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Older Adult Exam 1 > CKD > Flashcards

CKD Flashcards

1
Q

why is CKD increasing in incidence?

A
  • aging population

- increased prevalence of DM and HTN

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2
Q

what are some long term adverse outcomes from CKD?

A
  • impaired kidney function
  • end stage renal failure
  • death
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3
Q

ckd is associated with significant;y increased risk of which medical problems?

A
  • CVD

- stroke

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4
Q

what do the kidneys do?

A
  • regulate water
  • balance salts - sodium and potassium
  • acid base balance
  • calcium reabsorption/vitamin d activation
  • blood pressure
  • RBC production
  • filter waste/excrete medication
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5
Q

what happens to the kidney as we age? around what age does this declines accelerate?

A
  • kidney function slowly declines - natural process

- happens more rapidly after age 45

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6
Q

what factors can cause kidney injury?

A
  • infection (post-strep glomerulonephritis)
  • autoimmune process (lupus nephritis)
  • medications
  • volume depletion - n/v, diuretic use
  • obstruction
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7
Q

how does the kidney respond to injury?

A
  • increased filtration in remaining normal nephrons - adaptive hyperfiltration
  • additional homeostatic mechanisms permit serum concentrations of sodium, potassium, phosphorus, calcium, and total body water to remain w/in normal range, particularly among those with mild-moderate renal failure
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8
Q

pros/cons adaptive hyper-filtration? manifestations of hyper-filtration?

A
  • initially beneficial
  • often results in long term damage to glomeruli of remaining nephrons
  • manifested by proteinuria and an increase in circulating biomarkers or kidney disease (BUN/creatinine) and progressive renal failure
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9
Q

how is ckd defined?

A
  • presence of structural or functional abnormalities of the kidney for 3 or more months, irrespective of cause
  • persistence of kidney damage/decreased kidney function is necessary to distinguish it from acute kidney injury (aki) - in aki, appropriate eval for reversible causes should be performed
  • decline in gfr to <60 for > 3 months
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10
Q

what are some risk factors for ckd?

A
  • DM
  • HTN
  • CVD
  • HLD
  • obesity
  • metabolic syndrome
  • smoking
  • HIV
  • hep C
  • malignancy
  • fam hx ckd
  • sickle cell trait
  • urinary outflow obstruction
  • hx aki
  • persistent hematuria
  • tx w/ potentially nephrotoxic drugs like NSAIDs
    fam hx CKD, DM, HTN
  • african americans
  • hispanics
  • asians
  • pacific islanders
  • > 60 years old
  • recurrent kidney stone disease
  • frequent UTI
  • inflammatory disease like RA, SLE
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11
Q

what are the 2 most common causes of CKD?

A
  • DM, particularly type 2

- HTN

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12
Q

what is the initial presentation of diabetic kidney disease?

A
  • microalbuminuria
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13
Q

how does HTN cause CKD?

A

nephrosclerosis occurs from long standing periods of uncontrolled HTN, contributing to end organ damage

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14
Q

who should be screened for CKD?

A

all individuals should be assessed routinely

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15
Q

what methods are used to screen for ckd?

A
  • urine test for proteinuria - spot urine in the morning, measure albumin to creatinine ratio
  • blood test for creatinine, a by-product of muscle metabolism in blood, and GFR
  • BP monitoring, w/ goal <125-130/80
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16
Q

what factors are the 5 stages of CKD based on?

A
  • cause of kidney disease
  • 6 categories of eGFR
  • 3 categories of albuminuria
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17
Q

why stage patients with CKD?

A

staging guides clinicians in managing patients with ckd by identifying those that have the most severe disease who are, therefore, at greatest risk of progression and complications

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18
Q

what are the 3 categories of albuminuria?

A
  • A1, normal to mildly increased: < 30 mg/g or < 3 mg/mmol
  • A2, moderately increased: 30-300 mg/g or 3-30 mg/mmol
  • A3, severely increased: >300 mg/g or > 30 mg/mmol
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19
Q

what are the 6 categories of eGFR?

