Renal Pathophysiology Chapter 7

Objectives of Study

• Understand factors regulating potassium balance, focusing on transcellular distribution and urinary excretion.
• Recognize major causes of hyperkalemia, with emphasis on impaired urinary potassium excretion.
• Learn physiologic principles for therapies aimed at reversing hyperkalemia.
• Identify factors and mechanisms leading to lowered plasma potassium and urinary potassium wasting.
• Describe clinical implications of conditions such as Syndrome of apparent mineralocorticoid excess and various syndromes affecting potassium handling.

Case Presentation

• Patient: 49-year-old woman with moderate, recent-onset hypertension and mild muscle weakness.
• Lab results:
  • Plasma sodium (Na): 140 mEq/L
  • Plasma potassium (K): 3.1 mEq/L
  • Plasma chloride (Cl): 98 mEq/L
  • Total CO2: 32 mEq/L
  • Urine sodium: 80 mEq/L
  • Urine potassium: 60 mEq/L

Physiologic Effects of Potassium

• Total body potassium (K) approximately 3,000-4,000 mEq, with 98% intracellularly stored.
• Na-K-ATPase pump functions with a 3:2 ion transport ratio, influencing intracellular and extracellular potassium concentrations.
• Changes in K+ levels influence membrane potential, affecting Na-channel function.
• Abnormal potassium levels can cause muscle weakness and cardiac arrhythmias, largely dependent on the magnitude and rate of change.

Regulation of Potassium Balance

• Average extracellular volume is between 12-14 L; healthy plasma potassium levels range from 4-5 mEq/L.
• Daily potassium intake is 40-100 mEq; hyperkalemia avoided by increased cellular uptake via the Na-K-ATPase pump and enhanced renal excretion within 6-8 hours.

Urinary Potassium Excretion

• Glomerular filtration rate (GFR) is about 180 L/day, with a plasma potassium around 4.5 mEq leading to a filtered load of approximately 810 mEq.
• Significant passive reabsorption occurs in the proximal tubule and thick ascending loop of Henle.
• Secretion happens in principal cells of collecting ducts, where increased intracellular potassium alters luminal membrane potential.

Hyperkalemia

• Hyperkalemia can arise from decreased cell entry, increased cell release, or reduced urinary excretion.
• Distinct mechanisms involved in acute versus chronic hyperkalemia, including changes in Na-K-ATPase activity.
• Impaired urinary potassium excretion primarily due to hypoaldosteronism and decreased distal urinary flow, often linked to heart failure or advanced renal failure.

Hyperkalemia and Metabolic Acidosis

• Metabolic acidosis triggers an increase in hydrogen ions (H+), pushing potassium out of cells, leading to a rise of approximately 0.6 mEq/L of K per 0.1 pH unit decrease.
• Conditions such as chronic renal failure exacerbate hyperkalemia during metabolic acidosis.

Etiologies of Hyperkalemia

• Insulin deficiency: Leads to increased plasma potassium, particularly in uncontrolled diabetes where hyperosmolality impacts osmotic balance.
• Beta Adrenergic Blockade: Reduces potassium entry into cells.
• Muscle Breakdown: Intense exercise and trauma can cause liberation of intracellular potassium, further increasing serum levels.

This quiz focuses on the regulation of potassium balance, emphasizing transcellular distribution and urinary excretion. Designed for students of renal pathophysiology, it aims to deepen understanding of the factors influencing potassium homeostasis in the body.