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Renal Tubular Acidosis, Pediatric


Basics


Description


  • Renal tubular acidosis (RTA) is characterized by hyperchloremic metabolic acidosis in the setting of normal or near-normal glomerular filtration rate (GFR).
  • The acidification defect can be localized to the proximal tubule (type II RTA) resulting in incomplete bicarbonate reabsorption, or the distal tubule (type I or type IV RTA) resulting in impaired net acid secretion.
  • Type I and II RTA are associated with hypokalemia; type IV is associated with hyperkalemia.
  • Timing of onset and severity of presentation are variable, depending on the underlying cause of the acidification defect.
  • Type I RTA is associated with nephrocalcinosis, osteopenia, rickets and sometimes hearing loss.
  • Four different types of RTA are recognized:
    • Type I (classic, hypokalemic, distal)
    • Type II (proximal)
    • Type III (characteristics of both proximal and distal RTA, rare inherited disorder associated with mental retardation, osteopetrosis, and cerebral calcification)
    • Type IV (hyperkalemic, distal)
      • Associated with aldosterone deficiency or resistance to its renal effect

Epidemiology


RTA is a rare disorder. Increased prevalence is observed in areas where consanguinity is common. ‚  

Etiology


  • Genetic causes of proximal RTA:
    • Mutation in carbonic anhydrase II
    • Mutation in sodium bicarbonate cotransporter
  • Genetic causes of distal RTA:
    • Mutation in anion exchanger 1 (AE1) in alpha-intercalated cell
    • Mutation in H+-ATPase
    • Mutation in carbonic anhydrase II
  • Genetic causes of Fanconi syndrome/proximal RTA:
    • Lowe syndrome
    • Dent disease
    • Cystinosis
    • Tyrosinemia
    • Galactosemia
    • Hereditary fructose intolerance
    • Wilson disease
    • Fanconi-Bickel syndrome
    • Mitochondrial disorders
  • Acquired causes of proximal RTA:
    • Drugs:
      • Ifosfamide
      • Cisplatin/oxaliplatin
      • Valproic acid
      • Carbonic anhydrase inhibitor (e.g., acetazolamide)
      • Topiramate
      • Aminoglycosides
      • Antiretroviral therapy (tenofovir)
  • Acquired causes of distal RTA type I:
    • Autoimmune disorders
    • Drugs:
      • Lithium toxicity
      • Amphotericin
      • Ifosfamide
  • Acquired causes of distal RTA type IV:
    • Aldosterone resistance/deficiency
      • Diabetic renal disease
      • Obstructive uropathy
      • Adrenal insufficiency
    • Drugs:
      • Nonsteroidal anti-inflammatory medications
      • Heparin
      • Potassium-sparing diuretics
      • Angiotensin-converting enzyme inhibitor or angiotensin receptor blocker
      • Calcineurin inhibitors (e.g., tacrolimus or cyclosporine)
      • Trimethoprim
      • Pentamidine

Pathophysiology


  • With ingestion of a typical Western diet, healthy adults generate ¢ ˆ ¼1 mEq/kg net acid per day and infants and children ¢ ˆ ¼2 " “3 mEq/kg/day.
  • Under physiologic conditions, the proximal tubule is responsible for reclaiming 85 " “90% of filtered bicarbonate.
    • Bicarbonate reclamation in the proximal tubule is achieved by a sodium " “hydrogen ion antiporter, which secretes hydrogen ion into the urine resulting in generation of bicarbonate within the cell. Cellular bicarbonate is then transported into the bloodstream via an Na-HCO3 transporter on the basolateral membrane.
  • The distal tubule normally reclaims the remaining 10 " “15% of filtered bicarbonate and secretes a net amount of acid, both via hydrogen ion secretion.
    • In the distal tubule, hydrogen ion secretion occurs primarily via H+-ATPase.
    • Secreted hydrogen ions are buffered in the urinary lumen primarily by ammonia and excreted as ammonium ions.
  • In proximal RTA, mutations in the basolateral sodium bicarbonate cotransporter or in carbonic anhydrase prevent adequate bicarbonate reclamation in the proximal tubule.
    • Unreclaimed bicarbonate enters the distal nephron, which has limited capacity for bicarbonate reclamation, resulting in bicarbonaturia and non " “anion gap metabolic acidosis (usually serum bicarbonate does not decrease below 16 mEq/L).
  • In distal RTA, mutations in the basolateral anion exchanger or the H+-ATPase prevent bicarbonate transport into the bloodstream and hydrogen ion secretion into the lumen, respectively, resulting in impaired net acid secretion and non " “anion gap metabolic acidosis.
  • Proximal RTA can be associated with Fanconi syndrome in which there is general proximal tubular dysfunction leading to bicarbonaturia, glucosuria, phosphaturia, and tubular proteinuria.
  • Distal RTA type I is associated with urine pH >5.5
  • Distal RTA type IV is associated with either low aldosterone levels or aldosterone resistance and presents with hyperkalemic non " “anion gap metabolic acidosis.