A
  • G1, normal or high: > 90
  • G2, mildly decreased: 60-89
  • G3a, mildly to moderately decreased: 45-59
  • G3b, moderately to severely decreased: 30-44
  • G4, severely decreased: 15-29
  • G5, kidney failure: < 15
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20
Q

what does albuminuria tell us?

A
  • sensitive marker of CKD caused by DM, HTN, and glomerular disease
  • microalbuminuria is inherent in the diabetes disease process but can also be associated with non-renal conditions (i.e. obesity, inflammation, cancer)
  • increases vascular permeability
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21
Q

what is the BP goal for patients with CKD?

A

125-130/80 mmHg

less aggressive SBP of 135-140 in pts > 75+ with high burden of comorbidity or a DBP < 55-60 in older adults with postural hypotension

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22
Q

what is the tx for pts w/ proteinuria?

A

1st line: ACE-I or ARB
2nd line: loop or thiazide diuretic
3rd line: non-dihydropyridine CCB like nifedipine

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23
Q

what is the tx for pts w/o proteinuria but w/ edema?

A

1st line: loop diuretic
2nd line: ACE-I or ARB
3rd line: dihydropyridine CCB like amlodipine

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24
Q

what is the tx for pts w/o proteinuria and wo/ edema?

A

1st line: ACE-I or ARB
2nd line: dihydropiridine CCB
3rd line: diuretic

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25
Q

when do we prescribe non-dihydropiridine (nifedipine) vs dihydropyridine (amlodipine) CCBs?

A
  • w/ proteinuria: non-dihydropyridine, i.e. nifedipine

- w/o proteinuria: dihydropyridine, i.e. amlodipine

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26
Q

how does ACE-Is work?

A
  • angiotensin II is a potent chemical produced by the body that causes constriction of smooth muscle that surrounds blood vessels
  • ACE-Is slow the action of the enzyme ACE and thus reduce angiotensin II
  • result is dilation of blood vessels and reduction of BP
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27
Q

what is the glomerulus?

A

tiny, ball-shaped structure composed of capillary blood vessels actively involved in filtration of blood to form urine

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28
Q

what is gfr?

A
  • volume of plasma filtered from glomerular capillaries into Bowman’s capsule each minute, expressed in mL/min
  • gfr provides a great measure of filtering capacity of kidneys
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29
Q

how is gfr used clinically?

A

used to

  • evaluate degree of renal impairment
  • follow course of disease
  • assess response to therapy
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30
Q

what is the best measure of kidney function?

A

gfr

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31
Q

what is normal gfr? how does it change with age?

A
  • varies by age, sex, and body size
  • approx 120-130 in young adults
  • decreases by an avg of 1 per year after age 30
  • gfr < 60 means loss of approx 1/2 kidney function and increased prevalence of CKD complications
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32
Q

what variables do most formulas use to estimate gfr?

A
  • age
  • sex
  • race
  • weight
  • serum creatinine
33
Q

what 3 formulas estimate GFR? which was the original formula used? which one is used now? why?

A
  1. CKD-EPI equation: currently used because most accurate
  2. Modification of Diet in Renal Disease (MDRD)
  3. Cockcroft-Gault formula: original formula used
34
Q

what are some signs and symptoms of CKD?

A
  • often asymptomatic! may present in advanced stages w/o any symptoms at all*
  • weakness, fatigue
  • decreased appetite
  • difficulty with urination
  • foamy or dark urine
  • decreased libido
  • swelling - periorbital, LE, generalized
35
Q

what systems are affected by advanced stage kidney disease/uremia?

A
  • CV
  • GI
  • neurologic
  • metabolic
  • psychosocial
  • hematologic
36
Q

what are some CV complications of advanced stage kidney disease/uremia?

A
  • atherosclerosis
  • HTN
  • HF
  • pericarditis
  • pulmonary edema
37
Q

what are some GI complications of advanced stage kidney disease/uremia?

A
  • nausea
  • vomiting
  • anorexia
38
Q

what are some neurologic complications of advanced stage kidney disease/uremia?

A
  • peripheral neuropathy
  • muscle cramps
  • itching
39
Q

what are some metabolic complications of advanced stage kidney disease/uremia?

