CKD-AKI

Question 1

Definition of AKI

Answer 1

• Abrupt decline in GFR occurring over hours to days/weeks
• Associated with accumulation of waste products (urea and creatinine)
• Inability to maintain and regulate fluid, electrolyte and acid-base balance

• Increase in SCr by ≥ 26.5 μmol/L within 48 h, or
• Increase in SCr to ≥ 1.5x baseline, within 7 days, or
• Urine vol < 0.5 ml/kg/h for ≥ 6 h

Question 2

risk factors for AKI

Answer 2

• > 60yo
• Female
• Acute infection
• Pre-existing chronic respiratory or CVS disease
• Dehydration/volume depletion
• Pre-existing CKD -> AoCKD

Question 3

levels of urine output

normal, non oliguria, oliguria, anuria

Answer 3

• Normal urine output ≥ 1200 ml/day
• Non-oliguria: Urine output > 500 ml/day
• Oliguria: Urine output < 500 ml/day
• Anuria: Urine output < 50 ml/day

Question 4

Clinical presentation of AKI

Answer 4

• Reduced urine output
• Peripheral edema (due to fluid accumulation)
• Flank pain
• Lab abnormalities:
  a. Elevated SCr, BUN, K
  b. Metabolic acidosis (Low CO2)
  c. Urinalysis -> presence of casts, cells, crystals, WBC, RBC protein or abnormal specific gravity, fractional excretion of Na, urine osmolality

Question 5

types of AKI

Answer 5

• pre renal (from decreased prefusion to kidneys)
• intrinsic (from structural damage of kidneys)
• post renal (obstruction of urine flow after kidneys)

Question 6

Causes of pre renal AKI

abnormality and what causes the abnormalities

Answer 6

• volume depletion –> hemorrage, GI losses
• reduced cardiac output –> CHF/MI
• renal hypoperfusion –> thrombosis, emboli, drug induced (!!)

result in dec afferent arteriole pressure

Question 7

diagnosis and evaluation of pre renal AKI

clinical presentation and urine lab abnormalities

Answer 7

• Pt history (GI loss, diuresis)
• Physical Exam (orthostatic hypotension, tachycardia, poor skin turgor)
• Central venous pressure
• pt will have highly concentrated urine, low in Na, high SG (specific gravity), oliguria

Question 8

what drugs can cause pre renal AKI

Answer 8

• NSAIDs
• ACEi/ARB

PG inhibitor prevents afferent arteriole from dilating –> prevents increased RBF
ACEi prevents constriction of efferenct arteriole due to Ang II –> decrease pressure

Question 9

management of pre renal AKI

Answer 9

• no specific treatment
• Reverse of etiologic factors (treat pre-renal causes)
• Use of vasopressors with fluids in pts with vasomotor shock
• Supportive care

Question 10

types of intrinsic AKI

Answer 10

• Acute tubular necrosis (need to know)
• Acute interstitial nephritis (need to know)
• Glomerular damage
• vascular damage

Question 11

causes of ATN

Answer 11

drugs (radiocontrast, aminoglycoside, amphoterin B) / injury

• Injury causes tubule epithelial cell necrosis/apoptosis; hypoxia and inflammatory response; damaged tubular cells sloughed off
• Result: Loss of ability to concentrate urine, defective sodium reabsorption and reduction in GFR

Question 12

4 phases of ATN

Answer 12

• Initiating – ischemia/injury
• Oliguric – cant excrete waste
• Diuretic – increase urine, renal blood flow and GFR (reabsorb Na and concentrate urea)
• Recovery – return to normal

• Oliguria occurs in 70-80% of patients with ATN
• Volume is lower than necessary to excrete body waste products
• Anuria is less common
• Duration of oliguric phase is 1-2 weeks
• The longer the duration, the greater the risk of complications and the worse the outcome and prognosis

Question 13

management of ATN oliguric phase

Answer 13

• Diuretics (mostly loop like furosemide)
• CCB
• Water, Na, K, P acid-base balance
• Nutrition, drug dosage adjustment, dialysis

• CCB– Reverse renovascular constriction, increase renal blood flow, GFR
• Role is to increase urine output, fluid management
• Diuretic resistance is common –needs aggressive Na restriction, Combination diuretic therapy, IV dosing or continuous infusion of loop diuretics
• Avoid overdiuresis or use of diuretics in pre-renal AKI

Question 14

how does radiocontrast cause ATN?

