MDRD (more accurate estimated of glomerular filtration rate)

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27
Q

Can we use kidney function equations in dose adjustment for dialysis patients?

A

No, these equations become irrelevant in dialysis patients

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28
Q

What renal equation is used to make drug/dose adjustments?

A

Cockroft-Gault

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29
Q

What is the difference between indexed and non-indexed eGFR?

A

Indexed eGFR values assume BSA(body surface area) of 1.73m^2

Non-indexed eGFR are adjusted for patient’s BSA (use height and weight to calculate BSA)

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30
Q

Why is urea important in kidney function?

A

It is the breakdown product of protein

Filtered by the kidney, but is also reabsorbed, therfore its measurement underestimates GFR

Increases in renal impairment

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31
Q

What is proteinuria?

A

It is a general term for presence of increased amounts of protein in the urine

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32
Q

What the three levels of albuminura?

A

A1: Normal to mildly increased (less than 3mg/mmol)

A2: Moderately increased (between 3 and 30mg/mmol)

A3: Severely increased (more than 30mg/mmol)

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33
Q

What are some causes for transient albuminuria?

A
  • Recent major exercise
  • UTI
  • Febrile illness
  • Heart failure decompensation
  • Menstruation
  • Acute severe elevation in blood glucse and pressure
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34
Q

What is the purpose of urinalysis?

A

Provides information abut the physical and chemical composition of urine

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35
Q

What is being analyzed in a urinalysis test?

A
  • Colour, turbidity
  • Presence of cells, micro-organisms, “casts”, crystals
  • pH analysis and specific gravity
  • Glucose, ketones (indicative of diabetes/DKA)
  • Leukocyte esterase and nitrite
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36
Q

What are urinary casts?

A

They are collection of cells that form a “cast”-like structure molded by the shape of the tubule they passed through

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37
Q

What is acute kidney injury?

A

A sudden decline renal function (hours or days) as evidenced by changes in laboratory values (SCr, BUN, and urine)

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38
Q

What are the most important changes seen in acute kidney injury?

A

Increases in SCr

Reduced urine volume

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39
Q

What are the three classifications of acute kidney injury?

A

AKI is staged based on urine production:

  1. Anuric (less than 50mL/day)
  2. Oliguric (less than 500mL/day)
  3. Non-oliguric (greater than 500mL/day)
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40
Q

What are the two criteria used to stage acute kidney injury?

A
  1. RIFLE (Risk, Injury, Failure, Loss, ESRD)
  2. AKIN (Stage 1, Stage 2, Stage 3)
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41
Q

What are the limitations of acute kidney injury staging criteria?

A

They are both based on SCr and urine output, both of which are delayed in acute kidney injury

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42
Q

What is the clinical presentation of acute kidney injury?

A

Most patients are asymptomatic

Patients may present with:
- Signs and symptoms of dehydration (pre-renal)
- Malaise, anorexia, nausea, vomiting, pruritis (uremia)
- Severe abdominal or flank pain (kidney stone)
- Decreased force of urine stream (obstruction)
- Excessive urine foaming (protein in urine)

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43
Q

What are some risk factors for AKI?

A
  • Anything that reduces blood flow to the kidneys
  • Pre-existing renal dysfunction
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44
Q

What are the three types of acute kidney injury classified based on location of injury?

A
  1. Pre-renal (blood supply)
  2. Intra-renal or intrinsic (tubules, glomerulus, intersitium, vasculature)
  3. Post-renal (collecting tubule, ureter, bladder, urethra)
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45
Q

What are some characterstics of pre-renal AKI?

A

Most common cause of AKI (about 60% of cases)

Caused by inadequate blood supply to filter the blood (hypo-perfusion)

Kidneys themselves are healthy

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46
Q

What are the four main types of intra-renal/instrinsic AKI?

A

25-35% of AKI cases

  1. Acute tubular necrosis
  2. Acute interstitial nephritis
  3. Acute glomerulonephritis
  4. Vascular kidney injury
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47
Q

What are some characteristics of post-renal AKI?

A

Less than 5% of all cases

  • Urethral obstruction
  • Ureter obstruction
  • Bladder neck obstruction
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48
Q

How is AKI diagnosed?

A
  1. Laboratory data:
    - Increased SCr
    - Increased BUN
    - acidosis
    - Hyperkalemia
  2. Urinary Na+ concentration (fraction excretion of sodium)
    - Decreased with pre-renal AKI
    - Increased with tubular damage
  3. Urinalysis
    - Casts (seen in acute tubular necrosis)
    - Hematuria, proteinuria (glomerular injury)
    - Increased WBC (UTI/pyelonephritis)
    - Crystals (post-renal AKI)
  4. Other tests
    - Renal ultrasound
    - Kidney biopsy (invasive, only used if necessary)
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49
Q

What are the goals of therapy for treatment of AKI?

A
  1. Prevent further renal injury
  2. Minimize extra-renal complications
  3. Facilitate recovery of renal function back to baseline
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50
Q

How is pre-renal AKI treated?

A
  • Hydration with IV fluids (ex. isotoonic sodium chloride)
  • BP supposrt with vasopressors
  • Fluid removal in volume overload states (use diuretics)
  • Stop or hold drugs that impair kidney function/urine flow (ex. NSAIDs)
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51
Q

How is intra-renal/intrinsic AKI treated?

A
  • Discontinue offending agent
  • Manage underlying autoimmune disease
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52
Q

How is post-renal AKI treated?

A
  • Catheter to restore urine flow
  • Identify and remove obstruction
  • Adequate hydration when giving drugs with the potential to crystallize
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53
Q

What are some symptoms associated with mild-moderate hyperkalemia (5.1-7mmol/L)?

A
  • Weakness
  • Confusion
  • Muscle twitches
  • ECG changes (peaked T-waves)
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54
Q

What are some symptoms associated with severe hyperkalemia (more than 7mmol/L)?

A
  • ECG changes like widened QRS complex, small amplitude P waves, sine waves
  • Heart block
  • Ventricular tachycardia
  • Death
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55
Q

What are some treatment options for hyperkalemia?

A

MIld:
- May not require treatment
- Kayexalate (sodium polystyrene sulfonate)
- Furosemide

Severe:
- Calcium gluconate to stabilize myocardium
-To drive K+ into cells (Insulin, sodium bicarb, salbutamol)
- Kayexalate

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56
Q

How is metabolic acidosis treated?

