The Whys and Wherefores of ATN · Title: Microsoft PowerPoint - ACD19_day2-9_trk1-6-Pinson-2f Author: WWalsh Created Date: 5/11/2019 3:25:28 PM

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This is the Full Title of a Session

The Whys and Wherefores of ATN

Richard D. Pinson, MD, FACP, CCSPrincipalPinson and Tang, LLCHouston, TX

2019 Copyright, HCPro, a division of Simplify Compliance LLC, and/or session presenter(s). All rights reserved. These materials may not be copied without written permission.

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Learning Objectives

• At the completion of this educational activity, the learner will be able to:– Describe the evolution of the modern clinical concept of ATN– Define the current diagnostic criteria for ATN– Recognize undocumented ATN and compose an effective query for clarification of the diagnosis


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Agenda

• Anatomy of the kidney• Acute kidney injury (AKI)• Acute tubular necrosis (ATN)

– Diagnostic standards – Classical and current concepts/definition

• Documentation and coding implications• Polling questions• Clinical scenario and query• Q&A


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Kidney & Nephron Anatomy

Artist: Lydia Williamson Used with permission


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Acute Kidney Injury (AKI)

• Sudden reduction in kidney function usually within hours or days• Classified as:

– Pre‐renal: dehydration, volume depletion– Renal (intra‐renal): ATN, papillary necrosis, glomerulonephritis– Post‐renal: obstruction of ureters or bladder

• Diagnostic criteria (KDIGO, 2012):– Cr increase to > 1.5x baseline within 7 days or less; or– Cr increase by > 0.3 mg/dl within 48 hours or less;– Urine output < 0.5 ml/kg/hr for 6 hours

• Baseline unknown: lowest creatinine during admission assumed to be baseline


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Acute Kidney Injury (AKI) – Case Studies

• 79 yo female with CKD presents with nausea, vomiting, diarrhea x 3 daysCreatinine: 3.4 2.6 2.0

• 68 yo male with CHF Tx’d with Lasix 80 mg IVCreatinine: 0.9 1.3 1.0

• 45 yo female with pyelonephritisCreatinine: 1.4 1.0 1.1


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Acute Tubular Necrosis (ATN)

• A functional abnormality of the renal tubules due to toxic or ischemic injury– If severe, may sometimes progress to necrosis and sloughing of renal tubular cells– Actual histologic necrosis of renal tubules may occur in the most severe cases but is rare

– The defining feature of ATN is no longer considered to be necrosis (urine sediment may be normal)

• ATN is the cause of AKI in about 1/3 of hospitalized patients


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Classical Concept of ATN

• Profound and prolonged acute renal failure– Initial oliguric phase (low volume) with dramatic increase in creatinine levels– Subsequent prolonged oliguric plateau phase– Followed by a gradual polyuric (high‐volume) resolution phase frequently incomplete resulting in permanent chronic kidney disease

– Characteristic abnormal urine sediment:• Free renal epithelial (tubular) cells and casts• Muddy brown casts


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Classical ATN

0

0.5

1

1.5

2

2.5

3

3.5

Day 1 Day 2 Day 4 Day 6 Day 10 Day 14 Day 20 Day 25 Day 30 Day 60

Creatinine

Creatinine


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Current Clinical Concept of ATN

• ATN is a functional (not structural) abnormality of renal tubules– Ischemic or toxic injury

• Defining feature no longer considered to be necrosis

• Urinalysis usually unremarkable– Primarily used to exclude other causes of AKI

• Acute tubular injury (ATI) proposed but not widely employed– Necrosis is a misnomer for a functional abnormality


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ATN Diagnostic Criteria

• Meets criteria for AKI

• Defining criterion: Creatinine levels persistently increased for > 72 hrs despite adequate fluid resuscitation– Pre‐renal (e.g., dehydration) usually no more than 24–48 hrs

• Urine chemistry (optional/confirmatory):– Urinary sodium concentration > 40 meq/L

• Pre‐renal AKI usually < 20 meq/L– Fractional excretion of sodium (FENa) > 2%

• Pre‐renal AKI usually < 1%• Contrast‐induced ATN may be < 2%


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Current ATN: Tubular Dysfunction

0

0.2

0.4

0.6

0.8

1

1.2

1.4

1.6

1.8

Day 1 Day 2 Day 3 Day 4 Day 5

Creatinine

Creatinine


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Clinical Circumstances Associated With ATN

• IV contrast (always ATN)– “Contrast‐induced AKI”

• Hypotension/shock• Sepsis• Obstetrical complications (e.g., eclampsia, hemorrhage)• Prolonged surgery• Nephrotoxins• Rhabdomyolysis


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Nephrotoxic Drugs Causing ATN

• Acetaminophen (Tylenol)• NSAIDs• Aminoglycosides (e.g., gentamicin, tobramycin)• Tetracyclines• Acyclovir• Cisplatin• Cyclosporine


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Documentation and Coding Challenges

• AKI is assigned to code N17.9 (CC)• ATN is N17.0 (MCC)

– “Vasomotor nephropathy” = ATN– Toxic nephropathy = category N14 (non‐CC)

• ATN clinically underrecognized/underdiagnosed– 1/3 of inpatient AKI is due to ATN– All IV contrast‐induced AKI due to ATN

• Physician education is essential• Queries often necessary


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Polling Question 1: Definition of ATN

• The defining criterion for ATN is:– Increased creatinine > 2x baseline– Urinalysis showing “muddy brown” casts and renal tubular epithelial cells– Persistently elevated creatinine level for > 72 hours despite adequate fluid resuscitation

– None of the above


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Polling Question 2: Contrast‐Induced AKI

• Contrast‐induced AKI is always due to ATN.– Yes– No– Uncertain


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Query Example

• 45 yo with suspected coronary artery disease has cardiac cath with coronary angiography

• Creatinine– Admission = 1.0– Post‐procedure day 1 = 1.5– Day 2 = 1.6– Day 3 = 1.4– Day 4 = 1.3– Day 5 = 1.1

• Diagnosis: Contrast‐induced AKI


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Query

Dr. Smith:This patient has been diagnosed with contrast‐induced AKI following cardiac cath and coronary angiographyCreatinine levels are as follows:• Admission = 1.0• Post‐procedure day 1 = 1.5• Day 2 = 1.6• Day 3 = 1.4• Day 4 = 1.3• Day 5 = 1.1

Can you please clarify if the cause of contrast‐induced AKI is:• ATN• Prerenal• Other intra‐renal cause (please specify)• Other cause (please specify)• None of the above/not applicable


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Recommended Sources

• ICD‐10‐CM Official Guidelines for Coding and Reporting: FY 2019• KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney International

Supplements 2012; 2: 1–138• UpToDate.com: Etiology and diagnosis of prerenal disease and acute tubular

necrosis in acute kidney injury in adults• UpToDate.com: Pathogenesis, clinical features, and diagnosis of contrast‐

induced nephropathy• J Am Soc Nephrol 2008; 19: 871–875• Kidney Int 1996; 50: 811–818• Clin Geriatr Med 2009; 25: 331–358


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Thank you. Questions?

[email protected]

In order to receive your continuing education certificate(s) for this program, you must complete the online evaluation. The link can be found in the continuing education section at the front of the program guide.


The Whys and Wherefores of ATN · Title: Microsoft PowerPoint - ACD19_day2-9_trk1-6-Pinson-2f Author: WWalsh Created Date: 5/11/2019 3:25:28 PM

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