Lecture 14/15 AKI Flashcards
(30 cards)
What criteria must be met to define an AKI (stages)?
SCr ruses by > 26 micromol/L within 48 hours OR SCr rises > 1.5 fold from reference value which is known or presumed to have occurred within 7 days OR urine output is < 0.5 mL/kg/hr for > 6 consecutive hours
Stage 1: > 26 micromol/L within 48 hours OR increase 1.5-1.9 fold SCr OR < 0.5 mL/kg/hr for 6-12 hours
Stage 2: 2-2.9 fold SCr increase OR < 0.5 mL/kg/hr for > 12 hours
Stage 3: 3 fold SCr increase OR 354 micromol/L increase SCr OR commenced on renal replacement therapy (RRT) irrespective of stage OR < 0.3 mL/kg/hr for 24 hours or anuria for > 12 hours
What should be assessed when looking at AKIs?
PMHx: renal disease-related chronic conditions, HTN, diabetes
MedHx
Sx: changes in urinary habits, sudden weight gain, flank pain
Signs: edema (sometimes), colored or foamy urine, orthostatic hypotension, HTN
Lab Tests
other diagnostic tests, tests like SCr, Urea/BUN
What is prerenal AKI and possible causes?
most common cause of AKI (>60%), occurs over hours-days, generally result of renal hypoperfusion, glomerular filtration restored on reestablishment of more renal perfusion (no structural damage or injury to kidney itself)
Causes: hypovolemia - hemorrhage, GI fluid losses, renal fluid losses, extravascular
altered renal hemodynamics - low cardiac output state, systemic vasodilation (sepsis), renal vasoconstriction, impaired renal autoregulatory responses, hepatorenal syndrome
S&S of Prerenal AKI
thirst, orthostatic hypotension, dehydration - tachycardia, reduced jugular venous pressure, decreased skin turgor, dry mucous membranes
Lab and urine findings in prerenal AKI
increase in [Urea] and creatinine
Urine: hyaline casts, FeNa < 1%, UNa < 20 mmol/L, SG > 1.020 (1.010-1.025)
What is postrenal AKI and possible causes?
caused by obstruction of urine flow at any level of urinary tract, 5% of AKI cases, must occur in both kidneys at same time
Causes: physical barrier - kidney stones, prostate hypertrophy, cancer
drugs that crystallize - sulfonamide, methotrexate, acyclovir
S&S of Postrenal AKI and lab findings and urinalysis?
expresses pain, anuria, pyuria
Lab: UNa > 40 mmol/L, FeNa > 2%, increase in urea or no change
Urine - cellular debris, hematuria, possible WBCs (1+)
What is intrarenal AKI and possible causes?
occurs in 25-40% of AKI, acute injury to kidney itself (ex. nephron), either acute or chronic damage
damage to four possible sites - glomerulus, vascular/microvascular (renal arterioles/blood capillaries), tubules (ATN = acute tubular necrosis), interstitium (AIN = acute interstitial nephritis)
Causes: Drugs, other toxins, ischemia, infection, autoimmune diseases
Lab findings and urinalysis in intrarenal AKI?
Lab: UNa > 40 mmol/L, FeNa > 2%, increase or no change in urea
Urine: casts, cellular debris, protein, hematuria (2-4+), WBCs (2-4+)
What is the general tx of AKI (what is included, possible options)?
A. hydrate (IV fluids) - 0.9% NaCl > 200 mL/hr until SCr return to baseline
B. stop nephrotoxic agent - any drugs potential to cause renal failure or worsen it: ACEis or ARBs, NSAIDS, anticholinergic agents
C. treat underlying disease state
D. diuretics - loop - furosemide - metolazone (only if volume overload) - prevent pulmonary edema and HF, for pt who still have some urine output in AKI, controversial as some studies show worsening or no effect
E. dialysis (RRT), adjust med dosages/frequency for level of kidney fxn,, Advantages: correct electrolytes, treats fluid overloaded pt, removes uremic toxins,, Disadvantages: hypotension can exacerbate AKI, poor venous access makes it difficult, IV site is source of infection, kidney may not recover
Acronym for when to dialyze?→AEIOU,, A: Acid-base abnormalities (metabolic acidosis),, E: Electrolyte imbalance (hyperkalemia),, I Intoxications,, O: Fluid overload,, U: Uremia (decline in mental status, neuropathy)
What drugs can often cause prerenal AKIs?
ACEis, ARBs, NSAIDs, calcineurin inhibitors
What drugs can often cause intrarenal AKIs (types)?
Acute tubular necrosis (ATN) - amphotericin B, aminoglycosides, radiographic contrast dye
Acute interstitial nephritis (AIN) - penicillins, lithium
Chronic interstitial nephritis (CIN) - calcineurin inhibitors, lithium, NSAIDs
What drugs can often cause postrenal AKIs?
acyclovir, indinavir, sulfonamide antibiotics
How do ACEis and ARBs possibly cause prerenal AKIs, who is at higher risk, presentation, mech?
pt at higher risk: severe atherosclerotic disease, renal artery stenosis (bilateral), HF (acute, decompensated), CKD (severe later stages), volume depleted
Presentation: > 25-30% rise in SCr within 2-7 days following initiation, usually stabilizes in 1 week
Mech: first meds dilate efferent arteriole and reduce glomerular hydrostatic pressure = decrease GFR
For prerenal AKIs with ACEis and ARBs what are common urinalysis stats, management of the AKI, and how to prevent it in future?
