Laboratory Testing for CKD Patients with Acute Kidney Injury
Order a comprehensive metabolic panel with serum creatinine, electrolytes (Na⁺, K⁺, Ca²⁺, Mg²⁺, Cl⁻, bicarbonate), BUN, complete blood count, urinalysis with microscopy, and urine albumin-to-creatinine ratio immediately upon presentation. 1, 2
Essential Initial Laboratory Tests
Renal Function Assessment
Measure serum creatinine and calculate eGFR using the CKD-EPI equation to establish both baseline CKD status and degree of acute deterioration. 1 Do not rely on serum creatinine concentration alone—always calculate eGFR for accurate assessment. 1
Consider cystatin C-based eGFR when creatinine-based estimates appear discordant with clinical presentation, as creatinine equations are inaccurate in 16-20% of individuals with eGFR <60 mL/min/1.73 m². 1, 3 The 2012 CKD-EPI creatinine-cystatin C equation provides superior accuracy for confirmatory testing. 1
Review past creatinine measurements to determine duration of kidney disease (>3 months confirms CKD) and establish true baseline for AKI staging. 1 If no prior values exist, back-calculation from an assumed eGFR of 75 mL/min/1.73 m² is acceptable but may overestimate AKI severity in populations with high CKD prevalence. 1
Electrolyte and Metabolic Panel
Measure Na⁺, K⁺, Ca²⁺, Mg²⁺, Cl⁻, bicarbonate, BUN, and creatinine to identify life-threatening complications requiring urgent intervention. 1, 2 Monitor these every 4-6 hours initially in severe AKI. 2
Check serum potassium urgently because hyperkalemia >6.0 mmol/L with ECG changes is an absolute indication for emergent dialysis. 4
Assess for metabolic acidosis by measuring serum bicarbonate; severe acidosis with impaired respiratory compensation requires dialysis. 4
Urinalysis and Proteinuria Assessment
Perform urinalysis with microscopy to differentiate AKI etiology: muddy-brown casts suggest acute tubular necrosis, red-cell casts indicate glomerulonephritis, and white-cell casts point to interstitial nephritis. 2
Measure urine albumin-to-creatinine ratio (UACR) as the preferred method for proteinuria assessment. 1 An early morning sample is optimal. 1 UACR ≥30 mg/g requires confirmation with a repeat early morning sample. 1
Calculate fractional excretion of sodium (FENa) using spot urine sodium and creatinine: FENa <1% (or urine sodium <20 mEq/L) suggests prerenal azotemia, while FENa >2% (or urine sodium >40 mEq/L) indicates intrinsic renal injury such as ATN. 2
Hematologic Assessment
Order complete blood count to evaluate for anemia (common in CKD due to decreased erythropoietin) and thrombocytopenia. 1 Platelet count <50,000/mm³ increases hemorrhage risk and may require transfusion before invasive procedures. 1
Measure bleeding time or coagulation studies if invasive procedures are planned, as CKD patients have platelet dysfunction and those on hemodialysis receive anticoagulants with 1-4 hour half-lives. 1
Additional Tests Based on Clinical Context
Infection Evaluation
Obtain blood cultures, urine cultures, and chest radiograph when infection is suspected, as infection is a common AKI precipitant. 2 In cirrhotic patients, perform diagnostic paracentesis to rule out spontaneous bacterial peritonitis. 2
Initiate empiric broad-spectrum antibiotics promptly when infection is strongly suspected without awaiting culture results. 2
Mineral Bone Disease Screening (for eGFR <60 mL/min/1.73 m²)
Measure serum calcium and phosphorus every 3-6 months in Stage G3b CKD (eGFR 30-44 mL/min/1.73 m²). 3
Check parathyroid hormone (PTH) every 6-12 months in Stage G3b to screen for secondary hyperparathyroidism. 3
Medication Review
Conduct comprehensive medication review to identify nephrotoxic exposures including NSAIDs, ACE inhibitors, ARBs, diuretics, aminoglycosides, contrast agents, and chemotherapeutics. 2 All nephrotoxic medications must be discontinued immediately upon AKI diagnosis. 2
Verify dosing of all medications when eGFR <60 mL/min/1.73 m², as many drugs require renal dose adjustment. 3
Monitoring Frequency
Repeat serum creatinine and electrolytes every 4-6 hours initially in severe AKI (Stage 2-3) to track progression and identify complications. 2
Measure eGFR and UACR at least annually in stable CKD patients. 3 Increase frequency to every 3-6 months for those at higher risk of progression (eGFR <45 mL/min/1.73 m², UACR ≥300 mg/g, or rapid decline). 1
Common Pitfalls to Avoid
Do not use eGFR equations (MDRD or CKD-EPI) during acute changes in kidney function because they require steady-state creatinine and will be inaccurate in AKI. 1 These equations were validated only in stable CKD patients. 1
Avoid relying on urine output alone in cirrhotic patients due to frequent diuretic use and altered sodium handling. 2
Do not assume chronicity from a single abnormal eGFR or UACR as the finding could represent recent AKI or acute kidney disease rather than CKD. 1 Proof of chronicity requires either repeat measurements beyond 3 months or evidence from imaging (reduced kidney size, cortical thinning) or pathology (fibrosis, atrophy). 1
Recognize that baseline creatinine underestimates true GFR in cirrhotic patients due to reduced muscle mass; use ICA-AKI criteria (creatinine rise ≥0.3 mg/dL within 48 hours or ≥50% from baseline) without a fixed 1.5 mg/dL threshold. 2