A

Treat with sodium bicarbonate IV

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57
Q

What are some clinical manifestations that suggest patient may require dialysis?

A

AEIOU is a good acronym

A: Acidosis
E: Electrolyte abnormalities
I: Toxic Ingestions
O: Fluid Overload
U: Uremia

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58
Q

What is the prevalence of CKD?

A

1/10 Canadians live with CKD

ESRD has increased by 35% since 2009

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59
Q

Do most CKD patients recieve care from a nephrologist?

A

No, 95% of patients with CKD are managed in primary care

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60
Q

What is CKD?

A

Chronic Kidney Disease

Defined as progresssive loss of function occurring over several months to years

Long onset is what differentiates CKD from AKI

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61
Q

What happens to renal tissue in CKD?

A

Gradual replacement of normal kidney architecture with fibrosis

This fibrosis can progress to the point when dialysis or kidney transplantation may be required (ESRD)

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62
Q

What is the etiology of CKD?

A

CKD is an umbrella term for a number of kidney disorders that result in progressive reduction in kidney function

Diabetes: 45%
HTN: 25%
Immune/Inherited: 15%
Other: 15%

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63
Q

How does CKD impact indigenous people disproportionately?

A

2.6x higher rate of ESRD in diabetic patients

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64
Q

What are the diagnostic definitions for CKD?

A
  • GFR under 60mL/min for 3 months or more with or without kidney damage

OR

  • Kidney damage for more than 3 months with or without decreased GFR
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65
Q

What are some markers for kidney damage?

A
  • Albuminuria: ACR above 3mg/mmol
  • Urine sediment abnormalities (RBC casts)
  • Electrolyte and other abnormalities due to tubular disorders
  • Abnormalities detected by histology
  • Structural abnormalities detected by imaging
  • History of kidney transplantation
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66
Q

What is the screening process for CKD?

A
  • If eGFR is below 60, retest in 3 months
  • If urine ACR is more than 3, re-measure 1 or 2 times over the next 3 months

Review slide 108

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67
Q

What are some situations that warrant referral to nephrologists?

A
  • eGFR below 30, and ACR over 60
  • eGFR below 45, but rapid decline (-5ml/min within 6 months)
  • 5-year Kidney Failure Risk Equation over 5%
  • Inability to acheive BP targets
  • Significant electrolyte disorder
  • RBC casts or hematuria
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68
Q

What is the normal decline in GFR due to aging?

A

GFR decreases by 1mL/min every year after the age of 30

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69
Q

What are some risks associated with reductions in GFR due to aging?

A
  • Higher risk of AKI (careful about titrating/initiating drugs)
  • Medication accumulation with reduced GFR (need to make renal dose adjustments)
  • Less room to lose more kidney function in the event other comorbidities develop over time (Diabetes)
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70
Q

What are the definitions of the GFR staging categories in CKD?

A

G1: more than 90
G2: 60-89
G3a: 45-59
G3b: 30-44
G4: 15-29
G5: less than 15

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71
Q

What are the definitions of the albuminuria staging categories in CKD?

A

A1: less than 3 (normal to mildly increased)
A2: 3-30 (moderately increased)
A3: more than 30 (severely increased)

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72
Q

Is CKD asymptomatic in most cases?

A

Yes, especially in the early stages (Stage 1-2)

Symptoms only become more apparent in stages 3 and 4

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73
Q

What are some symptoms of CKD?

A
  • Low energy, fatigue, confusion
  • Foaming, tea-coloured, blood or cloudy urine
  • Shortness of breath
  • Pruritis
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74
Q

What stages of CKD are dealt with primary care?

A

eGFR between 30-60mL/min (stage 3a and 3b) are managed in primary care, especially if the patient has no other comorbidities

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75
Q

What stages of CKD are dealt with nephrologists?

A

eGFR below 30mL/min (stage 2 and 5)

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76
Q

What are the goals of treatment for CKD?

A
  • Delay progression of CKD
  • CV risk reduction
  • Treat complications of CKD
  • Renal replacement therapies (RRT)
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77
Q

What does the progression of CKD look like?

A

Average rate in GFR by 2.3 to 4.5mL/min/year

Lower GFR and greater albuminuria are both associated with a faster rate of progression

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78
Q

What types of CKD etiologies show faster disease progression?

A
  • DM
  • glomerular diseases
  • Polycystic kidney disease
  • Kidney disease in kidney transplant recipients
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79
Q

What types of CKD etiologies show slower disease progression?

A
  • Hypertensive kidney disease
  • Tubulointerstitial disease
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80
Q

What are some non-modifiable risk factors that are associated with faster progression of CKD?

A
  • African male
  • Male gender
  • Advanced age
  • Family history
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81
Q

What are some modifiable risk factors that are associated with faster progression of CKD?

A
  • Uncontrolled hypertension
  • Poor blood glucose control
  • Proteinuria
  • Smoking
  • Obesity
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82
Q

What are some interventions that can delay progression of CKD?

A
  1. BP control
  2. RAAS blockade
    - ACEi/ARB therapy
    - Non-steroid MRAs
  3. BP control in people with DM
    - SGLT2i
    - GLP1RAs
  4. Smoking cessation
  5. Avoidance of nephrotoxins
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83
Q

What is the impact of good blood pressure control in CKD patients?

A

Strict BP control delays progression of CKD

  • Untreated HTN: GFR declines by 12ml/min/yr
  • BP under 130/80: GFR declines by 1-2mL/min/year
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84
Q

What is the BP target for diabetic CKD patients?

A

less than 130/80

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85
Q

What patient group was excluded from the SPRINT trial (Blood pressure trial)?

A

Patients with DM

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86
Q

What is the acronym for the inclusion criteria for the SPRINT trial?

A

AARF

A: Age over 75
A: Atherosclerosis
R: Renal (CKD)
F: Framingham score over 15%

Only need to have one of the above to apply to qualify for the SPRINT trial

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87
Q

Do we have evidence that shows benefit of BP control on CKD progression in dialysis patients?

A

No, we only have inconclusive evidence from the SPRINT trial

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88
Q

What CKD patients groups may benefit from aggressive control of BP?

A
  • Age over 50
  • Patients without a high degree of comorbidities
  • Acheive BP control without requiring a large number of antihypertensives
  • Do not have issues with adverse effects (symptomatic hypotension)
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89
Q

What CKD patient groups are not expected to see benefot from aggressive BP control?

