Renal · Year 2 · from Renal
Case 3: Metabolic Alkalosis from Vomiting
Patient Presentation
A 28-year-old female presents to the emergency department with weakness, dizziness, and muscle cramps. Her roommate reports she has been vomiting frequently for several weeks and seems preoccupied with her weight.
History of Present Illness
- Self-induced vomiting after meals for 3 months
- Significant weight loss (15 pounds)
- Progressive weakness and lightheadedness
- Muscle cramps and tingling in hands
- Constipation
Physical Examination
- Blood pressure: 96/58 mmHg supine, 78/50 standing
- Heart rate: 102 bpm supine, 124 standing
- Dry mucous membranes, poor skin turgor
- Dental enamel erosions
- Positive Chvostek sign
- Calluses on knuckles (Russell sign)
Workup
Laboratory Studies:
- Serum potassium: 2.4 mEq/L (severely low)
- Serum bicarbonate: 38 mEq/L (elevated)
- Serum chloride: 84 mEq/L (low)
- BUN: 32 mg/dL (elevated)
- Creatinine: 1.3 mg/dL
- Calcium: 8.2 mg/dL
- Urine chloride: 8 mEq/L (low - chloride responsive)
- Urine pH: 5.5 (paradoxically acidic)
Diagnosis
Chloride-Responsive Metabolic Alkalosis with Severe Hypokalemia from Purging Behavior
Discussion
This case demonstrates the generation and maintenance of metabolic alkalosis:
- Generation vs. Maintenance: The lecture emphasizes this distinction. Vomiting generates alkalosis through HCl loss, but the kidney should excrete excess bicarbonate. Maintenance factors prevent this correction.
- Maintenance Factors: Volume depletion activates angiotensin II, stimulating proximal bicarbonate reabsorption. Chloride depletion limits the chloride-bicarbonate exchange needed to excrete bicarbonate. Hypokalemia increases hydrogen ion secretion and ammoniagenesis.
- Paradoxical Aciduria: Despite systemic alkalosis, urine pH is acidic because the kidney continues to secrete hydrogen ions due to the maintaining factors. This paradoxical aciduria indicates chloride-responsive alkalosis.
- Low Urine Chloride: The lecture notes that urine chloride <20 mEq/L identifies chloride-responsive alkalosis (vomiting, NG suction, prior diuretics). Chloride-resistant forms (hyperaldosteronism) have urine chloride >20 mEq/L.
- Hypokalemia Mechanism: Vomiting causes minimal direct potassium loss. The hypokalemia results from renal potassium wasting driven by the alkalosis and secondary hyperaldosteronism.
Treatment
- IV normal saline for volume and chloride repletion
- IV potassium chloride replacement (severe hypokalemia)
- Monitor electrolytes closely
- Psychiatry consultation for eating disorder
- Once stable, oral potassium chloride supplementation
- Nutritional rehabilitation
Clinical Pearl
In metabolic alkalosis from vomiting, urine chloride is more reliable than urine sodium for assessing volume status. Obligate bicarbonaturia carries sodium with it, making urine sodium elevated despite volume depletion. Paradoxical aciduria (acidic urine during alkalosis) signals that maintaining factors are present and the patient needs saline and chloride repletion.
Image Reference
For visual reference of renal acid-base concepts, see:
- Radiopaedia: Renal tubular acidosis - Clinical information and classification
- Wikimedia Commons: Acid-base balance - Diagrams of renal acid handling
- Radiopaedia: Nephrocalcinosis - Imaging findings in distal RTA
Learning Points
- Urine pH Distinguishes RTA Types: Distal RTA cannot acidify urine below pH 5.5 during acidosis; proximal RTA can acidify once the threshold is reached.
- Urine Anion Gap Assesses NH4+ Excretion: Negative gap indicates appropriate ammonium excretion (extrarenal acidosis); positive gap indicates impaired renal acid excretion (RTA).
- Fanconi Syndrome Components: Glucosuria with normal glucose, aminoaciduria, phosphaturia, uricosuria, and type 2 RTA indicate generalized proximal tubule dysfunction.
- Alkalosis Maintenance Requires Treatment: Addressing the maintaining factors (volume, chloride, potassium) is essential - the alkalosis will not correct with observation alone.
- Type 4 RTA is Hyperkalemic: Unlike types 1 and 2, type 4 RTA (hypoaldosteronism) causes hyperkalemia and mild acidosis from impaired ammonium production.