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🔍 1. 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.
AKI requires a documented baseline creatinine for clinical and coding validity. An isolated elevated creatinine on admission without a documented prior baseline or explicit provider diagnosis cannot support an N17.x code. CDI teams should query for baseline values and physician attestation when creatinine trends suggest AKI but documentation is incomplete. See CMS FY2026 IPPS Final Rule for clinical validity audit guidance.
🗂️ 2. 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):
| Formal / Clinical Name | Colloquial / Lay / Alternative Terms |
|---|---|
| Acute Kidney Injury (AKI) | Acute renal failure; ARF; kidney failure, acute |
| Acute Tubular Necrosis (ATN) | Tubular injury; ischemic ATN; nephrotoxic ATN; toxic nephropathy |
| Pre-renal AKI / Azotemia | Volume-responsive AKI; dehydration-related kidney failure; hemodynamic AKI |
| Intrinsic AKI | Parenchymal AKI; intrinsic renal failure; renal AKI |
| Post-renal AKI | Obstructive uropathy; urinary obstruction with AKI; hydronephrotic AKI |
| Contrast-Induced Nephropathy (CIN) | Contrast nephropathy; contrast-induced AKI (CI-AKI); radiocontrast nephropathy |
| Cardiorenal Syndrome Type 1 | Acute cardiac-induced AKI; heart failure–related AKI |
| Hepatorenal Syndrome (HRS) | Liver failure–related kidney failure (do NOT dual-code with N17.x — K76.7 is inclusive) |
| Pigment Nephropathy | Rhabdomyolysis-induced AKI; myoglobinuric AKI; hemoglobinuric nephropathy |
| AKI on CKD | Acute on chronic kidney disease; acute exacerbation of CKD; flare of CKD |
| Drug-Induced AKI / Nephrotoxic AKI | NSAID nephropathy; aminoglycoside nephrotoxicity; ACE-I/ARB–induced AKI |
| Postprocedural Renal Failure | Post-op AKI; surgical AKI; post-cardiac surgery AKI |
🩺 3. 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
Oliguria, azotemia, and electrolyte disturbances documented as manifestations of AKI are considered integral to the condition and should NOT be coded separately per ICD-10-CM Guideline I.B.5. However, hyperkalemia requiring specific treatment (e.g., kayexalate, IV calcium) may be coded separately (E87.5) when documented as a distinct clinical condition managed independently.
🧭 4. 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.
| Differential Diagnosis | Key Distinguishing Features | ICD-10-CM Code(s) |
|---|---|---|
| Pre-renal AKI (volume depletion) | FENa <1%, BUN:Cr >20:1, responds to IV fluids | N17.9 (if unspecified) or N17.8; also code cause (e.g., E86.0 dehydration) |
| Intrinsic AKI — ATN (ischemic or nephrotoxic) | FENa >2%, granular casts on UA, muddy brown casts; persists after volume correction | N17.0 |
| Intrinsic AKI — Acute Cortical Necrosis | Diffuse cortical infarction; typically post-obstetric, septic shock; very rare | N17.1 |
| Intrinsic AKI — Acute Medullary Necrosis | Papillary necrosis; associated with NSAIDs, sickle cell, DM, analgesic abuse | N17.2 |
| Glomerulonephritis / Vasculitis | RBC casts, nephrotic/nephritic syndrome, ANCA/anti-GBM positive | N00-N08 (acute glomerular diseases); N17.x if AKI results |
| Interstitial Nephritis (AIN) | Drug exposure, eosinophiluria, fever-rash triad | N10 (acute tubulo-interstitial nephritis) |
| Post-renal (Obstructive) AKI | Hydronephrosis on imaging, elevated post-void residual, bladder outlet obstruction | N13.x (hydronephrosis), N17.x if AKI present |
| CKD Exacerbation (not AKI) | Slowly rising Cr, no acute precipitant, at new stable baseline | N18.1–N18.6 (CKD by stage); no N17.x |
| Hepatorenal Syndrome (HRS) | Cirrhosis + ascites, low Na, FENa <0.1%, no structural kidney disease | K76.7 — do NOT add N17.x (inclusive) |
| Cardiorenal Syndrome Type 1 | Acute decompensated heart failure as precipitant; low CI, high CVP | N17.x + I50.x (heart failure) |
| Contrast-Induced Nephropathy (CIN) | Cr rise within 24–72h post-contrast; typically self-limiting | N14.11 + N17.x if AKI criteria met |
| Rhabdomyolysis with Pigment Nephropathy | Elevated CK, myoglobinuria, tea-colored urine, muscle pain/trauma | M62.82 + N17.x |
| Thrombotic Microangiopathy (TTP/HUS) | Microangiopathic hemolytic anemia, thrombocytopenia, Cr elevation | M31.1x (HUS), M31.19 (TTP); N17.x if AKI |
| Acute Urinary Retention mimicking AKI | No creatinine rise; bladder distension; resolves with catheterization | R33.x (retention of urine); N17.x only if Cr elevated |
📋 5. Clinical Indicators for Coders/CDI
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.
