Allison Clemens
April
ababaabhay
achoi2392
adhoward1

2025 PACUPrep BCCCP Preparatory Course Contrast‐Induced Nephropathy Contrast‐Induced Nephropathy: Pathophysiology, Prophylaxis, and Management

Lesson 16, Topic 2

In Progress

← Previous

Contrast‐Induced Nephropathy: Pathophysiology, Prophylaxis, and Management

Lesson Progress

0% Complete

Diagnosis and Classification of Contrast‐Induced Nephropathy

Learning Objective

Apply diagnostic and classification criteria to assess a patient with Contrast‐Induced Nephropathy (CIN) and guide initial management.

1. Clinical Manifestations and Initial Diagnostic Approach

Early recognition of CIN hinges on serial monitoring of kidney function and urine output; clinical signs are often subtle or absent.

A. Time Course of Serum Creatinine Rise (48–72 hours post-contrast)

Detectable increase at 24–48 hours, peak at 3–5 days, resolution by 7–10 days if no further insult.
Diagnostic thresholds: absolute rise ≥0.5 mg/dL or relative rise ≥25% from baseline within 48–72 hours.

B. Oliguria vs Non-oliguric Presentations

Oliguria (<0.5 mL/kg/h for ≥6 hours) occurs in <30% of CIN cases; most are non-oliguric.
Lack of oliguria does not rule out CIN—rely on creatinine trends.

C. Non-Specific Symptoms

Fluid overload signs (edema, pulmonary congestion) may reflect aggressive hydration or heart failure.
Nausea, malaise and fatigue are low‐specificity findings; always rule out other Acute Kidney Injury (AKI) causes (pre-renal, intrinsic, post-renal).

Key Clinical Pearl

CIN often presents without oliguria—monitor serum creatinine at defined intervals rather than relying on urine output alone.

2. Laboratory and Imaging Evaluation

Confirm CIN with serial laboratory measurements and exclude alternative AKI etiologies via urine studies and imaging.

A. Serum Creatinine Measurement

Baseline within 24 hours pre-contrast; account for muscle mass and fluid status.
Repeat at 24 hours and 48–72 hours post-exposure.
Diagnostic criteria: rise ≥0.5 mg/dL or ≥25% relative increase.

B. eGFR Estimation

CKD-EPI equation preferred over MDRD at GFR >60 mL/min/1.73 m².
Serum creatinine-based eGFR lags behind injury; consider cystatin-C if available.

C. Urinalysis and Urine Output Monitoring

Hourly measurement in high-risk patients; note oliguria definition above.
Fractional excretion of sodium (FENa) is confounded by diuretics and Chronic Kidney Disease (CKD).

D. Imaging Studies

Renal ultrasound: first-line to exclude obstruction (post-renal AKI).
Doppler ultrasound or non-contrast CT: when ultrasound is non-diagnostic or vascular causes suspected.

3. Classification Systems and Severity Scoring

Apply uniform AKI staging systems to CIN for risk stratification and management urgency.

A. Comparison of RIFLE, AKIN, and KDIGO Criteria

Comparison of AKI Classification Criteria for CIN
Criteria System	Serum Creatinine (SCr) Criteria	Urine Output (UO) Criteria	Timeframe
RIFLE	≥1.5× baseline OR ≥0.3 mg/dL increase	<0.5 mL/kg/h for 6 h	Up to 7 days
AKIN	Rise ≥50% OR ≥0.3 mg/dL increase	<0.5 mL/kg/h for 6 h	Within 48 hours
KDIGO	Combines SCr & UO: Stage 1 = SCr rise ≥0.3 mg/dL OR 1.5-1.9× baseline	Stage 1 = UO <0.5 mL/kg/h for 6–12h	48 hours – 7 days

B. KDIGO Staging (1–3)

KDIGO Staging for Acute Kidney Injury
KDIGO Stage	Serum Creatinine (SCr) Criteria	Urine Output (UO) Criteria
Stage 1	Increase ≥0.3 mg/dL OR 1.5–1.9× baseline	<0.5 mL/kg/h for 6–12 hours
Stage 2	2.0–2.9× baseline	<0.5 mL/kg/h for ≥12 hours
Stage 3	≥3.0× baseline OR ≥4.0 mg/dL OR initiation of Renal Replacement Therapy (RRT)	<0.3 mL/kg/h for ≥24 hours OR anuria for ≥12 hours

C. Integration with Risk Prediction Models

Use Mehran risk score (factors: baseline CKD, diabetes, volume of contrast, hypotension) to identify patients needing aggressive prophylaxis.
Combine staging and risk score to tailor monitoring frequency and interventions.

