Renal: AKI

• Elevation in nitrogenous waste products
• (ex. urea and creatinine)

• Symptoms assoc. w/ azotemic accumulations
• fatigue, anorexia, nausea, vomiting, pruritus, mental status changes, etc.

1-1.5 L / 24 hrs

> 500 mL/day

400-500 mL/day

< 50-100 mL/day

Any sudden onset injury or impairment of the kidney

• Hypoperfusion d/t:
• Intravascular volume depletion
• Reduced effective circulatory volume
• Vascular occlusion
• Drug induction

Direct renal damage

• thrombotic thrombocytopenic purpura
• hemolytic uremic syndrome
• renal artery thrombosis

• SLE
• glomerulonephritis
• post-infection

• Inflammatory, immunologic reaction within the
• renal interstitium resulting from drugs, infections or autoimmune disorders

• Causes 85% of intrinsic AKI
• Can result from extending pre-renal states or exposure to direct toxins
• uric acid, aminoglycosides, contrast media

• An obstruction of the urinary collection system
• BPH, improper catheter, cancers, fibrosis, nephrolithiasis

• Age (>65 y/o)
• Pre-existing renal dysfunction
• Volume depletion or dec. circulating volume 
• Serious infections
• Comorbidities  
• Exposure to nephrotoxins

• 1.5-1.9 times baseline
•           OR
• ≥ 0.3 mg/dL increase

< 0.5 mL/kg/h for 6-12 hours

2.0-2.9 times baseline

< 0.5 mL/kg/h for ≥ 12 hours

• 3.0 times baseline
• OR
• Increase in SCr to ≥ 4.0
• OR
• Initiation of renal replacement therapy
• OR
• In patients < 18 years: dec. in eGFR to < 35

• < 0.3 mL/kg/h for ≥ 24 hours
•           OR
• Anuria for ≥ 12 hours

• Need a baseline Scr level
• May be 1 to 2 day delay in SCr increase after injury
• Urine output can be variable
• Studied/validated in critically ill pop.

• Serial BUN, SCr, K⁺, BUN:SCr
• U/A
• Urine Na
• FE_Na

FE_Na =   (Urine Na x SCr / Serum Na x Urine Cr) x 100

• Renal ultrasound
• Catheter
• Kidney-ureter-bladder (KUB) X-ray
• Cystoscopy with retrograde pyelography
• Renal biopsy

• PE: Hypotension, dry mucus membranes, dec. CO, edema, ascites, etc.
• Urine Sediment: Normal
• Urine Na: <20
• FE_Na: <1
• BUN/SCr ratio: ≥ 20:1

• PE: Variable
• Urine Sediment: Granular and epithelial casts; RBCs; WBCs may be present in AIN
• Urine Na: >40
• FENa: >2
• BUN/SCr ratio: < 20:1

• PE: Prostatic enlargement, bladder distension, etc.
• Urine Sediment: Variable; cellular debris, RBCs, or crystals possible
• Urine Na: >40
• FENa: Variable
• BUN/SCr ratio: ~ 15:1

• Avoidance of nephrotoxins
• Maintain hemodynamic stability to avoid
• hypotension, hypovolemia, etc.
• ID and avoid risk factors when possible

Sodium bicarbonate + hydration (Alkalinizing agent)

N-Acetylcysteine (NAC) + hydration (Antioxidant effect / Neutralizes urine)

• Rapid identification of cause
• Removal or reduction of causative agents
• Prevent further kidney injury
• Prevent complications
• Regain renal function

• Stop nephrotoxic drugs
• Maintain adequate hemodynamic status
• Maintain glucose control
• Manage complications

• vasodilation; increase U/O
• not recommended

• vasodilation; increase U/O
• some use in crit. ill pts

• Inc. UO; Dec. renal ishemia risk
• Contoversial: harm/ototoxicity vs. minimal benefit

• Dec. vasoconstriction; natriuretic
• weak evidence for renal transplant pts

• antioxidant; dec. vasoconstriction
• weak evidence v. CIN w/hydration

• Antioxidant
• weak evidence in CIN

• May dec. ishemia risk
• needs more study

• Inc. vasodilation and perfusion
• may dec. need for dialysis
• needs more study

• A – Acid-base abnormalities
• E – Electrolyte imbalance
• I – Intoxications
• O – Overload of fluids    
• U – Uremia

• Minimize fluid intake
• Loop diuretics (Furosemide; also torsemide & bumetinide)
• Strategies to reduce diuretic resistance

• Initiate  @ 40-100 mg x 1 --> 200-1500 mg/day
• Cont. Infusion @ 10 mg/h dec. resistance and avoids high peaks

• Identify and eliminate/reduce potential cause
• Increase dose or use continusous infusion
• ADD Thiazide diuretics (Chlorothiazide 250–500 mg IV q12h)
• ADD Thiazide-like diuretics (Metolazone 5–10 mg PO q24h)

• Excessive sodium intake
• Inappropriate diuretic dose/regimen
• Reduced bioavailability
• Reduced renal blood flow
• Drugs (NSAIDs, ACE inhibitors)
• Hypotension          
• Intravascular depletion
• Increased sodium reabsorption
• Nephron adaptation to chronic diuretic Tx
• NSAIDs
• Heart failure
• Cirrhosis

• Most common complication of AKI
• Sx: Parasthesias, weakness, paralysis
• EKG changes: peaked T waves (5.5-6.0 mEq/L); prolongation of PR and QRS intervals (6.0-7.0 mEq/L); disappearance of P wave/merger with QRS and T wave (> 7.0 mEq/L)

Treat via Na restriction

• Most common cause of death
• Sepsis often leads to AKI

• HTN with intermittent hypotension
• CHF, arrythmias, and pulmonary edema

• Inc. bleed risk
• Stess ulceration
• N/V

• Altered mental status
• Seizures
• Somnolence

• Cardioprotective; stabilizes membrane voltage
• 10 mL 10% soln. IV push
• 1-3 min onset; 30 min duration

• 20-30 min infusion w/digoxin
• incompatible w/ Ca & Bicarb

• Redistribution: inc. cellular K+ & dec. plasma K+
• 10 U IV bolus w/50 mL D5W
• 10-30 min onset; 2-6 hr duration

• no D5W if BG > 250
• monitor BG closely

• Redistribution: inc. cellular K+ & dec. plasma K+
• 10-20 mg neb over 10 min
• 10-30 min onset; 2-4 hr duration

• 25% of pts do not respond
• tachycardia common

• elim. K⁺ in gut (exchanged for Na⁺)
• 15 g PO in sorbitol soln. 1-4 times/day OR
• 30-50 g retention enema in sorbitol (retain 30-60 min)
• 1-3 hr onset; 4-6 hr duration

• Sorbitol minimizes constipation but may -> bowel necrosis
• Enema has faster onset
• 1g binds ~ 1 g K⁺