Renal Physiology – Study Notes (Part 2)

Urine Osmolarity

• Range: 50–1400 mOsm/L

• Determined by how much free water the body must excrete.

• Maintains plasma volume without altering solute concentration.

Antidiuretic Hormone (ADH, Vasopressin)

• Secreted by: Posterior pituitary.

• Stimulus: ↑ plasma osmolarity (↑ solute concentration).

• Action:

  • Acts on distal tubule & collecting duct.

  • Increases free water reabsorption → concentrates urine.

• Obligatory urine volume:

  • Solute excretion ≈ 600 mOsm/day.

  • Max urine concentration ≈ 1200 mOsm/L.

  • Minimum urine volume ≈ 0.5 L/day (to excrete solutes).

• Clinical example: Seawater ingestion → too much salt intake → requires excessive urine output → worsens dehydration.

Disorders of ADH Regulation

SIADH (Syndrome of Inappropriate ADH Secretion)

• Pathophysiology: Too much ADH → water retention → dilutional hyponatremia.

• Causes:

  • CNS issues: head injury, hemorrhage, tumors.

  • Cancers: e.g., small-cell lung carcinoma.

  • Drugs: carbamazepine, antipsychotics.

• Findings:

  • Hyponatremia (Na < 110 mEq/L = CNS toxicity risk).

  • Concentrated urine.

• Treatment:

  • Fluid restriction.

  • Hypertonic saline (if severe).

  • Diuretics.

  • Correct Na < 0.5 mEq/L per hour to avoid central pontine myelinolysis (CPM).

Diabetes Insipidus (DI)

• Pathophysiology: Lack of ADH activity → impaired water reabsorption → excessive dilute urine.

• Types:

  1. Central (Neurogenic):

     • ↓ ADH secretion (pituitary damage: trauma, tumors, surgery, SAH).

     • Onset: 4–24 hrs after pituitary surgery.

     • Symptoms: polyuria, polydipsia, hypernatremia.

     • Treatment: Desmopressin (DDAVP), carbamazepine.

  2. Nephrogenic:

     • Normal ADH secretion, but kidney unresponsive.

     • ADH analogs ineffective → different treatments required.

• Findings:

  • Very dilute urine (low specific gravity, low urine osmolarity).

  • High serum osmolarity & sodium.

  • Large urine volumes (several 100s of mL/hr).

ADH Regulation

• Stimuli that ↑ ADH:

  • ↑ plasma osmolarity (Na+).

  • Hypovolemia, hypotension.

  • Nausea, hypoxia.

• ↓ ADH: Alcohol (→ diuresis).

• Contrast:

  • ADH: Retains free water only → changes osmolarity & Na+.

  • Aldosterone/Angiotensin II: Retain Na+ + water → minimal effect on osmolarity.

Potassium Physiology

• Normal plasma [K+]: 3.5–5.0 mEq/L.

• Distribution: 98% intracellular, 2% extracellular.

• Daily intake: ~100 mEq → mostly excreted renally, some in feces.

Regulation of K+ between ICF & ECF

• Shift K+ into cells: Insulin, aldosterone, β-stimulation, alkalosis.

• Shift K+ out of cells: Insulin deficiency, aldosterone deficiency, β-blockade, acidosis, cell lysis, strenuous exercise.

Renal Handling of K+

• Aldosterone: ↑ Na+ reabsorption, ↑ K+ secretion (via Na+/K+ ATPase).

• Increased tubular flow: ↑ K+ excretion.

• Acidosis:

  • Acute: ↓ K+ secretion (retention).

  • Chronic: ↑ K+ loss (via ↓ Na+ reabsorption).

Disorders of Potassium

Hyperkalemia

• Defined as: K+ > 5.5 mEq/L.

• Severity:

  • Mild: 5.5–6.0

  • Moderate: 6–7

  • Severe: >7 (life-threatening >8.5).

• Causes:

  • Renal failure.

  • ↓ Aldosterone.

  • Medications (K+-sparing diuretics).

  • Acidosis (H+ moves in, K+ moves out).

  • Cell destruction (lysis, trauma, exercise).

• Symptoms: Palpitations, muscle weakness.

• ECG changes:

  • Peaked T waves → widened QRS → sine wave → VFib/asystole.

Treatment of Hyperkalemia (Mnemonic: C BIG K Drop)

• C – Calcium gluconate (10 mL 10% IV over 10 min): cardiac protection.

• B – Beta agonists (albuterol); Bicarbonate (NaHCO₃): shift K+ into cells.

• I – Insulin (10 units IV) + G – Glucose (D50 IV): drive K+ into cells.

• K – Kayexalate (polystyrene resin): removes K+ via GI tract.

• D – Diuretics or Dialysis: excretion of K+.

✅ That closes out Part 2: ADH physiology, SIADH, Diabetes Insipidus, and Potassium balance.