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Chapter 15: Core Electrolyte Disorders

Urine Nephrology Now: A Primer for Students in Nephrology

Andrew Bland, MD

Hyponatremia: Complete Student Study Guide

Introduction to Hyponatremia

Hyponatremia (serum sodium <135 mEq/L) is the most common electrolyte disorder. It is crucial to conceptualize it as a disorder of water balance (too much water relative to sodium), primarily controlled by Antidiuretic Hormone (ADH), rather than a simple sodium deficit.

Systematic Diagnostic Approach

  1. Confirm True Hypotonic Hyponatremia: Measure serum osmolality (<275 mOsm/kg). Rule out pseudohyponatremia (normal osmolality) and hypertonic hyponatremia (high osmolality, e.g., hyperglycemia).
  2. Assess Volume Status: This is key to determining the cause. Is the patient hypovolemic, euvolemic, or hypervolemic?
  3. Check Urine Osmolality & Sodium:
    • Urine Osmolality < 100 mOsm/kg: ADH is appropriately suppressed. Think primary polydipsia or low solute intake (beer potomania).
    • Urine Osmolality > 100 mOsm/kg: ADH is active. This is the most common scenario.
  4. Urine Sodium:
    • < 30 mEq/L: Kidneys are conserving sodium. Suggests hypovolemia or hypervolemic states like heart failure/cirrhosis.
    • > 30 mEq/L: Kidneys are wasting sodium. Suggests euvolemic states like SIADH or renal salt wasting.

Serum Uric Acid: A low serum uric acid (<4 mg/dL) is a helpful clue that points towards SIADH.

Treatment Principles and Correction Rates

Avoid Osmotic Demyelination Syndrome (ODS)!

Overly rapid correction of chronic hyponatremia is dangerous. The brain adapts to chronic low sodium, and rapid correction can cause irreversible neurologic injury.

  • Correction Goal: Do not exceed 8-10 mEq/L in any 24-hour period. A safer target is 6-8 mEq/L per 24 hours, especially in high-risk patients (alcoholism, malnutrition, liver disease).
  • Acute/Symptomatic: For severe symptoms (seizures, coma), a rapid initial increase of 4-6 mEq/L with boluses of 3% hypertonic saline is warranted to alleviate cerebral edema. Once symptoms resolve, the correction rate must be slowed.

2024-2025 Treatment Updates

Modern Hyponatremia Management

  • Hypertonic Saline: Rapid intermittent boluses (100-150 mL of 3% saline) are now the standard for severe symptomatic cases, preferred over continuous infusions for better control.
  • Oral Urea: Now a mainstream, evidence-based therapy for chronic SIADH. It acts as an osmotic agent to promote free water excretion. Dosing is typically 15-60g per day.
  • SGLT2 Inhibitors: An emerging option, especially in heart failure. They induce osmotic diuresis via glucosuria, increasing free water clearance.
  • The dDAVP Clamp: A technique used to prevent overcorrection in high-risk scenarios. Prophylactic desmopressin (dDAVP) is given to "clamp" the kidneys' ability to excrete free water, allowing for controlled correction with hypertonic saline.

Hyperkalemia: Comprehensive Treatment Review

Emergency Management of Severe Hyperkalemia

Severe hyperkalemia (K+ > 6.5 mEq/L) or any level with ECG changes is a medical emergency. The treatment strategy is three-fold and should be initiated simultaneously.

Step 1: Stabilize the Cardiac Membrane (Immediate)

Calcium Gluconate or Calcium Chloride: This is the most critical first step. It does not lower serum potassium but protects the heart from arrhythmias.

  • Calcium Gluconate: 1-2 amps (10-20 mL of 10% solution) IV over 2-5 minutes. Safer for peripheral IVs.
  • Calcium Chloride: 1 amp (10 mL of 10% solution) IV. Contains 3x more elemental calcium but must be given through a central line to avoid tissue necrosis.

Onset: 1-3 minutes. Duration: 30-60 minutes.

Step 2: Shift Potassium Intracellularly (Temporary)

These measures buy time while definitive removal is arranged.

