Acute Kidney Dz Flashcards
RIFLE (Risk Inj Failure Loss EndStage Renal Dz=ESRD)
Can dx spectrum of kid impairment/injury
Based on changes in serum CREATININE and UO
Severity classes; Risk, Inj, Failure (FIF)
Outcome classes: Loss, ESRD
Acute Kidney Injury AKI
Sudden decline in rx , GFR -> to go hospital
- failure ot excrete metabolic waster
- inability to maint fluid and electrolytes balance
- impaired acid-base regulation
Dx criteria: AKIN: Acute Kid Inj Network
Modification of RIFLE
Risk category: addition of 0.3 mg or higher increase in serum CREAT
Missed Dx of Inj and Failuer in RIFLE
Dx Limitations
Concordance btw serum CREAT and UP not established
Poor correlation betw AKI stage and GFR
Relies on relative changes in serum Creat
Independent of cause of AKI
RIFLE
Risk: Incr Cr x1.5 or GFR decrby >25% UO50% UO 75% OR Cr>4.0 (with acute rise of 0.5)
UO 4wk
E: ESRD = end stage renal dz
AKIN
stage 1: inc Cr x 1.5 UO < 0.5 x 6 hr
stage 2: inc Cr x 2 UP 4 (with acute rise of .5) UO < .3 x 24 hr or ———————————————————anuria x 12 hr
Stage 3 = dialysis
Nonoliguric
Oliguric
Anuric
nonoliguric > 400 mL/24 hr
Oliguric < 400 / 24 hrs
Anuric < 100 / 24 hrs
3 sources of injury
Prerenal
Intrarenal
Postrenal
Prerenal injury
Inadequate perfusion to kidney: Vascular deplesion (decreased volume): ---------true: Hemmorhage, GI: V/D, NG tube, pancreatitis; Renal (DKA, Addison's dz (dicr Aldo: decr volume); Cutaneous (burns, sweating) ---------effective: decr. Effective Circulating Volume: normovolemic, hypervolemic; vasoDILATION (sepsis=dilate, cirrhosis causes Ascites, anaphylactic shock decr TPR); decr CO (aortic stenosis); renal vasoCONSTRICTION (renal artery stenosis, FMD=familial muscular dz)
NSAIDS and ACE-I/ARB affect which arteriole in the glomerulus
NSAIDS: Afferent arteriole
ACE ARB: Efferent
A doesn’t equal Afferent
Intrarenal injury
glomerular
interstitial
vascular
TUBULAR (most)
Tubular Intrarenal Injury
1) Ishemic due to HTN, Sepsis = Acute Tubular Necrosis
2) Nephrotoxic due to
- —- meds: aminoglycosides, Amphotericin B, Cisplatin, CONTRAST
- —- CAST nephropathy (pathology in nephrons): Mult Meyloma (rare)
- —- Rhabdomyolysis (often): 92 yo fell, ironman (inc myoglobin)
CONTRAST nephropathy
renal TUBULAR epithilial cell toxicity and renal ischemia of medulla
- # 2 cause of acute kid injury in hosp pts
- Risks: age, dehydration, PRE-EXIST RENAL DZ, REPEATED CONTRAST, comorbid DM, CHF
prevention of contrast nephropathy
HYDRATION is key
Acetylcysteine - antidote to tylenol
NaHCO3- sodium bicard - still controvercial
Postrenal Injury
OBSTRUCTION (most) due to : retroperitoneal fibrosis bladder outlet obstruction stones tumors (press on ureter, urethra, bladder, kidney) clots BPH (older men) Can have any or all
hypotension (decreased vol) would lead to
Acute Tubular necrosis (part of Intrarenal)
Increased BUN and Cr may bd due to
Effective Volume depletion (dehydration?) = type of prerenal inj
Matastasis can lead to
Obstruction (Postrenal injury)
Prerenal vascular (vol) depletion can be 2 types
True: GI, burn, sweating
Effective vol depletion: decr Effect circ vol
vasoDILATION (sepsis, cirrhosis, anaphylactic shock)
decr CO
renal vasoCONSTRICTION (renal artery stenosis, FMD)
Acute Interstitial Dz is going to be which: prerenal intra or post
intrarenal
primary blood exams performed in AKI
BUN ELECTROLYTES (high K, high Ca) CBC with diff: EOSINOPHILS to ro infection (interstitial nephritis) Phosphorus, high Uric Acidd (in ppl with gout)
2nd blood exams
Albumin, ANA, Anti DS DNA Ab, complement (low bc fighting), ANCA, ANti GMB, antistreptolysin O titler, Hep B and C - bc need to ro if want dialysis
UA sediment
Muddy brown CASTS: PATHOGNOMIC OF TUBULAR INJURY
Can get random electrolytes
Eosinophils (in Acute Interstitial Nephritis)
Urine prot/urine creat ration < 30 can be done by
24 hr or spot as effective
must be early morning sample
FENa Fractional Excretion of Na
3 % suggests intrarenal (ATN acute tubular necrosis)
BUN/creat ration is >20.1 and FENa is 3% in
<20.1 and FENa is 1-3 in
PRErenal
Intrinsic/intrarenal (Acute tubular necrosis)
POSTrenal
When to use radiology (CT and MRI)
little value in CR and MRI
CT may be used if retroperitoneas FIBROSIS (WHY?)