A
  • electrolyte abnormalities
  • metabolic acidosis
  • HLD
  • alterations in vitamin d/calcium/phopsphorus metabolism
  • mineral and bone density disorders
  • hyperparathyroidism
40
Q

what are some psychosocial complications of advanced stage kidney disease/uremia?

A
  • depression
  • fatigue
  • insomnia
  • suicide
  • sexual dysfunction
  • unemployment
41
Q

what are some hematologic complications of advanced stage kidney disease/uremia?

A
  • anemia
  • leukopenia
  • erythropoietin deficiency
42
Q

how do we evaluate and manage ckd?

A
  • determine etiology of CKD and evaluate for comorbidities
  • collect pt and fam hx
  • PE
  • BP
  • weight mgmt
43
Q

what is more likely than progression to dialysis in any stage of CKD?

A

death

44
Q

what should we assess to understand pt’s CVD risk?

A
  • smoking status
  • lipid levels
  • ECG to evaluate LVH
45
Q

what is the leading cause of kidney failure in the US?

A

DM

46
Q

what is the a1c goal in those with CKD w/o proteinuria?

A

7% - preserves GFR

47
Q

tighter control of a1c is associated with what?

A

more severe complications including hypoglycemia and death

48
Q

what lab workup should we do for patients with CKD?

A
  • renal function, at least annually for any patient at risk
  • fasting lipid profile, A1c
  • urine albumin to creatinine ratio (ACR)
  • BP
  • hgb if gfr < 45; calcium, phosphate, and parathyroid if gfr < 30
  • renal US - evaluate kidney size and assess for possible structural abnormalities
49
Q

how should we manage ckd?

A
  • tx reversible causes of kidney failure
  • prevent or slow progression of kidney disease
  • tx complications of renal failure
  • adjust drug doses when appropriate
  • identification of patients appropriate for dialysis or renal transplantation
50
Q

how many patients with ckd have htn?

A

approx 80-85%

51
Q

how does tx of htn affect ckd?

A

slow progression of proteinuric CKD and reduces rate of CV complications

52
Q

what meds should we use to tx htn in ckd?

A

aces or arbs

53
Q

what are the reversible causes of renal failure?

A

decreased renal perfusion

  • hypovolemia, i.e. vomiting, diarrhea, bleeding, diuretic use
  • hypotension, i.e. myocardial dysfunction
  • infection, i.e. sepsis
  • meds that lower gfr, i.e. NSAIDs, ACE-Is

administration of nephrotoxic drugs

  • frequent cause of worseing kidney function
  • common offenders are aminoglycosides, NSAIDs, radiographic contrast material

urinary tract obstruction

  • less common cause of worsening kidney function
  • patient often with no symptoms referable to kidney/no change in UA/UO
  • renal US often performed to r/o obstruction if pt has unexplained elevation of creatinine
54
Q

how do we slow the progression of ckd?

A
  • adequate BP control
  • reduce proteinuria
  • protein restriction
  • statin therapy
  • smoking cessation
55
Q

what are some complications of renal failure?

A

fluid and electrolyte imbalance

  • volume overload: Na and intravascular volume balance are usually maintained by homeostasis until GFR falls below 10-15mL/min
  • hyperkalemia
  • metabolic acidosis
  • mineral and bone disorders - hyperphosphatemia

tx of chronic metabolic acidosis w/ bicarbonate may slow progression to ESRD

56
Q

what are some clinical findings of CKD stages 3-5?

A
  • anemia
  • malnutrition
  • metabolic bone disease
  • neuropathy
  • reduce level of functioning and well being
57
Q

what kind of anemia do we normally see in ckd?

A
  • usually normocytic, normochromic

- important to r/o other causes of anemia too, like iron deficiency

58
Q

what causes anemia in ckd?

A

reduced production of hormone erythropoetin

59
Q

what causes malnutrition in ckd?

A
  • lower food intake
  • decreased intestinal absorption
  • metabolic acidosis
60
Q

how do we manage malnutrition in ckd?

