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Therapeutics Y2 Sem 2 > Kidney > Flashcards

Kidney Flashcards

1
Q

What are the three functions of the kidney?

A

Excretory
Endocrine
Metabolic

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2
Q

What is the term renal function mean?

A

Excretion, endocrine, metabolic functions

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3
Q

What is the purpose of 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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4
Q

How is the excretory function of the kidney achieved?

A

Filtration
Reabsorption
Secretion

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5
Q

How does blood enter the glomerulus?

A

Afferent arteriole

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6
Q

What is Glomerular Filtraiton?

A

Filtered via the hydrostatic pressure through the capillaries that form the glomerulus into the bowman capsule

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7
Q

What is the filtrate composed of?

A

~20% of plasma entering the glomerulus, fluids, electrolytes, small molecules

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8
Q

What is not in the filtrate or shouldnt be?

A

Largle molecules and proteins such as blood cells

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9
Q

How does blood leave the kidney/

A

Efferent arteriole

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10
Q

What is the composition of filtrate?

A

– Glucose
– Electrolytes
– Amino acids
– Water
– Urea
– Uric acid
– Creatinine
– Protein

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11
Q

What is the process of reabsorption/

A

Substances out of the renal tubules back into the blood capillaries

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12
Q

What is reabsorption include?

A

Water, NaCl, K, HCO3, urea, amino acids, glucose

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13
Q

Which substances are secreted?

A

H+, K+, uric acid, certain drugs

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14
Q

How are substances secreted?

A

Active transport mechanisms, Diffusion

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15
Q

Which ion is the kidney responsible for secreting for acid-base balance

A

H+

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16
Q

What is the kidney responsible for with respect to reabsorption

A

HCO3-, Bicarbonate

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17
Q

What is the response in Acidosis?

A

In response to excess acid, kidneys reabsorb all
filtered bicarbonate and produces new
bicarbonate

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18
Q

What is the response of alkalosis

A

In response to too little acid, kidneys excrete
bicarbonate to restore H+ concentration to
normal

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19
Q

The endocrine functions of the kidney involve?

A

Blood pressure control, RBC production

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20
Q

What are the Key renal blood pressure mechanisms?

A

RAAS, ADH, ANP

  • Renin-Angiotensin-Aldosterone System
    (RAAS)
  • Antidiuretic hormone (ADH)
  • Atrial natriuretic peptide (ANP)
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21
Q

What does increases renin lead to?

A

– Vasoconstriction
– Sodium and water retention

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22
Q

What does angiotensin II do?

A

evokes vasoconstriction of the efferent
arteriole, to increase glomerular hydrostatic pressure

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23
Q

What is Prostaglandin E2 and I2?

A

Produced by the kidney in response to
decreased blood flow

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24
Q

What does Prostaglandin E2 and I2 do?

A

Cause vasodilation, specifically of the afferent
arteriole, to increase renal perfusion

– Why NSAIDs decrease kidney function

  • Also promote the secretion of renin
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25
Q

What is aldosterone?

A

Primary role is to stimulate tubule reabsorption of
sodium

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26
Q

What does Aldosterone indirectly do?

A

– Increases potassium excretion
– Increases H+ excretion

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27
Q

What is ADH?

A

Secreted by the posterior pituitary in response to
increased blood sodium levels / low blood volume

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28
Q

What does ADH do?

A

Increases water permeability of the collecting
ducts, promoting water reabsorption

leads to kidneys excreting more concentrated urine

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29
Q

What is antidiuresis?

A

Very concentrated urine

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30
Q

What is ANP?

A

Released in response to increased stretch of
the heart muscle

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31
Q

What does ANP do?

A

Opposes the actions of RAAS by causing
vasodilation and increased renal excretion of
sodium (opposite effect of aldosterone)

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32
Q

What are the three main metabolic functions of the kidney?

A

i. Metabolism of endogenous compounds (e.g.,
insulin)
ii. Vitamin D activation
iii. Gluconeogenesis

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33
Q

In CKD Vitamin D activation is?

A

Impaired

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34
Q

What does Vitamin D insufficiencies lead to/

A

– Leads to disruption of the calcium-
phosphorus-parathyroid hormone balance
and renal bone disease

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35
Q

What is Gluconeogensis?

A

Production of glucose from amino acids

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36
Q

Why do we check renal functions?

A

Early recognition of CKD
Adjust Drug doses
Monitoring nephrotoxic medications

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37
Q

What is creatinine?

A

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

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38
Q

What happens tot he SCr when the GFR is low?

A

Increased as this is a measurement of Cr in the serum (Blood)

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39
Q

What is the equation for classifying the severity of kidney disease?

A

CKD-EPI

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40
Q

What is the CKD-EPI measurment?

A

The CKD-EPI Creatinine Equation for Glomerular Filtration Rate (GFR) estimates GFR based on serum creatinine.

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41
Q

What is the equation used for making renal dose adjustmemnts?

A

Cockcroft-Gault

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42
Q

What is the Cockcroft-Gault equation?

A

Calculates CrCl according to the Cockcroft-Gault equation. For use in patients with stable renal function to estimate creatinine clearance. (ml/min)

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43
Q

The CKD-EPI equation is used to estimate kidney
function in a patient receiving dialysis True of False?

A

False, Given that the machine is filtering, we can no longer estimate kidney function. It is no longer relevant. CKD-EPI is out of the door.

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44
Q

Which equations are generally utilized?

A

CKD-
EPI and Cockcroft-Gault equation

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45
Q

To calculate CrCl for the purpose of DRUG/DOSE
ADJUSTMENT, use

A

COCKROFT-GAULT

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46
Q

To calculate eGFR to STAGE CKD use,

A

CKD-EPI

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47
Q

Which key component was removed from the 2012 to 2021 CKD-EPI

A

Have removed ‘race’ from the equation

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48
Q

What is the normalized or indexed eGFR?

A

Uses the mean standardized BSA of 1.73m^2

Recommended for CKD staging/progression

Units mL/min/1.73m^2

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49
Q

What is the schwartz calculation used for?

A

GFR for pediatrics

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50
Q

What is urea?

A

BUN produces as a break down product of protein

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51
Q

Does Urea truly measure GFR?

A

No because it is reabsorbed

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52
Q

Is urea increased or decreased in renal impariemnt?

A

BUN is increased in renal impairment

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53
Q

What is BUN affected by?