Diagnosis


History


  • Failure to thrive in infants and children
  • Polyuria
  • Constipation
  • Anorexia
  • Symptoms of hypokalemia:
    • Muscle weakness
    • Constipation
  • Kidney stones
  • Intellectual disability
  • Propensity for fractures

Physical Exam


  • Constitutional: failure to thrive
  • Head: frontal bossing
  • Ears: deafness (associated with some forms of RTA)
  • Neurologic: developmental and cognitive delay
  • Skin: decreased turgor, prolonged capillary refill

Diagnostic Tests & Interpretation


  • Serum electrolytes
    • To identify metabolic acidosis with normal anion gap, and hypokalemia or hyperkalemia
    • Magnesium level (can be low in Fanconi syndrome)
    • Phosphorus level (can be low in Fanconi syndrome)
  • Serum creatinine: to evaluate GFR
  • Urine electrolytes
    • Urine anion gap, calculated as (urine sodium + urine potassium ¢ ˆ ’ urine chloride): typically >10 in distal RTA (type I or IV)
    • Urine phosphorus: Fractional excretion is high in Fanconi syndrome, resulting in hypophosphatemia.
  • Urinalysis
    • Urine pH is high in distal RTA, often >6.8 and can be elevated or normal in proximal RTA.
    • Look for glucosuria in setting of normal serum glucose.
  • Urine spot for calcium/creatinine ratio: Look for hypercalciuria (normal values are age-dependent).
  • 24-hour urine collection for citrate (typically low)

Imaging
  • Renal ultrasound: Evaluate for nephrocalcinosis and kidney stones.
  • Long bone films to look for signs of rickets or osteopenia

Differential Diagnosis


  • Renal insufficiency (earlier stages)
  • Diarrhea
  • Urinary diversion via bowel conduits
  • Acetazolamide use

Treatment


Medication


  • Alkali supplementation given as sodium or potassium bicarbonate or citrate (typically requires 5 " “8 mEq/kg/24 h in distal RTA and 5 " “15 mEq/kg/24 h in proximal RTA)
  • Thiazide diuretics (in proximal RTA) to induce volume depletion which can be sensed by the proximal tubule, resulting in increased proximal tubular reabsorption of bicarbonate
  • Mineralocorticoid supplementation (for those with select causes of type IV RTA)

Additional Therapies


General Measures
  • Vitamin D supplementation as needed
  • Phosphorus supplementation as needed (if concurrent Fanconi syndrome)

Ongoing Care


Follow-up Recommendations


  • Frequent monitoring of serum electrolytes
  • Close follow-up of linear growth
  • Renal ultrasound to monitor for evidence or progression of nephrocalcinosis

Prognosis


  • Can rarely progress to chronic kidney disease over time depending on etiology of RTA (as in cystinosis) or if associated with nephrocalcinosis
  • May be associated with development of nephrolithiasis

Additional Reading


  • Batlle ‚  D, Haque ‚  SK. Genetic causes and mechanisms of distal renal tubular acidosis. Nephrol Dial Transplant.  2012;27(10):3691 " “3704. ‚  [View Abstract]
  • Haque ‚  SK, Ariceta ‚  G, Batlle ‚  D. Proximal renal tubular acidosis: a not so rare disorder of multiple etiologies. Nephrol Dial Transplant.  2012;27(12):4273 " “4287. ‚  [View Abstract]
  • Karet ‚  FE. Mechanisms in hyperkalemic renal tubular acidosis. J Am Soc Nephrol.  2009;20(2):251 " “254. ‚  [View Abstract]

Codes


ICD09


  • 588.89 Other specified disorders resulting from impaired renal function

ICD10


  • N25.89 Other disorders resulting from impaired renal tubular function

SNOMED


  • 1776003 Renal tubular acidosis (disorder)
  • 24790002 Proximal renal tubular acidosis (disorder)
  • 236461000 Distal renal tubular acidosis (disorder)
  • 236463002 Hyperkalemic renal tubular acidosis

FAQ


  • Q: Can RTA be diagnosed in the setting of renal failure?
  • A: No. Typically, RTA is diagnosed in the setting of relatively preserved renal function. Renal function associated with non " “anion or anion gap acidosis typically occurs when GFR is <30 mL/min/1.73 m2.
  • Q: Does a urine pH <5.5 exclude RTA?
  • A: A low urinary pH excludes distal RTA but could still be consistent with a proximal RTA. However, urine pH as tested on urine dipsticks or formal urinalysis can be unreliable depending on duration between time of sample delivery and analysis.
  • Q: What are the available forms of alkali supplementation?
  • A: Alkali supplementation is best provided as a combination of sodium and potassium citrate or bicarbonate (except in distal RTA type IV, in which potassium alkali is avoided).
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