Renal Medicine Survival Guide
Acute Kidney Injury
Acute kidney injury (AKI) represents a rapid decline in kidney function, classified by the KDIGO staging system based on changes in serum creatinine and urine output.
KDIGO Staging
| Stage | Creatinine Change | Urine Output | Clinical Significance |
|---|---|---|---|
| 1 | 1.5-1.9× baseline OR ≥0.3 absolute increase | <0.5 mL/kg/h × 6-12 hours | Mild elevation, immediate evaluation needed |
| 2 | 2-2.9× baseline | <0.5 mL/kg/h × ≥12 hours | Moderate decline, intervention indicated |
| 3 | ≥3× baseline OR ≥4.0 absolute increase OR RRT initiated | <0.3 mL/kg/h × ≥24 hours OR anuria ≥12 hours | Severe, often requires renal replacement therapy |
Pathophysiology and Differential Diagnosis
Pre-renal AKI
Caused by inadequate renal perfusion from volume depletion, hypotension, or reduced effective circulating volume.
Common Etiologies: - Hypovolemia (GI losses, diuretics, hemorrhage) - Hypotension (sepsis, cardiogenic shock) - Decreased effective circulating volume (heart failure, cirrhosis, nephrotic syndrome)
Urinary Findings: - Fractional excretion of sodium (FeNa) <1% - BUN:creatinine ratio >20 - Urine sodium <20 mEq/L - Urine osmolality >500 mOsm/kg
Intrinsic Renal AKI
Direct kidney tissue injury from acute tubular necrosis (ATN), acute interstitial nephritis (AIN), or glomerulonephritis.
ATN (Ischemic or Nephrotoxic): - FeNa >2% - Muddy brown casts on urinalysis - Often irreversible if prolonged
AIN (Drug-Induced or Infection-Related): - WBC casts with eosinophiluria - Common offenders: NSAIDs, beta-lactams, sulfonamides, proton pump inhibitors - Rash and fever may accompany
Glomerulonephritis: - RBC casts on microscopy - Hematuria and proteinuria - May have systemic symptoms
Post-renal AKI
Obstruction to urine flow distal to the kidney, amenable to intervention.
Common Causes: - Benign prostatic hyperplasia (BPH) - Kidney stones - Malignancy - Urinary catheter obstruction
Key Finding: Hydronephrosis on renal ultrasound
Diagnostic Approach
Initial Workup
Obtain basic metabolic panel (BMP), urinalysis with microscopy, urine electrolytes for FeNa calculation, and renal ultrasound. Consider renal biopsy only if diagnosis remains unclear after non-invasive evaluation.
Essential Tests: - Serum creatinine (baseline and current) - BUN - Electrolytes (particularly potassium) - Urinalysis with microscopy - Urine electrolytes (sodium, osmolality) - Renal ultrasound to assess hydronephrosis and kidney size
Management Principles
Critical First Steps
Immediately identify and treat the underlying cause. Discontinue all nephrotoxic medications and address volume status appropriately.
General Approach:
- Identify etiology - Pre-renal vs intrinsic vs post-renal
- Stop nephrotoxins - ACE inhibitors, ARBs, NSAIDs, aminoglycosides
- Volume management - Aggressive fluid resuscitation for pre-renal; fluid restriction for intrinsic with oliguria
- Relieve obstruction - Percutaneous nephrostomy or foley placement for post-renal causes
- Supportive care - Control electrolytes, acid-base status, and fluid balance
Indications for Emergent Dialysis (AEIOU Mnemonic)
| Indication | Details | Time Frame |
|---|---|---|
| Acidosis | Severe metabolic acidosis unresponsive to medical therapy (usually pH <7.1) | Emergent |
| Electrolyte | Severe hyperkalemia refractory to medical management (K+ >6.5 with ECG changes) | Emergent |
| Ingestion | Toxic ingestions amenable to dialysis (methanol, ethylene glycol, salicylates) | Varies |
| Overload | Pulmonary edema unresponsive to diuretics | Urgent |
| Uremia | Uremic encephalopathy, pericarditis, or severe symptoms | Urgent |
Chronic Kidney Disease
Chronic kidney disease (CKD) is defined as reduced glomerular filtration rate (GFR) or kidney damage persisting for ≥3 months, staged by GFR.
