Kidney Disorders Flashcards
1
Q
What are the main functions of the kidney?
A
- Excretory
- Endocrine (renin, prostaglandins, kinins, erythropoeitin)
- Metabolic (vit D activ., gluconeogenesis, insulin metabolism)
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
3
Q
What are the components of renal excretion?
A
- Filtration
- Reabsorption
- Secretion
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
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
6
Q
What substances are reabsorbed?
A
Water and solutes including:
- NaCl, K+, HCO3-, urea, amino acids, glucose
7
Q
What substances are secreted by the kidneys?
A
H+, K+, uric acid, certain drugs
8
Q
What are the two secretion mechanisms?
A
- Active transport mechanism
- Diffusion across the membranes
9
Q
What are the mechanisms of acid-base balance in the body?
A
- Lungs (alveolar ventilation of CO2)
- Kidneys (H+ excretion, bicarbonate reabsorption, phsophate and amonia buffer systems)
10
Q
What do the kidneys do in acidosis?
A
Kidneys reabsorb all filtered bicarbonate and produces new bicarbonate
11
Q
What doe the kidneys do in alkalosis?
A
Kidneys excrete bicarbonate to restore H+ concentration to normal
12
Q
What are the endocrine functions of the kidney?
A
- Blood pressure control (renins, ADH, atrial natriuretic peptide)
- RBC production (erythropoeitin)
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
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)
15
Q
When are prostaglandins released by the kidneys?
A
In response to decreased blood flow
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
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
18
Q
What is the trigger for the release of antidiuretic hormone?
A
In respose to increased blood Na+ levels or low blood volume
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)
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)
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)
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
23
Q
What is the role of erythropoetin?
A
This hormone stimulates production of RBCs (increase O2 carrying capacity of the blood)
24
Q
What are the metabolic functions of the kidneys?
A
- Metabolism of endogenous compounds
- Vitamin D activation
- Gluconeogenesis (from amino acids, minimal process)
25
What is creatinine?
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
26
What renal equation is used to classify the severity of kidney disease?
CKD-EPI
It is an improved version of MDRD (more accurate estimated of glomerular filtration rate)
27
Can we use kidney function equations in dose adjustment for dialysis patients?
No, these equations become irrelevant in dialysis patients
28
What renal equation is used to make drug/dose adjustments?
Cockroft-Gault
29
What is the difference between indexed and non-indexed eGFR?
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)
30
Why is urea important in kidney function?
It is the breakdown product of protein
Filtered by the kidney, but is also reabsorbed, therfore its measurement underestimates GFR
Increases in renal impairment
31
What is proteinuria?
It is a general term for presence of increased amounts of protein in the urine
32
What the three levels of albuminura?
A1: Normal to mildly increased (less than 3mg/mmol)
A2: Moderately increased (between 3 and 30mg/mmol)
A3: Severely increased (more than 30mg/mmol)
33
What are some causes for transient albuminuria?
- Recent major exercise
- UTI
- Febrile illness
- Heart failure decompensation
- Menstruation
- Acute severe elevation in blood glucse and pressure
34
What is the purpose of urinalysis?
Provides information abut the physical and chemical composition of urine
35
What is being analyzed in a urinalysis test?
- Colour, turbidity
- Presence of cells, micro-organisms, "casts", crystals
- pH analysis and specific gravity
- Glucose, ketones (indicative of diabetes/DKA)
- Leukocyte esterase and nitrite
36
What are urinary casts?
They are collection of cells that form a "cast"-like structure molded by the shape of the tubule they passed through
37
What is acute kidney injury?
A sudden decline renal function (hours or days) as evidenced by changes in laboratory values (SCr, BUN, and urine)
38
What are the most important changes seen in acute kidney injury?
Increases in SCr
Reduced urine volume
39
What are the three classifications of acute kidney injury?
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)
40
What are the two criteria used to stage acute kidney injury?
1. RIFLE (Risk, Injury, Failure, Loss, ESRD)
2. AKIN (Stage 1, Stage 2, Stage 3)
41
What are the limitations of acute kidney injury staging criteria?
They are both based on SCr and urine output, both of which are delayed in acute kidney injury
42
What is the clinical presentation of acute kidney injury?
