Acute Renal Failure

An abrupt decrease in GFR occurring over hours to days (sometimes weeks). Assoc with acumulation of waste products including urea and creatinine.

Greater than or equal to 1200 ml/day

Urine output < 50 ml/day

UO < 500 ml/d

UO > 500 ml/day

• R: Risk of dysfunction. SCr up 50% or GFR down 25% and UO < 0.5 ml/kg/h x 6h
• I: Injury. SCr up 100% or GFR down 50% and UO < 0.5 ml/kg/hr x 12 h
• F: Failure. SCr up 200% or > 4 mg/dl or GFR down 75% and UO < 0.3 ml/kg/h x 24 h or anuria x 12 h
• L: Loss. ARF > 4 weeks
• E: End Stage Renal Disease. ESRD > 3 months

ARF caused by decreased renal perfusion in the absence of damage to parenchymal tissue. Often assoc with volume depletion or poor cardiac function. (Blood loss, dehydration)

Structural damage to the kidney - usually the tubule - d/t ischemia or toxicity. (contrast induced nephropathy)

D/T obstruction of urine flow downstream from the kidney. Usually not drug-induced. (Prostate, foley)

Prerenal ischemia d/t decreased renal perfusion secondary to sepsis, reduced CO, or surgery

• 1. acute blood loss
• 2. dehydration
• 3. hypoalbuminemia
• 4. diuretic therapy

Elevated blood levels of urea in the serum

Atherothrombi dislodged during a procedure or thromboemboli from pts with severe HF or AFib

Severe inflammatory processes as seen in SLE and poststreptococcal glomerulonephritis

Tubule Damage (acute tubular necrosis)

• 50% to renal ischemia
• 35% to exposure to direct tubule toxins

• 1. Inability to concentrate urine
• 2. Defective distal sodium reabsorption
• 3. Decreased GFR

2-3 weeks per phase

• medications
• bacterial or viral infections

• 1. Bladder outlet obstruction due to a prostatic process (enlarged prostate)
• 2. Improperly placed urinary catheter
• 3. Neurogenic bladder
• 4. Anticholinergic meds

• Urine sodium: < 20
• FENa %: < 1
• Urine/serum osmolality: > 1.5
• Urine/SCr: > 40:1
• BUN/SCr: >20

• Urine Sodium: > 40
• FENa %: > 2
• Urine/serum osmolality: < 1.3
• Urine/SCr: < 20:1
• BUN/SCr: approx 15

• Urine Sodium: > 40
• FENa %: variable
• Urine/serum osmolality: < 1.5
• Urine/SCr: < 20:1
• BUN/SCr: approx 15

Diuretics (mainly loops)

> 7 OR 6.1 - 6.9 if there are EKG changes

no

Calcium to protect/stabilize the heart. It antagonizes the action of K+ on cardiac membranes.

Decrease extracellular K+ by promoting its movement into cells using glucose, insulin, B2 receptor agonists, sodium bicarb), or enhance its removal using dialysis or exchange resins.

Inhibit renal Na+ reabsorption (incr K+ out in urine)

Resin exchanges Na+ for K+ (incr K+ elimination)

Raises cardiac threshold potential (reverses electrocardiographic effects)

Raises serum pH. (intracellular K+ redistribution - back into cell)

Insulin stimulates intracellular K+ uptake

Stimulate intracellular K+ uptake

Removal from serum (incr K+ elimination)

It puts pt at higher risk for lactic acidosis

• Vancomycin
• Aminoglycosides
• NSAIDS
• ACE inhibitors
• ARBs
• Amphotericin B
• Lithium
• Contrast dye
• COX inhibitors
• Acyclovir
• Loop diuretics
• Bactrim (can incr SCr without causing ARF, or can cause ARF)

• (e.g. gentamicin, tobramycin, amikacin, netilmicin)
• Progressive rise in SCr and decrease in CrCl after 6-10 days of therapy. Result of proximal tubular epithelial cell damage leading to obstruction of the tubular lumen.

Direct tubular toxicity and/or renal ischemia

Oxidative stress and renal tubular toxicity

• Patient Population: Not pregnant, Not children, No renal dysfunction, Normal weight, undergoing AG for any G- infection
• Clinical Outcomes: (resolution of s/s) Trend favoring SDD
• Microbiology Outcomes: No difference - indeterminant
• Nephrotoxicity: No significant difference, but a trend for SDD to be used - less toxic
• Other issues: Easy to clear infx were looked at - more serious might have been better.

• Is N-acetylcystine effective? Yes, but only with NS, not alone
• Theophylline? Not statistically. Yes, but very narrow therapeutic window
• Ascorbic acid? Yes
• Bicarbonate? Yes
• Furosemide? No, increased the risk
• Fenoldopam? No, increased the risk
• Mannitol? No, increased the risk
• Dopamine? Not really any benefit seen
• Issues with the meta-analysis - Some of the studies had low quality scores. Not all had the same risk factors. Volume and type of contrast makes a difference and this was not always controlled for.

• Definition of SCr change (nephrotoxicity): 0.05 increase of 50% on at least 2 consecutive days
• Important baseline characteristics: Pt weight > 101 kg. Trough value. Residents in ICU at time of onset.
• Rate of renal toxicity: if trough value was > 20, up to 33%
• Other issues: Need 7 days to see renal tox to vanco. If creatinine goes up the next day, it's probably d/t something else.

• Hemodynamically mediated.
• NSAIDs constrict the afferent arterioles into kidney.
• ACEs, ARBs dilate the efferent arterioles out of the kidney.
• No pressure inside kidney. Kidney needs pressure to work, so ARF.