What are the types of Renal Tubular Acidosis (RTA) that can occur in patients with Southeast Asian Ovalocytosis (SAO)?

Medical Advisory BoardAll articles are reviewed for accuracy by our Medical Advisory Board
Educational purpose only • Exercise caution as content is pending human review
Article Review Status
Submitted
Under Review
Approved

Last updated: February 2, 2026View editorial policy

Personalize

Help us tailor your experience

Which best describes you? Your choice helps us use language that's most understandable for you.

Types of Renal Tubular Acidosis in Southeast Asian Ovalocytosis

Patients with Southeast Asian Ovalocytosis (SAO) can develop distal renal tubular acidosis (Type 1 RTA), which occurs through autosomal recessive inheritance when SAO is combined with additional mutations in the anion exchanger-1 (AE1) gene. 1

Primary RTA Type Associated with SAO

Type 1 (Distal) RTA

  • SAO alone does not cause RTA - individuals with isolated SAO (27 bp deletion in exon 11 of the AE1 gene) maintain normal renal acidification capacity 1
  • Compound heterozygosity is required - dRTA develops only when SAO is inherited together with a second pathogenic AE1 mutation (such as G701D missense mutation in exon 17), creating autosomal recessive dRTA 1
  • The prevalence is striking: 81.8% of Malay patients with dRTA have SAO, compared to only 4% in healthy controls, indicating SAO significantly increases susceptibility to dRTA when combined with other genetic factors 2

Clinical Presentation in SAO-Associated dRTA

Metabolic Features

  • Normal anion gap metabolic acidosis (anion gap 8-12 mEq/L) with hyperchloremia 3, 4
  • Severe hypokalemia (potassium as low as 2.7 mmol/L) leading to proximal muscle weakness, paralysis risk, rhabdomyolysis, and cardiac arrhythmias 3, 4
  • Inability to lower urine pH below 5.5-6.3 despite systemic acidemia 4, 5

Renal Manifestations

  • Low ammonium (NH4+) excretion initially (26 micromol/min), though capacity for NH4+ production remains intact and can increase threefold with diuretic challenge 4
  • Nephrocalcinosis and nephrolithiasis from hypercalciuria, alkaline urine, and low urinary citrate 3, 6
  • Growth retardation in children and osteodystrophy 5, 6

Unique Finding in SAO-Associated dRTA

  • Paradoxically elevated urine-blood PCO2 difference (U-B PCO2 of 27 mm Hg when urine pH reaches 7.7 after bicarbonate loading), possibly from misdirection of AE1 to the apical membrane of type A intercalated cells 4

Other RTA Types NOT Associated with SAO

Type 2 (Proximal) RTA

  • Results from impaired bicarbonate reabsorption in the proximal tubule, not distal dysfunction 7
  • Associated with Fanconi syndrome features: aminoaciduria, glucosuria, phosphaturia, and uricosuria 3, 7
  • Not linked to SAO - the AE1 defect in SAO affects distal tubules, not proximal transport mechanisms 1

Type 4 (Hyperkalemic) RTA

  • Characterized by hyperkalemia as the dominant feature, with mild metabolic acidosis 3
  • Results from aldosterone deficiency or resistance, not AE1 dysfunction 8
  • Not associated with SAO - the pathophysiology is unrelated to anion exchanger abnormalities 3

Critical Diagnostic Pitfall

Do not assume all individuals with SAO have RTA - parents and family members with isolated SAO demonstrate completely normal renal acidification on NH4Cl loading tests 1. The key distinction is that autosomal recessive inheritance of two abnormal AE1 alleles (SAO deletion plus an additional mutation) is required for dRTA to manifest 1.

References

Guideline

Renal Tubular Acidosis Diagnosis and Clinical Features

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2026

Research

Distal renal tubular acidosis and high urine carbon dioxide tension in a patient with southeast Asian ovalocytosis.

American journal of kidney diseases : the official journal of the National Kidney Foundation, 1999

Research

Renal tubular acidosis.

Endocrinology and metabolism clinics of North America, 1990

Guideline

Characteristics of Type II Renal Tubular Acidosis

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Guideline

Renal Tubular Acidosis Treatment and Management

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

Have a follow-up question?

Our Medical A.I. is used by practicing medical doctors at top research institutions around the world. Ask any follow up question and get world-class guideline-backed answers instantly.