Acute Kidney Injury (AKI)

🔍 Definition

Acute Kidney Injury (AKI) is a rapid decline in renal function occurring over hours to days, characterized by an abrupt increase in serum creatinine, decrease in urine output, or both. AKI represents a spectrum of injury from mild, reversible azotemia to severe renal failure requiring renal replacement therapy (RRT). Per the KDIGO 2012 Clinical Practice Guideline for Acute Kidney Injury, AKI is defined by any of the following criteria:

• Increase in serum creatinine (Cr) by ≥0.3 mg/dL within 48 hours
• Increase in serum Cr to ≥1.5× baseline within the prior 7 days
• Urine volume <0.5 mL/kg/h for ≥6 hours

For ICD-10-CM coding purposes, AKI is classified under category N17 (Acute kidney failure). A physician/provider diagnosis is required; coders and CDI specialists may not assign AKI solely on lab values without a documented diagnosis.

🗂️ Alternative Terminology

Clinicians, nurses, and consultants use various terms for AKI. Coders must recognize all of the following as potentially codeable as N17.x (when documented by the treating provider):

🩺 Signs & Symptoms

AKI presents along a wide clinical spectrum. Early stages may be asymptomatic with only laboratory abnormalities, while advanced stages produce systemic manifestations of uremia and volume overload. Coders should note that signs and symptoms integral to a condition (e.g., oliguria in the setting of documented AKI) are not separately coded per ICD-10-CM Official Guidelines Section I.B.5.

• Oliguria/anuria — urine output <400 mL/24h (oliguria) or <100 mL/24h (anuria)
• Rising serum creatinine and BUN — azotemia
• Hyperkalemia — potentially life-threatening; may cause EKG changes and arrhythmias
• Metabolic acidosis — reduced bicarbonate, elevated anion gap
• Fluid overload — peripheral edema, pulmonary edema, hypertension
• Uremic symptoms — nausea, vomiting, anorexia, altered mental status (encephalopathy), pericarditis
• Hematuria / proteinuria — especially in glomerular etiologies
• Flank pain — in obstructive or vascular etiologies
• Electrolyte disturbances — hyperphosphatemia, hypocalcemia, hyponatremia

🧭 Differential Diagnosis

Accurate AKI coding depends on the provider’s determination of etiology (pre-renal, intrinsic, or post-renal) and exclusion of conditions that mimic AKI. CDI specialists should prompt clarification when the etiology is ambiguous.

📋 Clinical Indicators

The following clinical indicators should prompt a CDI review or query for AKI. Coders should not assign N17.x without provider documentation; however, clinical indicators support query generation per AHIMA and ACDIS guidelines.

🦴 Anatomy & Pathophysiology

The kidneys are paired retroperitoneal organs responsible for filtration of approximately 180 liters of plasma per day via approximately 1 million nephrons each. The nephron — comprising the glomerulus, proximal convoluted tubule (PCT), loop of Henle, distal convoluted tubule, and collecting duct — is the functional unit affected in AKI.

Pre-renal AKI

Decreased renal perfusion due to true volume depletion (hemorrhage, GI losses, insensible losses), effective arterial blood volume depletion (heart failure, cirrhosis, sepsis), or medications (NSAIDs blunting prostaglandin-mediated afferent arteriolar dilation; ACE-I/ARBs blocking angiotensin II–mediated efferent arteriolar constriction). The GFR falls reversibly with no structural tubular damage initially. Prolonged pre-renal state converts to ischemic ATN.

Intrinsic AKI — Acute Tubular Necrosis (ATN)

ATN is the most common form of intrinsic AKI and the most frequently coded subtype (N17.0). It arises from:

• Ischemia: Sustained hypoperfusion causes tubular epithelial cell death, particularly in the highly metabolically active S3 segment of the PCT and thick ascending limb of Henle — both highly susceptible to oxygen deprivation.
• Nephrotoxins: Aminoglycosides (proximal tubule accumulation), IV contrast agents, cisplatin, amphotericin B, myoglobin (rhabdomyolysis), hemoglobin (hemolysis), and NSAIDs.

Pathophysiologically, tubular cell necrosis leads to intratubular obstruction by cellular debris, backleak of filtrate, and a reduction in GFR via tubuloglomerular feedback mechanisms.

Intrinsic AKI — Other Forms

• Acute cortical necrosis (N17.1): Diffuse ischemic necrosis of the renal cortex sparing the medulla; associated with obstetric catastrophes (abruptio placentae, PPH), septic shock, and DIC. High mortality; often irreversible.
• Acute medullary/papillary necrosis (N17.2): Ischemia of the renal papillae; classically associated with NSAID abuse, sickle cell disease, DM, analgesic nephropathy, and urinary tract obstruction.
• Interstitial nephritis (N10): Immune-mediated tubulointerstitial inflammation; drug reactions (beta-lactams, PPIs, NSAIDs), infections, or autoimmune.

