Contents
Renal Anatomy & Physiology
Kidney Functions
- Fluid and electrolyte balance
- Acid-base regulation (excrete H+, reabsorb/generate HCO3)
- Waste product removal (urea, creatinine)
- Blood pressure regulation (RAAS, fluid balance)
- Erythropoietin production (stimulates RBC production)
- Vitamin D activation (calcium metabolism)
Nephron Structure
- Glomerulus: Filtration of blood
- Proximal tubule: Reabsorbs ~65% of filtered Na, water, glucose, amino acids
- Loop of Henle: Concentrating mechanism, creates medullary gradient
- Distal tubule: Fine-tuning of Na, K, regulated by aldosterone
- Collecting duct: Water reabsorption under ADH control
Renal Assessment Parameters
- GFR (Glomerular Filtration Rate): Best overall measure of kidney function
- Normal GFR: >90 mL/min/1.73m²
- Creatinine: Muscle metabolism byproduct, inversely related to GFR
- BUN (Blood Urea Nitrogen): Protein metabolism byproduct
- BUN:Creatinine ratio: Normal 10-20:1
- BUN:Cr >20:1 suggests prerenal cause
Acute Kidney Injury
AKI Definition (KDIGO)
- Increase in serum creatinine ≥0.3 mg/dL within 48 hours, OR
- Increase in creatinine ≥1.5x baseline within 7 days, OR
- Urine output <0.5 mL/kg/hr for 6 hours
- AKI is common in ICU (30-50% of patients)
Pre-Renal AKI
- Cause: Decreased renal perfusion (hypovolemia, heart failure, sepsis)
- BUN:Cr ratio >20:1
- FENa <1% (kidneys retaining sodium)
- Urine sodium <20 mEq/L
- Urine osmolality >500 mOsm/kg (concentrated urine)
- Treatment: Restore volume and perfusion
Intrinsic Renal AKI (ATN)
- Acute Tubular Necrosis: Most common intrinsic cause
- Causes: Prolonged ischemia, nephrotoxins (contrast, aminoglycosides, NSAIDs)
- BUN:Cr ratio 10-15:1
- FENa >2% (tubular damage impairs sodium reabsorption)
- Urine sodium >40 mEq/L
- Urine osmolality <350 mOsm/kg (unable to concentrate)
- Muddy brown casts on urinalysis
- Treatment: Remove offending agent, supportive care, may need dialysis
Post-Renal AKI
- Cause: Urinary tract obstruction (stones, BPH, tumor, clot)
- Must be bilateral or obstruct single functioning kidney
- Diagnosis: Hydronephrosis on ultrasound
- Treatment: Relieve obstruction (Foley, nephrostomy, stent)
- Watch for post-obstructive diuresis after relief
Chronic Kidney Disease
CKD Staging by GFR (mL/min/1.73m²)
- Stage 1: GFR ≥90 - Normal or high GFR with evidence of kidney damage
- Stage 2: GFR 60-89 - Mildly decreased GFR with kidney damage markers
- Stage 3a: GFR 45-59 - Mild to moderately decreased
- Stage 3b: GFR 30-44 - Moderate to severely decreased
- Stage 4: GFR 15-29 - Severely decreased (pre-dialysis planning stage)
- Stage 5: GFR <15 - Kidney failure (ESRD, dialysis or transplant needed)
- GFR calculation uses creatinine, age, sex, and race
Albuminuria Staging (mg/g creatinine)
- A1: <30 mg/g - Normal to mildly increased (low risk)
- A2: 30-300 mg/g - Moderately increased (microalbuminuria)
- A3: >300 mg/g - Severely increased (macroalbuminuria/proteinuria)
- Albuminuria indicates glomerular damage and predicts progression
- Both GFR stage AND albuminuria category determine overall risk
- Higher albuminuria = faster progression and higher cardiovascular risk
CKD Risk Stratification
- Green (low risk): G1-G2 with A1 - annual monitoring
- Yellow (moderate risk): G1-G2 with A2, or G3a with A1 - monitor every 6-12 months
- Orange (high risk): G3a with A2, G3b with A1-A2 - monitor every 3-6 months
- Red (very high risk): G4-G5 or any stage with A3 - monitor at least every 3 months
- Risk increases exponentially with lower GFR and higher albuminuria
CKD Complications
- Fluid overload: Edema, hypertension, pulmonary congestion