A

– dietary protein
– GI bleeding
– hydration status (HIGH urea means LOW water;
dehydration)

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54
Q

What is proteinuria?

A

This is a marker of kidney damage since protein should never pass the kidney membrane

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55
Q

What type of protein is lost in the urine

A

– ↑ albumin excretion sensitive to kidney damage from diabetes,
hypertension, glomerular diseases

LMW globublin in tubulointerstitial kidney disease

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56
Q

A small amount of albumin in the urine is

A

Normal

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57
Q

How do we screen albuminuria?

A

Albumin creatinine ratio (ACR)

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58
Q

What is the mg/mmol for A1

A

<3 mg/mmol

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59
Q

What is the mg/mmol for A2 category

A

3-30 mg/mmol

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60
Q

What is the mg/mmol for A3 category

A

> 30mg/mmol

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61
Q

What is Urinalysis

A

Provides info about the physical and chemical
composition of urine

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62
Q

What is the Urinalysis

A

Colour, cells, and crystals

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63
Q

What are the four different casts?

A

RBC, WBC, Fatty, and Granular

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64
Q

What is Urinary eosinophils indicate?

A

Interstitial neprhritis

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65
Q

What does glucose indicate in urine

A

Indicative of diabetes/DKA

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66
Q

What is leukocyte esterase and nitrite

A

positive in UTIs

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67
Q

Acute kidney injury is?

A

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

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68
Q

What is Anuric?

A

less than 50 mL/day urine output

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69
Q

What is Oliguric

A
  • less than 500 mL/day urine output
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70
Q

What is Non-Oliguric?

A
  • greater than 500 mL/day urine output
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71
Q

How long AKI take to develop and what develops

A

After development of AKI, may take up to 4 days
before an ↑ in SCr is observed

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72
Q

What is the criteria of AKI?

A

Change in SCr

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73
Q

Risk factors for AKI?

A

Anything that decreases blood flow to the kidneys

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74
Q

Most common causes of AKI

A

Pre-Renal
Intra-Renal or Intrinsic
Post-Renal

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75
Q

What is the most common form of AKI?

A

Pre-Renal AKI

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76
Q

What causes decreased kidney perfusion?

A

– Intravascular volume depletion (e.g., hemorrhage,
dehydration, burns, diuretic therapy)

– Decreased effective circulating volume (e.g., HF, cirrhosis)

– Hypotension (e.g., vasodilating medications, septic shock)

– Decreased glomerular filtration pressure (ACEi/ARBs +
NSAIDs)

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77
Q

What are the 4 types of intrinsic AKI?

A

Acute Tubular necrosis
Acute Interstitial nephritis
Acute Glomerulonephritis
Vascular kidney injury

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78
Q

What can cause intrinsic AKI?

A

Ischemia, Toxins, Disease

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79
Q

What are the causes of Post-renal KAI?

A

Nephrolithiasis (Kidney stones)
Prostate enlargement
Cervical cancer tumors
Drugs that crystallize

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80
Q

What drugs can crystallize and cause Post renal AKI?

A

Sulfonamides, Acyclovir, MTX

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81
Q

What are the lab values of AKI? (4)

A

Increases in SCr, BUN, acidosis, and hyperkalemia

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82
Q

What is FENa

A

Fractional excretion of sodium

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83
Q

FENa will ___ with pre-renal AKI

A

Decrease because of the activation of the RAAS system

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84
Q

FENa will ___ with tubular damage

A

Increase

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85
Q

What can be observed in urinalysis?

A

Cellular debris or casts

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86
Q

Other tests that can be done for the diagnosis of AKI

A

Renal ultrasound
Kidney biopsy
- invasive, only used if necessary

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87
Q

What is the goal of therapy for AKI?

A

Prevent further renal injury

Minimize extra renal complications

Facilitate recovery of renal function bake to baseline

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88
Q

Treatment for Pre-renal failure include (General)

A

Hydration
BP support
Fluid removal
Stop or hold drugs that impair kidney function/urine flow

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89
Q

Treatment for intrinsic renal failure

A

Discontinue offending agent
Manage underlying autoimmune disease

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90
Q

What is the post renal failure treatment?

A

Catheter to restore urine flow
Identify and remove obstruction
Adequate hydration when giving drugs with potential to crystallize

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91
Q

What is the #1 concern of AKI?

A

Hyperkalemia

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92
Q

What is the potassium range in an individual

A

3.5-5mmol/L

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93
Q

What do we see in AKI/CKD with respect to lab levels (Potassium)

A

Hyperkalemia

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94
Q

At what potassium level are we concerned with?

A

> 7mmol/L

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95
Q

What is the mild treatment of Hyperkalemia

A

Kayexalate, furosemide to increase urinary excretion

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96
Q

If severe hyperkalemia what do you do?

A

hospital

Just need to regulate everything

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97
Q

When do we Dialyze in AKI?

A

AEIOU
Acidosis, Electrolye abnormalities, Toxic ingestions, fluid overload, uremia

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98
Q

What are the clinical guidelines we use to help with Kidney related questions

A

KDIGO, Canadian society of nephrology, KDOQI (USA)

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99
Q

What are the 4 causes of CKD?

A

Diabetes, Hypertension, Immune/Inherited, Other etiology

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100
Q

What is the Definition of CKD?

A

GFR ≤ 60 mL/min/1.73m2 for 3 months or more,
with or without kidney damage

OR

Kidney damage for ≥ 3 months, with or without
decreased GFR, as evidenced by pathological
abnormalities, abnormalities in blood or urine, or as
seen by renal imaging

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101
Q

What is something we need to rule out with respect to CKD?

A

Remember low eGFR may be explained by an AKI –
may need to rule-out

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102
Q

What are the two ways we can stage CKD?

A

GFR and Albuminuria

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103
Q

What is the the values for he GFR for each category?

A
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104
Q

What are the Albuminuria categories for kidney function

A
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105
Q

HOw do we stage CKD?

A
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106
Q

How can CKD be staged?

A

Generally is asymptomatic hence screening required

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107
Q

What Can occur at stages 3 and 4 of CKD?

A

– Low energy, fatigue, confusion
– Foaming, tea-coloured, blood or cloudy urine
– Edema
– Shortness of breath
– Pruritis

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108
Q

Which stages of CKD are generally managed in primary care

A

Stage 3a-3b, 30-59ml/min

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109
Q

Which stages of CKD are generally managed with a nephrologist?

