Renal Pathophysiology Chapter 7

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.

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

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.

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.

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 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.

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.

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.