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)
43
What are some risk factors for AKI?
- Anything that reduces blood flow to the kidneys
- Pre-existing renal dysfunction
44
What are the three types of acute kidney injury classified based on location of injury?
1. Pre-renal (blood supply)
2. Intra-renal or intrinsic (tubules, glomerulus, intersitium, vasculature)
3. Post-renal (collecting tubule, ureter, bladder, urethra)
45
What are some characterstics of pre-renal AKI?
Most common cause of AKI (about 60% of cases)
Caused by inadequate blood supply to filter the blood (hypo-perfusion)
Kidneys themselves are healthy
46
What are the four main types of intra-renal/instrinsic AKI?
25-35% of AKI cases
1. Acute tubular necrosis
2. Acute interstitial nephritis
3. Acute glomerulonephritis
4. Vascular kidney injury
47
What are some characteristics of post-renal AKI?
Less than 5% of all cases
- Urethral obstruction
- Ureter obstruction
- Bladder neck obstruction
48
How is AKI diagnosed?
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)
49
What are the goals of therapy for treatment of AKI?
1. Prevent further renal injury
2. Minimize extra-renal complications
3. Facilitate recovery of renal function back to baseline
50
How is pre-renal AKI treated?
- 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)
51
How is intra-renal/intrinsic AKI treated?
- Discontinue offending agent
- Manage underlying autoimmune disease
52
How is post-renal AKI treated?
- Catheter to restore urine flow
- Identify and remove obstruction
- Adequate hydration when giving drugs with the potential to crystallize
53
What are some symptoms associated with mild-moderate hyperkalemia (5.1-7mmol/L)?
- Weakness
- Confusion
- Muscle twitches
- ECG changes (peaked T-waves)
54
What are some symptoms associated with severe hyperkalemia (more than 7mmol/L)?
- ECG changes like widened QRS complex, small amplitude P waves, sine waves
- Heart block
- Ventricular tachycardia
- Death
55
What are some treatment options for hyperkalemia?
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
56
How is metabolic acidosis treated?
Treat with sodium bicarbonate IV
57
What are some clinical manifestations that suggest patient may require dialysis?
AEIOU is a good acronym
A: **A**cidosis
E: **E**lectrolyte abnormalities
I: Toxic **I**ngestions
O: Fluid **O**verload
U: **U**remia
58
What is the prevalence of CKD?
1/10 Canadians live with CKD
ESRD has increased by 35% since 2009
59
Do most CKD patients recieve care from a nephrologist?
No, 95% of patients with CKD are managed in primary care
60
What is CKD?
Chronic Kidney Disease
Defined as progresssive loss of function occurring over several months to years
Long onset is what differentiates CKD from AKI
61
What happens to renal tissue in CKD?
Gradual replacement of normal kidney architecture with fibrosis
This fibrosis can progress to the point when dialysis or kidney transplantation may be required (ESRD)
62
What is the etiology of CKD?
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%
63
How does CKD impact indigenous people disproportionately?
2.6x higher rate of ESRD in diabetic patients
64
What are the diagnostic definitions for CKD?
- 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
65
What are some markers for kidney damage?
- 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
66
What is the screening process for CKD?
- 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
67
What are some situations that warrant referral to nephrologists?
- 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
68
What is the normal decline in GFR due to aging?
GFR decreases by 1mL/min every year after the age of 30
69
What are some risks associated with reductions in GFR due to aging?
- 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)
70
What are the definitions of the GFR staging categories in CKD?
G1: more than 90
G2: 60-89
G3a: 45-59
G3b: 30-44
G4: 15-29
G5: less than 15
71
What are the definitions of the albuminuria staging categories in CKD?
A1: less than 3 (normal to mildly increased)
A2: 3-30 (moderately increased)
A3: more than 30 (severely increased)
72
Is CKD asymptomatic in most cases?
Yes, especially in the early stages (Stage 1-2)
Symptoms only become more apparent in stages 3 and 4
73
What are some symptoms of CKD?