A

Stage 4-5 <30ml/min

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110
Q

What is the average rate of decline for individuals with CKD?

A

between 2.3 to 4.5
mL/min/1.73m2 per year in the MDRD study

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111
Q

What are associated with a faster rate of CKD progression?

A

Lower GFR and greater albuminuria

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112
Q

What diseases can cause quicker rates of kidney damage?

A

Diabetic nephropathy, glomerular diseases, polycystic
kidney disease, and kidney disease in transplant
recipients tend to progress more quickly

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113
Q

What diseases can cause slower progression of CKD?

A

Hypertensive kidney disease and tubulointerstitial
diseases tend to progress more slowly

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114
Q

What are non-modifiable factors of CKD?

A

African american race, male, advanced age, family history

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115
Q

What are modifiable factors of CKD?

A

– Uncontrolled hypertension
– Poor blood glucose control
– Proteinuria
– Smoking
– Obesity

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116
Q

How rapidly can untreated hypertension cause CKD decline?

A

12ml/min/year

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117
Q

If BP is less then 130/80 what GFR decline can we expect?

A

1-2ml/min/year

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118
Q

What are the blood pressure targets for individuals with high BP and CKD (Not on dialysis)

A

120

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119
Q

What is the target BP for individuals with kidney transplant?

A

130/80

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120
Q

What is the blood pressure targets for people with diabetic CKD?

A

130/80

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121
Q

What is the BP target for adults with polycystic kidney disease?

A

110

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122
Q

What is the BP target for high risk patients

A

<120

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123
Q

What is the acronym AARF?

A
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124
Q

Who is not suitable for blood pressure lowering?

A
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125
Q

What lifestyle recomendations from HTN Canada should be followed?

A

Salt restriction to 2000mg Sodium (5g of salt) per day

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126
Q

What other lifestyle recommendations are made for decreasing blood pressure?

A

Excersize, weight reduction, alcohol consumption

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127
Q

What are the first line BP agents for individuals with Kidney disease?

A

– ACE-i/ARBs
– diuretics
– long-acting CCBs

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128
Q

What factors should be considered for blood pressure management for individuals with kidney disease?

A

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

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129
Q

What is the first line treatment for HTN if a
patient has proteinuria?

A

a. ACE-i/ARBs

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130
Q

What are the benefits of Ace/Arbs?

A

Reduce BP and flomerular cap pressure,

Reduce proteinuria

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131
Q

For Diabetes and non diabetes what are the htn first line therapy for kidney disease with albuminuria guidelines?

A

– Diabetic kidney disease – if ACR > 3mg/mmol
(category A2, aka microalbuminuria)
– Nondiabetic proteinuric CKD – if ACR > 30mg/mmol
(category A3, aka macroalbuminuria)

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132
Q

What are the CI of Ace/Arb therapy

A

– Angioedema
– Bilateral renal artery stenosis
– Pregnancy

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133
Q

What precautions should be taken when on ace/arb therapy

A

– Intravascular fluid depletion
* Reduce/hold dose if severe vomiting, diarrhea, fluid depletion
– eGFR <30mL/min/m2
– Hypotension (caution if BP <110/70)
– Hyperkalemia (K+ > 5.5 mmol/L)

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134
Q

What are the monitoring parameters of ACE/ARB therapies? (4)

A
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135
Q

Why shouldnt Acei/Arb therapy be used in combination therapy?

A

Because it can lead to a worsened renal outcomes

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136
Q

Why should DRI not be used in CKD/Renal disease?

A

More adverse events including non fatal stroke, renal complications, hyperkalemia nad hypotension

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137
Q

What are the steroidal MRAs?

A

Spironolactone, eplerenone

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138
Q

What are the non-steroidal (Selective)

A

Finerenone

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139
Q

What is the benefit of Finerenone?

A

Much higher specificity for MR vs glucocorticoid androgen receptors

Reduction in albuminuria while javing less side effects

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140
Q

Which population should we consider using finerenone?

A

T2DM, eGFR >25ml/min, normal K+ levels and albuminuria >3

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141
Q

What is the concerning side effects associated with finerenone?

A

Hyperkalemia.

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142
Q

Which combination is generally recommended with finerenone

A

SGLT2 inhibitor, but not a lot of evidence

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143
Q

What is the usage of furosemide in CKD?

A

fluid retention, needs ot be dosed though every 6 hours

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144
Q

What is chlorthalidone>

A

Studied for stage 4 CKD. Hypokalemia and orthostasis though

Hypertensive agent

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145
Q

What is the benefit of using DHPCCBS?

A

Preferred over thiazides in combination with ace/arb therapy with patients with diabetes

Good CV benefits

No evidence for CKD progression slowing

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146
Q

What is the DHPCCB we should know?

A

Amlodipine?

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147
Q

What is the non-DHP CCBs?

A

Diltiazem and verapamil

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148
Q

What do nonDHP CCBs do?

A

Shown to decrease proteinuria but not to the same extent as ACEis

No evidence for slowing ckd progression

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149
Q

What role do BB play in CKD?

A

CV protection in patients with CKD, renal dose adjustement once CrCL approaches 30ml/min

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150
Q

What is clonidine?

A

Alpha 2 agonists that is good as adjunctive therapy for HTN bc no DIs with commonly used BP meds

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151
Q

What is the alpha 1 blockers?

A

Terazosin prazosin

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152
Q

What are terazosin and prazosin used for?

A

Adjunctive therapy for elevated BP in CKD patients

May consider in patients with prostatic hypertrophy

Alpha 1 antagonist

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153
Q

What are the direct vasodilators?

A

Hydralazine, Might be used as adjunct but MANY side effects

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154
Q

What is the Role of Proteinuria in CKD Progression?

A

Linked with progression of diabetic and non diabetic CKD

High risk of progressing to kidney failure

An indicator of subclinical cardiovascular disease

155
Q

What does microalbuminuria do?

A

Predicts loss of kidney function

156
Q

Why is it important to identify patients at category A2 albuminuria?

A

so appropriate therapy (ACE-i or ARB) can be instituted to slow progression

157
Q

What is considered mild proteinuria loss?

A

Mild 150-500mg (Cat 2)

158
Q

What is considered moderate proteinuria loss?

A

> 500mg Cat 3

159
Q

WhatWhat is considered nephrotic proteinuria loss?

