Chronic kidney disease (CKD) Flashcards

1
Q

What is one of the leading causes of death in the US?

A

kidney diseases

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2
Q

What is one of the leading causes of kidney failure (3/4 cases)?

A

DM and high BP

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3
Q

Chronic kidney disease is more prevalent in which populations?

A

Older, Women, Racial minorities, Lower socioeconomic status, DM and HTN

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4
Q

Median wait time for individuals first kidney transplant?

A

3.6 yrs

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5
Q

Characteristics of acute kidney disease?

A

Rapid loss of function, commonly reversible
-usually caused by: dehydration, blood loss, meds, IV contrast, obstruction

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6
Q

Characteristics of chronic kidney disease?

A

Progressive loss of function or presence of damage that lasts 3+ months, commonly irreversible
-usually caused by: long term chronic systemic/autoimmune/genetic diseases (DM, HTN, Lupus, PKD)

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7
Q

Chronic kidney disease results in an inability to maintain what?

A

Acid-base balance, fluid/electrolyte balance, excretion of nitrogenous waste

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8
Q

As CKD progresses, what happens to glomerular filtration?

A

Decreases

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9
Q

The most accurate measure of GFR is using what?

A

plasma or urinary clearance of an exogenous filtration marker (ex. insulin) *not routinely performed

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10
Q

Normal value for GFR?

A

90+

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11
Q

What value of GFR indicated a treatment plan for kidney failure (dialysis or kidney transplant)?

A

Below 15

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12
Q

In clinical practice, estimated GFR is calculated using what?

A

Endogenous filtration markers such as serum CR +/- cystatin C level, in combo w/ demographic factors such as age and gender

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13
Q

What is the recommended calculation of eGFR?

A

2021 CKD EPI equation

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14
Q

How does the 2021 CKD EPI equation estimate GFR?

A

Serum Cr, age, sex
(+/- cystatin)

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15
Q

Stage 0 of CKD?

A

Increased risk (DM, HTN, etc.) GFR: >/=90

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16
Q

Stage 1 of CKD?

A

Kidney damage w/ normal or inc. GFR (>/=90)

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17
Q

Stage 2 of CKD?

A

Kidney damage w/ mildly reduced GFR (60-89)

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18
Q

Stage 3 of CKD?

A

Moderately reduced GFR (30-59)

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19
Q

Stage 4 of CKD?

A

Severely reduced GFR (15-29)

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20
Q

Stage 5 of CKD?

A

Overt renal failure (dialysis) GFR: <15

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21
Q

Individuals may often remain _____ until kidney disease is far advanced?

A

Asymptomatic

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22
Q

PMH to gather for CKD?

A

BP and glucose control, family/personal hx of: HTN, DM, genetic/autoimmune kidney disease, abnormal kidney imaging/urine studies, cancer/chemo/radiation

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23
Q

Med history for CKD?

A

Review meds, potentially nephrotoxic agents (even if not currently taking)

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24
Q

Social history for CKD?

A

Human immunodeficiency, Hep C/B, IV drug use, STDs, occupational contaminants (lead, pesticides)
Pts w/ risk factors: test for presence of these viruses if underlying cause not clear

