| Acute kidney disease is seen when a sudden, major insult damages the kidneys. The principal causes are toxins (eg, ethylene glycol, aminoglycoside antibiotics, hypercalcemia, hemoglobinuria) and ischemia (eg, embolic showers from disseminated intravascular coagulation or severe prolonged hypoperfusion). |
| Clinical Findings: |
| Mild, acute kidney disease often goes unrecognized; severe initial or repeated bouts may lead to chronic kidney disease. The stages of acute and chronic kidney disease are the same (see
Chronic Kidney Disease). Most often, acute kidney disease is recognized in Stage IV and is characterized clinically by anorexia, depression, dehydration, oral ulceration, vomiting and/or diarrhea, or oliguria. Physical examination findings often reveal dehydration but otherwise are usually not remarkable, although pain is occasionally elicited on palpation of the kidneys, which may be normal-sized to slightly enlarged. |
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| Diagnosis: |
| A history of hypotension, shock, or recent exposure to known nephrotoxins in an animal with sudden-onset uremia (Stage IV) is the typical clinical picture of an animal with acute kidney disease. The presence of inappropriately concentrated urine (specific gravity 1.007-1.035) in the face of dehydration and/or azotemia suggests renal dysfunction. Differentiating between chronic and acute kidney disease (and establishing a specific cause in acute kidney disease) is important, as
the prognosis and specific therapy may differ. Animals with acute kidney disease usually have a compatible history and other urinalysis abnormalities; marked cylindruria is a frequent and definitive finding. Other urinalysis findings may include the presence of a large number of renal epithelial cells and leukocytes in the urine sediment, glucosuria, crystalluria, and/or myoglobinuria/hemoglobinuria. Animals with Stage III or IV acute kidney disease have increased serum urea
nitrogen, creatinine, and inorganic phosphorus concentrations and metabolic acidosis. Oliguria or anuria following rehydration, which is often associated with hyperkalemia, is a poor prognostic sign; in contrast, polyuric animals have a better prognosis, although they may become hypokalemic. Anemia is often, but not always, absent—a finding that may be helpful in differentiating acute from chronic kidney disease. |
| Following injury, the kidney has considerable potential for functional regeneration through the process of compensatory hypertrophy and adaptive hyperfunction. In animals with chronic kidney disease, it is likely that much of these processes has occurred prior to the initial diagnosis. In contrast, animals with acute kidney disease have considerably more potential for improvement of renal function, if they can be sustained through a uremic episode. The duration of the uremic
episode may be substantial with some nephrotoxins (eg, 1-3 wk with aminoglycoside antibiotics and 4-8 wk with ethylene glycol). A renal biopsy may be of value in assessment of the severity, extent, cause, and potential reversibility of the disease. |
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| Treatment: |
| If the cause is known, specific therapy should be instituted, eg, 4-methyl-pyrazole or ethanol for ethylene glycol toxicity in dogs (
Ethylene Glycol Toxicity: Introduction). Fluid therapy is indicated for all dehydrated and inappetant animals. A polyionic fluid such as lactated Ringer’s solution is satisfactory unless hyperkalemia is present, in which case normal saline is recommended. Sodium bicarbonate may be cautiously added to the fluids to correct acidosis. |
| In oliguric or anuric animals, therapy to promote increased urine volume is often recommended if the animal is well hydrated and urine production is <0.5 mL/kg/hr. This approach has been questioned because urine flow may increase without corresponding increases in renal blood flow and GFR. Administration of excess fluid to an animal in the maintenance phase of oliguric renal failure may result in life-threatening pulmonary and cerebral edema. Nonetheless, efforts to increase
renal blood flow and GFR may enhance urine production and do have a role in the management of these animals. For this therapy, urine production must be quantitatively monitored closely via an indwelling urethral catheter. Monitoring central venous pressure is advised to prevent overhydration. A sequential approach generally includes an initial slight overhydration by administration of a test dosage of 50 mL/kg of polyionic solution IV. If this fails to yield adequate urine flow
within 3 hr, further measures include osmotic diuresis (10% or 20% mannitol or dextrose, 0.5-1 g/kg, IV, as a slow bolus over 15-30 min, alternated with infusion of lactated Ringer’s solution, 30 mL/kg, IV, over 30 min). Subsequent measures generally include furosemide (2 mg/kg, IV, which can be doubled and then tripled at 2-hr intervals if urine production does not increase above the target of 0.5 mL/kg/hr). However, furosemide may worsen the severity of acute renal failure
caused by aminoglycosides. Finally, renal vasodilators (dopamine diluted in 5% dextrose, IV, to provide 1-5 g/kg/min) plus furosemide (2 mg/kg, IV) may be tried for 2 hr. Dopamine may lead to ventricular arrhythmias and its use as a renal vasodilator has been questioned, particularly in cats. High doses of dopamine may cause renal vasoconstriction. If attempts to restore urine flow fail, aggressive measures should be discontinued to avoid overhydration. Daily fluid therapy based
on maintenance and rehydration needs is continued until renal function and clinical condition improve. Feeding tube placement greatly facilitates patient management at this stage and should be implemented for any animal with marked renal azotemia (serum creatinine >10 mg/dL after rehydration). |
| A second therapeutic option, rather than the aggressive measures discussed above, is to proceed directly to fluid therapy with polyionic solutions while waiting for renal regeneration. Again, feeding tube placement for parenteral nutrition should be implemented in anorectic animals with marked azotemia. Peritoneal dialysis, hemodialysis, or euthanasia may be necessary if none of the above measures restores urine production. |
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