| Clinical Indicator | Threshold / Details | CDI Action |
|---|---|---|
| Serum creatinine rise | ≥0.3 mg/dL within 48h OR ≥1.5× documented baseline within 7 days | Query if no explicit AKI diagnosis documented; confirm baseline |
| Oliguria | UOP <0.5 mL/kg/h for ≥6–12h; documented in nursing flow sheets | Cross-reference with physician notes; query for AKI if not documented |
| Nephrology or renal consult ordered | Any inpatient nephrology consult for kidney function evaluation | Review consult note for AKI diagnosis; ensure attending attestation |
| IV fluid resuscitation for renal indications | Large-volume saline or LR given for “pre-renal” or “hydration for kidneys” | Query etiology (pre-renal vs. ATN) if AKI not explicitly documented |
| Renal replacement therapy (CRRT/HD) | Any acute dialysis order; CRRT initiated; IHD placed for AKI | Confirm N17.x; verify N99.0 vs. Z99.2; query stage |
| Foley catheter for strict I&O monitoring | Order comment references “renal monitoring” or “oliguria assessment” | Cross-reference with creatinine trend and nursing documentation |
| N-acetylcysteine (NAC) or sodium bicarb administration | Typically administered for contrast nephropathy prophylaxis or CIN treatment | Query for contrast-induced nephropathy; verify N14.11 |
| Elevated BUN:Creatinine ratio (>20:1) | Consistent with pre-renal azotemia or dehydration | Query provider for AKI vs. pre-renal azotemia with clinical significance |
| Creatinine normalization in documentation | “Cr improving with fluids” or “kidneys recovering” | Confirm AKI was present; document acute episode even if resolved |
| Discharge creatinine above admission baseline | Persistent Cr elevation at discharge suggests possible new CKD stage | Query for new CKD stage post-AKI resolution |
When serum creatinine rises ≥0.3 mg/dL within 48 hours or ≥1.5× documented baseline within 7 days AND no explicit AKI or acute renal failure diagnosis appears in provider documentation, initiate a concurrent CDI query. Request the provider document the clinical significance, etiology (pre-renal, ATN, post-renal, or combined), and KDIGO stage if applicable.
🦴 6. 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:
| KDIGO Stage | Serum Creatinine Criteria | Urine Output Criteria | Coding/Clinical Significance |
|---|---|---|---|
| Stage 1 | Cr rise ≥0.3 mg/dL within 48h OR 1.5–1.9× baseline within 7 days | UOP <0.5 mL/kg/h × 6–12h | Supports AKI diagnosis; typically N17.9 or N17.8 if etiology specified; MCC if documented |
| Stage 2 | 2.0–2.9× baseline creatinine | UOP <0.5 mL/kg/h × ≥12h | Moderate-severe; strengthens MCC argument; query for etiology if N17.9 |
| Stage 3 | ≥3.0× baseline OR Cr ≥4.0 mg/dL OR need for RRT | UOP <0.3 mL/kg/h × ≥24h OR anuria ≥12h | Severe; dialysis likely → PCS codes; N17.0 (ATN) most defensible; maximum MCC weight |
💊 7. 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)
| Medication Class | Mechanism of AKI | ICD-10-CM Code(s) | T-Code (Adverse Effect) |
|---|---|---|---|
| NSAIDs (ibuprofen, naproxen, ketorolac, indomethacin) | Inhibit prostaglandin synthesis → afferent arteriolar vasoconstriction; papillary necrosis with chronic use | N14.1 + N17.x; N17.2 if medullary necrosis | T39.311A–T39.399A (adverse effect) or T39.311D (initial); assign 5th/6th character per circumstance |
| ACE Inhibitors (lisinopril, enalapril, ramipril) | Efferent arteriolar dilation → reduced GFR; dangerous in bilateral RAS or volume depletion | N14.1 + N17.x | T46.4x1A adverse effect; T46.4x6A underdosing |
| ARBs (losartan, valsartan, irbesartan) | Same mechanism as ACE-I — RAAS blockade | N14.1 + N17.x | T46.5x1A adverse effect |
