CKD Flashcards

1
Q

CKD

A
  • GFR < 60 ml/min for more than 3 months
  • persistent proteinuria*, hematuria, or abnormal urinary sediment
  • progressive nephrosclerosis, irreversible reduction in nephron number
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2
Q

major function of nephron

A
  • glomerular filtration
  • tubular reabsorption (passive)
  • tubular secretion (active, mainly K)
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3
Q

hyperfiltration and CKD

A
  • DM or HTN causes hyperfiltration to maintain GFR
  • causes hypertrophy of viable nephrons
  • increased pressure and flow -> distortion glomerular architecture, sclerosis, loss of remaining nephrons
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4
Q

RAAS and CKD

A
  • RAAS and AII get activated to maintain GFR with hyperfiltration
  • AII causes altered pore sizes -> increased permeability -> protein leak -> microalbuminuria
  • AII and aldosterone are also proinflammatory and profibrotic independently
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5
Q

proteinuria and CKD

A
  • excessive proteins in urine are directly toxic to tubules

- causes tubular injury, inflammation, scarring

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6
Q

GFR

A
  • measure of how well kidneys are removing waste and excess fluid from blood
  • based on SCr, age, weight, gender, body size
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7
Q

normal GFR

A
  • > 90
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8
Q

GFR suggesting kidney dysfunction

A
  • < 60
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9
Q

GFR that qualifies for dialysis or transplant

A
  • < 15
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10
Q

serum creatinine

A
  • waste product from normal wear and tear produced by muscles at constant rate
  • excreted unchanged in kidneys
  • as kidney function decreases Cr levels rise
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11
Q

high serum creatinine levels

A
  • > 1.2 in women

- > 1.4 in men

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12
Q

BUN

A
  • measure of amount of nitrogen in blood that comes from waste product urea
  • urea made when protein is is broken down
  • as kidney function decrease, BUN increases
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13
Q

normal BUN

A
  • between 7-20
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14
Q

sx of CKD

A
  • no sx until stage 3 or 4
  • anemia, weakness, fatigue
  • decreased appetite with progressive malnutrition
  • sleep problems
  • decreased mental sharpness/ encephalopathy
  • muscle twitches/ cramps
  • pruritis
  • uremic syndrome
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15
Q

complications of progressive CKD

A
  • anemia
  • metabolic acidosis
  • derangement in vit d, ca, and p metabolism
  • volume overload
  • hyperkalemia
  • uremia
  • CV consequences*
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16
Q

approach to pt with new renal dysfunction

A
  • consider pre-renal, renal, and post-renal etiology
  • careful H&P
  • SCr/GFR
  • urine dipstick, microscopy, spot protein- proteinuria one of first signs
  • renal US, advanced imaging
  • urinalysis
  • consider checking for MM
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17
Q

lab data for CKD

A
  • 24 hour urine test*- compares urine Cr to SCr
  • urinalysis- protein/ albumin
  • urine microscopy- cells/ casts/ crystals
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18
Q

microalbuminuria definition

A
  • 30-300 mg/L
19
Q

macroalbuminuria definition

A
  • > 300 mg/L
20
Q

proteinuria

A
  • > 150-160 mg
  • 1-2 suggests kidney abnormality
  • > 3.5 in nephrotic range
21
Q

anemia and CKD

A
  • due to decreased EPO production
  • dx of exclusion- r/o all other causes
  • can give EPO stim agents if Hgb falls < 10
22
Q

vitamin D def and CKD

A
  • secondary to decreased active vit d (1,25- OH), very short half life
  • kidneys take vit D storage form (25-OH) and active it
  • measure storage vit D to assess kidneys- longer half life
23
Q

metabolic acidosis and CKD

A
  • secondary to decreased bicarb resorption and generation by kidneys
  • treat with bicarb supplementation
24
Q

bone disease and CKD

A
  • secondary to abnormalities in complex interaction between vit d, p, ca, and PTH
  • excessive bone resorption
  • state of bone quiescence- adynamic bone disease
  • results in fragile bone matrix and increased risk fx
25
Q

uremia and CKD

A
  • hundreds of toxins accumulate
  • urea and Cr elevated, used as surrogate marker for toxins
  • systemic inflammation increases
26
Q

Risk factors for dev CKD

A
  • DM*
  • HTN*
  • autoimmune disease
  • older age
  • AA or hispanic
  • family hx
  • previous episode AKI
  • proteinuria
  • abnormal urinary sediment
  • structural abnormalities of urinary tract
27
Q

stage I kidney disease

A
  • GFR > 90
28
Q

Stage II kidney disease

A
  • GFR 60-89
29
Q

stage III kidney disease

A
  • GFR 30-59
30
Q

Stage IV kidney disease

A
  • GFR 15-29
  • difficult to control HTN- require loop diuretics
  • hyperkalemia*
  • +/- uremia
  • refer to nephrologist
31
Q

Stage V kidney disease

A
  • GFR < 15 or dialysis
  • need renal replacement/ transplant
  • discuss end of life
  • once on dialysis > 50% mortality within 5 years
32
Q

what do most CKD pts die from

A
  • CV complications
33
Q

most common causes of ESRD

A
  • diabetic glomerular disease*
  • HTN nephropathy*
  • glomerulonephritis
  • autosomal dominant polycystic kidney disease
  • other cystic and tubulointerstitial nephropathy
34
Q

treatment for CKD

A
  • primary prevention
  • treat underlying disorder
  • dialysis
  • transplant
35
Q

when to refer pts to nephrologists

A
  • GFR < 30
  • rapidly progressive CKD
  • poorly controlled HTN despite four agents
  • rare or genetic causes CKD
  • suspected renal artery stenosis
36
Q

what is the leading cause of ESRD

A
  • DM
37
Q

DM and CKD

A
  • damages BV in kidneys
  • elevated blood glucose rises beyond kidneys capacity to resorb glucose
  • glucose concentration remains high in fluid -> increasing urine volume
38
Q

what is the goal hbA1C to reduce risk of CKD

A
  • < 7
39
Q

treatment for DM and CKD

A
  • primary prevention- diet/ exercise, weight loss
  • tight glucose control < 7
  • BP control < 130/80- delays onset of microalbuminuria
40
Q

diabetic nephropathy

A
  • diabetic pts with dev of renal injury

- first sign= microalbuminuria

41
Q

treatment for diabetic nephropathy

A
  • ACEI/ARB as first line tx even if normotensive

- diuretics are second line to aide in BP control

42
Q

what is the second leading cause of ESRD

A
  • HTN
43
Q

treatment for HTN and CKD

A
  • salt and water restriction
  • BP < 130/80
  • weight loss
  • pharm therapies- ACEI/ARB
44
Q

why should you be cautious when treating HTN nephropathy with ACEI/ARB

A
  • recommended CKD stages 1-3
  • expect worsening of Cr in up to 30% of pts or reduction in GFR 20% from baseline
  • if values continue to drop consult nephrology
  • contribute to hyperK