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25
Physical exam for CKD?
Evaluate for: -volume imbalance/third spacing (edema, inc. JVP) -microvascular injury (AV nicking, retinopathy --> chronic microvascular dz, peripheral neuropathy --> diabetic microvascular dz) Auscultate: -Abd bruit Palpate: -abnormal distal pulses (Renal artery stenosis/RAS) -enlarged kidneys (polycystic KD)
26
CBC/CMP findings in CKD?
Elevated BUN & Cr Hyperkalemia, Hyperphosphatemia, Hypocalcemia, Low hemoglobin/hematocrit
27
Urinalysis/microscopy for CKD?
Proteinuria/albuminuria, RBC/casts, WBC/casts
28
As kidney function decreases, what happens to Cr levels?
Increase (waste product develops from normal wear/tear on body muscles)
29
Normal levels of Cr vary depending on what?
Age, race, body size
30
What Cr level in men may be an early sign of kidneys not functioning properly?
>1.4
31
What Cr level in women may be an early sign of kidneys not functioning properly?
>1.2
32
BUN measures what?
Amount of nitrogen in blood (waste product of urea)
33
When is urea made in the body?
When protein is broken down
34
What happens to BUN levels as kidney function decreases?
Increase
35
Multiple lab abnormalities and declining GFR function may require what?
Direct evaluation and management by nephrologist to conduct serologic testing +/- renal bx
36
Lab data for albuminuria and proteinuria in CKD?
Albumin spot samples (common) or 24hr urine collection Mod inc: 30-300 (spot) and 300mg/24hrs Severely inc. >300 Dipstick urine Mod increase: 1+ Severe: >1+
37
Additional diagnostics for CKD?
EKG changes (electrolyte abnormalities) +/- US (CKD late stage: small echogenic kidneys bilaterally), r/o obstruction, r/o RAS
38
What to monitor in progression of CKD?
Proteinuria/Albuminuria, Cr/BUN, Na+ and volume, Posph/Calcium balance & PTH, Hematocrit/Erthropoietin (EPO), K+, Acid-base
39
The RAAS pathway is initiated in response to what?
Lifesaving measures, fluid/electrolyte imbalance
40
What does RAAS regulate?
Aldosterone secretion (aldosterone regulates blood volume, BP, Na+, K+, H+ in blood)
41
What causes the juxtaglomerular cells of the kidneys to increase renin?
Dehydration, Na+ deficiency, hemorrhage --> dec. in blood volume ---> dec. BP (Liver also releases angiotensinogen)
42
Increased renin/angiotensinogen will increase angiotensin I, leading to what?
ACE converting angiotensin I to angiotensin II in the lungs
43
Effects of angiotensin II?
Vasoconstricts arterioles (increasing BP until normal), acts on adrenal cortex (as well as extracellular K+) to inc. aldosterone
44
What does increased aldosterone lead to?
In kidneys, increase Na+ and water reabsorption/K+ and H+ excretion in urine ---> inc. blood volume to act on BP
45
What is tubuloglomerular feedback?
Macula densa (area of specialized cell) senses NaCl conc and GFR ---> works w/ RAAS to regulate renal BF/GFR *high NaCl: increased GFR *low NaCl: decreased GFR
46
When renal BF/GFR is reduced, or if there is a decrease/dilution of Na and Cl ion concentration in filtrate, what occurs?
Release of prostaglandins --> releases renin --> activates RAAS to inc. BP and volume --> increases retention of Na+, fluid via aldosterone
47
If afferent arterioles are constricted, what will happen in the capillaries?
BP will drop in capillaries of kidneys and GFR is reduced
48
When angiotensin II levels increase d/t activation of RAAS, most arteries in the body experience what? What do efferent arterioles do to compensate?
Vasoconstriction in order to maintain adequate systemic BP (reduced BF/pressure to the kidneys) TO compensate: efferent arterioles constrict to greater degree in response to elevated angio II
49
Efferent arteriole constriction increases what?
Hydrostatic pressure in glomerular capillaries/drives more filtrate into bowmans capsule, increasing the GFR *hyperfiltration
50
In initial nephron injury, the remaining functioning nephrons experience what?
Hyperfiltration (to compensate for loss of non-functioning units and maintain GFR)
51
What is a consequence of hyperfiltration by remaining functional nephrons?