CKD Stages
| Stage | GFR (mL/min/1.73m²) | Description | Kidney Function |
|---|---|---|---|
| G1 | ≥90 | Normal or high | Normal with kidney disease |
| G2 | 60-89 | Mildly decreased | Normal or mildly decreased |
| G3a | 45-59 | Mildly to moderately decreased | Mild-moderate decline |
| G3b | 30-44 | Moderately to severely decreased | Moderate-severe decline |
| G4 | 15-29 | Severely decreased | Severe decline, prepare for RRT |
| G5 | <15 OR on dialysis | Kidney failure | Requires RRT |
Complications of Chronic Kidney Disease
Monitor for Complications
CKD patients develop multiple metabolic and hematologic complications that require proactive management to prevent morbidity and mortality.
- Anemia - From erythropoietin deficiency; contribute to fatigue and cardiac strain
- Mineral and bone disease - Hyperphosphatemia, hypocalcemia, secondary hyperparathyroidism leading to bone loss and vascular calcification
- Metabolic acidosis - Accumulation of organic and inorganic acids
- Hyperkalemia - Impaired renal excretion of potassium
- Volume overload - Sodium and fluid retention, contributing to hypertension and pulmonary edema
- Uremic toxins - Accumulation causes uremic syndrome with neurologic and gastrointestinal manifestations
Management Strategy
Key Interventions
Blood pressure control and glycemic control form the foundation of CKD management. ACE inhibitors and ARBs provide cardio-renal protection beyond blood pressure lowering.
Pharmacologic Approach: - Blood pressure control - Target <120 mmHg; use ACE inhibitors or ARBs as first-line for proteinuria reduction - Glycemic control - Strict control in diabetes (HbA1c 7-8%) - Phosphate binders - Start when phosphate rises (calcium acetate, sevelamer, lanthanum) - Vitamin D supplementation - Calcitriol as GFR falls - Erythropoiesis-stimulating agents - For hemoglobin 10-12 g/dL (avoid targets >12) - Avoid nephrotoxins - NSAIDs, contrast, certain antibiotics
Diuretic Therapy
Diuretics are essential for managing volume overload in kidney disease, heart failure, and cirrhosis. Understanding their mechanism and escalation strategy optimizes outcomes.
Diuresis Escalation Algorithm
Follow this stepwise approach when initial diuretic therapy proves inadequate:
Diuretic Equivalency
Understanding equipotent doses ensures appropriate escalation:
| Agent | Equivalent Dose | Route Notes |
|---|---|---|
| Furosemide (Lasix) | 40 mg PO = 20 mg IV | Standard reference |
| Torsemide | 20 mg | 4× more potent than furosemide |
| Bumetanide | 1 mg | 40× more potent than furosemide |
Dosing Strategy
When escalating therapy, remember that 2.5× the patient's home dose is often needed to achieve initial diuresis. IV dosing is typically 40-50% of equivalent oral dose.
Adverse Effects by Diuretic Class
| Adverse Effect | Loop Diuretics | Thiazide Diuretics | K-Sparing Diuretics |
|---|---|---|---|
| Electrolyte abnormalities | ↓ Na, K, Mg | ↓ Na, K, Mg | ↑ K, ↑ H+ |
| Metabolic | ↑ Uric acid (gout) | ↑ Glucose, ↑ Lipids | Metabolic acidosis |
| Endocrine | — | Hyperglycemia | — |
| Other | Ototoxicity (high doses) | Pancreatitis, photosensitivity | Gynecomastia (spironolactone) |
Special Population Dosing
Adjust Strategy by Comorbidity
Different disease states require modified diuretic approaches to prevent complications.