- Low energy, fatigue, confusion
- Foaming, tea-coloured, blood or cloudy urine
- Shortness of breath
- Pruritis
74
What stages of CKD are dealt with primary care?
eGFR between 30-60mL/min (stage 3a and 3b) are managed in primary care, especially if the patient has no other comorbidities
75
What stages of CKD are dealt with nephrologists?
eGFR below 30mL/min (stage 2 and 5)
76
What are the goals of treatment for CKD?
- Delay progression of CKD
- CV risk reduction
- Treat complications of CKD
- Renal replacement therapies (RRT)
77
What does the progression of CKD look like?
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
78
What types of CKD etiologies show faster disease progression?
- DM
- glomerular diseases
- Polycystic kidney disease
- Kidney disease in kidney transplant recipients
79
What types of CKD etiologies show slower disease progression?
- Hypertensive kidney disease
- Tubulointerstitial disease
80
What are some non-modifiable risk factors that are associated with faster progression of CKD?
- African male
- Male gender
- Advanced age
- Family history
81
What are some modifiable risk factors that are associated with faster progression of CKD?
- Uncontrolled hypertension
- Poor blood glucose control
- Proteinuria
- Smoking
- Obesity
82
What are some interventions that can delay progression of CKD?
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
83
What is the impact of good blood pressure control in CKD patients?
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
84
What is the BP target for diabetic CKD patients?
less than 130/80
85
What patient group was excluded from the SPRINT trial (Blood pressure trial)?
Patients with DM
86
What is the acronym for the inclusion criteria for the SPRINT trial?
AARF
A: **A**ge over 75
A: **A**therosclerosis
R: **R**enal (CKD)
F: **F**ramingham score over 15%
Only need to have one of the above to apply to qualify for the SPRINT trial
87
Do we have evidence that shows benefit of BP control on CKD progression in dialysis patients?
No, we only have inconclusive evidence from the SPRINT trial
88
What CKD patients groups may benefit from aggressive control of BP?
- 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)
89
What CKD patient groups are not expected to see benefot from aggressive BP control?
- 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
90
What are some lifestyle modifications to help manage CKD?
- 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)
91
What are some first-line agents for BP control in CKD patients?
Consider comorbidities, stage of CKD, degree of albuminuria, type of CKD when selecting therapy
- ACEi/ARB
- Diuretics
- Long-acting CCBs
92
What is the best BP controlling agent for a CKD patient with proteinuria?
ACEi or ARBs are first line therapy for kidney diseases with albuminuria
- Reduce BP and glomerular capillary pressure (reduces mechanical damage to glomerulus)
93
What are some contraindications for ACEi/ARBs?
- Angioedema
- Bilateral renal artery stenosis
- Pregnancy
94
What are some important monitoring parameters when trying BP control in CKD patients?
- 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)
95
Should BP dose increases be stopped once patient acheived BP target for CKD patients?
No, titrate to maximum tolerated dose to get maximum reduction in proteinuria
96
Can ACEi and ARBs be used in combination to treat proteinuria in CKD patients?
No, although this combination is superior in reducing proteinuria and BP, **it actually worsened renal outcomes**.
97
What is the utility of Aliskren in the treatment of proteinuria in CKD patients?
Not used due to adverse events
98
What is the role of MRAs in CKD treatment?
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)
99
What is the most significant adverse effect that pharmacists need to monitor when using MRAs?
Hyperkalemia is a significant adverse effect that needs to be closely monitored when using MRAs
100
What is the difference between steroidal and non-steroidal MRAs?
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)
101
What are some limitations of finerenone (non-steroidal MRA)?
- 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
102
What is the role of diuretics in CKD treatment?
Most patients require diuretic therapy because fluid retention is an important contributor to HTN in CKD
103
What diuretic is initially started in CKD patients?
Thiazide diuretics (Chlorthalidone)
May switch or combine with loop diuretics (furosemide) if HTN becomes resistant to therapy
104
What is the impact of starting diuretics in CKD patients?
Significant reduction in SBP
105
What is the value of DHP-CCBs (amlodipine) in CKD patients?
BP-lowering agents in CKD
Used in combo with ACEi/ARB in diabetic patients with CKD
No evidence for slowing CKD progression
106
What is a drawback to DHP-CCBs in CKD treatment?