A
  • Age over 90 or live in a nursing home
  • Require more than 3 antihypertensives to acheive aggressive target
  • At risk of falls from pastural hypotension
  • DBP (less than 60mmHg)
  • SBP (between 120-129)
  • Severe HTN (SBP above 180)
  • Patients that do not feel the benefits outweigh the risks, cost, and effort
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90
Q

What are some lifestyle modifications to help manage CKD?

A
  • Salt restriction (below 5g, and towards 2g)
  • Exercise (30-60 min of moderate intensity)
  • Weight reduction (BMI within 18.5 to 25)
  • Limit alcohol consumption (1-2 drinks/day)
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91
Q

What are some first-line agents for BP control in CKD patients?

A

Consider comorbidities, stage of CKD, degree of albuminuria, type of CKD when selecting therapy

  • ACEi/ARB
  • Diuretics
  • Long-acting CCBs
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92
Q

What is the best BP controlling agent for a CKD patient with proteinuria?

A

ACEi or ARBs are first line therapy for kidney diseases with albuminuria

  • Reduce BP and glomerular capillary pressure (reduces mechanical damage to glomerulus)
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93
Q

What are some contraindications for ACEi/ARBs?

A
  • Angioedema
  • Bilateral renal artery stenosis
  • Pregnancy
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94
Q

What are some important monitoring parameters when trying BP control in CKD patients?

A
  • Check SCr, 2-4 weeks after initiation or dose change (less than 30% increase from baseline)
  • Check K+ (should be within 3.5-5mmol/L)
  • BP (assess target acheivement)
  • Urinary albumin: Creatinine ratio (ACR)
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95
Q

Should BP dose increases be stopped once patient acheived BP target for CKD patients?

A

No, titrate to maximum tolerated dose to get maximum reduction in proteinuria

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96
Q

Can ACEi and ARBs be used in combination to treat proteinuria in CKD patients?

A

No, although this combination is superior in reducing proteinuria and BP, it actually worsened renal outcomes.

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97
Q

What is the utility of Aliskren in the treatment of proteinuria in CKD patients?

A

Not used due to adverse events

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98
Q

What is the role of MRAs in CKD treatment?

A

Non-steroidal MRA (Finerenone) can be used as an adjunct therapy (ACEi/ARB are first line) for CKD patients that have the following cormorbidities:
- T2DM
- eGFR greater than 25mL/min
- Normal K+ levels (below 4.8)
- Albuminuria (ACR below 3)

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99
Q

What is the most significant adverse effect that pharmacists need to monitor when using MRAs?

A

Hyperkalemia is a significant adverse effect that needs to be closely monitored when using MRAs

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100
Q

What is the difference between steroidal and non-steroidal MRAs?

A

Steroid MRAs (Spironolactone & Eplerenone):
- non-selective
- not used in CKD treatment

Non-steroidal (Finerenone):
- Higher specificity for the mineralocorticoid receptor vs. glucocorticoid/androgen receptors
- Reduction in albuminuria with less side effects (gynecomastia)

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101
Q

What are some limitations of finerenone (non-steroidal MRA)?

A
  • Not covered by public plans (SPDP and NIHB)
  • Less evidence in patients using SGLT2i
  • Do not use in combo with steroidal MRAs for dual treatment of HF and CKD
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102
Q

What is the role of diuretics in CKD treatment?

A

Most patients require diuretic therapy because fluid retention is an important contributor to HTN in CKD

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103
Q

What diuretic is initially started in CKD patients?

A

Thiazide diuretics (Chlorthalidone)

May switch or combine with loop diuretics (furosemide) if HTN becomes resistant to therapy

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104
Q

What is the impact of starting diuretics in CKD patients?

A

Significant reduction in SBP

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105
Q

What is the value of DHP-CCBs (amlodipine) in CKD patients?

A

BP-lowering agents in CKD

Used in combo with ACEi/ARB in diabetic patients with CKD

No evidence for slowing CKD progression

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106
Q

What is a drawback to DHP-CCBs in CKD treatment?

A

May cause fluid retention and edema (mostly around the ankles due to peripheral vasodilation)

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107
Q

What is the role of non-DHP CCBs (diltiazem and verapamil) in the treatment of CKD?

A

Used in combo with ACEi/ARB for reducing proteinuria, because it has lower ability to reduce proteinuria on its own

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108
Q

What is a drawback to non-DHP CCB use in CKD treatment?

A

Constipation and bradyarrhythmia (especially when used in combination with beta blockers)

  • CYP 3A4 inhibitor (many DIs)
109
Q

Are beta-blockers used for first-line treatment for CKD?

A

No, due to inconsistent evidence for benefit in CKD

110
Q

What is the role of alpha-2 agonists in CKD treatment?

A

Valuable as adjunctive therapy (with ACEi/ARB) for HTN because no DIs with commonly used BP meds

Precaution in elderly patients due to CNS side effects

111
Q

What is the role of alpha-1 antagonists in CKD treatment?

A

Adjunctive treatment for elevated BP in CKD patients

Consider in patients with BPH

112
Q

What is the role of direct vasodilators (hydralazine) in CKD treatment?

A

Used often by the CKD clinic

No renal dose adjustment (useful in patients with CKD that have low GFR values)

113
Q

What is the definition of proteinuria?

A

More than 150mg protein lost in urine per day

Can be albumin or other plasma proteins

114
Q

What are the categories of proteinuria?

A

A2 (Mild): 150-500mg of protein in urine
A3 (Moderate): 500-3000g of protein in urine
Nephrotic range: More than 3000mg (3g) in urine or more than 2200mg (2.2g)/day

115
Q

What are some symptoms associated with nephrotic syndrome (severe loss of protein via urine)?

A

Associated with hyperlipidemia, hypoalbuminemia, generalized edema, thromboembolic risk, foamy urine

116
Q

What is the role of proteinuria in CKD progression?

A
  • Linked with progression of diabetic and non-diabetic CKD
  • High risk of progression to kidney failure
  • Indicates subclinical CV disease
117
Q

What condition is the most significant cause of nephrotic syndrome?

A

Diabetic nephropathy

118
Q

What is microalbuminuria?

A

It is an early indicator of kidney disease (small amount of albumin found in the urine)

ACEi/ARB therapy is initiated to slow progression into more severe forms of proteinuria

119
Q

Are ACEi/ARBs useful in CKD patients with no HTN?

A

Yes, they still reduce proteinuria by lowering glomerular pressure (constriction of afferent arteriole)

ACEi/ARBs are first line therapy for kidney diseases with proteinuria

120
Q

What is the role of SGLT2i’s in CKD treatment?

