CKD Flashcards
KDIGO AKI criteria
↑ 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
nephrotic v nephritic
Otic = damage to podocytes = holesItic = inflammation = bloody time
focal segmental glomerulosclerosis
1 seen clinicallyhypertension (always)nephrotic syndromeasymptomatic or microscopic proteinuriarenal insufficiency↑ risk progress to ESRD
FSGS dx
RENAL BIOPSY
FSGS tx
corticosteroids + immunosuppressant
IgA nephropathy
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
IgA nephropathy tx
BP control w ACE-I or ARBproteinurialt 1g - typically no txgt 1g - 6 mo steroid trial, maybe immunosuppressants
IgA s/s
often only manifestation is hematuria
IgA nephropathy and proteinuria relationship
lt 1g - typically no txgt 1g - 6 mo steroid trial, maybe immunosuppressants
primary glomerular disease x2
FSGSIgA nephropathyAcute GN, MCD, FSGS, MN, MPGN, IgA Nephropathy, Post Infectious GN, Anti‐GBM Nephritis
secondary glomerular disease example
SLESLE, Wegner’s Granulomatosis, Vasculitis, Goodpasture’s Syndrome, Hepatitis C, Hepatitis B, HIV
SLE + kidney relationship
nephropathy! secondary glomerular diseasemore females, and younger
SLE glomerular disease s/s
often present, not always: proteinurianephrotic syndromehematuria
SLE glomerular disease dx
renal biopsycomplement (see depression), anti-dsDNA, anti-nuclear ab (positive)
IgA nephropathy dx
RENAL BIOPSY
** renal biopsy as dx **
FSGSIgA nephropathySLEnephritic syndrome
nephrotic vs nephritic setting
OTIC: chronicITIC: acute (biopsy to dx/tx STAT)
nephrotic vs nephritic mechanism
OTIC: podocyte injury, changed architecture (scar, matrix deposition)ITIC: inflammation, GBM break, crescent formation
nephrotic vs nephritic onset
OTIC: insidiousITIC: abrupt
nephrotic vs nephritic edema
OTIC: largeITIC: small - mod
nephrotic vs nephritic BP
OTIC: normal - lowITIC: HIGH
nephrotic vs nephritic proteinuria
OTIC: LARGEITIC: small - mod
nephrotic vs nephritic hematuria
OTIC: eh maybe, maybe notITIC: MOD - LARGE
nephrotic vs nephritic RBC casts
OTIC: absentITIC: present
leading cause of CKD in US
DIABETIC KIDNEY DISEASE! (diabetic nephropathy)
** diabetic kidney disease dx **
CLINICAL PRESENTATION! often r/t poorly controlled DMACR- macro OR - micro + diab retinopathy or T1DM x10 years
** ACR is… **
albumin:creatinine ratiomacro: greater than 300 mg/gmicro: 30 - 300 mg/g
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
proteinuria and diabetic kidney disease
YES - think albumin!!!!ACR: micro or macroalbuminuria??
** 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
late stage 4 diabetic kidney disease tx nota bene
do not start ACE/ARBdc ACE/ARB if taking
** metformin + CKD mgmt **
creatinine: 1.5 (f) 1.4 ()AVOID METFORMIN. (lactic acid increase believed) change to glipizide.
hypertensive nephrosclerosis
2nd leading cause of CKD in USkidney damage d/t htn
hypertensive nephrosclerosis risk factors for ESRD progression
african americanadvancing agemalesmokerlipid abnormalitiesinsulin resistance
** hypertensive nephrosclerosis dx **
clinical - systemic signs of chronic, uncontrolled htn
hypertension goals - diabetic v non-diabetic
diab: less than 130/80non-diab 120/70
stage 4 CKD med nota bene
thiazides do not work!dc ACE/ARB (or don’t start)
AE procardia, hydralazine
LE swelling
** clonidine + CKD **
NO NO NO. missed dose = rebound hypertension- difficult to wean off
CKD stages mnemonic
90 / 60 / 30 / 15 / less(GFR)
CKD: refer to nephrology
proteinuriaGFR declinehematuriamultiple renal cysts (incidental or purposeful imaging)resistant hypertensionrecurrent renal stones → urology & nephrology!electrolyte abnormalities (ex: hypercalcemia, hypernatremia)
UA dipstick proteinuria equivalencies
mg/dL1+ 302+ 1003+ 300 - 5004+ 1000+
nephrotic range proteinuria
3g +
glucose usually not present in urine until…
serum glucose over 160-180
normal 24 hour urine protein content
less than 150
UA: leukocyte esterase and nitrite tell you
about pyuriareduction product from nitrites: E Coli, enterobacter, citrobacter, klebsiella, proteus
urine pH typically
6between 4.5 - 7
how much renal fxn lost before elevations of creat noted
60%
CKD + anemia
NORMALLYlow blood volume = erythropoetin to increase RBC creationCKD - depressed kidney fxn = no epo = anemia
anemia w CKD tx
iron PO if tolerated- give with vitamin CESA (epo stimulating agent)
increases absorption of PO Fe
Vit C
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)
CKD + chronic metabolic acidosis tx
bicarb supplement - NaBicarb, NOT baking soda
CKD + hyperuricemia tx
tx only if uric acid greater than 12REFER IF GOUT
** absolute indications for dialysis (ESRD) **
Uremic pericarditis/effusionUremicencephalopathyGI BleedingAnorexia/N/VProgressive Malnutrition
** 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
ESRD referrals
dialysis centersocial workRD
PD complications
- peritonitis- fluid/vol mgmt- hypoalbuminemia- glucose management (dialysate has lots of glucose)- non-compliance
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)
acute tubular necrosis: 3 phases of injury
oliguric
diuretic
recovery (post-oliguric)
ATN: oliguric phase
- UOP lt 400 ml/day
- increased BUN & creat
- electrolyte disturbances, acidosis, fluid overload (d/t kidney inability to excrete water)
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
ATN: recovery phase
- decreased edema
- normalization of fluid & electrolyte balance
- return of GFR to 70% or 80% of normal
ATN: treatment
- loop diuretics (Lasix)
- dialysis (until functional again)
- dopamine (increase perfusion, but no longer recommended)
chronic kidney disease definition
GFR under 60 for 3+ mos
+ “kidney damage”: pathologic abnormalities or markers of damage including abn blood/urine tests, imaging
CKD: stages 1-5
GFR 1 - 90+ 2 - 60 - 89 3 - 30 - 59 4 - 15 - 29 5 - under 15 (ESRD)
end stage renal disease definition
- renal fxn under 85%
- Stage V CKD: GFR under 15 OR dialysis
- uremia/CVD
pharm tx of choice for anemia s/t CKD
ESA erythropoesis stimulating agent