acute kidney injury - med.uth.edu · novo ckd, ckd progression, and in some cases death. acute...
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Acute Kidney Injury
Jade M Teakell, MD, PhD, FASN
Assistant Professor
Division of Renal Diseases and Hypertension
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Outline
• Scope
• Definition
• Tools to diagnose
• Etiology
• Treatments
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Why is this important?
• AKI occurs in 10-20% hospitalized patients
– 40-60% ICU patients
• 5% of ICU patients with AKI require renal replacement therapy (50% mortality).
• AKI is associated with an increased risk for de novo CKD, CKD progression, and in some cases death.
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Acute Kidney Injury Definition
20042007
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KDIGO Definition of AKI
• Increase in SCr by ≥0.3mg/dL within 48 hours
• Increase in SCr to ≥1.5x baseline, known or presumed to have occurred within prior 7 days
• Urine volume <0.5mL/kg/h for 6 hoursStage Serum Creatinine Urine Output
1 1.5–1.9 x baseline OR >0.3 mg/dL increase
<0.5mL/kg/h for 6-12h
2 2.0–2.9 x baseline <0.5mL/kg/h for >12h
3 3.0 x baseline OR >4.0 mg/dL increaseOR Initiation of RRT
<0.3mL/kg/h for >24h ORAnuria for >12h
2012
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Limitations of Serum Creatinine
• Low Sensitivity – cellular injury that does not affect GFR
• Low Specificity – creatinine can increase/decrease without change in GFR
• Delayed – rise is seen 2-3 days after drop in GFR
• Fluid therapy – may dilute serum creatinine delaying diagnosis
• Inter-laboratory Variation
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Work-up
• Basic Metabolic Panel
• Urinalysis with micro
• Fractional excretion of sodium (and/or Urea)
• Urine protein to creatinine ratio (UPC)*
• Autoimmune and infectious serology
• Renal ultrasound
• Renal Biopsy
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Urinalysis – Cells
Isomorphic RBCs Dysmorphic RBCs
Renal Tubular Epithelial Cells (RTE) Squamous Epithelial Cells
WBC
WBCs
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Urinalysis - Casts
Granular RBC
RTE WBC
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Fractional Excretion of Na/Urea
• FENa < 1% suggests prerenal disease, where reabsorption of almost all of the filtered Na is an appropriate response to decreased renal perfusion.
• FENa > 2% percent usually indicates ATN
𝑭𝑬𝑵𝒂 =𝑼𝑵𝒂 𝒙 𝑺𝑪𝒓
𝑺𝑵𝒂 𝒙 𝑼𝑪𝒓𝒙 𝟏𝟎𝟎%
• FEUN < 35% suggests prerenal disease
• FEUN can be more accurate than the FENa in patients receiving diuretics when the FENa is higher than expected for clinical prerenal disease
𝑭𝑬𝑼𝒓𝒆𝒂 =𝑼𝑼𝑵𝒙 𝑺𝑪𝒓
𝑩𝑼𝑵 𝒙 𝑼𝑪𝒓𝒙 𝟏𝟎𝟎%
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Fractional Excretion of Na - Limitations
• The FENa criterion of less than 1% to diagnose prerenal disease applies only to patients with a marked reduction in GFR and oliguria
• Single measurements of SCr may not provide an accurate estimate of the GFR.
• There are other causes of AKI other than prerenaldisease in which the FENa can be less than 1%.
• The FENa may be above 1% when prerenaldisease occurs in patients with CKD or any cause of sodium wasting, such as diuretic therapy.
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Renal Ultrasound
• Low yield in patients without risk factors or clinical concern for obstruction
• Risk Factors - history of hydronephrosis, recurrent urinary tract infections, a diagnosis consistent with obstruction, non-black race.– AND absence of: exposure to nephrotoxins,
congestive heart failure, or prerenal AKI
• RUS in AKI – 10-15% with hydronephrosis, but only 3-5% requiring intervention.
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Risk Factors for AKI
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Etiologies
AKI
Prerenal
Intrinsic
Acute Tubular Necrosis
Acute Interstitial Nephritis
Acute GN
Acute Vascular Syndromes
IntratubularObstruction
Postrenal
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Etiologies
AKI
Prerenal
Intrinsic
Acute Tubular Necrosis
Acute Interstitial Nephritis
Acute GN
Acute Vascular Syndromes
IntratubularObstruction
Postrenal
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Prerenal AKI
Renal Hypo-
perfusion
Incr Vasoconstriction
•↑ Angiotensin II
•↑ Adrenergic stim.