A

Drugs in this drug class have both CV and kidney benefits

SGLT2is can be used in the treatment of diabetic and non-diabetic CKD

121
Q

What is the prevalence of CKD amongst diabetes patients?

A

About 40% of patients with T2DM have CKD

T2DM is a significant comorbidity (most common cause of CKD and ESRD)

122
Q

How often are diabetes patients screened for CKD?

A

T1DM: 5 years after diagnosis
T2DM: At time of diagnosis

123
Q

Does progression of CKD accelerate with more severe proteinuria?

A

Yes

124
Q

What is the benefit of blood glucose control for CKD patients?

A

Good blood glucose control prevents and delays progression of diabetic nephropathy

125
Q

What are the A1C targets for most CKD patients?

A

Less than 7.0

Less than 6.5 may be appropriate in some due to greater need to reduce CKD risk

126
Q

What are some issues with using A1C in patients on dialysis?

A

Dialysis patients often develop anemia and bleeds, so this impacts the accuracy of the A1C readings

127
Q

What is first-line therapy for blood glucose control in diabetic CKD?

A

Combination of Metformin & SGLT2i

128
Q

Does metformin have kidney protective effects?

A

There is a lack of evidence for metformin having kidney protective effects

The evidence for using metformin in CKD patients lies in CV benefit

129
Q

Are metformin doses renally adjusted?

A

Yes

eGFR greater than 60: less than 2500mg/day

eGFR 25-59: less than 2000mg/day

eGFR 30-44: less than 1000mg/day

eGFR below 30: avoid

Peritoneal dialysis: 250mg/day

Hemodialysis: 500mg after dialysis

130
Q

Can metformin be initiated in patients with GFR below 30mL/min?

A

No, but a low dose (500mg/day) can be maintained if Metformin was started before GFR fell below 30mL/min

These patients are closely monitored at the CKD clinic

131
Q

What is the consequence of SGLT2i and ACEi/ARB combination therapy in CKD?

A

The two drugs have complimenting mechanisms of action and result in the following outcomes:
- Potential for normalization of intraglomerular pressure
- Potential additive intraglomerular pressure reduction
- Potential for long-term renal protection

132
Q

If A1C levels are normal, should SGLT2is be stopped if being used for CKD treatment?

A

No, reduce doses of other antihyperglycemics like sulfonylureas before stopping a SGLT2i

133
Q

What is the lowest GFR level where SGLT2i can be used in CKD treatment?

A

Not to be initiated if eGFR is below 20mL/min, but can be maintained until dialysis

134
Q

What happens to GFR after starting a SGLT2i?

A

It may decline by up to 30% (due to reduction in glomerular pressure from efferent arteriole dilation)

135
Q

What is the impact of SGLT2i on the progression of CKD?

A

Empagliflozin can delay dialysis by up to 10 years (significant difference vs. placebo)

136
Q

What are some adverse effects associated with SGLT2i use?

A
  • Thirst
  • Polyuria
  • Genital mycotic infections
  • Hypovolemia
  • lightheadedness
  • diabetic ketoacidosis
137
Q

What is the role of GLP1RAs (semaglutide) in CKD treatment?

A

Benefit primarily seen in diabetic CKD, unlike SGLT2i that show more broader benefit (diabetic and non-diabetic CKD)

138
Q

What are the benefits of GLP1RAs broadly?

A
  • Weight loss
  • CV risk reduction
  • Insulin-sparing (need to less insulin and other antihyperglycemics)
139
Q

What is the impact of smoking on CKD?

A

Increases the progression of CKD:
- Increased BP & HR
- Reduced renal blood flow (constriction)
- Vascular injury

140
Q

What are some examples of nephrotoxic drugs?

A
  • Avoid combo of ACEi/ARB, NSAIDs, and diuretic (triple whammy)
  • NSAIDs
  • Lithium
  • Aminoglycosides
  • Amphotericin B
  • Calcineurin inhibitors
  • Cisplatin
141
Q

What is suggestion for sick day management in CKD patients?

A

Due to acute illness and fluid inbalance, it is reccomended to hold potentially nephrotoxic or renally excreted drugs

142
Q

What is an important acronym for drugs that should be avoided in sick day management?

A

SADMANS

Sulfonylureas
ACEi
Diuretics, direct renin inhibitors
Metformin
ARBs
NSAIDs
SGLT2i

143
Q

What drugs from SADMANS are renally-cleared and accumulate on sick days?

A

Sulfonylureas and Metformin

144
Q

What drugs from SADMANS are nephrotoxic and should be avoided on sick days?

A
  • ACEi
  • Diuretics
  • Direct renin inhibitors
  • ARBs
  • NSAIDs
  • SGLT2i
145
Q

What happens to CV risk as GFR declines?

A

CV risk increases

146
Q

What is the leading cause of death in CKD patients?

A

Most patients with CKD will die from CV disease before requiring dialysis

This is why it is important to screeen CKD patients for CV risk factors

147
Q

Is CKD a statin-indicated condition?

A

Yes, regardless of LDL levels

If a patient is over 50, GFR below 60 or ACR more than 3, they are started on a statin

148
Q

What is the LDL target in CKD?

A

There is no specified LDL target

“Fire and forget” strategy

149
Q

What is the benefit of statins in CKD?

A

CV risk reduction and mortality, no benefits to slowing CKD progression

150
Q

What is a good statin choice for CKD patients?

A

Atorvastatin 80mg (no renal adjustment bc it is hepatically eliminated)

Atorvastatin is less dependent on renal clearance, which is why it is preferred in CKD patients

151
Q

What is the toxicity concern for statins in patients with CKD?

A

Rhabdomyolysis is a rare adverse effect seen with high doses of statins and this can damage the kidneys. Fortunately, this is a rare adverse effects.

The most significant adverse effect in myositis

152
Q

What are the first-line components of CKD treatment?

A
  1. SGLT2i and Metformin
  2. RAAS inhibitors (if patient also has HTN)
  3. Moderate-severe intensity statin
153
Q

Review slide 215 for CKD treatment guideline

A
154
Q

What are three main types of Renal Replacement Therapy?

A
  1. Hemodialysis (Intermediate HD)
  2. Peritoneal Dialysis (Continuous Renal Replacement Therapy)
  3. Kidney transplant
    - Preferred option for eligible patients
    - Subject to organ availability
155
Q

What is conservative care management?

