CKD Flashcards

1
Q

KDIGO AKI criteria

A

↑ creat 0.3+ within 48 hoursOR↑ creat greater than 1.5x baseline within last 7 daysORurine vol less than 0.5 mL/kg/h FOR 6 HOURS

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2
Q

nephrotic v nephritic

A

Otic = damage to podocytes = holesItic = inflammation = bloody time

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3
Q

focal segmental glomerulosclerosis

A

1 seen clinicallyhypertension (always)nephrotic syndromeasymptomatic or microscopic proteinuriarenal insufficiency↑ risk progress to ESRD

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4
Q

FSGS dx

A

RENAL BIOPSY

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5
Q

FSGS tx

A

corticosteroids + immunosuppressant

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6
Q

IgA nephropathy

A

2 seen clinicallyaka Berger’s - IgA settles in kidneys = glomerulonephritisoften only manifestation is hematuriagood BP w/o large proteinuria often doesn’t progress to ESRD

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7
Q

IgA nephropathy tx

A

BP control w ACE-I or ARBproteinurialt 1g - typically no txgt 1g - 6 mo steroid trial, maybe immunosuppressants

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8
Q

IgA s/s

A

often only manifestation is hematuria

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9
Q

IgA nephropathy and proteinuria relationship

A

lt 1g - typically no txgt 1g - 6 mo steroid trial, maybe immunosuppressants

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10
Q

primary glomerular disease x2

A

FSGSIgA nephropathyAcute GN, MCD, FSGS, MN, MPGN, IgA Nephropathy, Post Infectious GN, Anti‐GBM Nephritis

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11
Q

secondary glomerular disease example

A

SLESLE, Wegner’s Granulomatosis, Vasculitis, Goodpasture’s Syndrome, Hepatitis C, Hepatitis B, HIV

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12
Q

SLE + kidney relationship

A

nephropathy! secondary glomerular diseasemore females, and younger

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13
Q

SLE glomerular disease s/s

A

often present, not always: proteinurianephrotic syndromehematuria

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14
Q

SLE glomerular disease dx

A

renal biopsycomplement (see depression), anti-dsDNA, anti-nuclear ab (positive)

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15
Q

IgA nephropathy dx

A

RENAL BIOPSY

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16
Q

** renal biopsy as dx **

A

FSGSIgA nephropathySLEnephritic syndrome

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17
Q

nephrotic vs nephritic setting

A

OTIC: chronicITIC: acute (biopsy to dx/tx STAT)

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18
Q

nephrotic vs nephritic mechanism

A

OTIC: podocyte injury, changed architecture (scar, matrix deposition)ITIC: inflammation, GBM break, crescent formation

