Nephrology High-Yield: CKD, AKI, and Electrolytes for FNP Boards

Clinical High-Yield · 10 min read · April 28, 2026

Nephrology is a section that rewards systematic preparation. The boards test a specific, predictable set of renal content: CKD staging and management, the three categories of acute kidney injury, and the electrolyte disorders that require immediate recognition and treatment. Here is the high-yield content organized for maximum board efficiency.

Chronic Kidney Disease: Staging and Management

CKD is defined as kidney damage or GFR <60 mL/min/1.73m² for more than 3 months. The KDIGO staging system classifies CKD by GFR (G1–G5) and albuminuria (A1–A3). The boards test the GFR stages and the management milestones at each stage.

CKD Stages by GFR:

G1: GFR ≥90 (normal or high GFR with evidence of kidney damage)
G2: GFR 60–89 (mildly decreased)
G3a: GFR 45–59 (mildly to moderately decreased)
G3b: GFR 30–44 (moderately to severely decreased)
G4: GFR 15–29 (severely decreased)
G5: GFR <15 (kidney failure — dialysis or transplant)

Management milestones by stage:

All stages: Blood pressure control (target <130/80 in CKD), ACE inhibitor or ARB for proteinuric CKD (reduces progression), dietary protein restriction (0.8 g/kg/day), sodium restriction, smoking cessation, diabetes management.
G3b–G4: Monitor for anemia (erythropoietin deficiency — treat with ESA if Hgb <10), metabolic acidosis (treat with sodium bicarbonate if serum bicarbonate <22 mEq/L), secondary hyperparathyroidism (phosphate restriction, vitamin D supplementation), and hyperkalemia.
G4–G5: Nephrology referral, preparation for renal replacement therapy (dialysis or transplant).

Medications to avoid or dose-adjust in CKD: The boards test this extensively. Avoid NSAIDs (reduce GFR, cause fluid retention). Avoid metformin when GFR <30 (lactic acidosis risk). Avoid direct oral anticoagulants (DOACs) at low GFR levels (varies by agent). Dose-adjust: digoxin, gabapentin, many antibiotics (aminoglycosides, vancomycin, fluoroquinolones).

Board Pearl: ACE inhibitors and ARBs are renoprotective in CKD with proteinuria — but they can cause an initial rise in creatinine (up to 30% increase is acceptable) and hyperkalemia. A creatinine rise >30% or new hyperkalemia requires dose reduction or discontinuation.

Acute Kidney Injury: The Three Categories

AKI is defined as an abrupt increase in serum creatinine ≥0.3 mg/dL within 48 hours, or ≥1.5× baseline within 7 days, or urine output <0.5 mL/kg/hour for ≥6 hours. The boards test the three categories and their distinguishing features.

Prerenal AKI: Caused by decreased renal perfusion — dehydration, hemorrhage, heart failure, sepsis, NSAIDs (reduce prostaglandin-mediated afferent arteriolar dilation). Urine findings: concentrated urine (specific gravity >1.020, osmolality >500 mOsm/kg), low urine sodium (<20 mEq/L), FENa <1%. Treatment: correct the underlying cause — IV fluids for hypovolemia, treat heart failure, discontinue nephrotoxins.

Intrinsic (intrarenal) AKI: Caused by direct kidney damage. The most common cause is acute tubular necrosis (ATN), caused by ischemia (prolonged prerenal → ATN) or nephrotoxins (aminoglycosides, contrast dye, myoglobin in rhabdomyolysis). Urine findings: muddy brown granular casts (pathognomonic for ATN), isosthenuric urine (specific gravity ~1.010), FENa >2%. Other causes: acute interstitial nephritis (AIN) — caused by NSAIDs, antibiotics (penicillins, cephalosporins), PPIs; presents with fever, rash, eosinophilia, and eosinophiluria.

Postrenal AKI: Caused by urinary tract obstruction — BPH (most common in older men), kidney stones, pelvic malignancy, retroperitoneal fibrosis. Ultrasound shows hydronephrosis. Treatment: relieve the obstruction (Foley catheter for BPH, ureteral stent or nephrostomy for ureteral obstruction).

Electrolyte Disorders: The High-Yield Ones

Hyponatremia (Na <135 mEq/L): The most common electrolyte disorder in hospitalized patients. The boards test the classification and management.

Hyponatremia is classified by volume status:

Hypovolemic hyponatremia: low total body sodium and water (more sodium lost than water) — causes: vomiting, diarrhea, diuretics, adrenal insufficiency. Treatment: isotonic saline.
Euvolemic hyponatremia: normal total body sodium, excess water — causes: SIADH (most common), hypothyroidism, psychogenic polydipsia. Treatment: fluid restriction; demeclocycline or vasopressin receptor antagonists (tolvaptan) for SIADH.
Hypervolemic hyponatremia: excess total body sodium and water (more water retained than sodium) — causes: heart failure, cirrhosis, nephrotic syndrome. Treatment: fluid restriction, diuretics.

Correction rate: Correct sodium no faster than 8–10 mEq/L per 24 hours to prevent osmotic demyelination syndrome (central pontine myelinolysis). This is a high-yield board concept.

Hyperkalemia (K >5.5 mEq/L): The most dangerous electrolyte disorder — can cause fatal cardiac arrhythmias. EKG changes in order of severity: peaked T waves → prolonged PR → wide QRS → sine wave pattern → ventricular fibrillation.

Treatment sequence (from fastest to slowest acting):

Calcium gluconate (stabilizes cardiac membrane — does not lower potassium, acts in minutes)
Insulin + glucose (drives potassium into cells — acts in 15–30 minutes)
Sodium bicarbonate (drives potassium into cells in acidosis — acts in 15–30 minutes)
Albuterol nebulization (drives potassium into cells — acts in 30–60 minutes)
Kayexalate (sodium polystyrene sulfonate) or patiromer (removes potassium from the body — acts in hours)
Dialysis (for refractory hyperkalemia or renal failure)

Nephrotic vs. Nephritic Syndrome

Nephrotic syndrome: Massive proteinuria (>3.5 g/day), hypoalbuminemia, edema, hyperlipidemia, lipiduria (oval fat bodies, fatty casts on urinalysis). Causes: minimal change disease (most common in children — responds to steroids), focal segmental glomerulosclerosis (FSGS — most common in adults, associated with HIV and heroin use), membranous nephropathy (most common cause of nephrotic syndrome in adults overall — associated with hepatitis B, SLE, malignancy), diabetic nephropathy.

Nephritic syndrome: Hematuria (RBC casts on urinalysis — pathognomonic), proteinuria (less than nephrotic range), hypertension, oliguria, azotemia. Causes: post-streptococcal glomerulonephritis (PSGN — 1–3 weeks after strep throat or skin infection, low complement C3), IgA nephropathy (Berger's disease — hematuria during or immediately after URI, normal complement), lupus nephritis (low C3 and C4), Goodpasture syndrome (anti-GBM antibodies, pulmonary-renal syndrome).

The Bottom Line

Nephrology on the FNP boards rewards knowing your CKD stages and management milestones, your three AKI categories and their urine findings, and your electrolyte emergencies (hyperkalemia treatment sequence, hyponatremia correction rate). Know your nephrotic vs. nephritic syndrome distinction. Know which medications to avoid in CKD. Master these and nephrology becomes one of your most reliable sections.

→ Explore the FNP Board Review Book — every nephrology topic covered with board-focused clinical pearls and practice questions.