A

It is the option to symptomatically treat and skip RRT.

156
Q

What is the GFR target to initiate RRT in CKD patients?

A

There is no set GFR at which RRT is required (guided more by clinical status of patient)

Although most patients require RRT at GFR below 10mL/min

157
Q

What are some symptoms that suggest the need for RRT?

A
  • Serositis (eg. pericarditis), acid-base or electrolyte abnormalities, pruritis
  • Inability to control volume status or BP
  • Malnutritiom refractory to dietary intervention
  • Cognitive impairment
158
Q

What is the most common type of RRT?

A

Hemodialysis (75% of all RRT)

159
Q

In general, what happens in hemodialysis?

A

Patient’s blood is passed through an external filter to remove wastes and fluid

  • Solutes move from the blood across the filter into the dialysis solution down their concentration gradient
  • FIltered blood is then returned to the patient’s body
160
Q

How often is hemodialysis performed?

A

It is usually conducted 3x per week at the clinic for 3-5 hours for each visit

161
Q

Where are the access points for hemodialysis?

A

Requires chronic vascular access that withstand high bloof-flow rates
- Arteriovenous (AV) fistula
- Insertion of a synthetic AV graft
- Catheter in neck

162
Q

What is done to prevent blood from clotting in the dialysis machine?

A

Patients require systemic anticoagulation during the procedure

163
Q

Is hypertension a concern for patients on hemodialysis?

A

Massive fluid shifts during dialysis make patients more prone to hypotension

164
Q

What are some characteristics of the different types of RRT access to blood supply?

A
  1. Graft
    - Higher risk of infections
  2. Catheter
    - Prone to infections
  3. Fistula
    - Can take several months to heal before dialysis can be started
    - preferred method
165
Q

What are the two types of hemodialysis based on where it is given?

A
  1. Home-based
    - Greater accessibility
    - Lower flow rates are better tolerated
    - Lots of prerequisites (H20 quality, self-needling, self-machine troubleshooting, electrical and plumbing work
  2. Clinical-based
    - Only 13 clinics in Saskatchewan
    - Access to trained professionals
166
Q

What are some symptoms associated with hemodialysis?

A

Fatigue, hypotension, hypertension, cramps, N/V

167
Q

What are some issues with all types of vascular access?

A
  • Infection
  • Clotting
  • Bleeding

These issues are more common in patients with catheters vs. fistulas

168
Q

What nutrients need to be replaced following hemodialysis?

A

Water soluble vitamins (B, C) are removed during treatment
- All dialysis patients require a water-soluble vitamin formulation (Replavite)
- Avoid multivitamins contains minerals, Vitamin A or D

169
Q

What is in Replavite?

A
  • Vitamin B1, B2, B3, B6, B12
  • Folic Acid
  • Biotin
  • Vitamin C
170
Q

What are some nutrients that should be monitored in hemodialysis patients?

A

Monitor every 6-12 months
- Serum folate
- Vitamin B12

171
Q

What is the logic behind peritoneal dialysis?

A

Relies on the patient’s own peritoneal membrane to act as a filter for fluid and wastes

172
Q

What is the process of peritoneal dialysis?

A
  • 2-3L of dialysate is instilled in the peritoneal cavity through an indwelling catheter in the abdominal wall
  • Wastes and fluid diffues across the peritoneal membranes down their concentration gradient
  • Dialysate is drained and replaced with fresh solution
173
Q

What are the two main types of peritoneal dialysis?

A
  1. Continuous Ambulatory Peritoneal Dialysis (CAPD)
    - Manual exchange, usually 4-5x per day
    - Each exchange takes 30-40 minutes
  2. Automated Peritoneal Dialysis (APD)
    - Automated using a machine (called a ‘cycler’) while you sleep
    - Takes 8-10 hours
    - May also require fluid in abdomen during the day
174
Q

What are some advantages of peritoneal dialysis?

A

Added flexibility (only need to go to the CKD clinic every 1-2 months)

  • Preserves the last 10mL/min of GFR better than hemodialysis
175
Q

What are some disadvantages associated with peritoneal dialysis?

A
  • Patients must be able to perform self-care activities
  • Most common complication (Peritonitis)
    a. Inflammation and infection of the peritoneal lining results in reduced efficacy of peritoneal dialysis
176
Q

What is Continuous Renal Replacement Therapy (CRRT)?

A

Patients are hooked up to dialyser for continous periods of time (used in acute settings, not suitable for chronic RRT)

177
Q

What patient group us on Continuous Renal Replacement Therapy (CRRT)?

A

Patients on CRRT are usually in a poor condition and cannot tolerate the abrupt fluid shifts with intermittent hemodialysis

178
Q

What functions of the kidney are impaired in CKD?

A
  1. Fluid, electrolyte, and acid-base balance
  2. Metabolic waste removal
  3. Foreign body removal
  4. BP regulation
  5. Secretion of hormones
179
Q

What are the complications of CKD?

A
  1. Fluid and electrolyte abnormalities
    a. Na+ and H20 imbalance
    b. Metabolic acidosis
    c. Hyperkalemia
  2. Chronic kidney disease-mineral bone disease
  3. Anemia
  4. Other: CV, GI, Neuro complications
180
Q

What are the consequences of Na+ and H20 imbalance?

A

Symptoms become more evident in later stages of CKD

  • Weight gain
  • Hypertension
  • Peripheral and pulmonary edema
181
Q

How is Na+ and H20 imbalance treated?

A
  • Na+ and water restriction (less than 2g of Na+ and no more than 1-2 L of H20/day)
  • Diuretics (Furosemide +/- metolazone)
  • Stage 5 CKD (Dialysis)
182
Q

Why is Furosemide preferred in treatment of Na+ and water imbalance?

A

Efficacy continues to lower GFR values (useful in more advanced forms of CKD)

183
Q

What is the mechanism of loop diuretic resistance?

A

The loop diuretic prevent reabsorption at the loop of Henle, but to compensate this actions the body will absorb more in the distal convoluted tubule.

Metolazone (TZD) can be added to furosemide to inhibit the compensatory mechanism

184
Q

What is the consequence of using diuretics to manage Na+ and H20 imbalance?

A
  • Hyperkalemia (test every 1-2 weeks initiallt, reduce frequency to every 3-6 months when stable)
185
Q

What is metabolic acidosis?

