Acute Renal Insufficiency

AKI in ICU increases mortality

  • Common causes of AKI in ICU:
    • AKI in hospital much more likely to be d/t hypoperfusion and/or drug toxicity
    • Pre-renal: low MAP, AAA, RAS, RVT, abdominal compartment syndrome
    • Post-renal: stones, tumor, clot, trauma, BPH
      • Flush foley, check bladder scan, keeping in mind, obstruction could be proximal to bladder
    • Renal: ATN, AIN, other drug toxicity, GN
      • Trough levels à toxicity (peak levels à bactericide)
      • AIN: Use Hansel’s stain for urine eo’s, as Wright’s stain is pH dependent and can be falsely negative
    • Thoughts about evaluation of renal function to keep in mind:
      • Volume status: difficult to assess
        • Physical exam findings (mucous membranes, skin turgor) unreliable
        • Orthostatic BP more reliable, though affected by autonomic insufficiency (DM, elderly)
        • Fluid responsiveness marks diagnosis of pre-renal AKI
        • Response to passive leg raise predicts fluid responsiveness – this requires cardiac output monitor or stroke volume variation monitor
      • Urine volume usually parallels kidney perfusion; and urine osmolality tubular function/concentrating ability, but FENa and other laboratory indices to determine pre- versus intra-renal have poor specificity
        • Urine Na+ and FENa rely on intact tubular function at baseline
          • Be wary if CKD, hypoaldosteronism, metabolic alkalosis, diuretics
        • BUN
          • Note: BUN is surrogate marker for uremic toxins, of which there are many
          • Increased by high protein intake, rhabdo, GIB, corticosteroids, low GFR/volume depletion (reabsorbed with Na and H2O)
          • Decreased by low protein intake, liver disease, low muscle mass, increased GFR (pregnancy, aggressive volume resuscitation)
        • Cr
          • Also affected by muscle mass, but more consistent than BUN
          • Serum Cr elevations lag behind GFR, so GFR cannot be accurately estimated until Cr stabilizes
          • Drugs that compete with Cr at proximal tubule will cause serum Cr elevation not indicative of decreased GFR.
        • New AKI markers
          • Cystatin C
            • Proteinase inhibitor released by nucleated cells at constant rate and completely metabolized by proximal tubule
            • Precedes Cr elevation in AKI by 1-2 days
          • IL-18
          • KIM-1
          • NGAL
        • Best treatment is prevention! Second best is early recognition and action:
          • Renally dose meds
            • If a patient becomes oliguric, best to dose meds based on GFR of 0 (serum Cr lags behind GFR)
          • Avoid unnecessary nephrotoxic medicines
            • NSAIDs block PGE2, constricting afferent (pre-glomerular) arterioles, decreasing glomerular perfusion pressure. They also cause Na+, K+, and H2O retention.
            • ACE-I’s reduce systemic BP and dilate efferent (post-glomerular) arterioles, decreasing glomerular perfusion pressure
          • Prevent CIN: esp in pts with preexisting renal disease
            • Think ahead and bundle imaging studies when possible
            • Volume load with NaHCO3 or NaCl, +/- NAC
            • If ESRD, time imaging study within 24 hours of dialysis
          • Prevent tumor lysis syndrome
          • Once AKI recognized:
            • Limit non-essential IVF and concentrate IV meds when appropriate
            • Beware extra K+ and PO4 intake; start phos binders when indicated. If on tube feeds, make sure Nepro/other renal formulation
            • D/c Mg2+ supplements
            • Consider IVF challenge vs. Lasix (1 mg/kg) challenge
            • If ATN, monitor closely for electrolyte disturbances in polyuric phase (usually ~3 weeks after initial injury)—can be fatal
            • Minimize catabolism to decrease production of uremic toxins
              • Avoid corticosteroids, limit protein intake (<50 g/day)
            • Keep in mind that uremia inhibits platelets and factor VIII, predisposing to bleeding
              • DDAVP increases factor VIII; can also consider plt, cryo, FFP transfusions
              • Definitive tx is correcting uremia
            • Supplement folate, pyridoxine if on HD
          • Indications for emergent HD
            • A: life-threatening metabolic Acidosis
              • From increased production (sepsis, multiorgan failure), decreased renal excretion of organic acids, decreased reabsorption of bicarbonate
            • E: Electrolytes: refractory hyperkalemia or hypermagnesemia
            • I: Ingestion/dialyzable toxin
Dialyzable Toxins
I Isopropanol
S Salicylates
T Theophylline, Tylenol
U Uremia-inducing agents
M Methanol

Barbiturates, bromine

L Lithium
E Ethylene glycol
D Depakote (valproic acid)


  • O: refractory volume Overload causing respiratory compromise or severe soft tissue edema impairing barrier defense
  • U: symptomatic Uremia (pericarditis, uremic encephalopathy, seizures)
  • Types of HD
    • Differentiated by method (convection vs. diffusion), time-course (intermittent vs continuous), and access site (venovenous—preferred, arteriovenous—rare, or peritoneal)
    • HD = hemodialysis/intermittent hemodialysis
      • Combines convection and diffusion to achieve high rate of solute clearance
      • Electrolyte concentrations in “bath” adjusted for desired end-dialysis plasma concentrations
      • Prone to rapid solute (urea) shifts à hypotonic plasma à fluid shift out of vasculature and into cells à hypotension and cellular edema
      • Other causes of hypotension with HD: decreased preload, allergic reaction to dialysis membrane/bath material
        • Also, causes not directly related to HD (bleed, tamponade, MI)
      • Hypoventilation may occur with CO2 diffusion into dialysate
    • SLED = slow low-efficiency dialysis; usually 8-12h per session
      • Less rapid shifts than conventional HD and therefore better-tolerated in hemodynamically tenuous patient
      • Slow HD à lower body temperature à increased SVR
        • Can decrease temp of dialysate to take advantage, or warm dialysate to prevent
        • Note: could blunt fever
      • Slow ratesàmore prone to clot, necessitating anticoagulation, usually with heparin, and this anticoagulation usually has systemic effects
        • Argatroban can be used if HIT
        • Citrate is local option: citrate chelates Ca2+, inhibiting coagulation cascade. Is metabolized in liver to bicarbonate, therefore no systemic anticoagulation (assuming functioning liver). iCa2+ must be monitored closely and Ca2+ replaced via separate line.
        • For clotted catheter, may try 2mg alteplase in lumens *remove before resuming dialysis*
      • HF = hemofiltration
        • Uses convection only: movement across semi-permeable membrane via hydrostatic or osmotic pressure
        • Solutes carried passively across membrane; can be selectively replaced with electrolyte solution
        • Slower changes in plasma osmolality than HD
        • HF à increased plasma protein concentration à flux of water from cells into plasma (opposite effect from HD)
      • CVVH/CAVH = continuous venovenous hemofiltration/continuous arteriovenous hemofiltration = HF done continuously
      • SCUF = slow continuous ultrafiltration = HF done continuously and at low-flow rates
        • Used primarily for fluid removal
        • Same hypothermic and coagulant effects as SLED, but can’t change dialysate temp (because there is no dialysate).
      • Renal Dosing:
        • When on SLED,
          • once daily meds should be given after SLED completed.
          • BID meds should be given post-SLED then 12h later.
          • If monitoring drug/abx levels, check after SLED and redose as indicated
        • Again, if pt oliguric, dose for GFR of 0 (Cr lags GFR and is unreliable when kidney fxn in flux)