- Electrolyte imbalances: Hyperkalemia, hyperphosphatemia, hypocalcemia
- Metabolic acidosis: Impaired H+ excretion, reduced HCO3 generation
- Anemia: Decreased erythropoietin production (typically starts Stage 3)
- Renal osteodystrophy: Secondary hyperparathyroidism, bone disease
- Uremic syndrome: Encephalopathy, pericarditis, bleeding tendency, pruritus
- Cardiovascular disease: Leading cause of death in CKD patients
CKD Management Goals
- Blood pressure control: Target <130/80 mmHg (ACE-I or ARB preferred)
- Diabetes control: Target A1c <7% (individualize in advanced CKD)
- Protein restriction: May slow progression in advanced stages
- Avoid nephrotoxins: NSAIDs, aminoglycosides, IV contrast (with precautions)
- Anemia management: Erythropoiesis-stimulating agents when Hgb <10 g/dL
- Bone-mineral disease: Phosphate binders, vitamin D supplementation
- Prepare for RRT: Fistula planning when GFR <30 (Stage 4)
KDIGO AKI Staging Criteria
KDIGO Definition of AKI
- Increase in serum creatinine ≥0.3 mg/dL within 48 hours, OR
- Increase in creatinine ≥1.5x baseline within 7 days, OR
- Urine output <0.5 mL/kg/hr for 6 hours
- KDIGO = Kidney Disease: Improving Global Outcomes
- Standardized criteria for consistent AKI diagnosis
AKI Stage 1 (Mild)
- Creatinine: Increase ≥0.3 mg/dL OR 1.5-1.9x baseline
- Urine Output: <0.5 mL/kg/hr for 6-12 hours
- May be reversible with prompt treatment
- Focus on removing nephrotoxins and optimizing perfusion
AKI Stage 2 (Moderate)
- Creatinine: 2.0-2.9x baseline
- Urine Output: <0.5 mL/kg/hr for 12-24 hours
- Higher risk for progression to Stage 3
- Close monitoring of fluid balance and electrolytes
AKI Stage 3 (Severe)
- Creatinine: ≥3.0x baseline OR increase to ≥4.0 mg/dL
- Urine Output: <0.3 mL/kg/hr for ≥24 hours OR anuria for ≥12 hours
- OR: Initiation of Renal Replacement Therapy (RRT)
- High mortality, often requires dialysis
- May progress to ESRD
Clinical Application
- Always establish baseline creatinine for accurate staging
- Monitor BOTH creatinine AND urine output
- Early recognition allows for intervention before severe AKI
- Staging helps guide treatment intensity and prognosis
- Higher stages associated with increased mortality and length of stay
Dialysis
Indications for Dialysis (AEIOU)
- A - Acidosis (refractory metabolic acidosis)
- E - Electrolytes (hyperkalemia unresponsive to treatment)
- I - Intoxication (dialyzable toxins: methanol, ethylene glycol, lithium)
- O - Overload (fluid overload refractory to diuretics)
- U - Uremia (symptomatic: encephalopathy, pericarditis, bleeding)
Hemodialysis (HD)
- Intermittent: 3-4 hours, 3x/week typically
- CRRT (Continuous): For hemodynamically unstable ICU patients
- CRRT modes: CVVH (hemofiltration), CVVHD (diffusion), CVVHDF (both)
- Access: AV fistula (best long-term), AV graft, tunneled catheter
- Complications: Hypotension, arrhythmias, air embolism, bleeding
Peritoneal Dialysis
- Uses peritoneal membrane as dialysis membrane
- Dialysate instilled into peritoneal cavity, dwells, then drained
- Types: CAPD (manual exchanges), APD (cycler overnight)
- Advantages: Can do at home, preserves residual renal function
- Complications: Peritonitis (cloudy effluent, abdominal pain), catheter issues
Electrolyte Imbalances
Sodium Disorders
- Hyponatremia (<135 mEq/L): SIADH, heart failure, cirrhosis, thiazides
- Symptoms: Confusion, seizures, coma (especially if acute or severe)
- Treatment: Fluid restriction (SIADH), NS or hypertonic saline
- Correct slowly: Max 8-10 mEq/L per 24 hours to avoid osmotic demyelination
- Hypernatremia (>145 mEq/L): Water deficit, diabetes insipidus