A

> 3grams of albumin excretion or >2200mg/24hours

160
Q

What is Nephrotic syndrome?

A

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

161
Q

What are examples of kidney diseases associated with proteinuria?

A
  • Diabetic nephropathy
  • Hypertensive kidney disease
  • Primary glomerular diseases (e.g., Minimal Change
    Disease, focal and segmental glomerulosclerosis, IgA
    nephropathy)
  • Lupus nephritis
  • Post-streptococcal glomerulonephritis
162
Q

How is kidney disease associated with proteinuria sometimes treated?

A

Treated with steroids or immunosuppressants

163
Q

ACE-i/ARBs for select patients with
no hypertension why?

A

– Reduce glomerular capillary pressure and volume
– Possible direct effect on podocytes to ↓ proteinuria

164
Q

What is considered First-line therapy for kidney diseases with proteinuria?

A

– Diabetic or hypertensive kidney disease with category A2 or A3 albuminuria
– Other kidney diseases with proteinuria

165
Q

What is the potential new role for SGLT2i in proteinuria kidney disease?

A

Dapagliflozin was well tolerated and showed major improvement in those with ESKD

166
Q

What is the treatment recommendations in accordance to the CCS guidelines for CKD?

A
167
Q

How often is one screened for CKD with diabetes?

A
  • 5 years after diagnosis of T1DM
  • At time of diagnosis for T2DM
168
Q

What is the threshold of ACR used for staging nephropathy?

A
169
Q

What does blood glucose control do?

A

Prevents and delays progression of diabetic nephropathy

170
Q

What measurements will be less accurate in patients with advanced CKD? (G4-G5)

A

Hb A1C

171
Q

What does metformin do with respect to renal disease?

A

CV benefit

172
Q

What dosage of metformin do we see in individuals with eGFR 15-29ml/min?

A

500mg/day

173
Q

What is the dosing of metformin?

A
174
Q

What benefits does sglt2 inhibitors have in CKD?

A

Evidence for CV benefits AND for reducing the progression of CKD in patients with DM

175
Q

At what level does SGLT2 inhibitors not have glucose secreting effects in the kidneys?

A

eGFR >20ml/min

176
Q

When can SGLT2 inhibitors be initiated?

A
  • Not to be initiated if eGFR <20mL/min, but may be continued until dialysis
  • Can continue with a modest initial ↓ eGFR (≤30%)
177
Q

What are the dosages for SGLT2 inhibitors?

A
178
Q

Which SGLT2 inhibitor has the lowest eGFR?

A

Empagliflozin

179
Q

What evidence is their for GLP-1 agonists for kidney disease?

A

FLOW trial, but data is not yet available (used semaglutide as their study)

180
Q

What does smoking do with respect to CKD?

A

Smoking increases progression of CKD
– Mechanisms: ↑ BP & HR, ↓ renal blood flow
(constriction), vascular injury

181
Q

What nephrotoxins should be avoided in CKD?

A
  • NSAIDs, COX-2 inhibitors
  • lithium
  • aminoglycosides
  • amphotericin B
  • calcineurin inhibitors
  • cisplatin
182
Q

What drugs should you avoid combining with nephrotoxins?

A

Ace-i/Arb, NSAIDS, Diuretics

183
Q

When should dyslipidemia be treated?

> 50 years old with eGFR <60 & not on dialysis:

A

Tx with low-dose statin or statin/ezetimibe combo irrespective
of LDL level

184
Q

When should dyslipidemia be treated?

> 50 years old with CKD and eGFR >60

A

Tx with statin

185
Q

When should dyslipidemia be treated?

18–49 year old with CKD:

A

– Tx with statin treatment if estimated CV risk is >10% (high)
(e.g., prior CV event or diabetes)

186
Q

Do statins have benefit to slowing CKD progression?

A

No, but Fire and forget strategy is employed because of the CV risk reduction

187
Q

What are the issues with the usage of a statin in CKD?

A

Not well tested in your normal CKD population

188
Q

What is a concern with statins in CKD?

A

rhabdomyolysis

189
Q

For statin usage one might consider using general population doses for individuals with GFR category?

A
190
Q

What benefit is their for low dose ASA? in CKD

A
  • Low dose ASA (81 mg) has no role in primary
    CV prevention in patients with CKD
  • Would be used in secondary prevention (post-
    MI etc.)
191
Q

What are the two renal replacement therapies discussed?

A

HD, PD, Kidney transplant

192
Q

At what stage can complications of CKD be evidenct?

A

Stage G2

193
Q

With respect to Na and water imbalance what occurs in CKD?

A

Progressive loss of ability of the kidneys to excrete excess
water and sodium.

Therefore weight gain, hypertension, peripheral and pulmonary ededma

194
Q

When does sodium and water imbalance generally occur (Stage)

A

Stage 4 CKDW

195
Q

What is the treatment of Sodium and water imabalance?

A

– Sodium and water restriction
* 90mmol sodium (<2g) and 1-2L of fluid per day
– Diuretics: Furosemide +/- metolazone
– Stage 5: Dialysis

196
Q

What GFR are thiazide diuretics not effective

A

<30ml/min

197
Q

Which diuretics are preferred for water loss?

A

Furosemide, but also become less effective as kindye funciton declines

198
Q

Where does furosemide work?

A

Loop of Henle

199
Q

Where does Metolazone work?

A

Distal convulated tubule

200
Q

Why do we also treat with metolazone for add on therapy?

A

Synergistic diuresis with furosemide due to natriuretic
action at distal tubule

201
Q

What can occur with furosemide?

A

We can sometimes see resistancd

202
Q

What diuretic monitoring parameters are required?

A

Electrolytes (PotassiuM)

q1-2 weeks initially, every 3-6 months

203
Q

What is metabolic acidosis?

A

Characterized by a ↓ in the pH of the blood (acidemia) and a
↓ in serum bicarbonate levels (<22 mmol/L)

204
Q

How is metabolic acidosis exacerbated?

A

by hyperkalemia – further depresses NH3
production

205
Q

When is metabolic acidosis most prominent?

A

Stages 4-5 of CKD

206
Q

What is the treatment of metabolic acidosis?

A

Sodium bicarbonate tablets
* 325-500mg PO BID-TID (variable dose)

207
Q

What are the benefits of treatment of metabolic acidosis?

A

Decreases CKD progression, imporved nutritional status

208
Q

What is the concern with treating with sodium bicarbonate tablets?

