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Acute Renal Failureaka Acute Kidney Injury
Dr H Bierman
RIFLE criteria for diagnosis of AKI based on The “Acute Dialysis Quality Initiative”
Increase in SCr Urine output
Risk of renal injury
Injury to the kidney
Failure of kidney function
0.3 mg/dl increase
2 X baseline
3 X baseline OR> 0.5 mg/dl increase if SCr >=4 mg/dl
< 0.5 ml/kg/hr for > 6 h
< 0.5 ml/kg/hr for >12h
Anuria for >12 h
Loss of kidney functionEnd-stage disease
Persistent renal failure for > 4 weeksPersistent renal failure for > 3 months
Am J Kidney Dis. 2005 Dec;46(6):1038-48
Increase in Creatinine without AKI
• Inhibition of tubular creatinine secretionTrimethoprim, Cimetidine, Probenecid
• Interference with creatinine assays in the lab (false elevation)
glucose, acetoacetate, ascorbic acid, cefoxitinflucytosine
Increase in BUN without AKI
• Increased productionGI BleedingCatabolic states (Prolonged ICU stay)CorticosteroidsProtein loads (TPN-Albumin infusion)
Major Disease Categories Causing AKIDisease Category Incidence
Prerenal azotemia caused by acute renal hypoperfusion 55-60%
Intrinsic renal azotemia caused by acute diseases of renal parenchyma: -Large renal vessels dis. -Small renal vessels and glomerular dis. -ATN (ischemic and toxic) -Tubulo-interestitial dis. -Intratubular obstruccttion
35-40%
*>90%*
Postrenal azotemia caused by acute obstruction of the urinary tract <5%
Prerenal Azotemia
• Intravascular volume depletionbleeding, GI loss, Renal loss, Skin loss, Third space loss
• Decreased cardiac outputCHF
• Renal vasoconstrictionLiver Disease, Sepsis, Hypercalcemia
• Pharmacologic impairment of autoregulation and GFR in specific settings
ACEi in bilateral RAS, NSAIDS in any renal hypoperfusion setting
Acute Kidney Injury• Prerenal and ATN encountered most often in the
hospital setting: 70-75% in many studies• Most common diagnostic consideration is
therefore between these two conditions• Prerenal:
1. Intravascular volume depletion2. Hypotension3. Edematous states4. Localized renal ischemia
• ATN:1. All causes for prerenal, leading to post-ischemic ATN2. Toxins
Intrinsic Renal Azotemia• Large Renal Vessel Disease
Thrombo-embolic disease• Renal Microvasculature and Glomerular Disease
Inflammatory: glomerulonephritis, allograft rejectionVasospastic: malignant hypertension, scleroderma crisis, pre-eclampsia, contrastHematologic: HUS-TTP, DIC
• Acute Tubular Necrosis (ATN)IschemicToxic
• Tubulo-interestitial DiseaseAcute Interstitial Nephritis (AIN), Acute cellular allograft rejection, viral (HIV, BK virus), infiltration (sarcoid)
• Intratubular Obstructionmyoglobin, hemoglobin, myeloma light chains, uric acid, tumor lysis, drugs (indinavir, acyclovir, foscarnet, oxalate in ethylene glycol toxicity)
Postrenal azotemia
• Stones• Blood clots• Papillary necrotic tissue• Urethral disease
anatomic: posterior valvefunctional: anticholinergics, L-DOPA
• Prostate disease• Bladder disease
anatomic: cancer, schistosomiasisfunctional: neurogenic bladder
Initial diagnostic tools in AKI• History and Physical exam• Detailed review of the chart, drugs administered,
procedures done, hemodynamics during the procedures.• Urinalysis
SG, PH, protein, blood, crystals, infection• Urine microscopy
casts, cells (eosinophils)• Renal imaging
US, Retrograde Pyelogram, CT etc• Markers of CKD
iPTH, size<9cm, anemia, high phosphate, low bicarb• Renal biopsy
AKI: Diagnostic studies-urine• Urinalysis for sediment, casts• Response to volume repletion with return to
baseline SCr 24-72 hr c/w prerenal event• Urine Na; FENa FENa (%) = UNa x SCr x 100 SNa x UCr
– FENa < 1%: Prerenal– FENa 1-2%: Mixed– FENa > 2%: ATN
• Hansel’s stain
Urinalysis in Acute Kidney InjuryBiomarkers: AMI versus AKI
PrerenalPostrenalOncotic AKI
GlomerulopathyVasculitisThrombotic MA
PyelonephritisInterstitial nephritis
AINAthero-
embolic AKI
ATNMyoglobinHemoglobin
Uric acidToxinsDrugs
Plasma cell dyscrasia
HematuriaRBC castsproteinuria
WBCWBC casts
Eosinophils RTE cellsPigmented
casts
Crystalluria Non-albumin
proteinuria
Abnormal sedimentNormal/bland
Acute Kidney Injury
IMAGING STUDIES• Ultrasound: evaluates renal size, able to detect
masses, obstruction, stones• CT: detects masses, stones; caveat exists when