Glomerular capillary HTN
52
How does hyperfiltration further the RAAS cycle?
Efferent arteriole vasoconstriction causes stimulation of RAAS --> initiates cycle to inc. blood volume/BP --> causes further glomerular injury from inc. capillary pressure
53
What is glomerular pore size altered by?
Angio II (increases protein leak across glomerular BM) --> leads to inc. in glomerular permeability/excess protein filtration
54
What results as a consequence of repeated/continued activation of RAAS in kidney pathology?
Albuminuria/proteinuria
55
Excess protein excretion in the urine contributes to what?
Progressive kidney damage: proteins in urine are toxic to tubules (cause tubular injury, tubulointerstitial inflammation, scarring)
56
What are the underlying causes of injury that develop in the renal parenchyma?
Proinflammatory/Profibrotic effects of Angio II and aldosterone
57
What promotes fibrosis and scarring in the kidneys?
Inflammatory mediators
58
What ultimately occurs in kidney injury that promotes CKD?
glomerulosclerosis and tubulointerstitial fibrosis
59
Risk factors for CKD?
DM** (leading cause of CKD/ESRD), HTN, Glomerulonephritis, Tubulointerstitial nephritis, Genetic disease, Obstructive nephropathies, Vascular disease
60
What is a clinical diagnosis of a diabetic patient w/ renal injury?
DKD
61
What reduces the progression of kidney disease w/ DM?
Intensive insulin therapy to maintain HbA1c levels
62
Poorly controlled diabetes leads to what?
Renal injury w/ albuminuria +/- reduced GFR and activation/re-activation of RAAS pathway (leading to poor BP control)
63
Normal glucose handling in the kidneys?
Filtration of glucose w/ 100% reabsorption of glucose
64
Glucose handling w/ DM in the kidneys?
High filtered loads of glucose, filtered load exceeds reabsorption capacity, glucose excreted in urine, polyuria
65
What is diabetic nephropathy/diabetic kidney disease (DKD)?
Elevated blood glucose rises beyond kidneys capacity of reabsorption
66
What does non-reabsorbed glucose raise?
osmotic pressure, causing more water to be carried out --> inc. volume of urine--> dilutes NaCl in filtrate/signals RAAS
67
Treatment goal of poor glucose control?
Halt progression to diabetic nephropathy or DKD (glycemic control, BP control, lifestyle modifications)
68
DKD patients have a high rate of progression to what?
CKD, cardiovascular disease, mortality
69
Most common comorbidity in DKD?
HTN
70
Recommended BP in DKD?
<130/80 *reduced CV morbidity/mortality
71
Be flexible with target BP in DKD if patient is at risk for what?
Hypotension
72
In DKD, glycemic control slows disease progression to what?
ESRD
73
Target HbA1c in DKD?
6.5-8%
74
Be flexible with target HbA1c if patient with DKD is at risk for what?
Hypoglycemia
75
Pharmacologic tx for glycemic control in DKD?
Metformin (1st line, cost effective) SGLT2i (first line) GLP-1 RA (second line) other options: insulin/other antidiabetic agents
76
Pharmacologic tx for HTN control in DKD?
ACEi or ARB (1st line) *titrate to max dose tolerated, do not use both simultaneously *combo therapy w/ diff HTN agents may be necessary for BP control
77
Renal protective qualities of ACEi and ARBs?
Block RAAS pathway/delay DKD progression in pts w/ albuminuria and HTN
78
What other pharmacologic tx can be considered for DKD?
Statins
79
What is the secondary leading cause of ESRD?
Hypertensive nephropathy or hypertensive kidney disease
80
Sustained HTN leads to what?
Renal injury and worsening BP control
81
Mechanisms of HTN in CKD include what?
Volume overload, Sympathetic overactivity, salt retention, endothelial dysfunction, alterations in hormone systems that regulate BP
82
Treatment goal w/ HTN for kidney dz?
halt progression into Hypertensive nephropathy or hypertensive kidney disease
83
Target BP in Hypertensive nephropathy or hypertensive kidney disease?
<130/80
84
Treatment for pts with HTN and albuminuria in Hypertensive nephropathy or hypertensive kidney disease?
First line: ACEi and ARB 2nd/3rd line if volume overload: Loop diuretic +/- CCB