| Aminoglycosides (gentamicin, tobramycin) | Direct proximal tubular toxicity (lysosomal phospholipidosis) | N14.1 + N17.0 (ATN) | T36.5x1A adverse effect |
| IV Contrast Agents (iodinated) | Direct tubular toxicity + transient renal vasoconstriction | N14.11 + N17.x if AKI confirmed | T50.8x1A (adverse effect of diagnostic agents) |
| Vancomycin | Direct tubular nephrotoxicity; risk ↑ with trough >15 mcg/mL or with piperacillin-tazobactam combination | N14.1 + N17.0 | T36.8x1A |
| Amphotericin B | Membrane disruption of tubular epithelial cells; afferent vasoconstriction | N14.1 + N17.0 | T36.7x1A |
| Chemotherapy agents (cisplatin, carboplatin) | Direct PCT toxicity; platinum adduct formation | N14.1 + N17.0 | T45.1x1A |
| Calcineurin inhibitors (cyclosporine, tacrolimus) | Afferent arteriolar vasoconstriction; chronic nephrotoxicity | N14.1 + N17.x | T45.1x1A |
When AKI is drug-induced (adverse effect), code first the nephropathy code (N14.1 or N14.11 for contrast), then the AKI code (N17.x), then the adverse effect T-code per ICD-10-CM Guideline I.C.19.e.5.a. For FY2020+ cases, N14.11 specifically identifies contrast-induced nephropathy (new code added per FY2020 tabular additions). Do not use N14.0 (nephropathy due to analgesics) when contrast is the agent — use N14.11.
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.
Preview ends here. The full guide continues with FY2026 ICD-10-CM code sets, CPT surgical coding, MS-DRG mapping, reimbursement guidance, CDI query templates, and an audit checklist — all available to CCO Members.
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📘 8. ICD-10-CM Guidelines (FY2026)
AKI coding is governed by FY2026 ICD-10-CM Official Guidelines Section I.C.14 (Diseases of the Genitourinary System), specifically guideline I.C.14.a addressing acute kidney failure and chronic kidney disease.
Guideline I.C.14.a — AKI and CKD
Per ICD-10-CM Official Guidelines I.C.14.a:
- 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.
N17.9 is the highest-risk AKI code for clinical validation audits. Payers and RAC auditors scrutinize this code aggressively because it requires documented AKI without etiology specification. When N17.9 is assigned, auditors expect to find: (1) explicit AKI or acute renal failure diagnosis in provider documentation; (2) documented baseline creatinine supporting the KDIGO criteria; and (3) evidence of clinical management (nephrology consult, IV fluids, monitoring). When clinical documentation supports ATN or a specific AKI subtype, always pursue N17.0 or the more specific code. N17.9 should be a last resort, not a default. Per CMS IPPS guidance, query for etiology whenever N17.9 would be the only option.
Additional Coding Guidelines Applicable to AKI
- Postprocedural renal failure (N99.0): Use for AKI occurring as a complication of a procedure per Guideline I.C.14. Code additionally the underlying condition precipitating the AKI if applicable.
- 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, Urinary, Intermittent, Filtration
- 5A1D80Z — Performance, Urinary, Prolonged Intermittent, Filtration
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)
A frequent coding error is assigning only N17.x for AKI on CKD without the companion N18.x code, or conversely coding only the CKD stage and omitting the N17.x. Both codes are required per Guideline I.C.14.a. Failure to code both results in lost CC/MCC weight and inaccurate severity capture in MS-DRG grouping. CDI and coding teams should implement a concurrent query process flagging any N18.x case with creatinine rise meeting KDIGO Stage 1 criteria.
🔢 9. ICD-10-CM Code Set (FY2026)
All codes verified against the FY2026 ICD-10-CM Tabular List (effective October 1, 2025).