- Treatment: Free water replacement, correct slowly
Potassium Disorders
- Normal: 3.5-5.0 mEq/L
- Hyperkalemia (>5.0): Renal failure, acidosis, cell lysis, ACE-I/spironolactone
- ECG changes: Peaked T waves → widened QRS → sine wave → VF
- Treatment: Calcium gluconate (stabilize), insulin/glucose, albuterol, kayexalate, dialysis
- Hypokalemia (<3.5): Diuretics, vomiting, diarrhea
- ECG changes: Flattened T waves, U waves, prolonged QT
- Treatment: IV or oral potassium replacement, correct magnesium
Calcium & Phosphorus
- Inverse relationship: High phosphorus = Low calcium
- Hypercalcemia: Malignancy, hyperparathyroidism
- Symptoms: "Stones, bones, groans, psychiatric moans"
- Treatment: IV fluids, loop diuretics, bisphosphonates, calcitonin
- Hypocalcemia: CKD, hypoparathyroidism, low vitamin D
- Symptoms: Tetany, Chvostek sign, Trousseau sign, prolonged QT
- Treatment: IV calcium gluconate, treat underlying cause
Magnesium
- Normal: 1.5-2.5 mEq/L
- Hypomagnesemia: Alcoholism, diuretics, diarrhea, malnutrition
- Symptoms: Similar to hypocalcemia, arrhythmias, refractory hypokalemia
- Treatment: IV magnesium sulfate
- Hypermagnesemia: Renal failure, iatrogenic (MgSO4 for preeclampsia)
- Symptoms: Loss of DTRs, respiratory depression, cardiac arrest
- Treatment: IV calcium, dialysis if severe
AKI Lab Comparison
Pre-Renal vs ATN vs Post-Renal
- Pre-Renal: BUN/Cr >20:1, FENa <1%, Urine Na <20, Urine Osm >500
- ATN: BUN/Cr 10-15:1, FENa >2%, Urine Na >40, Urine Osm <350
- Post-Renal: BUN/Cr 10:1, FENa variable, variable urine output
Key Points
- FENa = (Urine Na × Plasma Cr) / (Plasma Na × Urine Cr) × 100
- FENa not reliable if patient on diuretics
- Urine microscopy helpful: Muddy brown casts = ATN
- Ultrasound: Look for hydronephrosis in post-renal
See a Renal question you can’t answer?
Here are 3 questions from our premium bank. The full rationale explains exactly why the right answer is right — and why the 3 distractors trap most test-takers.
BUN:Creatinine ratio is 10:1. Urine Sodium > 20. This is consistent with:
- Prerenal Failure
- Intrarenal Failure (ATN)
- Postrenal Failure
- Dehydration
Peaked T waves -> Widened QRS -> Sine Wave. This ECG progression indicates:
- Hypokalemia
- Hyperkalemia
- Hypocalcemia
- Hypercalcemia
What is the critical effect of severe hypophosphatemia on respiration?
- Bronchospasm
- Diaphragmatic weakness / Failure to wean
- Increased work of breathing
- Pulmonary edema
Practice Renal Questions
Test your renal knowledge with CCRN-style practice questions and detailed rationales.
Take Renal Quiz →Frequently Asked Questions
What percentage of the CCRN exam is renal?
Renal/genitourinary makes up 6% of the Adult CCRN exam — about 8 of the 125 scored questions.
What renal topics are tested on the CCRN exam?
Expect acute kidney injury (prerenal, intrarenal, and postrenal causes), CRRT versus intermittent hemodialysis, life-threatening electrolyte imbalances, rhabdomyolysis, and contrast-induced nephropathy prevention.
How is severe hyperkalemia treated on the CCRN exam?
Stabilize the myocardium first with IV calcium (gluconate or chloride), then shift potassium into cells with insulin plus dextrose and consider albuterol, and finally remove potassium with dialysis, loop diuretics, or potassium binders. EKG changes drive the urgency.
How should I study renal for the CCRN exam?
Focus on classifying AKI by cause using labs (BUN:creatinine ratio, urine sodium, FENa), the indications for emergent dialysis (AEIOU), and electrolyte emergency treatments. It is a small category, so high-yield facts and a set of practice questions cover it well.