PRE-RENAL AKI: DOES IT LEAD TO ATN. Sushma Bhusal
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1 PRE-RENAL AKI: DOES IT LEAD TO ATN Sushma Bhusal
2 CASE PRESENTATION CC : 31 AAM presented with Fatigue, malaise and body aches x 10 days HPI: STD testing done 2 weeks prior, all results negative Symptoms started the following day No clear precipitating cause ROS: Nausea, vomiting, poor po intake X 1 week Constipation x 1 week Low urine volume but no other urinary symptoms 1 pint of Vodka daily to help him sleep, last drink 4 days PTA
3 CASE PRESENTATION PMH: HTN, PTSD, ETOH use, Tobacco Use PSH: None FH: DM, HTN in Mom Social: Unemployed, Cigarette smoking, 1 pint ETOH daily, sexually active with one partner (polygamous)
4 Allergies: None CASE PRESENTATION Home Medications: Stopped one week prior Cholecalciferol 1000U po daily Folic acid 1 mg po dail Thiamine 100 mg po daily Lisinopril 20 mg/hctz 25 mg po daily
5 COURSE PRIOR TO RENAL TEAM EVALUATION Presenting Vitals: T 98.4, BP 81/54, HR 118, RR 15, O2 sat 100% RA Found with AKI, no obstruction on NCCT Patient deemed to be hypovolemic and given 2L of IV fluids
6 PHYSICAL EXAM Vitals: T 98.6, BP 116/74, HR 85, RR 18, O2 sat 100% RA General: Alert, oriented, no acute distress HEENT: oral mucosa dry CVS: S1S2+, RRR, no murmurs/rubs/gallops Resp: CTABL Abdomen: soft, non tender, non distended, BS+ all quadrants Back: No CVA tenderness Skin: No rash Ext: no joint swelling, edema
7 LABS CBC BMP ABG: ph PCO2 30 Po2-125 CPK : 51, Trop neg Calcium 10.5 Lactate: 0.6
8 LABS Urine studies UA: cloudy, SG 1.018, ph5.0, prot 1+, nit -, LE small, no blood Urine microscopy: hyaline casts, wbc 17, rbc 1 Urine lytes: Na 32, K 14, Cl 24, Urea 238 FENa: > 2% U P/Cr: 0.7/316 Urine tox: negative
9 IMAGING CXR: No acute Cardiopulmonary disease NCCT Abdomen and Pelvis Without contrast: Unremarkable, kidneys normal size, no hydronephrosis or calculus
10 DIFFERENTIALS: PRE RENAL AKI Hypovolemia Blood loss, GI loss, Skin 3 rd Space (bowel, pancreatitis, edema) Cardiovascular: low cardiac output Distributive (decreased SVR) Sepsis Hepatorenal Vasodilators Renal Renal artery stenosis Drugs (ACE inhibitors, non-steroidal) Rapid lowering of BP in severe hypertension
11 DIFFERENTIALS: ATN Ischemia Toxins: Myoglobin, Aminoglycosides, Radio-contrast agents Interstitial Nephritis Acute Glomerulonephritis and Vasculitis Post Renal
12 HOSPITAL COURSE Patient improved with IV fluids, total of 5 L Discharged to be followed up in clinic, never did x 2 At discharge the diagnosis was pre-renal renal failure
13 HOSPITAL COURSE
14 OBJECTIVES 1. Pathophysiology of pre-renal AKI: Failure of auto regulation 2. ATN: Is pre-renal failure a cause (difference in opinion) 3. Biomarkers in AKI: In brief
15 Pathophysiology of Pre-Renal AKI
16 AUTO-REGULATION OF RENAL BLOOD FLOW 1. Myogenic stretch Reflex 2. Tubulo-Glomerular feedback 3. Angiotensin II
17 AUTO-REGULATION OF RBF Abuelo NEJM, Aug 2007
18 TUBULO-GLOMERULAR FEEDBACK Okusa. Contrib Nephrol, 2011
19 AUTO-REGULATION OF RENAL BLOOD FLOW Badr NEJM, Sept 8, 1998
20 IMPAIRED AUTO-REGULATION Abuelo NEJM, Aug 2007
21 IMPAIRED RENAL AUTO-REGULATION Failure to decrease afferent arteriolar resistance 1. Structural changes Old age Atherosclerosis Ch HTN CKD Malignant HTN 2. Reduced vasodilatory PG NSAIDs Cox 2 inhibitors 3. Afferent art vasoconstriction Sepsis Hypercalcemia HRS CNI Radiocontrast Failure to increase efferent arteriolar resistance ACEI ARBS Renal Artery Stenosis Adapted from Abuelo NEJM, Aug 2007