| ICD-10-CM Code | Description | CC/MCC Status | Notes |
|---|---|---|---|
| N17.0 | Acute kidney failure with tubular necrosis (ATN) | MCC | Most clinically specific intrinsic AKI code; requires documentation of ATN (ischemic or nephrotoxic); most commonly coded subtype for intrinsic AKI |
| N17.1 | Acute kidney failure with acute cortical necrosis | MCC | Rare; obstetric catastrophes, septic shock, DIC; typically irreversible |
| N17.2 | Acute kidney failure with medullary necrosis | MCC | Papillary necrosis; NSAID-induced, sickle cell disease, diabetes, analgesic nephropathy |
| N17.8 | Other acute kidney failure (specified) | MCC | Specified AKI types not elsewhere classified; use when a specific type is documented but not captured by N17.0–N17.2 |
| N17.9 | Acute kidney failure, unspecified | MCC | ⚠️ AUDIT TRAP — Use only when no etiology or type is documented; always query for etiology first; high RAC scrutiny |
| N14.11 | Nephropathy induced by contrast media | CC | FY2020+ code; use for contrast-induced nephropathy; add N17.x if AKI criteria met; add T50.8x1A adverse effect code |
| N14.1 | Nephropathy induced by other drugs, medicaments, and biological substances | CC | For NSAID, ACE-I/ARB, aminoglycoside, vancomycin-induced nephropathy; add N17.x + T-code adverse effect |
| N99.0 | Post-procedural (acute) (chronic) kidney failure | MCC | Postprocedural AKI; use when AKI is a documented complication of a procedure; code additionally the specific procedure type if applicable |
| K76.7 | Hepatorenal syndrome | MCC | Do NOT additionally code N17.x — renal failure is inclusive within K76.7 per tabular inclusion note |
| M62.82 | Rhabdomyolysis | MCC | Pigment nephropathy trigger; code N17.x additionally for AKI when documented; sequence per circumstances of admission |
| N18.1 | Chronic kidney disease, stage 1 | — | Code with N17.x for AKI on CKD per Guideline I.C.14.a |
| N18.2 | Chronic kidney disease, stage 2 (mild) | — | Code with N17.x for AKI on CKD |
| N18.3 | Chronic kidney disease, stage 3 (moderate) | CC | Code with N17.x for AKI on CKD; CKD 3 is a CC driver |
| N18.31 | Chronic kidney disease, stage 3a | CC | FY2023 subcategory; GFR 45–59 |
| N18.32 | Chronic kidney disease, stage 3b | CC | FY2023 subcategory; GFR 30–44 |
| N18.4 | Chronic kidney disease, stage 4 (severe) | MCC | GFR 15–29; HCC 328 (v28 weight ~0.221) — code when AKI resolves to CKD 4 |
| N18.5 | Chronic kidney disease, stage 5 | MCC | GFR <15; HCC 327 (v28 weight ~0.320); code when pre-dialysis ESRD threshold reached post-AKI |
| N18.6 | End-stage renal disease (ESRD) | MCC | Dialysis-dependent CKD; HCC 326/328 + Z99.2 → HCC 326 (~0.436); requires chronic dialysis documentation |
| Z99.2 | Dependence on renal dialysis | CC | Code when patient is chronic dialysis-dependent; used with N18.6; maps to HCC 326 |
| R65.20 | Severe sepsis without septic shock | MCC | Code when sepsis + AKI qualifies as severe sepsis (organ dysfunction) |
| R65.21 | Severe sepsis with septic shock | MCC | Highest severity level; major MS-DRG driver |
All N17.x codes (N17.0 through N17.9) carry MCC (Major Complication or Comorbidity) status in the MS-DRG system. This means a documented and defensible AKI diagnosis can significantly affect DRG assignment, LOS expectations, and reimbursement. However, this high-value status also makes N17.x codes a primary target for clinical validation denials by commercial payers and Medicare RAC contractors. Documentation must robustly support the clinical criteria. See CMS Recovery Audit Program guidance for current AKI denial trends.
🔎 10. Indexing
The following index pathways from the FY2026 ICD-10-CM Alphabetic Index apply to AKI:
| Index Entry | Sub-Entry / Modifier | Code(s) |
|---|---|---|
| Failure, kidney, acute | (with tubular necrosis) | N17.0 |
| Failure, kidney, acute | (with cortical necrosis) | N17.1 |
| Failure, kidney, acute | (with medullary necrosis) | N17.2 |
| Failure, kidney, acute | (specified NEC) | N17.8 |
| Failure, kidney, acute | (unspecified) | N17.9 |
| Injury, kidney, acute (nontraumatic) | — | N17.9 (→ verify etiology) |
| Necrosis, tubular | (acute) | N17.0 |
| Necrosis, renal, cortical (acute) | — | N17.1 |
| Necrosis, renal, medullary (papillary) | — | N17.2 |
| Nephropathy, contrast media | — | N14.11 |
| Nephropathy, drug-induced | — | N14.1 |
| Nephropathy, analgesic | — | N14.0 |
| Failure, renal, postprocedural | — | N99.0 |
| Syndrome, hepatorenal | — | K76.7 |
| Rhabdomyolysis | (with AKI) | M62.82 + N17.x |
| AKI on CKD | — | N17.x + N18.x |
🏥 11. CPT (2026)
CPT codes for AKI-related procedures are governed by the AMA CPT 2026 code set. Renal replacement therapy coding is complex and requires documentation of the type of RRT (intermittent HD, CRRT, SLED, peritoneal dialysis), duration, and clinical setting.