A

Characterized by a reduction in the pH of the blood and a reduction in serum bicarbonate levels

Potentially due to impaired excretion of acids and/or reabsorption of bicarbonate

186
Q

Why does metabolic acidosis occur in patients with CKD?

A

The kidneys produce less ammonia to buffer the H+ in the blood, resulting in H+ retention

This is further exacerbated by hyperkalemia which further depresses ammonia production

187
Q

What are the consequences of reduced buffer capacity in metabolic acidosis?

A

The accumlated H+ ions are buffered by bicarbonate, protein (muscle wasting), and by phosphates (in bone)

188
Q

How is metabolic acidosis in CKD treated?

A

Sodium bicarbonate tablets

Benefits: Reduces CKD progression, improved nutritional status

Concern: Possibility of sodium loading (not to the same extent as NaCl)

189
Q

What is hyperkalemia?

A

An inability to maintain a normal serum potassium of 3.5-5mmol/L

190
Q

What causes hyperkalemia in CKD?

A

Decreased potassium excretion

191
Q

What are some factors that can exacerbate hyperkalemia?

A
  • Metabolic acidosis (intracellular –> extracellular K+ shift, H+ in blood is exchanged for K+ in cell)
  • Excessive potassium intake
  • ACEi/ARBs
  • NSAIDs
192
Q

What are some signs of mild-moderate hyperkalemia (5.1-7mmol/L)?

A
  • Weakness
  • Confusion
  • Muscle and respiratory paralysis
  • ECG changes (6-7mmol/L)
193
Q

What are some signs of severe hyperkalemia (more than 7mmol/L)?

A
  • ECG changes (7-8mmol/L)
    a. widened QRS, small amplitude P wave
  • ECG changes (8-9mmol/L)
    a. sinus waves
  • ECG changes (more than 9mmol/L)
    a. Heart block, ventricular tachycardia, sudden cardiac death
194
Q

How is hyperkalemia treated?

A
  • Lifestyle modification (drugs and diet)
  • Sodium polystyrene sulfonate (Kayexalate)
195
Q

What is the mechanism of action for sodium polystyrene sulfonate?

A

It is an example of a cation exchange resin
- Removes K+ ions by exchanging it for Na+ ions
- Not absorbed by the GI tract

196
Q

What are some adverse events associated with sodium polystyrene sulfonate?

A

Poorly tolerated

GI symptoms (nausea, constipation, etc.)

Significant drug binding interactions, ensure dosing of other drugs is spaced out

Newer K+ binding agents have fewer adverse events

197
Q

What agents are used to treat severe hyperkalemia (more than 7mmol/L)?

A

Review slide 258

198
Q

What is CKD-MBD?

A

Also referred to as: renal osteodystrophy or renal bone disease

A systemic disorder of mineral and bone metabolism manifested by either one, or a combination of the following:

  • Abnormalities of Ca2+, phosphorus, PTH, or vitamin D metabolism (ie. minerals)
  • Abnormalities in bone turnover, mineralization, volume, linear growth, or strength (ie. bone metabolism)
  • Vascular or other soft tissue calcification
199
Q

What is the mechanism of action for CKD-MBD?

A
  • Increased serum phosphate (due to reduced excretion)
  • Decreased serum calcium (due to reduced absorption caused by reduced Vit D, whose precursors are made in the kidney in smaller amounts in CKD)
  • Increased PTH (due to negative feedback loop)
200
Q

How is CKD-MBD diagnosed?

A
  1. Biochemical abnormalities
    - Serum Ca2+, phosphorus, PTH, alkaline phosphatase
  2. Bone abnormalities
    - Bone biopsy (needed for definitive diagnosis)
    - Bone mineral scanes (DEXA scans)
  3. Vascular calcification
    - Perform ECG
201
Q

When should CKD patients be monitored for signs of CKD-MBD?

A

Ca2+, PO4, and PTH abnormalities only appear in later stages of CKD (Stage G4-G5)

202
Q

What is the consequence of hyperphosphatemia in CKD patients?

A

Increased risk of all-cause mortality in CKD G3a to G5D

203
Q

What are the consequences of low calcium levels?

A

Contribute to secondary hyperparathyroidism and renal osteodystrophy, and prolong QT interval

204
Q

What are the consequences of elevated serum calcium?

A

Associated with higher mortality and risk of CV events in CKD patients

205
Q

What are the definitions of calcium lab values?

A

Ionized calcium = free/”active” calcium (most reliable reading)

Total calcium = (free/ionized + calcium bound to albumin)

Corrected calcium = (Ca2+ adjusted for albumin values)

206
Q

When should elevated PTH be treated in CKD patients?

A

PTH should be progressively rising or persistently high to initiate treatment (2-9x upper limit of normal)

207
Q

What are the different types of CKD-MBD (renal osteodystrophy)?

A
  1. Hyperparathyroid bone disease (high bone turnover)
  2. Adynamic bone disease (low bone turnover)
  3. Osteomalacia (reduced vit D activity)
208
Q

What is the activity of the hormone FGF-23?

A

Fibroblast growth factor 23

  • Promotes PO4 excretion in kidneys
  • Stimulates PTH to PO4 renal excretion
  • Suppresses formation of calcitriol and excretion of phosphate in the kidneys (reduced calcitriol and elevated phosphate)
209
Q

What is the activity of the hormone PTH?

A

Increased Ca2+ reabsorption and PO4 excretion in the kidneys

Increased Ca2+ mobilization from bone

210
Q

What are the roles of FGF-23 and PTH, and how do they change in CKD-MBD?

A

They help maintain serum Ca and PO4 levels in healthy patients

In patients with more advanced CKD, the kidneys fail to respond to these hormones and causes Ca+ and PO4 to worsen

211
Q

What are the consequences of sustained hyperparathyroidism?

A
  • Persistent Ca2+ resorption from bone (high bone turnover)
  • Parathyroid gland hyperplasia and becomes resistant to exogenous calcitriol therapy
212
Q

What is calciphylaxis?

A

Calcification and occlusion of small blood vessels

Leads to ulceration, gangrene, secondary infection (sepsis), and is associated with a high mortality rate

213
Q

How are elevated phosphate levels reduced?

A
  • Restrict dietary phosphate
  • Phosphate binders (in addition to dietary restriction)
  • Intensfied dialysis schedules
214
Q

How is hyperparathyroidism supresssed?

A
  • Vitamin D therapy (Calcitriol)
  • Calcimimetics (Cinacalcet)
  • Parathyroidectomy
215
Q

When do phosphate binders need to be taken?

