Acute kidney injury
Acute kidney injury (AKI; acute renal failure; acute nephritis) is a collective term for any acute renal disease.
The term has replaced the historical term acute renal failure for renal damage occurring over a short period of time (hours to days) because it is thought to better describe the pathophysiologic changes and duration of the different phases of injury.
Acute kidney injury is caused by ischemia or chemical injury to the circulatory, filtration, tubulointerstitial or excretory system of the kidney, resulting in uremia and elevated levels of creatinine and other metabolic wastes and electrolyte, fluid and acid-base balance. Following ischemia, the reperfusion of the kidney results in a repair process involving proliferation of proximal tubular epithelial cells as well as cell migration and differentiation. In severe ischemia, repair progresses to scar formation and fibrosis of individual nephron with associated loss of function.
Renal ischemia is a common intra-operative and post-operative cause, and when the mean arterial pressure is less than 70 to 80 mm Hg, renal perfusion is compromised.
Clinically, acute renal injury can be classified into three broad stages of initiation (immediately following renal insult), maintenance (oliguria and uremia which may persist for weeks) and recovery (renal repair with marked polyuria).
There are numerous causes, including:
- - Amyloidosis
- - Ectopic ureter
- - Ureteral stenosis
- - Fanconi's syndrome
- - Polycystic kidney disease
- - Renal agenesis
- - Renal cystadenocarcinoma - associated with dermatofibrosis in German Shepherds
- - Renal dysplasia
- - Renal hypoplasia (Ask-Upmark kidney)
- - X-linked hereditary nephropathy - Cocker Spaniel
- - Familial juvenile glomerulonephropathy (autosomal-recessive) - French Mastiff, Bull Terrier
- - Ethylene glycol, Zinc coins
- - Algal blooms
- - Drugs - Gentamycin, cisplatin, melamine and cyanuric acid feed additives
- - hemoglobinuria, myoglobinuria, hypercalcemia
- Secondary renal disease
- - Psychogenic polydipsia
- - Diabetes insipidus
- - Diabetes mellitus
- - Hyperadrenocorticism
- - Hypoadrenocorticism
- - Nephrotic syndrome
Clinically affected dogs usually present with acute anorexia, lethargy, vomiting, oral ulcers, uremic breath and 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. Ultrasonography may reveal irregularly shaped or smaller kidneys. Normal sized kidneys are usually compared to vertebral length (renal:vertebral ratios usually 1.3 - 2.7)
Blood results usually show hyperphosphatemia and elevated levels of blood creatinine and BUN and marked proteinuria, and urine examination findings of hematuria, cylindruria with renal epithelial cells and leukocytes in the urine sediment are considered definitive findings.
Diagnosis is usually based on evidence of exposure to toxins, presence of renal disease and hematological findings of markedly increased blood urea nitrogen and creatinine. Other blood abnormalities usually reflect underlying causes of renal disease.
Staging of renal function in acute renal failure is usually based on the International Renal Interest Society (IRIS) categories:
|Stage||Creatinine level||Blood pressure||Clinical signs|
|Stage 1||≤ 140 μmol/L||≤ 160 mm Hg||Asymptomatic|
|Stage 2||140 - 200 μmol/L||~160 mm Hg||Asymptomatic|
|Stage 3||180 - 440 μmol/L||≥160 mm Hg||Uremic breath, dehydration, vomiting, dehydration|
|Stage 4||≥ 440 μmol/L||≥160 mm Hg||Uremic breath, dehydration, vomiting, dehydration, moribund|
Renal ultrasonogrpahy or CT imaging are often employed to help visualize the physical extent of gross renal damage. Renal biopsies are indicated in patients hemodynamically stable enough to submit to general anesthesia.
Dehydrated patients should be rehydrated before general anesthesia or administration of potentially nephrotoxic substances.
Aggressive use of intravenous fluids or intermittent hemodialysis are essential for renal recovery in the short-term and minimizing loss of nephron activity. Use of diuretics such as furosemide are indicated in oliguric patients.
Nutritional support is critical in anorectic patients.
Response to intravenous fluids should be monitored with repeated measurements of urine output, urinalysis, and urine chemistry results.
Improved success rates have been noted in dogs with acute kidney injury secondary to leptospirosis.
Following recovery, a predisposition to developing chronic renal disease requires regular monitoring of blood creatinine levels on a 6 monthly basis.
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