Answer 14

• Mechanism: alter renal hemodynamics, cause renal ischemia, direct toxicity
• Progressive increase in SCr within 24-48h after contrast administration, usually peaks within 5 days

Increased risk for death or prolonged hospitalization

Question 15

risk factors for radiocontrast induced ATN

Answer 15

• preexisting CKD, DM, HTN, CHF, metabolic syndrome, hyperuricemia
• age
• volume depletion
• concomitant administration of nephrotoxins, use high volume/ionic high osmolar contrast media

• nephtoxins: discontinue NSAIDs, AG, ampho B, high dose loop diuretics (prevent over diuresis), antivirals, metformin (prevent lactic acidosis)
• use isotonic/non ionic/low osmolar contrast

Question 16

prevention of CIN

Answer 16

• Use lowest possible dose in pts at risk
• Use iso- or low osmolar contrast media rather than high osmolar agents
• IV Hydration is key
• N-acetylcysteine (NAC)

• IV hydration:
  
  • Normal saline, Hypotonic saline (0.45% NaCl), Sodium bicarbonate
  • Start at least 1 h before and continue for 3-6 h after
• NAC: prevent nephropathy
  
  • Antioxidant effects
  • More recent trials do not show consistent benefit (< commonly used now)

Question 17

how does aminoglycoside induce ATN

Answer 17

• AG include Amikacin, gentamicin, tobramycin
• Accumulates in renal cortex causing tubular epithelial cell damage and obstruction
• Onset: 5-7 days

Question 18

risk factors for AG induced ATN

Answer 18

• Elderly
• CKD, DM
• Volume depletion/hypotension, sepsis, shock
• Concomitant administration of nephrotoxins
• AG therapy > 3 days, multiple dosing, high serum conc (gentamicin > 2 mcg/mL)

Question 19

How to prevent AG induced ATN

Answer 19

• use less nephroxic drugs
• use extended interval dosing (od instead of bd etc)
• prolong dosing interval

• use concentration dependent killing for antibiotics for post antibiotic effects and minimise time dependent toxicity

Question 20

How prevent amphoterin B induced ATN

Answer 20

• Continuous infusion
• Alternate-day dosing rather than daily
• Use lipid formulations
• use other antifungals eg azoles

Question 21

Difference in urine in pre renal and intrinsic AKI

urine sediment, SG, osmolarity, urine to plasma osmolarity, Na, urea to sCr, FeNa

Answer 21

• Pre renal vs intrinsic
• urine sediment: normal, numerous casts
• specific gravity: >1.015, < 1.010
• urine osmolarity: >500, < 350
• urine to plama osmolarity: >1.5, < 1.2
• urine Na (mEq/L): < 20, >40
• urea to sCr ratio: > 40:1, < 20:1
• FeNa(%): < 1, > 2

Question 22

Causes of post renal urine obstruction

Answer 22

• bladder obstruction (prostatic hypertrophy, infection, cancer, improperly placed catheter)
• Ureteral (cancer with abdominal mass)
• Nephrolithiatis (stones from oxalate/uric acid)

Question 23

Treatment of postrenal AKI

Answer 23

• relief of obstruction
• alpha blockers for passage or kidney stones

Question 24

General management of AKI

Answer 24

• hemodynamic support, volume replacement
• remove underlying cause
• maintain water and Na and electrolyte and acid base balance
• drug dosage adjustment