A

Possibility of sodium loading

209
Q

When can hyperkalemia occur in CKD?

A

Generally stages 4-5 of CKD

210
Q

What is hyperkalemia generally caused by?

A

primarily due to decreased potassium excretion

211
Q

What are some of the exacerbating factors of potassium?

A

– metabolic acidosis
– excessive potassium intake from diet
– potassium sparing diuretics
– ACE-i/ARBs
– prostaglandin inhibitors (NSAIDs)

212
Q

What is considered mild hyperkalemia?

A

5.1-9 mmol/L

213
Q

What is considered severe hyperkalemia?

A

> 7mmol/L

214
Q

What does severe hyperkalemia cause?

A

Tachycardia, t wave peaking. just bad heart stuff

215
Q

What is the treatment of hyperkalemia?

A

potassium binders (remove K+ in GI tract)

216
Q

What is kayexalate?

A

– Cation exchange resin: Removes K+ ions by exchanging it
for Na2+ ions

– Not absorbed by the GI tract

217
Q

What is CKD-MBD?

A

Abnormalities of calcium, phosphorus, PTH, or
vitamin D metabolism

Abnormalities in bone turnover, mineralization,
volume, linear growth, or strength

Vascular or other soft tissue calcification

218
Q

What occurs in CKD-MBD?

A

Increased Serum phosphate

Decreased serum calcium

Decreased vitamin D

Increased Pth

219
Q

What causes increase serum phsophate?

A

Increase kidney excretion, also calcium binds to excess phosphate in the blood

220
Q

What causes decreased serum calcium?

A

Due to decreased GI absorption due to decreasted vitamin D

221
Q

Why do we see decreased vitamin D in CKD-MBD?

A

Because the final synthesis step to active calcitriol occurs in the kidneys

222
Q

What causes increase parathyroid hormone?

A

Negative feedback loop from increase calcium

223
Q

When should CKD-MBD be monitored?

A

CKD G4-5

224
Q

What does increasing serum concentrations of PO4 associate with?

A

CKD G3a-G5D, mortality

225
Q

Is there benefit in treatment to prevent hyperphosphatemia?

A

No

226
Q

What is considered increased with respect to phosphate? in ND-CKD

A

> 1.49mmol/L

227
Q

What is considered increased with respect to phosphate? in HD/PD-CKD

A

> 1.78mmol/L

228
Q

Why is the range threshold higher for HD/PD-CKD?

A

Because of how hard it is to regulate

229
Q

What do low levels of calcium contribute to?

A

secondary hyperparathyroidism
and renal osteodystrophy, and prolong the QT interval

230
Q

What do elevated serum concentrations of calcium associate with?

A

higher mortality and risk of CV events in CKD patients

231
Q

What occurs in symptomatic hypocalcemia?

A

Numbness, tingling, myalgia

232
Q

What is Ionized calcium?

A

This is the active calcium

233
Q

What is the total calcium?

A

free (ionized) + calcium
bound to albumin

234
Q

What is the corrected calcium

A

calcium adjusted for
albumin levels

235
Q

What can albumin do with respect to calcium?

A

With variable concentrations of albumin we can see variable bound calcium/unbound

236
Q

What is Severe HPT associated with?

A

calciphylaxis, CVD, neuromuscular disturbances, and
death in CKD stages 3-5D

237
Q

When should PTH be treated?

A

– PTH should be progressively rising or persistently high in
order to initiate treatment

238
Q

What are the three different types of renal osteodystrophy syndromes that may occur?

A

Hyperparathyroid bone disease
Adynamic bone disease
Osteomalacia

239
Q

What is Hyperparathyroid bone disease?

A

(high bone turnover disease)
* ↑ bone turnover, ↑ PTH levels (secondary HPT)

240
Q

What is adynamic bone disease?

A

(low bone turnover disease)
* ↓ bone turnover, normal or ↓ PTH levels

241
Q

What is osteomalacia?

A

↓ vitamin D activity

242
Q

What causes PTH increases (What pathways)

A
243
Q

What does FGF-23 stand for?

A

fibroblast growth factor 23

244
Q

What does FGF-23 do?

A

Initially maintain serum Ca & PO4 levels, at the expense of persistently high levels

245
Q

How does FGF-23 work?

A

– Promotes PO4 excretion in kidneys
– Stimulates PTH to ↑ PO4 renal excretion
– Suppresses formation of calcitriol to ↓ PO4
absorption from GI tract

246
Q

What does PTH do in the long run?

A

– ↑ Ca reabsorption and PO4 excretion in the kidneys
– ↑ Ca mobilization from bone

247
Q

In advanced CKD the kidneys fail to respond to?

A

FGF-23 and PTH, therefore Ca and PO4 worsen

248
Q

What does sustained Hyperparathyroid lead to?

A

Persistent calcium resorption form bone leading to high bone turnover

249
Q

What occurs during high bone turnover (Osteitis fibrosis cystica)

A
  • Bone pain and fragility
  • Bone marrow fibrosis (can lead to EPO resistance)
  • Also, refractory pruritis
250
Q

What does Calciphylaxis lead to

A

Calcification and occlusion of small blood vessels

Ulceration, gangrene, secondary infection and high rates of mortality

251
Q

How do we decrease phosphate in hyperparathyroid bone disease?

A

– Restrict dietary phosphate
– Phosphate binders
– Intensified dialysis schedules

252
Q

How do we suppress PTH?

A

Vitamin D
Calcimimetics
parathyroidectomy

253
Q

How do phosphate binders work?

A

All work by binding to dietary PO4 in the GI
tract → eliminated in feces

254
Q

When do phosphate binders need to be taken?

A

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

– Patient counseling is important

255
Q

What are calcium based binders used for?

A

As a phosphate binder and it can raise calcium

256
Q

What is the typical dose of calcium based binders?

A

500mg of elemental calcium po TID with meals

257
Q

What are the guidelines with respect to total recommended dose for calcium based bunders?

A

Not entirely known, needs to be monitored even in patients without hypercalcemia

258
Q

What are the adverse effects of calcium?

A

Constipation, stomach cramps, potentially hyper calcemia if co-administered with calcitriol

259
Q

What is calcitriol?

A

Vitamin D analogue that reverses low calcium

260
Q

What/Why are aluminum or magnesium phosphate bunders/

A

OTC antacids and not recommended for chronic use because of the risk of accumulation and toxicity

261
Q

What is sevelamer HCL?