May cause fluid retention and edema (mostly around the ankles due to peripheral vasodilation)
107
What is the role of non-DHP CCBs (diltiazem and verapamil) in the treatment of CKD?
Used in combo with ACEi/ARB for reducing proteinuria, because it has lower ability to reduce proteinuria on its own
108
What is a drawback to non-DHP CCB use in CKD treatment?
Constipation and bradyarrhythmia (especially when used in combination with beta blockers)
- CYP 3A4 inhibitor (many DIs)
109
Are beta-blockers used for first-line treatment for CKD?
No, due to inconsistent evidence for benefit in CKD
110
What is the role of alpha-2 agonists in CKD treatment?
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
What is the role of alpha-1 antagonists in CKD treatment?
Adjunctive treatment for elevated BP in CKD patients
Consider in patients with BPH
112
What is the role of direct vasodilators (hydralazine) in CKD treatment?
Used often by the CKD clinic
No renal dose adjustment (useful in patients with CKD that have low GFR values)
113
What is the definition of proteinuria?
More than 150mg protein lost in urine per day
Can be albumin or other plasma proteins
114
What are the categories of proteinuria?
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
What are some symptoms associated with nephrotic syndrome (severe loss of protein via urine)?
Associated with hyperlipidemia, hypoalbuminemia, generalized edema, thromboembolic risk, foamy urine
116
What is the role of proteinuria in CKD progression?
- Linked with progression of diabetic and non-diabetic CKD
- High risk of progression to kidney failure
- Indicates subclinical CV disease
117
What condition is the most significant cause of nephrotic syndrome?
Diabetic nephropathy
118
What is microalbuminuria?
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
Are ACEi/ARBs useful in CKD patients with no HTN?
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
What is the role of SGLT2i's in CKD treatment?
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
What is the prevalence of CKD amongst diabetes patients?
About 40% of patients with T2DM have CKD
T2DM is a significant comorbidity (most common cause of CKD and ESRD)
122
How often are diabetes patients screened for CKD?
T1DM: 5 years after diagnosis
T2DM: At time of diagnosis
123
Does progression of CKD accelerate with more severe proteinuria?
Yes
124
What is the benefit of blood glucose control for CKD patients?
Good blood glucose control prevents and delays progression of diabetic nephropathy
125
What are the A1C targets for most CKD patients?
**Less than 7.0**
Less than 6.5 may be appropriate in some due to greater need to reduce CKD risk
126
What are some issues with using A1C in patients on dialysis?
Dialysis patients often develop anemia and bleeds, so this impacts the accuracy of the A1C readings
127
What is first-line therapy for blood glucose control in diabetic CKD?
Combination of Metformin & SGLT2i
128
Does metformin have kidney protective effects?
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
Are metformin doses renally adjusted?
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
Can metformin be initiated in patients with GFR below 30mL/min?
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
What is the consequence of SGLT2i and ACEi/ARB combination therapy in CKD?
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
If A1C levels are normal, should SGLT2is be stopped if being used for CKD treatment?
No, reduce doses of other antihyperglycemics like sulfonylureas before stopping a SGLT2i
133
What is the lowest GFR level where SGLT2i can be used in CKD treatment?
Not to be initiated if eGFR is below 20mL/min, but can be maintained until dialysis
134
What happens to GFR after starting a SGLT2i?
It may decline by up to 30% (due to reduction in glomerular pressure from efferent arteriole dilation)
135
What is the impact of SGLT2i on the progression of CKD?
Empagliflozin can delay dialysis by up to 10 years (significant difference vs. placebo)
136
What are some adverse effects associated with SGLT2i use?
- Thirst
- Polyuria
- Genital mycotic infections
- Hypovolemia
- lightheadedness
- diabetic ketoacidosis
137
What is the role of GLP1RAs (semaglutide) in CKD treatment?
Benefit primarily seen in diabetic CKD, unlike SGLT2i that show more broader benefit (diabetic and non-diabetic CKD)
138
What are the benefits of GLP1RAs broadly?
- Weight loss
- CV risk reduction
- Insulin-sparing (need to less insulin and other antihyperglycemics)
139
What is the impact of smoking on CKD?
Increases the progression of CKD:
- Increased BP & HR
- Reduced renal blood flow (constriction)
- Vascular injury
140
What are some examples of nephrotoxic drugs?