22 Abuelo NEJM, Aug 2007
23 PRE-RENAL AZOTEMIA: A FLAWED PARADIGM IN CRITICALLY ILL SEPTIC PATIENTS? Contrib Nephrol 2007; 156: 1-9 Bellomo et al
24 PRE-RENAL AZOTEMIA: A FLAWED PARADIGM Widely known concept Applied to describe two overlapping processes: Trigger outside the kidney No parenchymal disease, functional, rapidly reversible, if not: ATN (structural) Assumption: Cannot arise denovo
25 PRE-RENAL AZOTEMIA: A FLAWED PARADIGM Questions before concept is accepted 1. How does one know when pre- renal AKI becomes ATN 2. How much structural injury needed to be able to say kidney has transitioned from pre- renal to ATN 3. Treatment implications of accurate classification 4. Availability of experimental data that these pathophysiological states exist in severe sepsis
26 WHEN DOES PRE- RENAL AKI BECOMES ATN No consensus criteria defining either ATN or Pre-renal AKI When no line can be defined, how to know when crossed? Biopsy vs clinical course: No biopsies available What duration of progressive pre renal azotemia before
27 HOW MUCH STRUCTURAL INJURY NEEDED If ATN assumed patchy, how many necrotic cells to call ATN? No. of necrotic cells correlate with duration and ability to resolve quickly Can both coexist What is rapid response to treatment?
28 TREATMENT IMPLICATIONS OF ACCURATE CLASSIFICATION Academic rather than clinical? Classification guides clinicians to appropriate treatments
29 AVAILABILITY OF EXPERIMENTAL DATA Urine analytes and derived variables can D/D between ATN and Prerenal AKI: Not supported by histopath Tubular casts: viable cells, not necrotic Animal studies: urinary chemistries due to loss of cell polarity and translocation of ATPase, not cell death Urinary findings may D/D sustained from rapidly resolving AKI: May be true in ward patients
30 Biomarkers: Where do we stand?
31 BIOMARKERS OF AKI AKI still remains a cause of significant morbidity and mortality Barriers to translating animal studies to patients: heterogeneity with regards to underlying etiology Comorbidities complex pathophysiology late timing of experimental interventions Search for kidney troponin still on Current Biomarkers: NGAL, KIM1, L-FABP, IL8, Cystatin C, TIMP-2, IGFBP7
32
33 METHODS Prospective study, 161 patients Inclusion Criteria: All patients hospitalized with AKI Exclusion criteria: no baseline Cr, inadequate follow up or post obstructive renal failure Urinary NGAL levels checked at enrollment and 2 days later along with other parameters Composite outcome: Step up of RIFLE, RRT, Death
34 Kidney Intl Aug 2008
35 SUB STRATIFICATION OF RIFLE SEVERITY BY NGAL LEVELS
36 URINARY NGAL LEVELS AND OUTCOMES Kidney Intl. Aug 2008
37 Test AUC FOR DIFFERENT BIOMARKERS Diagnosis of intrinsic AKI (vs pre-renal AKI) Prediction of composite outcome (unfavorable clinical course) U- NGAL 0.87 ( ) *** 0.71 ( ) *** U-NGAL/U Cr 0.89 ( ) *** 0.71 ( ) *** Serum Cr 0.74( ) ***, # 0.61( ) *, & RIFLE Class 0.72 ( ) ***, # 0.56( ) # FUrea 0.59( ) # 0.49( ) # FENa 0.54( ) # 0.45( ) # BUN/Cr 0.71( ) *,# 0.48( ) #
38 SOME OTHER STUDIES
39 CONCLUSIONS Our patient was a classic case of pre-renal renal failure by any criteria!! Hope to see biomarkers in our clinical practice
40
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