| The form of metabolic acidosis that occurs in Stages II-IV of acute and chronic kidney disease, referred to as uremic acidosis, is due to reduced urine-acidifying ability of diseased kidneys. In uremic acidosis, although the ability of some individual tubular cells to reabsorb bicarbonate and/or secrete hydrogen ions may be normal, there is generally far less total cell mass present. Acid accumulates if the animal is under metabolic or dietary acid pressure, which is common in
carnivores and is particularly problematic in cats, which are often fed acidifying maintenance diets. |
| Rare renal tubular defects in dogs and cats may result in hyperchloremic metabolic acidosis, referred to as renal tubular acidosis. Two types of renal tubular acidosis have been described in dogs and one in cats. In Type I (distal), the ability of the distal tubule to secrete hydrogen ions against a concentration gradient is defective; in Type II (proximal), the ability to reabsorb bicarbonate in the proximal tubule is reduced. Type I has been reported in both species; Type II has
also been described in dogs in conjunction with other proximal tubular defects in acquired (gentamicin nephrotoxicosis and an idiopathic form) and heritable (Fanconi syndrome, see
Fanconi Syndrome) forms. |
| Type I renal tubular acidosis has been associated with demineralization of the skeleton (due to buffering of excess hydrogen ions) and nephrolithiasis (due to hypercalciuria from bone resorption) in dogs. Diagnosis is based on the presence of hyperchloremic metabolic acidosis with a urinary pH that is inappropriately high for the degree of systemic acidosis in the absence of bacterial urease modification of urine. Failure to produce acid urine after oral ammonium chloride loading
is diagnostic; however, this test is contraindicated in animals that are already severely acidotic. Type II renal tubular acidosis is diagnosed by demonstrating increased urinary fractional excretion of bicarbonate when plasma bicarbonate levels are normal or decreased; this test is not practicable in the clinical setting and diagnosis is presumptively based on history, signalment, and clinical pathology findings. |
| Therapy consists of oral administration of an alkalinizing agent sufficient to maintain normal blood pH (1 mEq bicarbonate equivalent/kg/day for Type I and 1-6 mEq bicarbonate equivalent/kg/day for Type II, PO). Therapy is more problematic in dogs with Type II renal tubular acidosis, because supplemental bicarbonate is readily lost in the urine. |
