Disease of the kidney can be generally classified as acute or chronic. It leads to a loss of ability to concentrate or dilute tubular filtrate, to eliminate nitrogenous wastes and to maintain acid-base status.
Acute renal injury
Acute renal injury is characterized by a deterioration in renal function over hours to days, resulting in a failure of the kidney to excrete nitrogenous waste and maintain fluid, electrolyte and acid-base status. Acute renal injury can be corrected, however it may progress to chronic renal disease. Acute renal injury can result from the following causes:
- Decreased renal perfusion from prerenal causes (e.g. hypovolemia due to dehydration).
- Intrinsic renal disease. This can be due to acute tubular necrosis (nephrosis) or inflammation (nephritis).
- Nephrosis: Acute tubular necrosis is usually due to traumatic, ischemic or toxic injury. Ischemia is the most common cause of acute renal failure in animals and can be primarily due to prerenal causes. Most cases of ischemic renal tubule injury are reversible if the underlying cause is corrected, unless there has been extensive necrosis or vessel injury. Examples of nephrotoxins that produce acute renal failure are aminoglycosides (all species), acorns (large animals) and ethylene glycol (companion animals).
- Nephritis: Renal failure in nephritis probably results from vasculitis or vascular compression secondary to interstitial infiltrates. Causes include leptospirosis, Rocky Mountain Spotted Fever, ehrlichiosis and bacteremia.
- Post-renal causes. This is usually due to outflow obstruction or rupture.
Chronic renal disease
Chronic renal disease is due to slowly progressive, chronic deterioration of kidney function and may be preceded by acute renal injury in some (but not all) cases. Chronic kidney disease progresses through four stages.
- Stage 1 – Decreased renal reserve
- During this period, there may be an upward trend in urea and creatinine, but are still within reference intervals. There are no clinical signs, but the kidneys are less able to compensate for dehydration or decreased perfusion.
- Stage 2 – Chronic renal insufficiency
- Additional loss of renal function will lead to decreased urine concentrating ability and polyuria, eventually accompanied by azotemia. However, other clinical signs of uremia are not yet present.
- Stage 3 – Chronic renal failure
- Clinical signs of uremia accompanied by worsening azotemia develop as the kidney disease progresses. At this stage, the animal is considered to be in stage 3, or chronic renal failure. These animals may also develop additional laboratory abnormalities such as metabolic acidosis.
- Stage 4 – End-stage renal disease
- The kidney can no longer produce much urine and the animal becomes oliguric and severely uremic, with very severe changes on serum chemistry. The oliguria and severe lab changes can be similar to the presentation of animals with acute renal injury, but animals in the end stage of chronic kidney disease will have a longer time course of disease that included a period of polyuria.
An acute exacerbation of renal disease may occur in some patients with chronic renal failure (“acute on chronic” renal failure). The most common cause of chronic renal failure in large animals is glomerulonephritis. In small animals, both glomerulonephritis and amyloidosis can produce chronic renal failure. Some breeds are predisposed to amyloidosis, e.g. Sharpei, Beagles, Oriental and Siamese cats. In addition, many breeds suffer from inherited renal dysplasias which result in chronic renal failure, e.g. Samoyeds, Bull Terriers and Soft-coated Wheaten Terriers. Often proteinuria is the first sign of renal disease in breeds with inherited renal disease. Both acute and chronic renal failure have similar laboratory features, including azotemia, hyperphosphatemia, and metabolic acidosis with a high anion gap. Differentiation of acute renal injury from chronic renal disease can be difficult but can be accomplished by assessment of clinical signs, laboratory features and history.
|Acute renal injury||Chronic renal disease|
|History||Ischemic episode, toxicant exposure, trauma, nephrotoxic drugs||May have had previous episodes of acute renal failure|
|Clinical signs||Good body condition, acute onset of vomiting, diarrhea, lethargy and depression. Anuria or oliguria is usually present.||Long standing signs of polyuria, polydipsia, nocturia, vomiting and diarrhea|
|Kidneys||Normal to large, with smooth contours, may be painful||Small with irregular contours|
|Packed cell volume||Normal or increased||Mild to moderate non-regenerative anemia|
|Urine sediment||Usually abnormal: Glucosuria, mild proteinuria, granular casts||Severe proteinuria, granular and waxy casts may be seen, glucosuria is less common.|
|Serum creatinine||Previously normal||Previously elevated|
|Serum potassium||Normal to increased||Normal to decreased, unless anuric or oliguric|
|Metabolic acidosis||Severe||Less severe|
|Histopathology||Acute tubular necrosis or inflammation||Interstitial fibrosis, chronic inflammation, glomerulosclerosis, amyloidosis|