A

Must be taken at the beginning of a meal (within the first few bites)

Taken multiple times per day with meals

Patients still need to restrict their dietary intake of phosphates

216
Q

What type of phosphate binders are first-line in CKD-MBD?

A

Calcium-based binders, due to low cost, good efficacy

Limited by their potential to contribute to hypercalcemia (may need to substitute for a non-Ca2+ based binder like Sevelamer)

217
Q

What is the benefit of Vitamin D therapy in CKD-MBD?

A

It can help reduce elevated PTH levels seen in CKD-MBD

(Vit D stimulates absorption of Ca2+, which inhibits PTH synthesis)

218
Q

What are some drawbacks to Vitamin D therapy in CKD-MBD?

A
  • Increased risk of hypercalcemia and hyperphosphatemia (increased production in FGF-23)
  • Uncertain if fracture or mortality risk is reduced by Vitamin D therapy
219
Q

What is the recommendation for Vitamin D therapy in secondary hyperparathyroidism in CKD-MBD?

A

Should not be routinely used in patients not on dialysis or for patients with severe and progressive hyperparathyroidism

220
Q

How are doses of Vitamin D therapy initiated and adjusted in patients with hyperparathyroidism in CKD-MBD?

A
  • Serum Ca and PO4 levels should be in range before initiating therapy
  • Dose adjustments based on serum Ca, PO4, and PTH levels
221
Q

What is the impact of calcimimetics on hyperparathyroidism in CKD-MBD?

A
  • Increase sensitivity of the parathyroid glan to calcium
  • Directly reduces PTH without increasing serum Ca or PO4
  • Potential for hypocalcemia
222
Q

What patient groups use calcimimetics in CKD-MBD therapy?

A

Used in dialysis patients only, usually as an adjunct to Vitamin D therapy

223
Q

What are some examples of antiresorptive treatment?

A

Denosumab (Prolia) and Bisphosphonates

224
Q

What is the impact of antiresorptive treatments in CKD-MBD treatment?

A

May increase bone mineral density and reduce fracture risk

Usually used in patients with higher GFRs (more than 30mL/min)

225
Q

What is parathyroidectomy?

A

Excision of the parathyroid gland

Usually performed in ESRD or patient is not responding to pharmaceutical treatments for CKD-MBD

226
Q

What is the consequence of a parathyroidectomy?

A

Post-operation, hungry bone syndrome can develop

Increased bone building consumes Ca2+, PO4, and PTH resulting in low levels of these minerals and hormones in the blood

227
Q

What is adynamic bone disease?

A

Low bone turnover disease

Associated with fractures and calcification

Caused by excessive Ca2+ and Vitamin D supplementation (PTH becomes too low) or over-suppression of PTH

228
Q

What is osteomalacia?

A

Inadequate mineralization of Ca2+ and PO4 (softening of bone)

Due to reduced production of calcitriol (or deposition of aluminum in the bones)

229
Q

What is vascular calcification?

A

Seen in high and low bone turnover disease

Vascular smooth cells change into an osteoblast-like cell (changes to gene expression)

230
Q

Review slide 297 for a summary of the different anemia-relevant lab values

A
231
Q

What type of anemia is associated with CKD patients?

A

In CKD, we see normochromic, normocytic anemia due to reduced erythropoietin stimulation in CKD

232
Q

What is the cause of iron deficiency in patients with CKD?

A
  • Erythropoiesis stimulating agents can increase iron demands
  • Reduced GI absorption of iron
  • Blood loss in hemodialysis
233
Q

What are the benefits of erythropoiesis stimulating agents (ESA) in CKD treatment?

A
  • Practically eliminated the need for blood transfusions
  • Reduced fatigue, symptoms of anemia (quality of life)
234
Q

What are the disadvantages of erythropoiesis stimulating agents (ESA) in CKD treatment?

A
  • Failed to improve CV outcomes
  • Associated with increased risk of stroke and other thromboembolic events
235
Q

What are the anemia target lab values in CKD patients using ESA therapy?

A

HgB: 100-110 g/L (do not aim for 120-130 due to increased risk of thromboembolic events due to ESA therapy)

Tsat%: Maintain 20%

Serum ferritin: more than 100mcg/L(non-dialysis) & more than 200mcg/L(hemodialysis patients)

236
Q

When is IV iron used to supplement iron deficiency in patients on ESA therapy for CKD?

A
  • Patient is intolerant, unresponsive, or non-compliant to oral iron
  • Recommended 1st line in hemodialysis patients
237
Q

What is Erythropoietin?

A

It is a hormone produced by kidney cells (production becomes deficient in CKD) when they sense decreased blood oxygenation

Stimulates development and maturation of RBCs

238
Q

What are the two main ESA agents?

A

Both are available as single-use pre-filled syringes

Epoeitin alfa (Eprex)
- Resembles endogenous erythropoeitin

Darbepoetin alfa (Aransep)
- Second-generation molecule (longer half-life)

239
Q

How is ESA therapy monitored?

A
  • Serum iron, TIBC, Tsat, ferritin (every 1-3 months)
  • Hemoglobin (every 1-2 weeks intially, then monthly)
    If HgB is more than 100g/L (non-HD) or more than 110g/L (HD), hold or reduce dose
240
Q

What are some adverse effects associated with ESA therapy?

A

Overall well-tolerated if monitored adequately

Other adverse events are due to unchecked elevated hemoglobin (HTN, flu-like symptoms, thrombosis, etc)

241
Q

What is erythropoietin resistance?

A

It is an incomplete or lack of response to ESA (if this continues a transfusion may be required)

Caused primarily by iron deficiency, but vitamin deficiency, bleeding, and inflammation can also contribute to erythropoietin resistance

242
Q

What is the role of hypertension in CKD?

A

HTN is both a cause and consequence of CKD (due to activation of RAAS)

90% of patients have HTN by stage 5 CKD

243
Q

What are some contributing factors for HTN in CKD patients?

A
  • Salt and water retention
  • Activation of RAAS
  • ESA therapy
  • Hyperparathyroidism
  • Renal vascular disease
244
Q

What are some conditions experienced by CKD patients that can cause heart failure?

A
  • Anemia (increased tachycardia)
  • LVH
  • HTN (fluid overload)
  • CAD
245
Q

What causes most neurological complications associated with CKD?

A

Uremia (build up of urea in the blood)

246
Q

What are some characteristics of chronic pruritis in CKD patients?

