Week 14 AKI and CKD

dinosaur1234's version from 2015-04-24 15:21


Question Answer
Definition of AKIGFR decrease >25% or 1.5 fold increase in SCr; urine output <0.5 ml/kg/h for at least 6 hours
Categories of AKIprerenal, intrinsic, and post renal
Pre-renal AKIdecreased perfusion due to volume depletion; DOC for tx is IV fluids; can be caused by NSAIDs/ACE combo; s/sx hypotension, sepsis, decreased CO, diabetes insipudis, hypoalbuminemia, D/V
Post-renal AKIkidney is initially undamaged; mostly caused by bladder output obstruction (BPH, anticholinergics, etc.)
Intrinsic AKIassociated with kidney damage; removal of offending agents does NOT necessarily result in prompt recovery of renal function; tx is removing offending drug and IV fluids if dehydrated
SCrnormal metabolic product of muscle; more likely to be higher in males than females; used to calculate CrCl
BUNless specific indicator of kidney function and is a reflection of ingested protein and muscle catabolism; can be elevated by protein intake, TPN, steroids, fever, dehydration, and GI bleed
Norma BUN to SCr ration10 to 1 up to 20 to 1
Anuricurine output <50 ml/d
Oliguricurine output <500 ml/d
Nonoliguircurine output >500 ml/d
Lab findings in AKIurine sediment, urinary RBC, urinary WBC, BUN/Scr
When do you see urinary RBCintrinsic AKI
When do you see urinary WBCintrinsic AKI
When do you see elevated BUN/SCrpre-renal AKI
Cause of community acquired AKIcaused by renal hypoperfusion from volume depletion associated with dehydration, V/D; can be secondary to HF or meds
Causes of hospital and intensive care AKIischemic or toxic acute tubular necrosis
RF for AKIpresence of underlying CKD, multisystem organ failure, preexisting chronic condition, bone marrow or solid organ transplantation, age >65, sepsis, drugs, infection, surgery, malignancy
How do NSAIDs impact kidney functioninhibit PGs which therefore causes afferent arteriole vasoconstriction and reduces GFR
How to ACE/ARBs impact kidney functionthey block Ang 2 which causes vasodilation of the efferent arteriole, reducing GFR
Ways to prevent AKIhydration! Antioxidants, glycemic control (for pt with diabetes), w/d of causative agents
Antioxidantsascorbic acid- benefits not consistent; N-acetylcysteine is reserved only for those with contrast induced nephrotoxicity
Treatment of AKIremove offending drugs; 250-500 ml NS over 15-30 min if dehydrated; blood products if a result of anemia
Def of CKDGFR <60 ml/min for at least 3 months
Stage 1 CKDkidney damage with normal or increased GFR (>90)
Stage 2 CKDmild reduction in GFR- 60-89
Stage 3 CKDmoderate reduction in GFR- 30-59
Stage 4 CKDsevere reduction in GFR (15-29)
Stage 5 CKDkidney failure- GFR <15 or dialysis
RF for CKDsystemic inflammation, dyslipidemia, glomerulonephritis, diabetes, HTN, proteinuria, obesity
Interventions in CKDglucose control, control of BP, management of hyperlipidemia, management of anemia
Complications of CKDelectrolyte imbalance (inc P, dec Ca), anemia, bone disease, HTN
Management of hyperphosphatemiacalcium acetate or calcium carbonate (not appropriate if pt s hypercalcemic); Forrenol or sevelame (phosphate binders)
Management of hypocalcemiaCa supplements +/- calcitriol
Management of anemiairon supplements or ESA
Iron supplementsPO has reduced absorption as CKD progresses; give IV if stage 4 (sucrose, dextran, ferric gluconate)
Iron with highest risk of anaphylaxisiron dextran
When to use ESA and targetgive if Hg <10; target is 11-12; evaluate iron status before and during treatment and maintain iron repletion
Management of Vit D deficiencyif stage 1-3 can give PO vit D; in advanced stages need to give vit analog- Calcitriol or doxercalciferol
Management of high PTHsame as vit D deficiency + calcimimetic agent (Cinacalcet [Sensipar])
MOA of cinacalcetdecreased PTH by increasing sensitivity to Ca on parathyroid gland; don’t initiate if Ca <8.4
BP goalpre-dialysis is <140/90; post dialysis is <130/80
Why ACE/ARBs still recommended in CKDdecrease sympathetic nerve activity; decrease arterial stiffness; greater regression of LVH
Can you give diuretics in CKDin stages 1-3, still have some urine output, so okay to give furosemide for volume overload