Disorders of Sodium and Potassium Metabolism

Outline

1. Review of sodium and potassium metabolism

2. Paradigm for analyzing pathophysiology

3. Abnormalities of potassium balance

4. Abnormalities of sodium and water balance

5. Example cases

Major Mediators of Sodium and Water Balance

Angiotensin II

Aldosterone

Antidiuretic hormone (ADH)

Renin-Angiotensin-Aldosterone Axis

Angiotensin II 1. Stimulates production of aldosterone

2. Acts directly on arterioles to cause vasoconstriction

3. Stimulates Na+/H+ exchange in the proximal tubule

Aldosterone 1. Stimulates reabsorption of Na+ and excretion of K+ in the late distal tubule

2. Stimulates activity of H+ ATPase pumps in the late distal tubule

Role of ADH (antidiuretic hormone)Synthesized in the hypothalamus and stored in the posterior pituitary

Released in response to plasma hyperosmolality and decreased effective circulating volume

Actions of ADH 1. Increases the water permeability of the collecting tubule

2. Mildly increases vascular resistance

Overview of Biochemical Homeostasis

Overview of Potassium Balance

Etiologies of Hyperkalemia

Excessive Dietary Intake

Decreased Urinary Excretion

Decreased GFR

Aldosterone deficiency

Adrenal insufficiency

ACE inhibitors

Hyporeninemic hypoaldosteronism

Diabetic nephropathy

Aldosterone resistance

Potassium sparing diuretics

Internal Redistribution

Transmembrane Shift

Acidosis

Exercise

Cell Lysis

Rhabdomyolysis

Tumor lysis syndrome

Etiologies of HypokalemiaPoor Intake

Increased Urinary Excretion

Decreased reabsorption in loop of Henle

Furosemide

Increased excretion in the late distal tubule

Increased delivery of Na+ to the late distal tubule

Furosemide, thiazides, and acetazolamide

Proximal RTA

Reduced function of the K+/H+ ATPase

Distal RTA

Hyperaldosteronism

Primary hyperaldosteronism

Adrenal adenoma

Adrenal hyperplasia

Secondary hyperaldosteronism

Renovascular hypertension

Renin-secreting tumor

Increased GI Losses

Diarrhea

Laxative abuse

Vomiting / NG drainage

Increased Transcutaneous Losses

Copious sweating

Transmembrane Shift

Alkalosis

Insulin treatment for DKA

High catecholamine states

Overview of Sodium Balance

Etiologies of Hyponatremia

Poor Intake of Sodium

Increased Urinary Loss of Sodium

Diuretics

Proximal RTA

Aldosterone deficiency/resistance

Increased GI Loss of Sodium (Fluid loss must be followed by repletion with free water).

Vomitting

Diarrhea

Increased Transcutaneous Loss of Sodium (Fluid loss must be followed by repletion with free water).

Excessive Intake of Water (1° polydipsia)

Psychosis

Decreased Urinary Excretion of Water

Decreased GFR

Increased ADH

Decreased effective circulating volume

True volume depletion (any cause)

Apparent volume depletion

Heart failure

Cirrhosis

SIADH

Reset osmostat

Transmembrane Shift of Water

Hyperglycemia

Primary Sodium Loss Primary Water Excess

Etiologies of Hypernatremia

Primary Sodium Excess

Excess Intake of Sodium

Decreased Urinary Excretion of Sodium

Hyperaldosteronism

Primary Water Loss

Poor Intake of Water

Impaired access to water (i.e. infants, elderly patients with dementia or whom are bedbound)

Impaired thirst sensation

Hypothalamic lesions

Increased Urinary Loss of Water

ADH deficiency (Central DI)

ADH resistance (Nephrogenic DI)

Increased GI Loss of Water

Increased Transcutaneous Loss of Water

Transmembrane Shift of Water (most often due to rapid production of intracellular lactate)

Case 1Mrs. L is a 62 y/o woman with a past medical history significant only for hypertension. She has a 45 pack year smoking history. She comes to the urgent care clinic today complaining of a cough and shortness of breath for the past week. Her physical exam is notable for both mild wheezing and rhonchi, more pronounced on the right side than the left.

Labs include the following:

Na 126 Cl 95 BUN 12Glucose 102

K 4.4 HCO3 25 Cr 1.4

Her CBC shows mild normocytic anemia.

Case 2

Mr. R is an 85 y/o man with advanced dementia who was sent to the ER from his skilled nursing facility for non-responsiveness since the morning nursing shift started about 8 hours ago. The remainder of his past medical history is unknown. Aside from his mental status, his physical exam is remarkable for a HR of 110 and BP of 100/50.

Labs include the following:

Na 164 Cl 126 BUN 50Glucose 98K 4.8 HCO3 28 Cr 2.6

Case 3Miss K is a 28 y/o woman who presents for her first routine clinic visit. She has no complaints, and her medical history is unremarkable. On physical exam you note that her BP is 162/94.

You send her for some routine labs which find the following:

Na 147 Cl 105 BUN 12Glucose 102

K 2.8 HCO3 32 Cr 0.7

UA unremarkable.

Case 4Mr. W is a 65 y/o man with a past history significant for CHF secondary from an MI 4 years ago. He comes to general medicine clinic today for a routine appointment. He states that he was complaining of some mild dyspnea on exertion at his cardiology appointment 2 weeks ago. In response, his cardiologist told him to double one of his medications, which the patient did, but at the moment he can’t remember which medication this was. He does report that his shortness of breath is now better.

Routine fasting labs reveal the following:

Today Na 128 Cl 89 BUN 32 Glucose 135K 3.1 HCO3 32Cr 1.4

2 months ago Na 132 Cl 97 BUN 24 Glucose 128K 3.8 HCO3 27Cr 1.2