A
  • Affects 40% of patients with ESRD
  • No clear cause, making treatment a challenge (potentially due to high urea or PTH)

Difelikefalin (Korsuva) is a peripheral kappa opioid receptor agonist and is the only therapy officially indicated for pruritus in hemodialysis patients

247
Q

What is the definition of drug-induced kidney disease?

A

Adverse functional or structural change to kidney after administration of a drug, chemical, or biological product

Kidney injury due to a disease process needs to be ruled out, drug-induced kidney disease occurs in patients with healthy kidneys.

248
Q

What are some mechanisms for drug-induced kidney disease?

A
  1. Indirect nephrotoxicity (disruption of renal blood flow, pre-renal)
  2. Direct kidnet injury/damage (intra-renal)
    - Acute tubular necrosis
    - Intersititial nephritis
    - Glomerulonephritis
  3. Obstructive uropathy (post-renal)
  4. Others
249
Q

What are some drugs that can make changes to renal blood flow, a risk factor for drug-induced kidney disease?

A

-ACEi/ARB
- SGLT2i
- NSAIDs
- Calcineurin inhibitors

250
Q

What patient group is at most significant risk for drug-induced kidney diseases following administration of drug that changes renal blood flow?

A

HF, renal artery stenosis, volume depletion, CKD, other nephrotoxins

251
Q

How can risk for drug-induced kidney disease caused by drugs that change renal blood flow be effectively managed?

A
  • Recognize and address other risk factors (HF, CKD, other nephrotoxins)
  • Titrate slowly from a small initial dose (monitor regularly)
  • Monitor SCr, BUN, electrolytes
  • Reduce dose or d/c therapy
252
Q

What are some drugs that can cause damage to the renal tubules (intra-renal damage)?

A
  • Aminoglycosides
  • Radiographic contrast media
  • Cisplatin
  • Calcineurin inhibitors
  • Specific antivirals
253
Q

What is the most common type of drug-induced kidney disease in the hospital?

A

Acute tubular necrosis

  • Ischemic or toxic cellular injury to renal tubules
254
Q

How can acute tubular necrosis be mitigated following administration?

A
  • Discontinue nephrotoxin
  • Maintaining adequate hydration is an important preventative measure for many of these drugs
  • Monitor SCr, BUN, electrolytes
255
Q

What are some drugs that can cause damage to the tissues that surround the tubules (intra-renal, interstitial nephritis)?

A
  • Penicillins/Cephalosporins
  • Ciprofloxacin
  • NSAIDs
  • PPI
  • Loop diuretics
  • Allopurinol
256
Q

What is acute interstitial nephritis?

A

Immune-mediated kidney injury associated with hypersensitivity reactions (allergic reactions)

Idiosyncratic

Injury usually occurs 7-14 days after administration

257
Q

How is acute interstitial nephritis managed?

A
  • Discontinue nephrotoxin (if done early, kidney function can return to normal)
  • Monitor SCr, BUN, and symptoms of AIN (fever, rash, arthralgia, eosinophilia)
258
Q

What is chronic interstitial nephritis?

A

It is a progressive (months to years) and it is irreversible

ex. Lithium and calcineurin inhibitors can cause chronic interstitial nephritis

259
Q

What are some drugs that can cause a blockage in the tubules (obstructive nephropathy)?

A
  • Sulfonamides
  • Acyclovir
  • Methotrexate
  • Oral phosphate solution
  • Triamtene
  • Ciprofloxacin
260
Q

How can obstructive nephropathy occur?

A

Directly by drugs: precipitated drug crystals (ex. acyclovir, ciprofloxacin)

Indirectly by drugs: tissue degradation products related by drug (myoglobin in rhabdo, uric acid crystals, RBC casts)

Precipitated minerals: calcium phosphate or calcium oxalate

261
Q

What are some risk factors for obstructive nephropathy?

A

Associated with inadequate hydration (causes supersaturation and drop in urine pH, more acidic)

262
Q

How is obstructive nephropathy managed?

A
  • High urine volume (drink more water)
  • Urinary alkinization
263
Q

What are some drug dosing issues in patients with CKD?

A
  • Reduced excretion of drugs and/or their metabolites
  • Increased sensitivity to drugs (highly albumin-bound drugs in hypoalbuminemia)
  • Diminished tolerance to side effects (especially in the elderly)
  • Loss in efficacy (especially with SGLT2i and TZDs)
264
Q

What equation is used to determine the degree to which drug elimination will be effected in renal impairment usually estimated from CrCl?

A

Cockroft-Gault

*CKD-EPI is only used to stage CKD

Do not use either equation alone to make therapy changes, also reflect on clinical factors

265
Q

At what creatinine clearance, do pharmacists need to start considering dose adjustments?

A

When CrCL falls below 60mL/min

266
Q

What are some clinical considerations before making therapy changes in patients with renal impairment?

A
  • Is the drug safe and effective in patients with renal dysfunction (is drug accumulation tolerable?)
  • Is the drug nephrotoxic (any available substitutes)
  • Does the clinical situation warrant an immediate effect/benefit from the drug
  • If benefit is not immediately required, can the dose be titrated?
267
Q

What is the step-wise process for adjusting drug doses according to renal impairment?

A
  1. Take a thorough med history
  2. Stermine the degree of renal impairment (CrCL, GFR, use multiple equations to compare values)
  3. Assess the drug being added
    - Indication, dose, interval, duration of therapy
    - Primary method of ADME
    - Potential for nephrotoxicity
    - AE, risks for drug accumulation
  4. Choose less nephrotoxic drugs wherever possible
  5. Determine appropriate dose for degree of renal impairment
  6. Monitor and reassess drug therapy
  7. Monitor SCr and reassess drug dosing periodically (continuously and over time)
268
Q

Is estimating creatinine clearance from SCr useful in dialysis patients?

A

No, because creatinine is removed in HD or PD

CrCl is generally considered to be 10mL/min in dialysis patients

269
Q

What are some basic management strategies for CKD?

A
  1. Control BP and manage CVD (ACEi/ARB, statin, ASA)
  2. Reduce albuminuria (ACEi/ARB, SGLT2i, control BG, weight loss, lower dietary Na+ intake)
  3. Manage diabetes (individualize A1C targets, adjust med doses)
  4. Limit nephrotoxins and adjust med doses (sick-day management)
  5. Monitor for and manage CKD complications (PTH, serum phosphorus, Ca2+, VitD, HgB, iron status)

PHAR 255 (15 decks)

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