| CPT Code | Description | Global Period | Notes / Documentation Requirements |
|---|---|---|---|
| 36555 | Insertion of non-tunneled centrally inserted central venous catheter; younger than 5 years of age | 0 days | For CVC/dialysis access placement in pediatric AKI; document age, indication, site, guidance used |
| 36556 | Insertion of non-tunneled centrally inserted central venous catheter; age 5 years and older | 0 days | Non-tunneled CVC for HD access in AKI; document indication, laterality, site; pair with 76937 for US guidance |
| 36800 | Insertion of cannula for hemodialysis, other purpose (separate procedure); vein to vein | 0 days | AV cannula for acute dialysis access; document type of vessel accessed and reason |
| 90935 | Hemodialysis procedure with single physician evaluation | 0 days | Single outpatient HD session with one evaluation; document duration, access site, patient response |
| 90937 | Hemodialysis procedure requiring repeated evaluation(s) | 0 days | HD session requiring multiple evaluations (hemodynamic instability, etc.); document each evaluation |
| 90940 | Hemodialysis access flow study to determine blood flow in grafts and arteriovenous fistulae | 0 days | Flow study for AV access evaluation; document flow rate results |
| 90945 | Dialysis procedure other than hemodialysis (e.g., peritoneal dialysis, hemofiltration) with single physician evaluation | 0 days | Peritoneal dialysis, CRRT; document modality, duration |
| 90947 | Dialysis procedure other than hemodialysis with repeated evaluations | 0 days | CRRT or PD requiring multiple evaluations; document each physician encounter |
| 90951–90962 | End-Stage Renal Disease (ESRD) related services, monthly (adult, various age ranges) | Monthly | ESRD monthly capitation; applicable when AKI resolves to ESRD; document date of ESRD determination |
| 90963–90966 | ESRD-related services, home dialysis (pediatric) | Monthly | Pediatric ESRD monthly services; document age and dialysis modality |
| 50200 | Renal biopsy, percutaneous, by trocar or needle | 0 days | Renal biopsy for AKI etiology workup (GN, interstitial nephritis); document indication, laterality, imaging guidance; add 76942 for US guidance |
| 82565 | Creatinine; blood | N/A | Lab code for serum creatinine; frequently ordered in AKI monitoring; document serial values and dates |
| 82575 | Creatinine; clearance, endogenous | N/A | CrCl / GFR calculation; useful for AKI staging and drug dosing adjustment |
| 81000 | Urinalysis, by dip stick or tablet reagent for bilirubin, glucose, hemoglobin, ketones, leukocytes, nitrite, pH, protein, specific gravity, and urobilinogen; non-automated, with microscopy | N/A | UA with microscopy for AKI workup (casts, RBCs, WBCs); document findings |
| 81001 | Urinalysis; automated, with microscopy | N/A | Automated UA with microscopy |
| 81003 | Urinalysis; automated, without microscopy | N/A | Dipstick only; use 81000/81001 when microscopy results are clinically relevant to AKI workup |
| 82043 | Albumin; urine, microalbumin, quantitative | N/A | Microalbumin for proteinuria quantification; relevant in post-AKI CKD assessment and ESRD monitoring |
Continuous renal replacement therapy (CRRT) and intermittent hemodialysis (IHD) are reported differently. CRRT (90945/90947) is used for critically ill AKI patients with hemodynamic instability. IHD (90935/90937) applies to intermittent sessions. Slow Low-Efficiency Dialysis (SLED/SLEDD) also uses 90945/90947. Document the specific modality clearly to support accurate CPT assignment. For ICD-10-PCS inpatient procedural coding, CRRT is 5A1D70Z or 5A1D80Z per the FY2026 ICD-10-PCS code set.
🧾 12. HCPCS (2026)
HCPCS Level II codes support billing for dialysis supplies, erythropoiesis-stimulating agents (ESAs), IV iron, and other renal-related products per CMS HCPCS 2026.