When can you use gadolinium with GFR
> 30
Which is the go to scan
CT (do after labs) - no contrast, bed side, non-invasive -> see obstruction right away (necrosis, stone, tumor), infection (pyelonephritis)
Biopsy in Acute Kid Dz
Not needed to dx AKI
Use if unexplained Chronic Kid Dz, unexp worsening Acute KInj, Nephrotic syndrome, Acute nephritic symdrome.
DON”T if: solitary native kid, bellding diathesis (anticoag dz), hydronephrosis, pyelonephritis (bc can spread infection), renal tumor can spread
Biopsy is CI in
solitary native kid, bellding diathesis (anticoag dz), hydronephrosis, pyelonephritis (bc can spread infection), renal tumor can spread
In captain Ohagan: takes thiazide, hx bladder CA and BCG?, UTI one week ago tx with Bactrim:
present to ED with fever, dysuria, BP low, HR high, H/H low, BUN high, Cr 1.9 then 2.2, WBC high, UA: large leukocytes, WBC, TooNumerousToCount (TNTC), few RBC
Dx: sepsis due to UTI but Cr goes up to 2.2 on day 3;
First tx with vol resuscitation to improve BP and HRvc hypoThyroid???
Order: Phosphorus, Uric Acid, LDH (hemolytic anemia) WNL (within normal limits)
Urinary sediment: muddy brown granular casts = intrinsic/tubular
FEna 4% > 3 so intrarenal
US neg for pyelonephritis
Brown muddy casts are a sign of which type of renal injury
Tubular injury (intrarenal)
Which type of renal injury would be corrected with fluid resuscitation
Prerenal
Mngt of acute Kid injury
Volume/hydration
Avoid nephrotoxins: NSIADS, Lasix decreases K, RENAL DOSING OF ACE
Has decreased albumin so feed then
If uremia - kid failure and dialysis or kid replacement
Meds concerns
Vancomycin Getamycin (aminoglycoside?), ACE i, K+ supplements (want to decrease K?) OTC NSAIDS, supplements (DVT prophylaxic meds have to be renally dosed)
Meds that cause false + rise in Cr?
Trimethoprim (Bactrim)
Cefoitin (pepsid)
Nutrition
Protein restriction is controversial bc AKI have protein deficit RESTRICT FLUID (could have fluid overload bc of kid dysfx) LOW K (due to vomiting and diahrrehia?)
Complication mngt
-volume depletion
-volume overload
-Electrolytes:
HYPERK+ is number 1, most impt
HYPOCa and Hyperphosphate
-metabolic acidosis
-uremia leads to bleeding disorders
When to tx HyperK
- makes BP go up
- peaked T waved
- tx based on clin presentation/findings
- EKG finding determine urgency (get baseline EKG)
3 principles of HyperK mngt
-stabilize cardio if EKG changes (for ppl with K >5.5): IV Calcium fast (shot) or Ca Gluconate if can wait
-Chasers: Drive extracellular K into cells with insuline and sugar D50W, Beta 2 Agonist (albuterol), NaHCO3- sod bicard (controversial)
-Remove excess K with
diuretics - Lasix if produce urine,
Cation exchange resins (KYEXALATE (bind to K and poop out)),
dialysis
If Hyper K >5.5 and peaked T wave
actively tx,
if flat P wave, then what ?
K uptake by cells is increased by
Beta 2 agonists - albuterol
insulin plus sugar d50W
poss sod bicarb
Kayexalate does what?
cation exchange resin - binds K and poop out
Albuterol, beta 2 agonist does what?
moves K into cells to tx HyperK
Incidations for Dialysis
AEIOU
Acid-base disturbance (met acidosis)
Electrolyte abnormalities (HyperK with EKG changes)
Ingested toxins
Overload (fluid) refractory to diuretics (common)- bc not responding
Uremia (not just BUN) : with AMS (altered mental status), Seizures, Pericarditis
Most likely cause of death in AKI
INFECTION is 1
- Cardiovascular events
- GI, pulm, neuro complication
- HyperK or dialysis related