Post-renal AKI

Urinary tract obstruction at any level (ureteral, bladder outlet, or urethral) causes increased intratubular pressure transmitted back to Bowman’s space, reducing GFR. Common causes include BPH, prostate cancer, retroperitoneal fibrosis, bilateral ureteral obstruction, and obstructed urinary catheter. Rapid decompression is key to recovery.

KDIGO Staging — Clinical Reference

The KDIGO AKI staging system is the clinical standard used by providers. ICD-10-CM does not have stage-specific codes within N17, but KDIGO stage should inform CDI queries and MS-DRG severity capture:

💊 Medication Impact / Treatment

Pharmacologic management of AKI is primarily supportive. Several medication classes are directly implicated in AKI causation and must be documented by providers as drug-induced nephropathy to allow appropriate ICD-10-CM coding of drug-adverse effect or underdosing codes per ICD-10-CM Guideline I.C.19.e.

Nephrotoxic Medications (Causative of AKI)

Supportive Pharmacologic Management (AKI Treatment)

• Loop diuretics (furosemide, bumetanide): Convert oliguric to non-oliguric AKI; facilitate fluid management; do NOT improve recovery or mortality in ATN.
• Vasopressors (norepinephrine, vasopressin): Maintain MAP ≥65 mmHg in sepsis-associated AKI; vasopressin preferred in hepatorenal syndrome (with albumin).
• Erythropoiesis-stimulating agents (ESAs): Epoetin alfa (J0885), darbepoetin (J0881) for anemia of CKD context post-AKI; HCPCS codes relevant for ESRD-associated management.
• IV Iron (ferric carboxymaltose — J1439; ferumoxytol — J0596; iron sucrose — J1756): Adjunct to ESA therapy in ESRD/CKD setting.
• Sodium bicarbonate: Manages metabolic acidosis; used prophylactically for contrast nephropathy.
• N-Acetylcysteine (NAC): Prophylaxis for contrast nephropathy (evidence mixed; still commonly ordered).
• Kayexalate / Patiromer / Sodium Zirconium Cyclosilicate (SZC): Management of AKI-associated hyperkalemia.

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📘 ICD-10-CM Guidelines

AKI coding is governed by FY2027 ICD-10-CM Official Guidelines and Tabular List conventions. Guideline I.C.14.a addresses chronic kidney disease staging and related CKD concepts; acute renal failure/AKI with CKD is explicitly addressed in the hypertensive CKD and hypertensive heart-and-CKD guidelines and should be coded in addition to CKD when documented, with sequencing based on the circumstances of the encounter.

Guideline I.C.14.a — AKI and CKD

Per FY2027 ICD-10-CM Official Guidelines I.C.14.a and the related hypertensive CKD guidance:

• When a patient has AKI and CKD, codes for both the AKI (N17.x) and the CKD stage (N18.1–N18.6) should be assigned.
• Sequencing is determined by the circumstances of admission (which condition was chiefly responsible for the hospital encounter). If the patient was admitted for AKI exacerbating underlying CKD, sequence the AKI first. If the CKD was the primary reason and AKI is a complication, sequence accordingly.
• The AKI and CKD codes are NOT mutually exclusive — both must be coded when both are documented.
• Do NOT use a “combination” code for AKI on CKD — there is no single code for this; the dual-code approach is required.

Additional Coding Guidelines Applicable to AKI

• Postprocedural kidney failure (N99.0): Use for AKI/acute renal failure documented as a clinically significant complication of a procedure per the complications-of-care guideline. Code additionally the specific type of kidney disease/failure and other underlying or precipitating condition when applicable and documented.
• Hepatorenal syndrome (K76.7): This code is inclusive of renal failure in the context of liver disease. Do NOT additionally code N17.x — the renal component is captured within K76.7 per the tabular inclusion note.
• Rhabdomyolysis (M62.82): When rhabdomyolysis causes AKI, code M62.82 first (or sequence per circumstances), then code N17.x for the resulting AKI (N17.0 for ATN is most appropriate given pigment nephropathy mechanism).
• Contrast-induced nephropathy: Code N14.11 (nephropathy induced by contrast media, FY2020+). Add N17.x if AKI criteria are also met. The T-code for adverse effect of the contrast agent should also be assigned.
• Sepsis-associated AKI: Code sepsis first (A41.x or appropriate sepsis code), followed by N17.x for AKI as an organ dysfunction. This combination typically triggers Severe Sepsis (R65.20/R65.21) — a critical MCC/MS-DRG driver.
• Bilateral ureteral obstruction with AKI: Code the obstruction (N13.x) plus N17.x when AKI criteria are met.
• Dialysis-dependent patients: When patient is on chronic renal dialysis, use Z99.2 (dependence on renal dialysis) as an additional code. For complications of dialysis catheters, use T82.4xxA or T85.6xxA per catheter type.
• CRRT procedural coding (ICD-10-PCS): Continuous renal replacement therapy during AKI is coded as:
  • 5A1D70Z — Performance of Urinary Filtration, Intermittent, Less than 6 Hours Per Day
  • 5A1D80Z — Performance of Urinary Filtration, Prolonged Intermittent, 6–18 Hours Per Day 5A1D90Z — Performance of Urinary Filtration, Continuous, Greater than 18 Hours Per Day