Urine: low volume, UNa < 20 mmol/L, FeNa < 1%, specific gravity > 1.010, no casts or cellular elements (high urea and creatinine)
Management: d/c these meds, supportive tx
Prevention: obtain baseline SCr and K+ and monitor them regularly, start low doses and titrate dose gradually for these meds, avoid other drugs like NSAIDs which may alter renal blood flow, maintain hydration, temporarily stop drugs in setting of stressed kidneys
How do NSAIDs possibly cause prerenal AKIs, who is at higher risk, presentation, mech?
pt at higher risk: CKD, HF, elderly, ACEi/this combo, indomethacin most likely to impair renal fxn (low dose ASA doesn’t impair renal fxn)
Presentation: pt presents with low urine volume, edema/weight gain and elevated SCr, K+ and urea
Mech: in pt with altered renal perfusion the compensatory response is to release PGs, inhibition of COX-2 inhibits this response therefore inhibiting afferent arteriole dilation and reducing GFR
For prerenal AKIs with NSAIDs what are common urinalysis stats, management of the AKI, and how to prevent it in the future?
Urine: low volume, UNa < 20 mmol/L, FeNa < 1%, specific gravity > 1.010, no casts or cellular elements (high urea and creatinine)
Management: d/c these meds, supportive tx
Prevention: obtain baseline SCr and K+ and monitor them regularly, start low doses and titrate dose gradually for these meds, avoid other drugs like NSAIDs which may alter renal blood flow, maintain hydration, temporarily stop drugs in setting of stressed kidneys
How do NSAIDs possibly cause prerenal AKIs, who is at higher risk, presentation, mech?
pt at higher risk: CKD, HF, elderly, ACEi/this combo, indomethacin most likely to impair renal fxn (low dose ASA doesn’t impair renal fxn)
Presentation: pt presents with low urine volume, edema/weight gain and elevated SCr, K+ and urea
Mech: in pt with altered renal perfusion the compensatory response is to release PGs, inhibition of COX-2 inhibits this response therefore inhibiting afferent arteriole dilation and reducing GFR
For prerenal AKIs with NSAIDs what are common urinalysis stats, management of the AKI, and how to prevent it in the future?
Urine: low volume, UNa < 20 mmol/L, FeNa < 1%, increase in SG, no casts or cellular debris, high urea and creatinine
Management: d/c offending agent, supportive tx
Prevention: avoid prolonged use in elderly, HF, CKD
avoid concomitant prolonged use with ACEi or ARB, start with low dose and titrate, monitor BP and SCr regularly
What are acute tubular necrosis intrarenal AKIs (types)?
most common form of intrarenal AKI, course - oliguric phase: within 24 hours and lasting 1-3 weeks, diuretic phase: usually indicates renal recovery
mortality rates range from 50-70%, complete recovery of renal fxn may not return
Types: 1. nephrotoxic - endogenous or exogenous, myoglobin, aminoglycosides (gentamicin, tobramycin), CT contrast dye
- Sepsis associated - ischemia and toxin related
How do aminoglycosides possibly cause intrarenal acute tubular necrosis AKIs, who is at higher risk, presentation, mech?
includes gentamicin, tobramycin
pt at risk: dehydrated, sepsis, ischemia, pre-existing renal impairment, concomitant nephrotoxins, sustained high this serum levels and large cumulative doses, long term this tx (> 14 days)
Presentation: increase in SCr 6-10 days
Mech: epithelial cell damage in proximal tubular cells, direct signaling of cell death of proximal tubule cells, toxicity related to cationic charge (neomycin > gentamicin/tobramycin > amikacin > streptomycin)
For intrarenal acute tubular necrosis AKIs with aminoglycosides what are common urinalysis stats, management of AKI, and how to prevent it in the future?
Urine: muddy brown epithelial cell casts and free epithelial cells, UNa > 40 mmol/L, FeNa > 3%, SG around 1.010,, Management: d/c this, supportive tx - correct volume and metabolic acidosis, hemodialysis/RRT
Prevention: avoid hypovolemia, avoid prolonged tx, TDM, avoid nephrotoxins, alternate dosing, avoid high risk pt - elderly, pre-existing renal failure
How does amphotericin B possibly causes intrarenal acute tubular necrosis AKIs, risk factors, mech, prevention?
antifungal used to treat systemic fungal infections
Risk factors: cumulative dose, pre-existing kidney disease, concurrent nephrotoxics, dehydration or volume depletion, conventional this vs liposomal formulations
Mech: direct toxicity to cells in distal nephron, cell death and necrosis, impairs kidney ability to filter and concentrate urine
Prevention: hydration, use of liposomal formulations, limiting dose and duration, monitoring renal fxn, avoiding concurrent nephrotoxins
What is acute interstitial nephritis, presentation, mech?
up to 3% of all AKIs
Presentation: fever, rash, pyuria/hematuria, oliguria, other - metabolic acidosis, hyperkalemia, salt wasting
occurs around 14 days after exposure to drug
Mech: hypersensitivity rxn, lymphocytic inflammation of the interstitium
