RN Alterations in Kidney Function and Elimination: What Are the Key Assessment Findings?

The core answer

This ATI/med-surg assessment covers how the kidneys fail and how nurses recognize and manage it. The high-yield facts:

• AKI lab pattern: rising BUN and serum creatinine, falling GFR, and decreased urine output (oliguria < 400 mL/day). Potassium rises (hyperkalemia) as the kidneys stop excreting it — a life-threatening priority because of cardiac arrhythmia risk.
• Nephrotoxic drugs: aminoglycoside antibiotics (gentamicin, tobramycin), NSAIDs, IV contrast dye, ACE inhibitors (in some contexts), and amphotericin B. Nurses monitor renal labs when these are used.
• Fluid overload management: loop diuretics such as furosemide, fluid and sodium restriction, daily weights, and monitoring for pulmonary edema.

AKI vs. CKD

The most-tested distinction is between acute and chronic kidney disease:

• Acute kidney injury (AKI) is a sudden (hours to days) drop in kidney function. It is often reversible if the cause is corrected. It is classified by cause: prerenal (decreased perfusion — hypovolemia, heart failure), intrarenal/intrinsic (direct kidney damage — nephrotoxins, acute tubular necrosis), and postrenal (obstruction — stones, enlarged prostate).
• Chronic kidney disease (CKD) is a gradual, irreversible loss of nephrons over months to years, staged by GFR. End-stage renal disease (GFR < 15) requires dialysis or transplant. CKD brings anemia (low erythropoietin), bone disease (altered calcium/phosphorus and vitamin D), and metabolic acidosis.

Interpreting the labs

• BUN (normal ~10–20 mg/dL): rises in kidney impairment, but also with dehydration, high protein intake, and GI bleeding — so it is less specific than creatinine.
• Serum creatinine (normal ~0.6–1.2 mg/dL): a more specific marker of kidney function because it is produced at a steady rate and cleared by the kidneys. A rising creatinine strongly indicates declining function.
• GFR: the best overall measure of kidney function; it falls as disease worsens. A BUN:creatinine ratio > 20:1 suggests a prerenal cause (dehydration), whereas a ratio near 10–15:1 with high both suggests intrarenal damage.

Ruling out common misconceptions

• "Urine output increases in AKI" — usually false; the oliguric phase shows decreased output. (A diuretic/recovery phase later can produce high output.)
• "BUN alone confirms kidney failure" — no; BUN can rise from dehydration or GI bleeding, so pair it with creatinine and GFR.
• "AKI and CKD are the same" — no; AKI is sudden and often reversible, CKD is gradual and permanent.
• "Give potassium for kidney patients" — dangerous; failing kidneys retain potassium, so hyperkalemia (not hypokalemia) is the usual threat, and potassium is typically restricted.

Nursing priorities

Monitor intake and output and daily weights, track potassium and watch for peaked T waves on ECG, restrict fluids and dietary potassium/phosphorus as ordered, hold or dose-adjust nephrotoxic drugs, and prepare for dialysis when indicated (severe hyperkalemia, fluid overload, acidosis, or uremia). Applying pathophysiology — rather than memorizing isolated flashcards — is what lets you answer the scenario-based questions correctly.