85
Both ACEi and ARBs reduce what?
Glomerular permeability barrier to proteins (limit proteinuria, filtered protein-dependent inflammatory signals) and decrease glomerular intra-capillary pressure
86
Caution with ACEi and ARBs w/ Cr and GFR?
Expect worsening Cr levels up to 30% and acute reduction in GFR from baseline a few days after starting meds (safe to continue if values stabilize after initial rise)
87
Caution with ACEi and ARBs w/ K+ levels?
Expect raise in K+ levels if hyperkalemia (>6mmol/L), stop any other harmful drugs (reduce K+ sparing drugs) If it still continues: stop ACEi/ARB
88
Monitoring w/ ACEi & ARBs?
Monitor serum Cr and K+ conc. prior to initiation, w/in 1 week of starting, w/in 1 week of increase in doses After: monthly, q3 months, then quarterly
89
Common ADRs w/ ACEi & ARBs?
Hypotension, cough (ACEi), hyperkalemia, headache, dizziness, fatigue, nausea
90
Contraindications of ACEi or ARBs?
-Previous angioedema or renal artery stenosis -Pregnancy category D: avoid
91
When should kidney disease be referred to a nephrologist?
eGFR <60 (stage 3), GFR <30 (CKD stage 4 and beyond), persistent albumin/Cr ratio (>/= 300), abnormal urine microscopy, hx of systemic autoimmune/genetic dz, large/cystic kidneys on imaging/exam, rapid progression of loss of kidney function, difficulty managing labs, Single kidney w/ eGFR <60, resistant HTN, pregnancy, young pt w/ unclear cause of CKD
92
ESRD treatment?
Dialysis, transplant
93
Dialysis is an artificial replacement for what?
Lost kidney function in those w/ CKD stage 5
94
Dialysis is regarded as a holding measure for what patients?
Those awaiting kidney transplant
95
Dialysis is sometimes the only supportive measure in which patients?
Those in which kidney transplant is not appropriate
96
Dialysis process?
Using machine patients blood is pumped through blood compartment of dialyzer --> exposed to partial permeable membrane (thousands of tiny synthetic hollow fibers) --> solution flows around outside of fibers/water & wastes move between --> cleansed blood returns to body via circuit
97
How is ultrafiltration achieved in dialysis?
Increasing hydrostatic pressure across dialyzer membrane (apply negative pressure to dialysate compartment of dialyzer) *allows several excess L's of fluid to be removed during typical 4 hr treatment
98
What is peritoneal dialysis?
Sterile solution containing glucose (dialysate) is run through a tube into peritoneal cavity --> peritoneal membrane acts as partially permeable membrane
99
What is the process of peritoneal dialysis?
Diffusion/osmosis drive waste products & excess fluid through peritoneum into dialysate until dialysate approaches equilibrium w/ body's fluids --> dialysate then drained, discarded, replaced w/ fresh dialysate *repeated 4-5x a day (automatic systems can run more frequently overnight)
100
How is the net effect of removal of waste products of salt and water similar in hemodialysis and peritoneal dialysis?
Because peritoneal dialysis is carried out for such a long period of time
101
Organ donors for kidney transplant may be in what condition?
Living, brain dead, or dead via circulatory death
102
How long after cessation of heart beat may a kidney be recovered from a donor?
24 hrs
103
How does kidney transplant remove the need for dialysis?
Transplanted kidney takes over work of both failure kidneys *often kidney will start making urine as soon as bloodflow starts
104
Indication for kidney transplant?
ESRD regardless of primary cause
105
Majority of kidney transplant recipients are on ______ at time of transplant?
Peritoneal or hemodialysis
106
Who may undergo pre-emptive kidney transplant before dialysis is needed?
Those with chronic renal failure who have a living donor available
107
Complications of kidney transplant?
Rejection (immune response to transplanted organ) with possible need for immediate removal of organ
108
When possible, kidney transplant rejection can be reduced by what?
Serotyping to determine the most appropriate donor-recipient match & use of immunosuppressant drugs