A

Useful in patients with hypercalcemia or when
not controlled with Ca-based binders

262
Q

What are the AE of sevelamer HCL?

A

GI Tolerability problems

263
Q

What is lanthanum?

A

Similar to sevelamer, just a chewable form

264
Q

Was is Sucroferric oxyhydroxide

A

Newest calcium-free binder that is iron based, but does not contribute ti iron intake.

Can cause black stools and nausea similar to AE

265
Q

What does vitamin D therapy aid in?

A

Helps suppress PTH levels

266
Q

How does vitamin D therapy suppress PTH levels?

A

– Stimulates absorption of Ca in the GI tract (neg.
feedback to ↓ PTH)

– Directly acts on parathyroid gland to suppress PTH
synthesis

267
Q

What is the risk of vitamin D therapy?

A

↑ risk of hypercalcemia & hyperphosphatemia
– Causes an ↑ in FGF-23 levels

268
Q

What is the uncertainties of vitamin D therapy?

A

Uncertain if it decreases fractures or mortality?

269
Q

Should Vitamin D therapy be used in dialysis therapy?

A

No, Should not be routinely used in patients not on
dialysis – reserve for severe & progressive HPT

270
Q

What are the Vitamin D analogues?

A

Calcitriol

Alfacalcidol

271
Q

What are the AE of of Calcitriol and alfacalcidol?

A

Hypercalcemia, hyperphosphatemia
* Serum Ca and PO4 levels should be in range prior to initiating
therapy

272
Q

What are calcimimetics?

A

– Increase sensitivity of the parathyroid gland to calcium
– Directly lowers PTH concentrations without increasing
serum Ca or PO4 (useful in hypercalcemia)
– Uncertain if ↓ fracture risk, cardiac events or mortality

273
Q

What is the one calcimimetic available?

A

Cinacalcet

274
Q

What is the issue with Cincacalcet?

A

Cost, Adverse effect of nausea vomiting diarrhea and HYPOcalcemia

275
Q

What is antiresorptive treatment?

A

May ↑ BMD and ↓ fracture risk

276
Q

What is prolia used for?

A

Hypercalcemia but can lead to hypocalcemia

277
Q

What are the bisphosphonates used for?

A

– May induce/exacerbate low bone turnover

– Use with caution at CrCl <35 mL/min (rarely nephrotoxic)

278
Q

What are the bisphosphonates used?

A

alendronate

279
Q

What is prolia?

A

Poses risk of hypocalcemia but may increase BMD and decrease fracture risk.

Denosumab requires monitoring though

280
Q

What is important with respect to hyperparathyroid bone disease treatment?

A

Monitoring, PTH levels tested monthly and drug interactions

281
Q

What is a Parathyroidectomy?

A

Partial removal of parathyroid gland

Reserved for patients where PTH, calcium, phosphate abnormalities not medically correctable

“Hungry bone syndrome”

282
Q

What is Adynamic bone disease

A

Decreased bone turnover, normal or decreased PTH levels

283
Q

What is Osteomalacia?

A

Decreased vitamin D activity

284
Q

What causes adynamic bonse disaese?

A

Lack of osteobalsts/osteoclasts stimulation (Leading to no bone remodeling)

285
Q

What does adynamic bone disease result from?

A

Caclium and vitamin D supplementation and oversuppression of pTH (Possible an overtreatment of secondary hyperparathyroidiusm)

286
Q

What is osteomalacia?

A

Softening of bone

287
Q

What is the treatment of osteomalacia

A

Stopping aluminum containing phosphate binders

288
Q

What is vascular calcification?

A

Vascular smooth muscle cells change into an osteoblast-
like cell
* Increased prevalence of cardiovascular calcification in
patients with CKD

289
Q

Where is vascular calcification used for?

A

Seen in high and low bone turnover disease

290
Q

What is reviewed in anemia related CKD? (4)

A

Hgb, reticulocyte count, transferrin saturation (TSAT), ferritin

291
Q

What is the definition of anemia in CKD patients generally>

A

Normochromic, normocytic, – Anemia = Hgb < 130 g/L in males and < 120 g/L in females

292
Q

What causes the anemia seen in ESRD/CKD?

A

Hypo-proliferative, decreased reticulocytes

Generally decreased because of a loss of erythropoeitin generation in the kidneys

293
Q

What are some other causes of anemia in CKD/ESRD?

A

Decreasesd RBC half life in uremia, blood loses, bone marrow fibrosis or deficiencies in iron, folate, vit b12

294
Q

Where is iron deficient anemia generally seen?

A

Stage 4-5 CKD dueu to decrease GI absorption inflammation, frequent blood tests and blood loss in Hemodialysis

Increase in iron demands with ESA therapy

295
Q

What is absolute iron deficiency?

A

Decreased TSAT and decreased Ferritin

Total iron stores in the body are LOW

296
Q

What is functional iron deficiency?

A

Decreased TSAT, normal or increased ferritin

Might be anemia of chronic disease and adding iron may not always help

297
Q

What are the signs and symptoms of anemia?

A

– Weakness, lethargy, malaise
– Shortness of breath on exertion
– Impaired memory and concentration
– Feeling cold

298
Q

Why should we treat anemia?

A

– Decreases patient quality of life
– Risk factor for adverse outcomes (e.g., LVH, CVD)

299
Q

What are the pros of Erythropoiesis Stimulating Agents?

A

– Practically eliminated need for blood transfusions
– ↓ fatigue, symptoms of anemia (QofL)

300
Q

What are the cons of Erythropoiesis Stimulating Agents (ESAs)

A

– Failed to improve CV outcomes
– Associated with increased risk of stroke and other
thromboembolic events
* Especially if treated to higher Hgb target values

301
Q

What are the hemoglobin targets for treatment in anemia? why? (HGB)

A

100-110hgb. This is because their are more risks associated with higher targets and getting higher may not be possible

302
Q

What are the hemoglobin targets for treatment in anemia?? (TSAT)

A

Maintain >20% and to avoid iron overload

303
Q

What are the hemoglobin targets for treatment in anemia? why? (Serum ferritin)

A

> 100mcg/L (non-dialysis CKD and PD) and >200mcg/L (HD)

– Limit to avoid iron overload. Complicated b/c an acute phase
reactant – levels may be falsely elevated

304
Q

What else should be maintained in anemia?