| HCPCS Code | Description | Typical Use / Notes |
|---|---|---|
| A4651–A4932 | Dialysis supplies range (catheters, needles, dialysate, blood tubing, etc.) | Outpatient dialysis supplies; document type of dialysis access and supply category |
| Q4081 | Injection, Epoetin alfa, 100 units (ESRD use) | ESA for ESRD-associated anemia; document Hgb level, dose, frequency; requires MUE compliance |
| J0885 | Injection, Epoetin alfa (for non-ESRD use), 1000 units | Non-ESRD epoetin; CKD anemia not on dialysis; document Hgb, diagnosis |
| J0887 | Injection, Epoetin beta, 1 mcg | Mircera (epoetin beta); CKD/ESRD anemia; document dose and indication |
| J0881 | Injection, Darbepoetin alfa, 1 mcg (non-ESRD) | Long-acting ESA; once every 1–4 weeks; document Hgb trending and response |
| J0882 | Injection, Darbepoetin alfa, 1 mcg (ESRD use) | Darbepoetin for dialysis patients; document per dose billed in units administered |
| Q5105 | Injection, Epoetin alfa, biosimilar (Retacrit), 100 units (ESRD use) | Biosimilar ESA; same clinical indications as Q4081; must document biosimilar use |
| Q5106 | Injection, Epoetin alfa, biosimilar (Retacrit), 1000 units (non-ESRD use) | Non-ESRD biosimilar epoetin; document brand, dose, indication |
| J1439 | Injection, Ferric carboxymaltose, 1 mg (Injectafer) | IV iron for CKD/ESRD iron deficiency anemia; high-dose formulation; document Hgb, ferritin, TSAT |
| J1756 | Injection, iron sucrose, 1 mg (Venofer) | IV iron sucrose; commonly used in dialysis patients; document dose and iron studies |
| J0596 | Injection, ferumoxytol, 1 mg (Feraheme) | IV iron for CKD patients; anaphylaxis risk; document allergy history and monitoring |
| A4660 | Sphygmomanometer/blood pressure apparatus w/cuff and stethoscope | Home dialysis supply; document home dialysis status |
| E1510–E1699 | Hemodialysis equipment (home hemodialysis machine range) | Durable medical equipment for home HD; document ESRD status, home HD training completed |
📚 13. AHA Coding Clinic (Recent Guidance)
The AHA Coding Clinic for ICD-10-CM/PCS provides official coding advice. The following represent significant guidance items relevant to AKI coding:
| Issue / Year | Topic | Key Guidance |
|---|---|---|
| Coding Clinic, Q4 2019 | Contrast-Induced Nephropathy | With the addition of N14.11 in FY2020, contrast-induced nephropathy should be coded to N14.11. If AKI criteria are additionally met, also assign N17.x. Prior guidance using T80.89xA is superseded. |
| Coding Clinic, Q3 2020 | AKI on CKD Sequencing | Reaffirmed that both N17.x and N18.x should be coded when AKI and CKD coexist; sequencing determined by principal diagnosis criteria and circumstances of admission. Neither code excludes the other. |
| Coding Clinic, Q1 2021 | Rhabdomyolysis with AKI | When rhabdomyolysis causes AKI, assign M62.82 for the rhabdomyolysis and N17.x for the resulting AKI. Sequence according to the reason for the encounter. The AKI code is NOT redundant — it captures organ dysfunction for severity purposes. |
| Coding Clinic, Q2 2022 | Clinical Validity — AKI | AKI must be documented by the treating provider. A creatinine elevation alone does not justify N17.x assignment. Coders and CDI specialists may use clinical indicators to generate compliant queries but cannot independently assign the diagnosis. |
| Coding Clinic, Q3 2023 | Hepatorenal Syndrome | K76.7 remains inclusive of renal failure in the setting of liver disease. Do not additionally code N17.x with K76.7. Type 1 and Type 2 HRS are both classified to K76.7 pending further ICD-10-CM expansions. |
| Coding Clinic, Q1 2024 | Postprocedural Renal Failure | N99.0 is appropriate for procedurally-caused AKI (post-cardiac surgery, post-contrast procedure with documented AKI). Code the underlying procedure category additionally. Do NOT use N99.0 if the AKI pre-existed the procedure or was unrelated. |
| Coding Clinic, Q2 2024 | CRRT ICD-10-PCS Coding | Continuous renal replacement therapy is coded to 5A1D70Z (intermittent filtration) or 5A1D80Z (prolonged intermittent filtration). The PCS code depends on the duration and frequency of sessions as documented by the provider. |
AHA Coding Clinic represents the official and authoritative guidance for ICD-10-CM/PCS coding questions. It supersedes payer-specific policies on code assignment when the two conflict. CDI and coding teams should maintain a Coding Clinic subscription and reference the most recent guidance when AKI coding questions arise.