Heart Failure: - Increase frequency before increasing dose - May require BID IV dosing - Combine with dietary sodium restriction
Nephrotic Syndrome: - Use 2-3× standard doses - Diuresis is often limited by low serum albumin - Consider IV albumin before diuretic in select cases
Cirrhosis: - Use spironolactone:furosemide ratio of 2.5:1 to prevent hypokalemia - Target weight loss ≤0.5 kg/day to avoid acute renal failure - Higher doses of spironolactone needed to block aldosterone
IV Furosemide Dosing Strategy
Use this formula to estimate appropriate initial IV dose in patients with reduced renal function:
$$\text{Initial IV Lasix dose (mg)} = 30 \times \text{Creatinine (mg/dL)}$$
Then titrate based on response, doubling dose every 2-4 hours if needed.
Intravenous Fluid Composition and Management
Selection of appropriate IV fluids is critical for resuscitation and maintenance therapy. Understanding electrolyte content and osmolality guides clinical decision-making.
IV Fluid Electrolyte Composition
| Solution | Na⁺ (mEq/L) | K⁺ (mEq/L) | Cl⁻ (mEq/L) | HCO₃⁻ (mEq/L) | Glucose (g/L) | Osmolality (mOsm/L) |
|---|---|---|---|---|---|---|
| D5W | 0 | 0 | 0 | 0 | 50 | 253 |
| Half-normal saline (½NS) | 77 | 0 | 77 | 0 | 0 | 154 |
| Normal saline (NS) | 154 | 0 | 154 | 0 | 0 | 308 |
| Lactated Ringer's (LR) | 130 | 4 | 109 | 28 | 0 | 275 |
| 3% hypertonic saline | 513 | 0 | 513 | 0 | 0 | 1026 |
| Normal plasma | 135-145 | 3.5-5 | 100-110 | 22-26 | 80-100 | 280-295 |
Classification of IV Solutions
By Tonicity Relative to Plasma:
- Hypotonic (osmolality <280) - D5W, ½NS; distribute to intracellular space; useful for hypernatremia but risk of cerebral edema
- Isotonic (osmolality 270-310) - NS, LR; remain in extracellular space; first-line for resuscitation
- Hypertonic (osmolality >310) - 3% NaCl; pulls fluid from intracellular to extracellular space; reserved for symptomatic hypernatremia or cerebral edema
By Composition:
- Crystalloids - Small electrolytes and glucose; cheap, rapid distribution, large volumes needed
- Colloids - Large molecules (albumin, dextran, hetastarch); expensive, stay intravascular longer, controversial efficacy in sepsis
Maintenance Fluid Calculations
Holliday-Segar Formula (pediatric and applicable to adults):
$$\text{First 10 kg} = 4 \text{ mL/kg/hour}$$ $$\text{Next 10 kg} = 2 \text{ mL/kg/hour}$$ $$\text{Remaining weight} = 1 \text{ mL/kg/hour}$$
Simplified Adult Formula:
$$\text{Maintenance rate (mL/hr)} = \text{Weight (kg)} + 40$$
Calculation Example
A 70 kg patient requires: 70 + 40 = 110 mL/hr maintenance fluid (approximately 2.6 L/day)
Third-Spacing Concept
Third spacing refers to accumulation of fluid in non-functional spaces (interstitium) that is unavailable for perfusion:
- Ascites - Portal hypertension increases Starling forces
- Burn injuries - Increased capillary permeability from inflammation
- Bowel obstruction - Fluid sequestration in bowel wall and lumen
- Peritonitis - Inflammatory response causes interstitial edema
Clinical Implication
Patients with third spacing may appear to have adequate intravascular volume on exam while being profoundly intravascularly depleted. Aggressive fluid resuscitation may be necessary despite peripheral edema or ascites.
Management Strategy: - Recognize third-spacing and compensate with additional IV fluids - Monitor for overload (pulmonary edema, peripheral edema) while ensuring adequate perfusion - Reassess volume status frequently, especially in critically ill patients