Renal Tubular Acidosis (RTA)
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Renal Tubular Acidosis (RTA) is a group of disorders where the kidneys fail to acidify the urine appropriately, leading to systemic metabolic acidosis. It is characterized by a Normal Anion Gap (Hyperchloraemic) Metabolic Acidosis. It is classified into Type 1, 2, and 4 (Type 3 is a rare obsolete term).
Clinical Scenario: The Stunted Child with Stones
A 6-year-old girl is investigated for failure to thrive and recurrent renal stones (nephrocalcinosis). Bloods show Bicarbonate 14 mmol/L (Low), Potassium 2.8 (Low). Urine pH is 6.5.
Key Teaching Points
- **Diagnosis**: **Type 1 (Distal) RTA**.
- **Clues**: Low K+, Acidosis, High Urine pH (>5.5), Stones.
- **Contrast**: Type 2 (Proximal) causes Rickets but not stones. Type 4 causes Hyperkalaemia.
- **Mechanism**: The distal tubule cannot secrete H+, so calcium precipitates in alkaline urine.
Image Integration Plan
| Image Type | Source | Status |
|---|---|---|
| Management Algorithm | AI-generated | PENDING |
| Nephron Diagram (Sites of RTA) | AI-generated | PENDING |
| X-Ray (Nephrocalcinosis) | Web Source | PENDING |
| X-Ray (Rickets) | Web Source | PENDING |
[!NOTE] Image Generation Status: Diagrams illustrating the H+ secretion and HCO3- resorption pumps are queued.
The "RTA Table" (Essential for Exams)
| Feature | Type 1 (Distal) | Type 2 (Proximal) | Type 4 (Hyperkalaemic) |
|---|---|---|---|
| Defect | Cannot excrete H+ | Cannot reabsorb HCO3- | Low Aldosterone |
| Urine pH | > 5.5 (Always) | Variable (often <5.5) | < 5.5 |
| Potassium | Low | Low | High |
| Stones | Yes (Ca Phosphate) | No | No |
| Bones | Rare | Yes (Rickets) | Rare |
- Type 1: Often Autoimmune (Sjogren's) in adults, Genetic in kids.
- Type 2: Rare isolated. Usually part of Fanconi Syndrome.
- Type 4: Most common form in adults (Diabetic Nephropathy).
- Type 1 (Distal):
- Alpha-intercalated cells in distal tubule fail to secrete H+.
- Urine remains alkaline (>5.5).
- Citrate reabsorption increases -> Low urinary citrate -> Stones (Nephrocalcinosis).
- Type 2 (Proximal):
- Proximal tubule fails to reabsorb filtered Bicarbonate (normally 85-90%).
- Large amounts of bicarb lost in urine (Bicarbonaturia) initially.
- Distal acidification is intact, so once plasma bicarb falls, urine can be acidified (<5.5).
- Type 4 (Hyperkalaemic):
- Aldosterone normally stimulates H+ and K+ secretion in exchange for Na+.
- Lack of aldosterone/resistance leads to H+ retention (Acidosis) and K+ retention (Hyperkalaemia).
- General: Short stature? Dehydration?
- Musculoskeletal: Evidence of rickets (bow legs, beaded ribs)?
- Eyes: Kayser-Fleischer rings (if Wilson's disease causes Type 2).
- Bloods:
- ABG: Metabolic Acidosis. Normal Anion Gap. High Chloride.
- Potassium: Low (1 & 2) or High (4).
- Bicarbonate: Low (usually <15 in Type 1, 12-20 in Type 2).
- Urine:
- pH: Check early morning fresh sample.
- Urinary Anion Gap: (Na + K) - Cl. Positive in RTA (failure to excrete NH4+). Negative in GI loss (Diarrhoea).
- Glucose/Protein: Present in Fanconi Syndrome (Type 2).
- Imaging:
- US/XR KUB: Nephrocalcinosis (Type 1).
Type 1 (Distal)
- Alkali Replacement: Sodium Bicarbonate or Potassium Citrate (preferred as it corrects K+ and Citrate prevents stones). High doses needed.
- Outcome: Excellent if treated early. Nephrocalcinosis is permanent.
Type 2 (Proximal)
- Alkali Replacement: Extremely high doses needed (10-15 mmol/kg) because as you give bicarb, the kidney just wastes it.
- Vitamin D / Phosphate: Treat bone disease.
- Treat Underlying Cause: e.g., Myeloma, Wilson's.
Type 4 (Hyperkalaemic)
- Diet: Low Potassium.
- Medication:
- Fludrocortisone: If mineralocorticoid deficiency (Addison's).
- Loop Diuretics: Increase K+ excretion.
- Stop offending drugs (Spironolactone, NSAIDs, ACEi if safe).
- Nephrocalcinosis.
- CKD.
- Arrhythmia (Hypo/Hyperkalaemia).
- Growth Retardation.
- Depends on underlying cause.
- Genetic forms require lifelong replacement.
- KDIGO Guidelines.
- Rare Renal Disease Registry.
What is RTA? Is it a condition where the kidneys are unable to filter acid out of the blood. Normally, the body produces acid from food, and the kidneys pee it out. In RTA, the acid stays in the blood ("Acidosis").
Is it dangerous? Acid in the blood can dissolve bones (leading to rickets) and stop children growing properly. It also messes up salt levels (like potassium) which are vital for the heart. In one type (Type 1), it causes chalky stones to form inside the kidney tissue.
How is it treated? We simply replace the "base" that is missing to neutralize the acid. This usually involves taking Bicarbonate or Citrate medicine (a salty tasting liquid or tablet) several times a day. Once the acid level is normal, children usually catch up on growth and bones heal.
- Rodriguez Soriano J. Renal tubular acidosis: the clinical entity. J Am Soc Nephrol. 2002.
- Both, et al. Clinical approach to renal tubular acidosis in adult patients. J Nephrol. 2014.