💰 14. HCC / Risk Adjustment (v28)
Per the CMS-HCC Model v28 (effective CY2024, fully phased in CY2026), AKI and CKD codes have distinct HCC mapping profiles:
| ICD-10-CM Code | Description | HCC v28 Category | RAF Weight (v28 approx.) | Risk Adjustment Impact |
|---|---|---|---|---|
| N17.0 | AKI with tubular necrosis | Does NOT map to HCC v28 | 0.000 | No direct HCC RAF impact; but MCC for MS-DRG and SOI/ROM scoring |
| N17.1 | AKI with acute cortical necrosis | Does NOT map to HCC v28 | 0.000 | No direct HCC RAF impact |
| N17.2 | AKI with medullary necrosis | Does NOT map to HCC v28 | 0.000 | No direct HCC RAF impact |
| N17.8 | Other AKI (specified) | Does NOT map to HCC v28 | 0.000 | No direct HCC RAF impact |
| N17.9 | AKI, unspecified | Does NOT map to HCC v28 | 0.000 | No direct HCC RAF impact; all the more reason to query for etiology |
| N18.3 / N18.31 / N18.32 | CKD Stage 3 (a/b) | HCC 329 | ~0.087 | Low-moderate RAF; code when AKI resolves to new CKD 3 baseline |
| N18.4 | CKD Stage 4 | HCC 328 | ~0.221 | Moderate RAF; code when post-AKI kidney function stabilizes at GFR 15–29 |
| N18.5 | CKD Stage 5 (non-dialysis) | HCC 327 | ~0.320 | High RAF; code when post-AKI GFR <15 without initiating dialysis |
| N18.6 + Z99.2 | ESRD + Dialysis Dependence | HCC 326 / HCC 328 | ~0.436 (HCC 326) | Highest CKD RAF; both codes required; Z99.2 maps to HCC 326; N18.6 maps to HCC 328 |
| K76.7 | Hepatorenal Syndrome | HCC 27 (Cirrhosis) — via K76.x | ~0.303 | HRS maps through liver disease HCC; significant RAF impact |
While N17.x codes do NOT directly map to an HCC v28 category, their importance for inpatient quality and reimbursement is substantial: (1) MS-DRG MCC driver — N17.x as MCC significantly elevates DRG weight and reimbursement; (2) SOI/ROM scoring — AKI drives Severity of Illness (SOI) and Risk of Mortality (ROM) Level 3–4 in APR-DRG systems (e.g., 3M APR-DRG); (3) Hospital-Acquired Condition (HAC) reporting — when AKI develops post-admission without prior documentation, it may trigger HAC flags; (4) Post-AKI CKD stage — when AKI does NOT fully resolve and the patient is discharged with a new CKD stage, THAT CKD stage DOES map to HCC (N18.4 → HCC 328, N18.5 → HCC 327, N18.6 → HCC 326). CDI teams should perform post-discharge reviews to document new CKD stage in the discharge summary.
✍️ 15. 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.
| # | Query Scenario | Clinical Trigger | Query Language (Sample) |
|---|---|---|---|
| 1 | AKI Etiology Clarification (Pre-renal vs. ATN vs. Post-renal) | Serum Cr rose from [baseline] to [peak]; nephrology consulted; IV fluids administered; no explicit etiology documented | “The patient’s serum creatinine increased from [X] to [Y] during this hospitalization. Based on the clinical picture, please clarify the etiology of the acute kidney injury, if present: (a) Pre-renal azotemia (volume/hemodynamic), (b) Acute tubular necrosis (ischemic or nephrotoxic), (c) Post-renal (obstructive), (d) Combined etiology — specify, (e) Other — specify, (f) Clinically undetermined.” |
| 2 | ATN vs. Unspecified AKI — Specificity Query | N17.9 coded; clinical indicators suggest ATN (granular casts, FENa >2%, nephrotoxin exposure, prolonged hypotension) | “The patient was diagnosed with acute kidney injury. Clinical documentation includes [granular casts on UA / nephrotoxin exposure / prolonged hypotension — select applicable]. Does this represent acute tubular necrosis (ATN)? (a) Yes — acute tubular necrosis, ischemic type, (b) Yes — acute tubular necrosis, nephrotoxic type, (c) Yes — ATN, mixed ischemic/nephrotoxic, (d) No — AKI without tubular necrosis, please specify type, (e) Clinically undetermined.” |
| 3 | AKI on CKD — Sequencing & CKD Stage | Patient has known CKD; creatinine acutely elevated above baseline during hospitalization; both AKI and CKD present but stage not documented in discharge summary | “The patient has documented CKD. During this hospitalization, serum creatinine increased acutely from the patient’s apparent baseline of [X]. Please confirm: (a) What is the patient’s underlying CKD stage (Stage 1–5 or ESRD)? (b) Is acute kidney injury (AKI) also present as an acute event superimposed on CKD? If yes, please specify etiology. (c) Clinically undetermined.” |
| 4 | Clinical Validity Support — Baseline Creatinine Confirmation | Creatinine elevated on admission; no documented prior baseline; provider diagnosis of AKI present but clinical validity may be challenged | “Documentation indicates a diagnosis of acute kidney injury. To support clinical validity for this diagnosis, please confirm and document: (a) The patient’s baseline creatinine prior to this admission (date/value): _______; (b) Whether the current creatinine represents an acute increase meeting AKI criteria (≥0.3 mg/dL rise within 48h OR ≥1.5× baseline within 7 days); (c) If no baseline is available, please document how the AKI diagnosis was established clinically.” |