•↑ Vasopressin
Volume Depletion
Congestive Heart Failure
Liver Failure
Sepsis
Decr Vasodilation
•↓ Prostaglandins
•↓ Nitric Oxide
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Volume Depletion
• Isotonic Fluid Volume Deficit
– Serum Na level remains wnl
• Decreased Cardiac Output
– Decreased blood pressure, decreased organ/tissue perfusion
• Compensation
– Neural – baro/chemoreceptors -> ↑SNS, ↑RR
– Hormonal – renin (RAAS), epi/norepi, ADH
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Volume Depletion
• Extra-Renal Losses
– Blood loss, third-spaced fluids, NPO, AMS
– GI – vomiting, diarrhea,
– Skin – excessive sweating, extensive burns, fever
• Renal Losses
– Intrinsic – salt-wasting, DI, diuretic phase of AKI
– Extrinsic – excess diuretics, osmotic diuresis
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Impaired Autoregulation can lead to “normotensive” prerenal AKI
Abuelo 2007 NEJM
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Congestive Heart Failure
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Advanced Liver Failure
Peripheral and splanchnic vasodilatation with inadequate increase in cardiac output
Activation of RAAS, SNS, Vasopressin
Renal Vasoconstriction Salt/Water Retention
Ascites / Edema
HRS
SBPHemorrhage
InfectionOver Diuresis Large vol para
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Prerenal AKI Treatment
• Correction of volume depletion (crystalloids)
• Discontinuation or Dose Adjustment– NSAIDS
– RAAS inhibitors
– CNIs
• Mgmt of “Effective” Volume Depletion– Diuresis in CHF
– Improving MAP in HRS treatment
– Antibiotics in Sepsis
• Recongnize and Treat Abd Compartment Syndrome
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Etiologies
AKI
Prerenal
Intrinsic
Acute Tubular Necrosis
Acute Interstitial Nephritis
Acute GN
Acute Vascular Syndromes
IntratubularObstruction
Postrenal
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Intrinsic Renal
VasculatureVasoconstrictionFocal ischemiaVasodilationThrombosisCoagulationInflammationIntermittent flow
MicroenvironmentInnate immunityAdaptive immunityCellular dysfunctionParacrine factorsAutocrine factors
TubulesApoptosisNecrosisMitochondrial
dysfunctionBack-leak DetachmentObstruction
Systemic factorsProinflammatory
cytokinesAntiinflammatory
cytokines
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Acute Tubular Necrosis
Abuelo 2007 NEJM
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Acute Tubular Necrosis
• Ischemic– Prolonged prerenal azotemia– Hypotension, shock– Cardiopulmonary arrest– Cardiopulmonary bypass
• Septic– Cytokine mediated inflammation– Endothelial stress/injury
• Nephrotoxic– Abx (aminoglycosides, vancomycin, amphotericin)– Chemotherapy (cisplatin, mtx)– Contrast?
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Sepsis-related AKI/ATN
Mechanisms
• Pro-Inflammatory state
• Cytokine-mediated Cell Injury
• Systemic Vasodilation
• Impaired Microcirculation
Schrier 2004 NEJM
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Toxins
There is no role for pre- or post-HD for prevention of CIN
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Acute Interstitial Nephritis
• Lymphocytic infiltration of the interstitium– Drugs (Abx, PPIs, NSAIDs, furosemide, etc)
– Infection
– Malignancy
– Systemic Diseases (SLE, Sjogren’s, TINU, etc)
• Classic Triad (rare) – fever + rash + eosinophilia
• Pyuria, WBC Casts
• Role of glucocorticoids is uncertain (no RTCs)
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Urine Eos?
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Glomerulopathies
• Nephritic (proliferative) pattern is an activeurine microscopy with RBC casts and/or dysmorphic red cells and a variable degree of albuminuria.
