2.2 Acute Kidney Injury & Chronic Kidney Disease Staging

Acute Kidney Injury & Chronic Kidney Disease Staging

Renal failure spans a spectrum from acute, reversible declines in excretory function to permanent parenchymal destruction culminating in end-stage renal disease (ESRD). Distinguishing acute kidney injury (AKI) from chronic kidney disease (CKD)—and recognizing acute insults superimposed on chronic impairment—is critical for tailoring dialytic intensity, planning vascular access, and avoiding fatal complications.

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Acute Kidney Injury: KDIGO Criteria & Staging

Acute Kidney Injury (AKI) is an abrupt decline in glomerular filtration resulting in azotemia and fluid-electrolyte dysregulation. The Kidney Disease: Improving Global Outcomes (KDIGO) criteria define AKI by any one of three parameters:

1. Serum creatinine increase by $\ge 0.3\text{ mg/dL}$ within 48 hours; OR
2. Serum creatinine increase to $\ge 1.5\times\text{ baseline}$ within the prior 7 days; OR
3. Documented urine output $< 0.5\text{ mL/kg/h}$ for 6 consecutive hours.

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AKI Classification: Prerenal, Intrinsic, and Postrenal

AKI is classified clinically into three anatomical categories:

1. Prerenal Azotemia

Prerenal AKI reflects reduced renal perfusion, often from volume loss, reduced effective arterial volume or vascular factors. Urine indices can support assessment but cannot establish the cause independently.

2. Intrinsic (Intrarenal) AKI

Intrinsic AKI reflects injury to renal tissue, including tubular, interstitial, glomerular or vascular disease.

• Acute tubular injury: Ischemia and nephrotoxic exposure can injure tubular cells. Granular casts support the diagnosis, but FeNa, urine concentration and BUN/creatinine ratios vary with context.
• Acute Interstitial Nephritis (AIN): Drug-induced allergic inflammation (beta-lactams, PPIs, NSAIDs) which may produce pyuria or white-cell casts. Urine eosinophils are neither sensitive nor specific enough to confirm the diagnosis.
• Acute Glomerulonephritis (AGN): Inflammatory injury with hematuria, dysmorphic RBCs, RBC casts, and proteinuria.

3. Postrenal (Obstructive) AKI

Results from urinary outflow obstruction (BPH, malignancy, stones, blocked catheter). Retrograde hydrostatic pressure transmits into Bowman's space, opposing filtration. Imaging helps evaluate obstruction, although early obstruction may not produce obvious hydronephrosis. Prompt decompression can improve function; recovery depends on the cause and duration.

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Chronic Kidney Disease: KDIGO 2024 Staging

Chronic Kidney Disease (CKD) is structural or functional kidney damage persisting at least three months.

KDIGO Staging Matrix (CGA Classification)

• GFR Categories (mL/min/1.73 m²): G1: $\ge 90$ (normal/high); G2: $60–89$ (mild); G3a: $45–59$ (mild-moderate); G3b: $30–44$ (moderate-severe); G4: $15–29$ (severely decreased); G5: $< 15$ (kidney failure/ESRD).
• Planning in advanced CKD: Teach modality options, preserve suitable veins and arrange individualized access evaluation based on kidney-failure risk and the patient’s ESKD Life-Plan. Fistula maturation varies; neither a GFR category nor elapsed weeks alone establishes readiness for cannulation.
• Albuminuria (UACR): A1: $< 30\text{ mg/g}$ (mild); A2: $30–300\text{ mg/g}$ (moderate); A3: $> 300\text{ mg/g}$ (severe macroalbuminuria).

The CKD-EPI 2021 race-free equation eliminates race multipliers from eGFR calculation, ensuring equitable care and transplant waitlisting.

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Leading Etiologies of Kidney Failure

Diabetes and hypertension are common causes of chronic kidney disease, but the nurse must also recognize glomerular disease, inherited disorders such as autosomal dominant polycystic kidney disease, chronic obstruction, recurrent infection, and drug or toxin injury. Diabetes produces albuminuria and progressive nephron loss; hypertension can be both a cause and a consequence of renal disease. Hematuria with active sediment suggests a different investigation from isolated longstanding albuminuria. Family history, prior creatinine measurements, medication exposure and imaging help distinguish chronic disease from a reversible acute component.

Fractional excretion indices are supporting data rather than diagnostic verdicts. Diuretics can raise fractional sodium excretion; fractional urea excretion is also affected by illness, sepsis and timing. Neither a low nor high value replaces examination, urine microscopy, obstruction assessment or response to treatment. Anuria with a distended bladder requires prompt obstruction evaluation, not automatic classification as irreversible kidney failure.

Progressive G4 disease warrants education about hemodialysis, peritoneal dialysis, transplantation and conservative care. Access planning follows the individual’s kidney-failure risk, vessel anatomy, expected course and treatment preferences. It does not require every G4 patient to undergo fistula surgery on the same timetable. Protect suitable veins while the nephrology and access teams develop the patient’s ESKD Life-Plan.

Indications for Urgent Kidney Replacement Therapy

The mnemonic AEIOU organizes indications: refractory acidosis, dangerous electrolyte disturbance, selected dialyzable intoxications, refractory fluid overload, and symptomatic uremia. It is a reasoning aid, not a set of universal laboratory orders. Severe hyperkalemia with ECG changes requires immediate stabilization while arranging definitive potassium removal. Pulmonary edema despite appropriate medical therapy, uremic encephalopathy, pericarditis and some toxic exposures may justify urgent therapy.

Decisions consider the whole clinical picture, laboratory trends and available treatment. A potassium result, BUN value or pH alone is not an automatic universal dialysis threshold. Suspected poisoning requires poison-control/toxicology consultation because dialyzability and treatment indications differ between agents. Rising BUN without symptoms is evaluated differently from a patient with seizures or a pericardial rub. Once urgent dialysis is ordered, verify the prescription, access, anticoagulation plan and monitoring intensity rather than accelerating clearance without an order.

Sources checked 2026-10-10: KDIGO CKD and AKI