Renal Tubular Acidosis

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Renal Tubular Acidosis

 

Renal Tubular Acidosis – a syndrome characterized by hyperchloremic metabolic acidosis due either to decreased bicarbonate reabsorption from the proximal renal tubule (proximal or type 2 RTA) or decreased hydrogen ion secretion in the distal tubule (distal, classic or type 1 RTA) in patients with normal or near normal glomerular filtration rate and absence of diarrhea.

  • Aldosterone deficiency or resistance can cause type 4 distal RTA leading to hyperkalemia. Proximal RTA has not been documented as an isolated entity in dogs but has been observed as part of Fanconi syndrome.
  • The following discussion is limited to classic distal RTA. In distal RTA, the urine cannot be maximally acidified despite moderately to markedly decreased plasma bicarbonate concentration as a consequence of impaired hydrogen secretion in the collecting ducts. Urine pH typically is above 6.0 (normally urine pH should be 4.5–5.0 in the presence of systemic acidosis).

 

SIGNALMENT

  • Reported in 8 dogs and 4 cats
  • No apparent breed or sex predilection
  • Age range at time of diagnosis, 1–12 years

 

SIGNS

  • Associated with acidemia and may include lethargy, muscle weakness (may be related to hypokalemia), inappetence, nausea, weight loss, stunted growth, and neurologic signs.
  • Other signs depend on the associated diseases (e.g., pyelonephritis).
  • Panting.
  • Polyuria and polydipsia (usually associated with hypokalemia or calciuresis).
  • Vomiting.
  • Hematuria and dysuria (secondary to urolithiasis).
  • Osteomalacia associated with chronic metabolic acidosis (not yet reported in dogs and cats).

 

CAUSES & RISK FACTORS

  • May be primary (i.e., inherited), or secondary to hypercalciuria, toxins, drugs (e.g., amphotericin B), altered calcium metabolism causing nephrocalcinosis (e.g., hypervitaminosis D, primary hyperparathyroidism), autoimmune (e.g., immune-mediated hemolytic anemia, systemic lupus erythematosus, renal transplant rejection), hypergammaglobulinemic disorders (e.g., multiple myeloma, systemic lupus erythematosus), and tubulointerstitial nephropathies.
  • In cats, distal RTA has been associated with pyelonephritis (2 cases), hepatic lipidosis (1 case), and idiopathic with secondary hyperaldosteronism (1 case).
  • In dogs, clinical cases were idiopathic or associated with immune-mediated hemolytic anemia (3 cases), leptospirosis (1 case), or experimentally-induced renal ischemia.

 

DIAGNOSIS

DIFFERENTIAL DIAGNOSIS

Consider other causes of hyperchloremic (normal anion gap) metabolic acidosis (e.g., diarrhea, carbonic anhydrase inhibitors, ammonium chloride, cationic amino acids, post-hypocapnic metabolic acidosis, dilutional acidosis, hypoadrenocorticism). Small bowel diarrhea is the most important differential diagnosis.

 

CBC/BIOCHEMISTRY/URINALYSIS

Results vary depending on associated diseases.

Hypokalemia (due to increased renal excretion) in some animals; may be severe enough to cause muscle weakness.

Alkaline urine (pH > 6.0); rule out urease-positive urinary tract infection (e.g. Staphylococcus aureus, Proteus spp.) as a cause of alkaline urine.

 

OTHER LABORATORY TESTS

Evaluation of blood gases and serum electrolytes indicates hyperchloremic (normal anion gap) metabolic acidosis. Urine pH is > 6.0 in distal RTA versus < 5.5 in proximal RTA.

 

IMAGING

Radiography—may detect uroliths or osteomalacia (uncommon).

 

DIAGNOSTIC PROCEDURES

  • The key diagnostic feature is normal anion gap metabolic acidosis accompanied by an inappropriately alkaline urine pH (> 6.0).
  • Ammonium chloride tolerance test—administer 200 mg/kg PO in dogs; measure urine pH before and at hourly intervals for 5 hours; empty the bladder hourly. Urine pH in normal dogs decreases to < 5.5 within 4 hours. Avoid this test if severe acidosis is present.
  • Type 1 and 2 RTA can be differentiated based on response to NaHCO3 infused at 0.5–1.0 mEq/kg/h. Fractional excretion of bicarbonate will increase markedly in type 2 RTA.

 

TREATMENT

  • Individualize depending on the nature and severity of associated conditions.
  • Typically, less bicarbonate is needed to resolve metabolic acidosis associated with distal RTA than is needed to resolve acidosis associated with proximal RTA.
  • Hypokalemia may resolve with bicarbonate or citrate administration alone, or additional potassium supplementation may be required.

 

MEDICATIONS

DRUG(S)

Potassium citrate alone or in combination with sodium citrate (depending on the serum potassium concentration) at a total dosage of 1–5 mEq/kg/day PO, divided into two doses, or sodium bicarbonate at 10–50 mg/kg q8–12h PO (1–3 mEq/kg/day).

Potassium supplementation—potassium gluconate; cats, 2–8 mEq/day divided q12h PO; dogs (depending on body size), 2–44 mEq/day divided q12h PO, if required.

 

CONTRAINDICATIONS/POSSIBLE INTERACTIONS

Citrate should be avoided in patients with renal failure receiving aluminum hydroxide because citrate increases intestinal permeability and can lead to excessive aluminum absorption.

 

FOLLOW-UP

  • Serial blood gas analyses (e.g., every 3–5 days) until acid-base status has normalized.
  • Monitor serum electrolytes, especially potassium, as needed.
  • Long-term prognosis depends on the nature and severity of associated conditions; may be reasonably good in patients without other diseases, but little information exists on the long-term course of this disease in dogs and cats.

 

MISCELLANEOUS

ABBREVIATIONS

NaHCO3 = sodium bicarbonate

RTA = renal tubular acidosis

 

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