• Nephrotic (non-proliferative) pattern is proteinuria, usually in the nephrotic range (>3.5 g per 24 hours), and an inactive urine microscopy with very few cells or casts*
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Glomerulopathies
General Pathogenic Mechanisms
Structural GBM Abnormalities
Thin Basement Membrane
Alports
Endothelial Injury /
Thrombosis
HUS
TTP
Antibody-Mediated
Anti-GBM
ANCA Vasculitis
Complement Dysregulation
MPGN
Atypical HUS
C3 Glomerulopathy
Immune Complex-Mediated
Membranous
Lupus Nephritis
IgAN
Podocyte Injury
MCD
FSGS
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Acute Vascular Syndromes
• Thrombotic Microangiopathy (TMA)– Hemolytic Uremic Syndrome (HUS)
• Diarrhea, Shiga/Vero Toxin associated
• Supportive Care, Dialysis if indicated
– Thrombotic Thrombocytopenic Purpura (TTP)• ADAMS13 Deficiency (autoimmune or hereditary)
• Autoimmunue - Supportive care, PLEX, adjuvant steroids/rituximab, rare splenectomy
– Atypical HUS (aHUS)• Complement dysregulation (hereditary or acquired)
• Supportive care, PLEX, immunosuppression, Eculizumab
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Intra Tubular Obstruction
• Protein
– Myeloma light chain cast nephropathy
• Crystals
– Uric acid
– Oxalate
– Medications
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Etiologies
AKI
Prerenal
Intrinsic
Acute Tubular Necrosis
Acute Interstitial Nephritis
Acute GN
Acute Vascular Syndromes
IntratubularObstruction
Postrenal
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Post-Renal AKI
• Obstruction within the kidney leading to dilatation of individual calyces or caliectasis
– stones, transitional cell carcinoma, blood clots, and sloughed papillae
• Obstruction at or distal to the renal pelvis leading to pelviectasis, hypdronephrosis/ureter
– stones, malignancy, external compression, blood clots, infection (fungus ball), bladder dysfunction
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A. Stone in renal pelvis B. CaliectasisC. Lymphatomatous infiltration
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Urinary Tract Obstruction
Symptoms
• Pain
• Change in UOP
• Hypertension
• Hematuria
Lab Findings
• Elevated creatinine
• Hyperkalemia / RTA
• Hematuria/pyuria
Treatment = Relieve the pressure!
• Percutaneous nephrostomy (PCN)
• Ureteral stent / Lithotripsy
• Foley / Suprapubic Catheter
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Natural History AKI
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Natural History AKI
AKI
CKD
Disease ModifiersSeverity of AKIDuration of AKINo. of EpisodesStage of CKDProteinuria
Risk FactorsAgeRace / EthnicityGenetic FactorsDiabetes MellitusHypertensionMetabolic syndrome
OutcomesCardiovascular eventsKidney EventsESRDDisabilityDiminished QOLDeath
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References
• KDIGO Clinical Practice Guideline for Acute Kidney Injury• Cerdá J, et al. “Epidemiology of acute kidney injury.” CJASN. 2008; 3(3): 881-6.• Wang HE, et al. “Acute kidney injury and mortality in hospitalized patients.” AJN. 2012; 35(4): 349-
55.• Parazella MA, et al. “Diagnostic Value of Urine Microscopy for Differential Diagnosis of Acute Kidney
Injury in Hospitalized Patients.” CJASN. 2008; 3(6): 1615–1619.• Carvounis CP, et al. “Significance of the fractional excretion of urea in the differential diagnosis of
acute renal failure.” KI. 2002; 62(6): 2223-9.• Podoll AS, et al. “Clinical utility of gray scale renal ultrasound in acute kidney injury.” BMC Nephrol.
2013; 14: 188.• Abuelo JG, et al. “Normotensive ischemic acute renal failure.” NEJM. 2007; 357(8): 797-805.• Schrier RW, et al. “Acute Renal Failure and Sepsis.” NEJM. 2004; 351(2): 159-169.• Muriithi AK, et al. “Utility of urine eosinophils in the diagnosis of acute interstitial nephritis.” CJASN.
2013; (11): 1857-62.• McGrogan A, et al. “The incidence of primary glomerulonephritis worldwide: a systematic review of
the literature.” NDT. 2011; 26(2): 414-30.• Chawla LS, et al. “Acute kidney injury and chronic kidney disease as interconnected syndromes.”
NEJM. 2014; 371(1): 58-66.