A

Normal serum Vitamin B12 and folic acid levels (also causes of anemia)

305
Q

What are the ways we can treat anemia?

A
  • Correct blood loss (e.g., treat GI bleeding)
  • Replace vitamin, iron deficiencies
  • Erythropoiesis-Stimulating Agent (ESA) Therapy
  • Dialysis to correct uremia (as applicable)
  • Blood transfusions if required
306
Q

What should be avoided before all causes of anemia have been addressed?

A

ESA therapy

307
Q

Most patients receiving ESA therapy will require ___

A

Iron supplementation

308
Q

What may iron supplementation do?

A

Iron supplementation may further ↑ Hgb or allow a ↓ in the
ESA dose (even when TSAT and ferritin are already at target)

309
Q

For CKD patients not on dialysis or using PD, select the
route of iron administration (PO/IV) based on:

A

– severity of iron deficiency (difference in bioavailability!)
– availability of venous access
– response to prior oral iron therapy
– side effects with prior oral or IV iron therapy
– patient compliance
– Cost

310
Q

How long is an oral ion suggested to be used in patients not on dialysis or using PD?

A

1-3 months prior to initiating IV therapy

311
Q

In HD patients and most/many PD patients IV route for iron administration is generally?

A

Requried

312
Q

What are the oral formulations of iron/

A

FF,FS,FG, Feramax

313
Q

Generally what amount of iron is required for individuals requiring iron dosing?

A

100mg-200mg elemental iron daily in 2-3 divides doses

314
Q

What are the AE of Iron supplementation in iron?

A

stomach cramping, constipation, nausea, vomiting,
diarrhea, dark stools, heartburn, staining of teeth (liquid)

  • Drug interactions – calcium, etc.
315
Q

When is Iron supplementation delivered subcu utilized?

A

– Intolerant, unresponsive, non-compliant to oral iron
– Recommended 1st line in hemodialysis (HD) patients

316
Q

What are the AE of IV iron?

A

– Hypersensitivity reactions → anaphylaxis, shock
* Primarily an issue with iron dextran
– Hypotension (can be minimized by decreasing the rate of infusion)
– Infection

317
Q

What is Erythropoetin?

A

Hormone produced by kidney cells when they
sense decreased blood oxygenation

318
Q

What does Erythropoeitin do?

A

Stimulates the development and maturation of
red blood cells

Increase Oxygen carrying capacity of the blood

Restore tissue oxygenation

319
Q

What happens to erythropoeitin in CKD?

A

Generally decreases due to loss of function of kidney

320
Q

What are the treatments available for Erythropoeitin therapy

A

Epoetin and Darbepoetin

321
Q

What is Epoetin alfa?

A

– Resembles endogenous erythropoeitin
– Shorter half-life

322
Q

What is Darbepoetin alfo?

A

– Second-generation molecule
– Longer half-life

323
Q

What is the generally dosing of eprex?

A

50-100 units/kg IV or subcut 2-3 x weekly

324
Q

What is the general dosing of Aranesp?

A

0.45 mcg/kg weekly IV or subcut weekly

325
Q

What is the goal of therapy of Erythropoetin therapy/

A

– Reach Hgb target (~110 g/L) within 2 to 4 months, then maintain

– Gradual ↑ Hgb by ~10 g/L every month, to target

326
Q

What dose adjustment management should be impolred if Hgb rise is inadequate?

A

<10 g/L) after 4 weeks ↑ dose by ~25%

327
Q

What dose adjustment management should be implored if Hgb rise is excessive?

A

(>10g/L) in 2 weeks ↓ dose by ~25%

328
Q

Why should you not adjust the dose of erythropoetin therapy more then every 1 to 2 months

A

Delays in changes in the Hgb levels as it takes 2-6 weeks

329
Q

What parameters are monitored during Erythropoeitin Therapy?

A

– Serum iron, total iron binding capacity, iron
saturation, ferritin: every 1-3 months
– Hemoglobin: every 1-2 week initially, then monthly

330
Q

What is the goal of Hgb levels for someone on Erythropoetin Therapy?

A

– Hgb > 100 g/L (non-HD) or > 110 g/L (HD) : hold or ↓
dose

331
Q

What are the adverse effects of Erythropoeitin Therapy?

A

– Well-tolerate
– Hypertension (5-24%) – dose-dependent
– Flu-like symptoms (transient)
– Thrombosis – HD access site, VTE (5-10%)
– STROKE, MI, death → avoid Hgb >110g/L
– Pure Red Cell Aplasia (PRCA) (<1%)

332
Q

What are the causes of erythropoietin “resistance”

A

– Iron deficiency
– Vitamin deficiency (e.g., B12, folate)
– Bleeding
- Inflammation/infection
– Aluminum toxicity
– Inadequate dialysis

333
Q

What is the definition of Erythropoeitin resistance?

A

Incomplete or lack of response to ESA (Eprex >300U/kg/week or Aranesp 1.5 mcg/kg/wk

334
Q

What is Hypoxia-inducible factor prolyl
hydroxylase inhibitors?

A

Inhibit enzyme that degrades hypoxia-
inducible factor = Improves iron mobilization
into serum, ↑ endogenous EPO production,
which ↑ Hgb (without causing a spike in EPO)

335
Q

What can be used for the treatment of HIF PHIs?

A

Daprodustat (Jesduvroq®) approved by FDA in
2023, for treatment of anemia in patients
receiving dialysis

336
Q

How is HIF-PHIs therapy administered/adverse effects?

A
  • Dose: 1-24 mg po daily
  • AE: possible risk of malignancy
337
Q

What are the cardiovascular complications that may arise due to CKD?

A
  • Hypertension
  • Left Ventricular Hypertrophy (LVH)
  • Heart Failure
  • Hyperlipidemia
  • Pericarditis
  • Others:
    – CAD, ACS, valvular heart disease, cardiomyopathy,
    dysrhythmias, PVD
338
Q

Hypertension is ___ and a ___ of CKD

A

Cause and consequence

339
Q

How does hypertension progress in CKD?

A

General progression from stage 1-3

340
Q

What percent of patients have hypertension once they have reached stage 5 CKD?

A

90%

341
Q

What are the contributing factors of Hypertension in CKD?