- **Avoid combo of ACEi/ARB, NSAIDs, and diuretic (triple whammy)**
- NSAIDs
- Lithium
- Aminoglycosides
- Amphotericin B
- Calcineurin inhibitors
- Cisplatin
141
What is suggestion for sick day management in CKD patients?
Due to acute illness and fluid inbalance, it is reccomended to hold potentially nephrotoxic or renally excreted drugs
142
What is an important acronym for drugs that should be avoided in sick day management?
SADMANS
**S**ulfonylureas
**A**CEi
**D**iuretics, **d**irect renin inhibitors
**M**etformin
**A**RBs
**N**SAIDs
**S**GLT2i
143
What drugs from SADMANS are renally-cleared and accumulate on sick days?
Sulfonylureas and Metformin
144
What drugs from SADMANS are nephrotoxic and should be avoided on sick days?
- ACEi
- Diuretics
- Direct renin inhibitors
- ARBs
- NSAIDs
- SGLT2i
145
What happens to CV risk as GFR declines?
CV risk increases
146
What is the leading cause of death in CKD patients?
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
Is CKD a statin-indicated condition?
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
What is the LDL target in CKD?
There is no specified LDL target
"Fire and forget" strategy
149
What is the benefit of statins in CKD?
CV risk reduction and mortality, no benefits to slowing CKD progression
150
What is a good statin choice for CKD patients?
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
What is the toxicity concern for statins in patients with CKD?
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
What are the first-line components of CKD treatment?
1. SGLT2i and Metformin
2. RAAS inhibitors (if patient also has HTN)
3. Moderate-severe intensity statin
153
Review slide 215 for CKD treatment guideline
154
What are three main types of Renal Replacement Therapy?
1. Hemodialysis (Intermediate HD)
2. Peritoneal Dialysis (Continuous Renal Replacement Therapy)
3. Kidney transplant
- Preferred option for eligible patients
- Subject to organ availability
155
What is conservative care management?
It is the option to symptomatically treat and skip RRT.
156
What is the GFR target to initiate RRT in CKD patients?
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
What are some symptoms that suggest the need for RRT?
- Serositis (eg. pericarditis), acid-base or electrolyte abnormalities, pruritis
- Inability to control volume status or BP
- Malnutritiom refractory to dietary intervention
- Cognitive impairment
158
What is the most common type of RRT?
Hemodialysis (75% of all RRT)
159
In general, what happens in hemodialysis?
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
How often is hemodialysis performed?
It is usually conducted 3x per week at the clinic for 3-5 hours for each visit
161
Where are the access points for hemodialysis?
Requires chronic vascular access that withstand high bloof-flow rates
- Arteriovenous (AV) fistula
- Insertion of a synthetic AV graft
- Catheter in neck
162
What is done to prevent blood from clotting in the dialysis machine?
Patients require systemic anticoagulation during the procedure
163
Is hypertension a concern for patients on hemodialysis?
Massive fluid shifts during dialysis make patients more prone to hypotension
164
What are some characteristics of the different types of RRT access to blood supply?
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
What are the two types of hemodialysis based on where it is given?
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
What are some symptoms associated with hemodialysis?
Fatigue, hypotension, hypertension, cramps, N/V
167
What are some issues with all types of vascular access?
- Infection
- Clotting
- Bleeding
These issues are more common in patients with catheters vs. fistulas
168
What nutrients need to be replaced following hemodialysis?
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
What is in Replavite?
- Vitamin B1, B2, B3, B6, B12
- Folic Acid
- Biotin
- Vitamin C
170
What are some nutrients that should be monitored in hemodialysis patients?
Monitor every 6-12 months
- Serum folate
- Vitamin B12
171
What is the logic behind peritoneal dialysis?
Relies on the patient's own peritoneal membrane to act as a filter for fluid and wastes
172
What is the process of peritoneal dialysis?
- 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
What are the two main types of peritoneal dialysis?
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
What are some advantages of peritoneal dialysis?
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
What are some disadvantages associated with peritoneal dialysis?
- 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
What is Continuous Renal Replacement Therapy (CRRT)?