| 5 | Contrast-Induced Nephropathy (CIN) Query | Patient received IV contrast (CT or angiography); creatinine rose ≥0.3 mg/dL within 24–72h of procedure; NAC or bicarb given; no CIN documented | “Following the administration of IV contrast media on [date], the patient’s serum creatinine increased from [X] to [Y]. Does this represent: (a) Contrast-induced nephropathy (N14.11), (b) Contrast-induced nephropathy with resulting acute kidney injury — please specify AKI type/etiology, (c) Creatinine elevation unrelated to contrast media — specify etiology, (d) Clinically undetermined.” |
| 6 | Drug-Induced Nephropathy (NSAID / ACE-I / ARB / Aminoglycoside) | Patient on nephrotoxic medication at admission or during hospitalization; creatinine rise documented; provider notes “possible drug effect” or “hold NSAID/ACE-I” | “The patient’s renal function declined during or following treatment with [medication name/class]. Please clarify whether the kidney injury represents: (a) Nephropathy induced by [drug class] — specify if adverse effect of correct drug, underdosing, or therapeutic level complication; (b) Pre-renal AKI secondary to medication effect (e.g., ACE-I/NSAID hemodynamic mechanism); (c) Acute tubular necrosis (nephrotoxic type); (d) Unrelated to the listed medication; (e) Clinically undetermined.” |
| 7 | Post-AKI New CKD Stage — Discharge Documentation Query | Creatinine does not return to prior baseline at discharge; patient did not have previously documented CKD or was at lower stage; discharge summary does not address long-term renal function | “At the time of discharge, the patient’s serum creatinine is [X], which remains above the prior baseline of [Y]. Based on the current eGFR of [Z] mL/min/1.73m², please document the patient’s renal status at discharge: (a) AKI resolved — creatinine expected to return to prior baseline; (b) AKI resolved with new CKD — specify stage (Stage 1 / 2 / 3a / 3b / 4 / 5); (c) AKI ongoing at discharge — specify management plan; (d) Pre-existing CKD at known stage [X] — no change; (e) Clinically undetermined.” |
| 8 | Rhabdomyolysis with AKI — Etiology Documentation | Elevated CK (>1000 U/L); myoglobinuria; dark urine documented; creatinine rising; provider has documented “rhabdo” but AKI not specified | “The patient has documented rhabdomyolysis (CK [X] U/L, myoglobinuria). Serum creatinine increased from [baseline] to [peak]. Does this clinical picture represent acute kidney injury as a result of pigment nephropathy/rhabdomyolysis? (a) Yes — acute kidney injury with tubular necrosis due to rhabdomyolysis; (b) Yes — AKI without tubular necrosis due to rhabdomyolysis; (c) Creatinine elevation is not clinically significant / does not represent AKI; (d) Clinically undetermined.” |
One of the highest-yield post-discharge CDI opportunities in AKI cases is querying for a new CKD stage when the discharge creatinine has not returned to the pre-admission baseline. Even a partial recovery resulting in CKD Stage 3 (N18.31/N18.32) or CKD Stage 4 (N18.4) carries HCC value under v28 (~0.087–0.221 RAF) and accurately reflects the patient’s ongoing medical complexity. Implement a concurrent/retrospective review process flagging all AKI encounters with discharge creatinine >1.2× the documented admission baseline.
🧑⚕️ 16. 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
- Tight glycemic control: Target glucose 110–149 mg/dL in ICU per KDIGO guidance
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; PCS 5A1D70Z or 5A1D80Z
- 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)
🎓 17. 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
Discharge instructions referencing “kidney injury,” “renal failure,” “dialysis,” “fluid restriction due to kidneys,” or “low potassium diet” that are NOT accompanied by a corresponding ICD-10-CM diagnosis code in the discharge summary represent a CDI opportunity. Review nursing discharge notes, dietary consults, and patient education printouts as supplementary sources to identify underdocumented diagnoses — then initiate compliant physician query rather than independently coding from these sources per AHIMA Standards of Ethical Coding.
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 FY2026 ICD-10-CM (effective October 1, 2025). 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: April 2026 · Next scheduled review: October 2026 (FY2027 update)
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