A
  • Salt and water retention
  • Activation of RAAS
  • Recombinant erythropoeitin therapy (ESA)
  • Hyperparathyroidism
  • Renal vascular disease
342
Q

What are the therapies for hypertension/

A

Same as the prevention therapies (Ace/Arb therapy)

343
Q

What is the most common structural cardiac abnormality in CKD patients?

A

LVH

344
Q

What are the risk factors for LVH?

A

– Hypertension, fluid retention
– Anemia
– Diabetes
– Older age
– Abnormalities in calcium/phosphate homeostasis
– Uremia

345
Q

Generally what does LVH lead to?

A

Leads to: Decreased diastolic compliance, ischemic heart
disease, HF

346
Q

What is the treatment of LVH?

A

– Management of hypertension, fluid overload
– Treatment of anemia
– Manage calcium, phosphorus, PTH levels as per CKD-
MBD

347
Q

In CKD patients heart failure can be precipitated by?

A

– Anemia
– LVH
– Hypertension, fluid overload
– CAD

348
Q

How are the neurological complications of CKD addressed?

A

Generally occurs in ESRD

Dialysis or change dialysis prescription is generally implored

349
Q

What are the treatments for pruritis?

A

Tx (with variable success): gabapentinoids,
capsaicin, sertraline, antihistamines, Uremol lotion

350
Q

What specific agent can be used for the treatment of chronic pruritis?

A

Difelikefalin (Korsuva®):
* Peripheral kappa opioid receptor agonist

351
Q

What is the definition of DIKD?

A

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

352
Q

What is the diagnosis that generally leads to the DIKD diagnosis?

A

– Changes in SCr or urine output consistent with an AKI
– Kidney injury temporally associated with use of a
nephrotoxic drug
– Kidney injury due to a disease process ruled out

353
Q

When discussing DIKD we are generally referring to individuals who had a?

A

Healthy kidney and not CKD

354
Q

Does DIKD happen to people with CKD?

A

yes!

355
Q

What are the many presentations of DIKD?

A
  • Metabolic acidosis
  • Changes to serum electrolytes
  • Proteinuria
  • Pyuria
  • Hematuria
  • Rise in SCr (or reduced eGFR)
  • Decreased (or increased) urine output
  • Symptoms: malaise, anorexia, nausea, vomiting, volume
    overload (shortness of breath or edema)
356
Q

What is the MOA of drug induced nephrotoxicity?

A

Indirect
Direct
Obstructive
Others

357
Q

What are the indirect nephrotoxicities?

A

-Disruption of renal blood flow (pre-renal)

358
Q

What are the direct kidney injury/damage types?

A
  • Acute tubular necrosis
  • Interstitial nephritis
  • Glomerulonephritis
359
Q

What are the obstructive uropathy damage types?

A

Bladder, Tubules??

360
Q

What medications may affect the pre-renal blood flow?

A

ACE/ARB, SGLT2 inhibitors, NSAIDS, Calcineurin inhibitors

361
Q

What changes occur to renal blood flow (pre-renal_

A

Acute decrease in GFR, Kidney recieves 25% of resting cardiac output

362
Q

Who is at risk of Pre-renal blood flow complications?

A

– Heart failure, renal artery stenosis, volume depletion, CKD,
other nephrotoxins

363
Q

What is the management for pre-renal blood flow issues?

A

Recongize and address, Start low and go slow, monitor SCr, BUN, Electrolytes, Watch for concurrent diuretics and hypotensive agents
Dose decrease of stop therapy as needed

364
Q

What drugs may cause DKI/damage via intra-renal? (Tubular specific)

A

Aminoglycosides
Radiographic contrast media
Cisplatin
Amphotericin B
Calcineurin inhibitors (cyclosporine, tacrolimus)
Adefovir, cidofovir, tenofovir
Zoledronate

365
Q

What is acute tubular necrosis?

A
  • Ischemic or toxic cellular injury to renal tubules
  • Generally dose-dependent
  • Maintaining adequate hydration is an important
    preventative measure for many drugs
366
Q

Who are the at risk patients of Intra-renal injury?

A

Patients predisposed to renal injury
* Pre-existing CKD, older, multiple nephrotoxic drugs

367
Q

What is the management for direct kindye injury/damage (Intra-renal)?

A
  • Discontinue nephrotoxin
  • Hydration may be necessary
  • Monitor SCr, BUN, electrolytes
368
Q

What medicaitons cause direct kidney injury/damage intrarenally, acute intersitial nephritis

A

Penicillins/Cephalosporins
Ciprofloxacin
NSAIDs
PPIs
Loop diuretics
Allopurinol
Phenytoin

369
Q

What is acute intersitial nephritis?

A

Mainly immune related

370
Q

What is the management of Acute Interstitial Nephritis>?

A
  • Discontinue nephrotoxin, provide corticosteroids (maybe)
  • Monitor SCr, BUN and symptoms of AIN for improvement
371
Q

What is chronic interstitial nephritis?

A

Progressive (months to years) and irreversible

372
Q

What causes chronic interstitial nephritis?

A

Lithium (↑ duration), calcineurin inhibitors

373
Q

What can cause obstructive nephropathy?

A

Obstructive Nephropathy
Sulfonamides
Acyclovir
Methotrexate
Oral phosphate solution
Triamterene
Ciprofloxacin

374
Q

What can cause blockages in obstructive nephropathy?

A

Precipitated drug crystals

375
Q

myoglobin release may occur in obstructive nephropathy due to?

A

rhabdomyolysis

376
Q

Uric acid release may occur in obstructive nephropathy due to?

A

Crystials with tumor lysis syndrome

377
Q

RBC casts release may occur in obstructive nephropathy due to?

A

Glomerular hemorrhage

378
Q

Generally obstructive nephropathy is?

A

Dose-dependent
Associated with inadequate hydration (causes
supersaturation and ↓ urine pH)
Solubility may be affected by either alkaline or
acidic urine

379
Q

What is the management of Obstructive Nephrophathy?

A

– High urine volume
– Urinary alkalinization

380
Q

Renal impairment can affect drug

A

ADME

381
Q

Which changes in CKD have the most lcinical relevance?

A

Distribution and reduced elimination

382
Q

Drug distribution is impacted by (CKD)

A

edema, ↓ protein binding,
uremia and metabolic acidosis

383
Q

Drug elimination is impacted by

A

↓ filtration and alterations
in tubular secretion and reabsorption

384
Q
A

Therapeutics Y2 Sem 2 (17 decks)

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