A
  • assess weight, serum albumin level, and dietary history every 6-12 mo in stage 3 and every 1-3 mo in stages 4-5
  • refer to dietician
  • limit protein intake
  • reduce sodium < 2g/day
  • fluid restriction in ESRD
61
Q

what causes metabolic acidosis in ckd?

A

primarily due to impaired renal ammonia synthesis and acid secretion

62
Q

how often does metabolic acidosis affect ckd patients and what are some SE of it?

A
  • 20% of pts in stages 4-5
  • malaise
  • fatigue
  • acceleration of bone disease
  • impaired synthesis of vitamin D
  • muscle catabolism
  • inflammation
63
Q

how do we assess metabolic bone disease in those with ckd?

A
  • alk phosphatase
  • calcium
  • phosphorus
    consider
  • DEXA
  • vitamin d
  • PTH
64
Q

what is the pathophysiology of metabolic bone disease in those with CKD?

A

as phosphorus levels rise, calcium is pulled from the bone causing bone disorders

65
Q

what pharmacological interventions can we use to tx/prevent metabolic bone disease?

A
  • phosphate binding drugs in advanced disease

- calcium and vitamin D supplements may be indicated

66
Q

how does metabolic bone disease present clinically?

A
  • fractures
  • pain
  • decreased mobility
  • decreased strength
67
Q

how does neuropathy present in ckd and what can we do to assess it?

A
  • paresthesias
  • sleep disturbances
  • RLS
    consider
  • sleep study
  • nerve conduction studies
68
Q

how do we assess functioning and well being in someone with ckd?

A

evaluate once and PRN

  • assess social support
  • health literacy assessment
  • kidney disease QOL scale (KDQOL) - 36 item survey related to symptoms and burden of kidney disease
69
Q

what does supportive care for older people with advanced ckd entail?

A
  • pathway where RRT is not chosen but patients continue to receive healthcare from renal team
  • aka “maximum conservative mgmt” or “non-dialytic care”

emerging themes in lit review are:

  • shared decision making
  • QOL
  • role of educational resources
70
Q

why is it important to think about drug dosing in ckd?

A
  • inappropriate dosing in patients with ckd can cause toxicity and/or ineffective therapy
71
Q

how do we adjust dosing in patients with ckd?

A
  • loading doses don’t need to be adjusted for ckd patients

- guidelines for maintenance dosing often include dose reduction, lengthening the dosing interval, or both

72
Q

what are some adverse renal effects of NSAIDs?

A
  • acute renal failure/acute kidney injury
  • nephrotic syndrome w/ interstitial nephritis
  • CRF w/wo glomerulopathy, interstitial nephritis, and papillary necrosis
73
Q

how does risk of AKI change with use of NSAIDs

A

risk is 3x higher in those that use NSAIDs than in those that don’t

74
Q

what are some other adverse effects of NSAIDs?

A
  • decreased potassium excretion - causes hyperkalemia
  • decreased sodium excretion - causes peripheral edema, elevated BP, decompensation of HF
  • blunts effect of antihypertensives
75
Q

how do COX2 inhibitors compare to traditional NSAIDs in terms of adverse renal effects

A

less GI side effects but renal effects are the SAME

76
Q

should we give NSAIDs to those with ckd?

A
  • short term use generally safe in patients who are well hydrated and have good renal function
  • avoid in chf, htn, and dm
  • long term use should be avoided if possible - check creatinine every 2-4 weeks after initiation of therapy in at risk patients
77
Q

are herbal remedies ok to take in ckd

A
  • many pose a risk to ckd patients
  • may contain undisclosed amounts of potassium or heavy metals that are toxic to kidneys
  • may have vasoconstrictive compounds that can cause HTN
78
Q

what are some indications for nephrology referral?

A
  • acute or complex cvd
  • anemia of ckd
  • difficult to manage adverse SE of meds
  • hyperkalemia (K > 5.5 despite tx)
  • refractory proteinuria
  • resistant HTN
  • stage 4 CKD - GFR < 30
  • unexplained decrease in GFR

Older Adult Exam 1 (7 decks)

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