Patients are hooked up to dialyser for continous periods of time (used in acute settings, not suitable for chronic RRT)
177
What patient group us on Continuous Renal Replacement Therapy (CRRT)?
Patients on CRRT are usually in a poor condition and cannot tolerate the abrupt fluid shifts with intermittent hemodialysis
178
What functions of the kidney are impaired in CKD?
1. Fluid, electrolyte, and acid-base balance
2. Metabolic waste removal
3. Foreign body removal
4. BP regulation
5. Secretion of hormones
179
What are the complications of CKD?
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
What are the consequences of Na+ and H20 imbalance?
Symptoms become more evident in later stages of CKD
- Weight gain
- Hypertension
- Peripheral and pulmonary edema
181
How is Na+ and H20 imbalance treated?
- 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
Why is Furosemide preferred in treatment of Na+ and water imbalance?
Efficacy continues to lower GFR values (useful in more advanced forms of CKD)
183
What is the mechanism of loop diuretic resistance?
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
What is the consequence of using diuretics to manage Na+ and H20 imbalance?
- Hyperkalemia (test every 1-2 weeks initiallt, reduce frequency to every 3-6 months when stable)
185
What is metabolic acidosis?
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
Why does metabolic acidosis occur in patients with CKD?
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
What are the consequences of reduced buffer capacity in metabolic acidosis?
The accumlated H+ ions are buffered by bicarbonate, protein (muscle wasting), and by phosphates (in bone)
188
How is metabolic acidosis in CKD treated?
Sodium bicarbonate tablets
Benefits: Reduces CKD progression, improved nutritional status
Concern: Possibility of sodium loading (not to the same extent as NaCl)
189
What is hyperkalemia?
An inability to maintain a normal serum potassium of 3.5-5mmol/L
190
What causes hyperkalemia in CKD?
Decreased potassium excretion
191
What are some factors that can exacerbate hyperkalemia?
- Metabolic acidosis (intracellular --> extracellular K+ shift, H+ in blood is exchanged for K+ in cell)
- Excessive potassium intake
- ACEi/ARBs
- NSAIDs
192
What are some signs of mild-moderate hyperkalemia (5.1-7mmol/L)?
- Weakness
- Confusion
- Muscle and respiratory paralysis
- ECG changes (6-7mmol/L)
193
What are some signs of severe hyperkalemia (more than 7mmol/L)?
- 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
How is hyperkalemia treated?
- Lifestyle modification (drugs and diet)
- Sodium polystyrene sulfonate (Kayexalate)
195
What is the mechanism of action for sodium polystyrene sulfonate?
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
What are some adverse events associated with sodium polystyrene sulfonate?
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
What agents are used to treat severe hyperkalemia (more than 7mmol/L)?
Review slide 258
198
What is CKD-MBD?
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
What is the mechanism of action for CKD-MBD?
- 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
How is CKD-MBD diagnosed?
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
When should CKD patients be monitored for signs of CKD-MBD?
Ca2+, PO4, and PTH abnormalities only appear in later stages of CKD (Stage G4-G5)
202
What is the consequence of hyperphosphatemia in CKD patients?
Increased risk of all-cause mortality in CKD G3a to G5D
203
What are the consequences of low calcium levels?
Contribute to secondary hyperparathyroidism and renal osteodystrophy, and prolong QT interval
204
What are the consequences of elevated serum calcium?
Associated with higher mortality and risk of CV events in CKD patients
205
What are the definitions of calcium lab values?
Ionized calcium = free/"active" calcium (most reliable reading)
Total calcium = (free/ionized + calcium bound to albumin)
Corrected calcium = (Ca2+ adjusted for albumin values)
206
When should elevated PTH be treated in CKD patients?
PTH should be progressively rising or persistently high to initiate treatment (2-9x upper limit of normal)
207
What are the different types of CKD-MBD (renal osteodystrophy)?
1. Hyperparathyroid bone disease (high bone turnover)
2. Adynamic bone disease (low bone turnover)
3. Osteomalacia (reduced vit D activity)
208
What is the activity of the hormone FGF-23?
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
What is the activity of the hormone PTH?