IVCD is considered• MRI/MRA: can detect RAS; use of Gadolinium
carries uncertain R/B ratio in AKI 2° potential hemodynamic changes similar to IVCD, and NFD
• In the AKI setting, U/S provides most information with the most favorable R/B ratio
AKI: Acute Tubular Necrosis• Non-oliguric vs. Oliguric
• Prognosis worse with oliguric ATN in most series• Ischemic insult: medulla most susceptible to
hypoxic event, cellular ATP depletion, oxidative injury
• AKI/ARF phase of ATN: 7-21 days on average• Recovery phase of ATN: also known as diuretic
phase• High urine output (>3-4 L)• K, Mg, PO4 wasting
• Associated with high FENa
AKI: Acute Tubular Necrosis
• Saline loading effective in lowering ATN risk from drugs/pigments/toxins; sometimes limited in post-ischemic ATN, particularly if CO/CI compromised
• Maintenance of CO, BP, avoid new insults • Preventative agents have shown promise in
animal models, but poorly translated to clinical situations• Dopamine, fenoldopam, mannitol, statins, loop diuetics
• Identification of high risk AKI patients is essential to prevention: DM, CKD, CVD, poor nutrition
Acute Kidney Injury: AIN causes
DRUGS• ACEI• Allopurinol• Cephalosporins• Cimetidine• Fluoroquinolones• Loop diuetics• NSAIDS• PCN• Phenytoin• Rifampin• Sulfonamides• Tegretol• Thiazides
INFECTION• Bacterial
– Agents causing pyelonephritis– Legionella– Brucella– Yersinia
• Viral– Hantavirus– HIV– CMV,EBV,HSV
AKI: Glomerulonephritis (RPGN)/Systemic Vasculitis
• Immune-Complex Mediated
• SLE• Cryoglobulinemic vasculitis• Henoch-Schönlein purpura• Post-strep GN
• Direct Ab attack• Anti-GBM disease• Goodpasture’s syndrome
• Pauci-immune vasculitis• Microscopic polyangiitis• Wegener’s granulomatosis• Churg-Strauss syndrome
• Thrombotic Microangiopathy
• TTP• HUS• Scleroderma renal crisis• Preeclampsia• Malignant hypertension
Treatment of AKI• Treatment is largely supportive in nature!• Pharmacologic treatments under study:
– Dopamine: no benefit– Atrial Natriuretic Peptide (ANP) or ANP-analogue
(Anaritide): promising– Human Insulin like growth factor 1: no benefit
• Renal Replacement therapy remains the cornerstone of management of minority of patients with severe AKI
Nephron Clin Pract 2009;112:c222-c229
Is there a role for diuretics in the treatment of AKI in ICU setting?
• PICARD Study: Cohort study of 552 pts in 4 UC hospitals: no effect on in hospital mortality or longterm renal outcome
• Improved urine output and shorter duration of RRT (none has clinical relevance in ICU pts)
• But diuretics continue to be used for volume control in AKI in ICU setting!
JAMA. 2002 Nov 27;288(20):2547-53Crit Care Resusc. 2007 Mar;9(1):60-8
When to do renal biopsy in AKI ?
• Any evidence of glomerular disease -nephrotic range proteinuria-sub-nephrotic range proteinuria with hematuria -RBC cast
• AKI in renal allograft
• Determine the prognosis and chance of recovery of renal function in dialysis dependent AKI.
• Whenever potential Bx result can change the management or prognosis.
Acute Kidney Injury
INDICATIONS FOR RENAL REPLACEMENT THERAPY• Consensus generally includes:
1. Refractory volume overload2. Severe metabolic acidosis; HCO3 may be variable, but
declining level; also falling pH to 7.1-7.23. Hyperkalemia, with levels > 6.5, or documented rapid rise
refractory to medical therapy4. Major uremic target organ manifestations i.e. pericarditis,
progressive neuropathy, seizure, or unexplained AMS5. Platelet dysfunction, bleeding diasthesis6. AKI in setting of dialyzable drug/toxin
Acute Kidney Injury: conclusions• Major advances in understanding AKI, but no clear
definition that guides research on prophylaxis, prognosis• AKI still carries high M/M risk, especially in ICU setting• Improving volume status, hemodynamics rapidly aids in
minimizing ischemic AKI risk; volume resuscitation, relief of urinary obstruction can be done concurrently
• Patient history, hosp chart review, routine labs, UA may establish cause in 40-60% of AKI
• Serologies and consideration of Bx are also adjuncts• Advent of urinary biomarkers of ischemic tubular injury
i.e. urine NGAL, will be next front in redefining AKI
Thank you!
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