  • Insulin and Glucose: 10 units of regular insulin with 25g of dextrose (1 amp of D50) IV. Onset is 15-30 minutes. Be cautious of hypoglycemia, especially in CKD patients.
  • Beta-Agonists: High-dose nebulized albuterol (10-20 mg). Additive effect with insulin.
  • Sodium Bicarbonate: Generally reserved for patients with concurrent severe metabolic acidosis.

Step 3: Remove Potassium from the Body (Definitive)

  • Loop Diuretics: Effective if the patient has residual kidney function and is volume overloaded.
  • Potassium Binders:
    • Kayexalate (SPS): Oldest agent, slow onset. Carries a risk of colonic necrosis, especially with sorbitol.
    • Patiromer (Veltassa) & SZC (Lokelma): Newer, safer binders for acute and chronic management. SZC has a faster onset (1 hour).
  • Dialysis: The most effective and rapid method of potassium removal, especially in patients with kidney failure. However, practical delays in initiation are common.

Urinary Obstruction: A Reversible Cause

Always consider urinary obstruction (e.g., from an enlarged prostate) in a patient with AKI and hyperkalemia. A bedside bladder scan can be diagnostic. Placing a Foley catheter can be both diagnostic and therapeutic, often rapidly resolving the hyperkalemia.

Hypercalcemia: Evaluation and Treatment

Systematic Evaluation

The first step is to confirm true hypercalcemia by correcting for albumin (Corrected Ca = Measured Ca + 0.8 × [4.0 - albumin]). The most crucial subsequent test is a **PTH level**.

The VITAMINS TRAP Mnemonic for Non-PTH Mediated Hypercalcemia

Primary Causes (VITAMINS)
  • V - Vitamins: Vitamin D or Vitamin A intoxication.
  • I - Immobilization: Prolonged bed rest increases bone resorption.
  • T - Thyrotoxicosis: Increased bone turnover.
  • A - Addison's Disease: Volume depletion and hemoconcentration.
  • M - Milk-Alkali Syndrome: Excessive intake of calcium carbonate.
  • I - Inflammatory/Infiltrative Disorders: Granulomatous diseases like sarcoidosis or tuberculosis (due to extrarenal 1α-hydroxylase activity).
  • N - Neoplasms: PTHrP-secreting tumors, osteolytic metastases (myeloma, breast), or lymphomas producing 1,25-vitamin D.
  • S - Sarcoidosis: A key example of an inflammatory disorder.
Additional Causes (TRAP)
  • T - Thiazides: Decrease urinary calcium excretion.
  • R - Renal Failure: Can lead to tertiary hyperparathyroidism.
  • A - Adrenal Insufficiency: Another way to remember Addison's disease.
  • P - Primary Hyperparathyroidism: Note: This is a PTH-mediated cause, but included for completeness of the mnemonic; it would be ruled out by a low PTH level.

Acute Management of Severe Hypercalcemia (Ca > 14 mg/dL or symptomatic)

Treatment Algorithm for Hypercalcemic Crisis

  1. IV Fluids - First and Foremost: Aggressive volume expansion with normal saline (e.g., 200-300 mL/hr) is the cornerstone of therapy. It restores GFR and enhances renal calcium excretion.
  2. Calcitonin: Provides rapid but transient reduction in calcium (onset 4-6 hours). Useful as a bridge therapy while awaiting the effects of other agents. Tachyphylaxis occurs in 48-72 hours.
  3. Bisphosphonates: The mainstay for malignancy-associated hypercalcemia. Zoledronic acid is most potent. Onset is 24-48 hours. Ensure patient is well-hydrated to reduce risk of ATN.
  4. Loop Diuretics: Use with extreme caution and ONLY after volume repletion is complete. No longer routinely recommended.
  5. Denosumab: An option for bisphosphonate-refractory hypercalcemia.
  6. Glucocorticoids: Effective for hypercalcemia due to vitamin D-mediated causes (e.g., granulomatous diseases, lymphomas).
  7. Dialysis: Reserved for severe cases with associated renal failure.
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Andrew Bland, MD - Chapter 15: Core Electrolyte Disorders
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