Increased Ca2+ reabsorption and PO4 excretion in the kidneys
Increased Ca2+ mobilization from bone
210
What are the roles of FGF-23 and PTH, and how do they change in CKD-MBD?
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
What are the consequences of sustained hyperparathyroidism?
- Persistent Ca2+ resorption from bone (high bone turnover)
- Parathyroid gland hyperplasia and becomes resistant to exogenous calcitriol therapy
212
What is calciphylaxis?
Calcification and occlusion of small blood vessels
Leads to ulceration, gangrene, secondary infection (sepsis), and is associated with a high mortality rate
213
How are elevated phosphate levels reduced?
- Restrict dietary phosphate
- Phosphate binders (in addition to dietary restriction)
- Intensfied dialysis schedules
214
How is hyperparathyroidism supresssed?
- Vitamin D therapy (Calcitriol)
- Calcimimetics (Cinacalcet)
- Parathyroidectomy
215
When do phosphate binders need to be taken?
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
What type of phosphate binders are first-line in CKD-MBD?
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
What is the benefit of Vitamin D therapy in CKD-MBD?
It can help reduce elevated PTH levels seen in CKD-MBD
(Vit D stimulates absorption of Ca2+, which inhibits PTH synthesis)
218
What are some drawbacks to Vitamin D therapy in CKD-MBD?
- Increased risk of hypercalcemia and hyperphosphatemia (increased production in FGF-23)
- Uncertain if fracture or mortality risk is reduced by Vitamin D therapy
219
What is the recommendation for Vitamin D therapy in secondary hyperparathyroidism in CKD-MBD?
Should not be routinely used in patients not on dialysis or for patients with severe and progressive hyperparathyroidism
220
How are doses of Vitamin D therapy initiated and adjusted in patients with hyperparathyroidism in CKD-MBD?
- Serum Ca and PO4 levels should be in range before initiating therapy
- Dose adjustments based on serum Ca, PO4, and PTH levels
221
What is the impact of calcimimetics on hyperparathyroidism in CKD-MBD?
- Increase sensitivity of the parathyroid glan to calcium
- Directly reduces PTH without increasing serum Ca or PO4
- Potential for hypocalcemia
222
What patient groups use calcimimetics in CKD-MBD therapy?
Used in dialysis patients only, usually as an adjunct to Vitamin D therapy
223
What are some examples of antiresorptive treatment?
Denosumab (Prolia) and Bisphosphonates
224
What is the impact of antiresorptive treatments in CKD-MBD treatment?
May increase bone mineral density and reduce fracture risk
Usually used in patients with higher GFRs (more than 30mL/min)
225
What is parathyroidectomy?
Excision of the parathyroid gland
Usually performed in ESRD or patient is not responding to pharmaceutical treatments for CKD-MBD
226
What is the consequence of a parathyroidectomy?
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
What is adynamic bone disease?
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
What is osteomalacia?
Inadequate mineralization of Ca2+ and PO4 (softening of bone)
Due to reduced production of calcitriol (or deposition of aluminum in the bones)
229
What is vascular calcification?
Seen in high and low bone turnover disease
Vascular smooth cells change into an osteoblast-like cell (changes to gene expression)
230
Review slide 297 for a summary of the different anemia-relevant lab values
231
What type of anemia is associated with CKD patients?
In CKD, we see normochromic, normocytic anemia due to reduced erythropoietin stimulation in CKD
232
What is the cause of iron deficiency in patients with CKD?
- Erythropoiesis stimulating agents can increase iron demands
- Reduced GI absorption of iron
- Blood loss in hemodialysis
233
What are the benefits of erythropoiesis stimulating agents (ESA) in CKD treatment?
- Practically eliminated the need for blood transfusions
- Reduced fatigue, symptoms of anemia (quality of life)
234
What are the disadvantages of erythropoiesis stimulating agents (ESA) in CKD treatment?
- Failed to improve CV outcomes
- Associated with increased risk of stroke and other thromboembolic events
235
What are the anemia target lab values in CKD patients using ESA therapy?
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
When is IV iron used to supplement iron deficiency in patients on ESA therapy for CKD?
- Patient is intolerant, unresponsive, or non-compliant to oral iron
- Recommended 1st line in hemodialysis patients
237
What is Erythropoietin?