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19
Q

nephrotic vs nephritic onset

A

OTIC: insidiousITIC: abrupt

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20
Q

nephrotic vs nephritic edema

A

OTIC: largeITIC: small - mod

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21
Q

nephrotic vs nephritic BP

A

OTIC: normal - lowITIC: HIGH

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22
Q

nephrotic vs nephritic proteinuria

A

OTIC: LARGEITIC: small - mod

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23
Q

nephrotic vs nephritic hematuria

A

OTIC: eh maybe, maybe notITIC: MOD - LARGE

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24
Q

nephrotic vs nephritic RBC casts

A

OTIC: absentITIC: present

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25
leading cause of CKD in US
DIABETIC KIDNEY DISEASE! (diabetic nephropathy)
26
** diabetic kidney disease dx **
CLINICAL PRESENTATION! often r/t poorly controlled DMACR- macro OR - micro + diab retinopathy or T1DM x10 years
27
** ACR is... **
albumin:creatinine ratiomacro: greater than 300 mg/gmicro: 30 - 300 mg/g
28
consider differentials for diabetic kidney disease if what are seen...
- absence of diabetic retino/neuro pathy- urine sediment- DM less than 5 years- little to no proteinuria
29
proteinuria and diabetic kidney disease
YES - think albumin!!!!ACR: micro or macroalbuminuria??
30
** diabetic kidney disease treatment for proteinuria **
ACE or ARB- low dose 2.5 mg lisinopril- check BMP 1 week (hyper K, AKI)DONT START / DO DC... IF LATE STAGE 4 good for normotensive albuminuric DM pts if BP can tolerate
31
late stage 4 diabetic kidney disease tx nota bene
do not start ACE/ARBdc ACE/ARB if taking
32
** metformin + CKD mgmt **
creatinine: 1.5 (f) 1.4 ()AVOID METFORMIN. (lactic acid increase believed) change to glipizide.
33
hypertensive nephrosclerosis
2nd leading cause of CKD in USkidney damage d/t htn
34
hypertensive nephrosclerosis risk factors for ESRD progression
african americanadvancing agemalesmokerlipid abnormalitiesinsulin resistance
35
** hypertensive nephrosclerosis dx **
clinical - systemic signs of chronic, uncontrolled htn
36
hypertension goals - diabetic v non-diabetic
diab: less than 130/80non-diab 120/70
37
stage 4 CKD med nota bene
thiazides do not work!dc ACE/ARB (or don't start)
38
AE procardia, hydralazine
LE swelling
39
** clonidine + CKD **
NO NO NO. missed dose = rebound hypertension- difficult to wean off
40
CKD stages mnemonic
90 / 60 / 30 / 15 / less(GFR)
41
CKD: refer to nephrology
proteinuriaGFR declinehematuriamultiple renal cysts (incidental or purposeful imaging)resistant hypertensionrecurrent renal stones → urology & nephrology!electrolyte abnormalities (ex: hypercalcemia, hypernatremia)
42
UA dipstick proteinuria equivalencies
mg/dL1+ 302+ 1003+ 300 - 5004+ 1000+
43
nephrotic range proteinuria
3g +
44
glucose usually not present in urine until...
serum glucose over 160-180
45
normal 24 hour urine protein content
less than 150
46
UA: leukocyte esterase and nitrite tell you
about pyuriareduction product from nitrites: E Coli, enterobacter, citrobacter, klebsiella, proteus
47
urine pH typically
6between 4.5 - 7
48
how much renal fxn lost before elevations of creat noted
60%
49
CKD + anemia
NORMALLYlow blood volume = erythropoetin to increase RBC creationCKD - depressed kidney fxn = no epo = anemia
50
anemia w CKD tx
iron PO if tolerated- give with vitamin CESA (epo stimulating agent)
51
increases absorption of PO Fe
Vit C
52
renal osteodystrophy/mineral bone disease
NORMALLY kidney works with parathyroid gland to manage Ca & PO4CKD- can't secrete = hyperphosphatemia = less calcium- 2ndary hyperparathyroidism (gland keeps secreting PTH trying to fix)
53
CKD + chronic metabolic acidosis tx
bicarb supplement - NaBicarb, NOT baking soda
54
CKD + hyperuricemia tx
tx only if uric acid greater than 12REFER IF GOUT
55
** absolute indications for dialysis (ESRD) **
Uremic pericarditis/effusionUremicencephalopathyGI BleedingAnorexia/N/VProgressive Malnutrition
56
** relative indications for dialysis (ESRD)
↑ serum CrGFR under 10‐15 ml/minRefractory lyte abnormalities (remember K can be managed without dialysis!!)Volume Overload not otherwise manageable
57
ESRD referrals
dialysis centersocial workRD
58
PD complications
- peritonitis- fluid/vol mgmt- hypoalbuminemia- glucose management (dialysate has lots of glucose)- non-compliance
59
acute tubular necrosis: general definition
d/t ischemia r/t poor perfusion OR nephrotoxic drugs; if sufficient to cause tubular ischemia, will result in loss of tubular fxn nephrotoxic drugs - include contrast, also cause vasoconstriction leading to ischemia/loss function (pre-tx with fluids, may add bicarb)
60
acute tubular necrosis: 3 phases of injury
oliguric diuretic recovery (post-oliguric)
61
ATN: oliguric phase
- UOP lt 400 ml/day - increased BUN & creat - electrolyte disturbances, acidosis, fluid overload (d/t kidney inability to excrete water)
62
ATN: diuretic phase
occurs when cause of AKI corrected - renal tubule scarring/edema - increased GFR - daily UOP 400+ ml - possible electrolyte depletion from excretion of more H2O & osmotic effects of high BUN
63
ATN: recovery phase
- decreased edema - normalization of fluid & electrolyte balance - return of GFR to 70% or 80% of normal
64
ATN: treatment
- loop diuretics (Lasix) - dialysis (until functional again) - dopamine (increase perfusion, but no longer recommended)
65
chronic kidney disease definition
GFR under 60 for 3+ mos | + "kidney damage": pathologic abnormalities or markers of damage including abn blood/urine tests, imaging
66
CKD: stages 1-5
``` GFR 1 - 90+ 2 - 60 - 89 3 - 30 - 59 4 - 15 - 29 5 - under 15 (ESRD) ```
67
end stage renal disease definition
- renal fxn under 85% - Stage V CKD: GFR under 15 OR dialysis - uremia/CVD
68
pharm tx of choice for anemia s/t CKD
ESA erythropoesis stimulating agent