4. Clinical Decision Algorithms

Structured workflows ensure timely detection and intervention for CIN.

A. Workflow Outline

1. Pre-Contrast Risk Assessment

(eGFR, comorbidities, contrast volume)

2. Document Baseline

(SCr, contrast details)

3. Implement Prophylaxis

(Moderate-high risk; e.g., IV isotonic saline)

4. Monitor Post-Contrast

(SCr at 24h, 48-72h; hourly UO)

5. Diagnose CIN if Criteria Met

Exclude other causes
(Urinalysis, ultrasound)

6. Stage per KDIGO & Escalate Care

(Hydration, avoid nephrotoxins,
RRT consult if needed)

Figure 1: Clinical Workflow for Contrast-Induced Nephropathy. This diagram outlines a systematic approach from pre-procedure risk assessment and prophylaxis to post-procedure monitoring, diagnosis, staging, and management escalation for CIN.

B. Trigger Points

Initiate prophylactic hydration for risk score ≥6 (e.g., Mehran score).
Nephrology consult for KDIGO stage 2–3 or persistent oliguria.

C. Documentation and Team Communication

Record all monitoring data and decisions in ICU flow sheet or patient chart.
Clearly communicate CIN diagnosis, stage, and plan during handoffs.

Key Takeaway

A protocolized approach—encompassing pre-contrast risk stratification, timed monitoring, prompt staging according to standardized criteria, and clear interdisciplinary communication—is crucial for optimizing outcomes in patients at risk for or developing CIN.

References

Shams E, Mayrovitz HN. Contrast-Induced Nephropathy: A Review of Mechanisms and Risks. Cureus. 2021;13(5):e14842.
Mamoulakis C, Tsarouhas K, Fragkiadoulaki I, et al. Contrast-induced nephropathy: basic concepts, pathophysiological implications and prevention strategies. Pharmacol Ther. 2017;180:99-112.
Morcos SK, Thomsen HS, Webb JA. Contrast-media-induced nephrotoxicity: a consensus report. Eur Radiol. 1999;9(8):1602-1613.
Thomsen HS, Morcos SK. Contrast media and the kidney: ESUR guidelines. Br J Radiol. 2003;76(908):513-518.
Mueller C, Buerkle G, Buettner HJ, et al. Prevention of contrast media-associated nephropathy: randomized comparison of hydration regimens. Arch Intern Med. 2002;162(3):329-336.
Wagener G, Jan M, Kim M, et al. Association between increases in urinary neutrophil gelatinase-associated lipocalin and acute renal dysfunction after adult cardiac surgery. Anesthesiology. 2006;105(3):485-491.
Aspelin P, Aubry P, Fransson SG, et al. Nephrotoxic effects in high-risk patients undergoing angiography. N Engl J Med. 2003;348(4):491-499.
Tepel M, van der Giet M, Schwarzfeld C, et al. Prevention of radiographic-contrast-agent-induced reductions in renal function by acetylcysteine. N Engl J Med. 2000;343(3):180-184.
Manske CL, Sprafka JM, Strony JT, et al. Contrast nephropathy in azotemic diabetic patients undergoing coronary angiography. Am J Med. 1990;89(5):615-620.
Hou SH, Bushinsky DA, Wish JB, et al. Hospital-acquired renal insufficiency: a prospective study. Am J Med. 1983;74(2):243-248.

2025 PACUPrep BCCCP Preparatory Course

Pulmonary

Participants 432