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
What are the two main ESA agents?
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
How is ESA therapy monitored?
- 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
What are some adverse effects associated with ESA therapy?
Overall well-tolerated if monitored adequately
Other adverse events are due to unchecked elevated hemoglobin (HTN, flu-like symptoms, thrombosis, etc)
241
What is erythropoietin resistance?
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
What is the role of hypertension in CKD?
HTN is both a cause and consequence of CKD (due to activation of RAAS)
90% of patients have HTN by stage 5 CKD
243
What are some contributing factors for HTN in CKD patients?
- Salt and water retention
- Activation of RAAS
- ESA therapy
- Hyperparathyroidism
- Renal vascular disease
244
What are some conditions experienced by CKD patients that can cause heart failure?
- Anemia (increased tachycardia)
- LVH
- HTN (fluid overload)
- CAD
245
What causes most neurological complications associated with CKD?
Uremia (build up of urea in the blood)
246
What are some characteristics of chronic pruritis in CKD patients?
- 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
What is the definition of drug-induced kidney disease?
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
What are some mechanisms for drug-induced kidney disease?
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
What are some drugs that can make changes to renal blood flow, a risk factor for drug-induced kidney disease?
-ACEi/ARB
- SGLT2i
- NSAIDs
- Calcineurin inhibitors
250
What patient group is at most significant risk for drug-induced kidney diseases following administration of drug that changes renal blood flow?
HF, renal artery stenosis, volume depletion, CKD, other nephrotoxins
251
How can risk for drug-induced kidney disease caused by drugs that change renal blood flow be effectively managed?
- 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
What are some drugs that can cause damage to the renal tubules (intra-renal damage)?
- Aminoglycosides
- Radiographic contrast media
- Cisplatin
- Calcineurin inhibitors
- Specific antivirals
253
What is the most common type of drug-induced kidney disease in the hospital?
Acute tubular necrosis
- Ischemic or toxic cellular injury to renal tubules
254
How can acute tubular necrosis be mitigated following administration?
- Discontinue nephrotoxin
- Maintaining adequate hydration is an important preventative measure for many of these drugs
- Monitor SCr, BUN, electrolytes
255
What are some drugs that can cause damage to the tissues that surround the tubules (intra-renal, interstitial nephritis)?
- Penicillins/Cephalosporins
- Ciprofloxacin
- NSAIDs
- PPI
- Loop diuretics
- Allopurinol
256
What is acute interstitial nephritis?
Immune-mediated kidney injury associated with hypersensitivity reactions (allergic reactions)
Idiosyncratic
Injury usually occurs 7-14 days after administration
257
How is acute interstitial nephritis managed?
- Discontinue nephrotoxin (if done early, kidney function can return to normal)
- Monitor SCr, BUN, and symptoms of AIN (fever, rash, arthralgia, eosinophilia)
258
What is chronic interstitial nephritis?
It is a progressive (months to years) and it is irreversible
ex. Lithium and calcineurin inhibitors can cause chronic interstitial nephritis
259
What are some drugs that can cause a blockage in the tubules (obstructive nephropathy)?
- Sulfonamides
- Acyclovir
- Methotrexate
- Oral phosphate solution
- Triamtene
- Ciprofloxacin
260
How can obstructive nephropathy occur?
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
What are some risk factors for obstructive nephropathy?
Associated with inadequate hydration (causes supersaturation and drop in urine pH, more acidic)
262
How is obstructive nephropathy managed?
- High urine volume (drink more water)
- Urinary alkinization
263
What are some drug dosing issues in patients with CKD?
- 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
What equation is used to determine the degree to which drug elimination will be effected in renal impairment usually estimated from CrCl?
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
At what creatinine clearance, do pharmacists need to start considering dose adjustments?
When CrCL falls below 60mL/min
266
What are some clinical considerations before making therapy changes in patients with renal impairment?
- 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
What is the step-wise process for adjusting drug doses according to renal impairment?
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
Is estimating creatinine clearance from SCr useful in dialysis patients?
No, because creatinine is removed in HD or PD
CrCl is generally considered to be 10mL/min in dialysis patients
269
What are some basic management strategies for CKD?
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)