Clinical Validity Considerations (FY2026 Emphasis)

Per CMS FY2026 IPPS Final Rule and related AHIMA clinical validity guidance, AKI must meet these documentation requirements to withstand audit:

• A documented baseline serum creatinine (pre-admission or early hospitalization value) that provides context for interpreting the elevated inpatient creatinine
• Explicit provider documentation linking the creatinine elevation or oliguria to a clinical diagnosis of AKI or acute renal failure
• Evidence of clinical evaluation and/or management directed at the AKI (not merely “monitoring” creatinine)
• Provider documentation of etiology or type when the clinical picture supports a more specific code (ATN, contrast-induced, drug-induced, obstructive)

🔢 ICD-10-CM Code Set (Tabular)

All codes verified against the FY2027 ICD-10-CM Tabular List (effective October 1, 2026).

🔎 Indexing

The following index pathways from the FY2027 ICD-10-CM Alphabetic Index apply to AKI:

🏥 CPT

CPT codes for AKI-related procedures are governed by the AMA CPT 2027 code set. Renal replacement therapy coding is complex and requires documentation of the type of RRT (intermittent HD, CRRT, SLED, peritoneal dialysis), duration, physician/QHP evaluations, and clinical setting.

🧾 HCPCS

HCPCS Level II codes support billing for dialysis supplies, erythropoiesis-stimulating agents (ESAs), IV iron, and other renal-related products per the applicable CMS HCPCS Level II quarterly update file.

📚 AHA Coding Clinic

The AHA Coding Clinic for ICD-10-CM/PCS provides official coding advice. The following represent significant guidance items relevant to AKI coding:

💰 HCC / Risk Adjustment

Per the CMS-HCC Model v28 (effective CY2024, fully phased in CY2026), AKI and CKD codes have distinct HCC mapping profiles:

✍️ CDI Query Templates

All query templates below conform to AHIMA and ACDIS compliant query format: non-leading, multiple-choice options offered with a “clinically undetermined” option, based on documented clinical indicators.

🧑‍⚕️ Treatments (Clinical)

Clinical management of AKI is guided by the KDIGO AKI Clinical Practice Guidelines and KDOQI clinical practice recommendations. CDI specialists should understand treatment context to recognize appropriate documentation triggers and clinical validity indicators.

General Supportive Management (All AKI Types)

• Volume optimization: IV fluid resuscitation (crystalloid preferred — isotonic saline or balanced solutions such as lactated Ringer’s) for volume-depleted pre-renal AKI; restrict fluids if volume overloaded
• Hemodynamic monitoring: MAP target ≥65 mmHg; vasopressors (norepinephrine) for vasodilatory sepsis-AKI
• Electrolyte management: Hyperkalemia (kayexalate, sodium bicarbonate, insulin/glucose, calcium gluconate, hemodialysis for refractory cases); hyperphosphatemia (phosphate binders); metabolic acidosis (sodium bicarbonate for pH <7.15)
• Nephrotoxin removal: Hold NSAIDs, ACE-I/ARBs in AKI episodes; renally dose-adjust or hold antibiotics; avoid iodinated contrast when alternatives available
• Nutritional support: Avoid protein restriction; 0.8–1.0 g/kg/day protein (non-catabolic), up to 1.7 g/kg/day in hypercatabolic/dialysis patients
• Glycemic control: Avoid severe hyperglycemia while minimizing hypoglycemia; many current hospital standards target 140–180 mg/dL for most critically ill patients, with more stringent targets only for selected patients when safely achievable

Renal Replacement Therapy (RRT)

Indications for urgent RRT in AKI (regardless of stage) include: refractory hyperkalemia (K+ >6.5 mEq/L), severe metabolic acidosis (pH <7.1), symptomatic uremia (encephalopathy, pericarditis), and refractory volume overload. RRT modality selection:

• Intermittent Hemodialysis (IHD): Standard modality for hemodynamically stable patients; 3–5 sessions/week; CPT 90935/90937
• Continuous Renal Replacement Therapy (CRRT): Preferred in hemodynamically unstable patients; ICU-based; CPT 90945/90947; for ICD-10-PCS, document daily filtration duration to support 5A1D70Z (less than 6 hours per day), 5A1D80Z (6–18 hours per day), or 5A1D90Z (greater than 18 hours per day)
• Sustained Low-Efficiency Dialysis (SLED/SLEDD): Hybrid modality; CPT 90945/90947; growing use in intermediate-acuity patients
• Peritoneal Dialysis (PD): Used in some AKI cases; CPT 90945/90947; requires PD catheter insertion

Etiology-Specific Treatments

• Contrast-induced nephropathy prevention: Pre-procedure IV hydration with isotonic saline; NAC (evidence mixed); minimize contrast volume; use iso-osmolar contrast agents
• Rhabdomyolysis AKI: Aggressive IV hydration (target UOP 200–300 mL/h); urinary alkalinization (sodium bicarbonate) to prevent myoglobin cast formation; early dialysis if severe
• Obstructive AKI: Urgent ureteral stenting, percutaneous nephrostomy (CPT 50432/50433), or Foley catheter decompression; address underlying obstruction (BPH — alpha-blockers; ureteral stones — ureteroscopy/lithotripsy)
• Glomerulonephritis-associated AKI: Pulse corticosteroids (methylprednisolone); cyclophosphamide; plasma exchange for anti-GBM/ANCA vasculitis
• Sepsis-AKI: Early antibiotics (within 1 hour per Sepsis-3); source control; EGDT fluid resuscitation; ARDS-protective ventilation if concurrent lung injury
• Hepatorenal syndrome: Terlipressin (vasopressin analog) + albumin infusion (most evidence); norepinephrine + albumin (ICU); TIPS procedure (selected cases); liver transplant (definitive treatment for type 2 HRS)

🎓 Patient Education / Summary

The following represents a patient-friendly summary of Acute Kidney Injury for inclusion in discharge education and health literacy resources. CDI specialists and coders may use this section to understand what patients are counseled about, which informs query scope and documentation gaps.

What Is Acute Kidney Injury?

Acute kidney injury (AKI) means your kidneys suddenly stopped working as well as they should. This can happen for many reasons — including getting dehydrated, having an infection, taking certain medications, or having a procedure that affected the kidneys. Most people recover from AKI, but it’s important to follow up because AKI can sometimes lead to lasting kidney problems (chronic kidney disease, or CKD).

Warning Signs That Require Immediate Medical Attention

• Making much less urine than usual, or no urine at all
• Swelling in your legs, ankles, or around your eyes
• Feeling confused, very tired, or having trouble breathing
• Muscle cramps or weakness (can signal dangerous potassium levels)
• Nausea and vomiting that won’t stop

After AKI: What to Expect

• Follow-up blood tests: Your doctor will check your creatinine and kidney function levels 7–14 days after discharge and again at 3 months. National Kidney Foundation AKI patient resources provide guidance on follow-up expectations.
• Medication changes: Some medications (NSAIDs, certain blood pressure medications) may be held or changed while your kidneys recover. Do NOT restart these without your doctor’s guidance.
• Diet: Low-sodium, low-potassium diet if instructed; limit protein if your kidneys are still recovering; stay well hydrated unless your doctor tells you to restrict fluids.
• Dialysis: If you needed dialysis in the hospital, your doctor will tell you whether this is temporary (expected to stop as kidneys recover) or may become long-term. Learn more about dialysis types from the National Kidney Foundation.
• CKD risk: Even after AKI resolves, you have a higher risk of developing CKD or having another AKI episode. Annual kidney function tests are recommended by KDIGO guidelines.

Patient Resources

• National Kidney Foundation — Acute Kidney Injury Patient Information
• KDIGO AKI Guidelines (patient summary available)
• NIDDK (NIH) — Acute Kidney Injury
• CDC — Chronic Kidney Disease and AKI basics

About this Guide

This Clinical Documentation Guide is published by CCO Academy and is intended for credentialed coding, CDI, and clinical documentation professionals. Content is updated for FY2027 ICD-10-CM (effective October 1, 2026). All code assignments should be verified against the official ICD-10-CM Tabular List, AHA Coding Clinic, and applicable payer-specific policies. This guide does not constitute legal, medical, or compliance advice.

Last reviewed: October 2026 · Next scheduled review: October 2027 (FY2028 update)