Renal damage and disease can be caused by acute or chronic insults to the kidney. The terms renal disease and renal damage
are used to denote the presence of renal lesions; these terms however imply nothing about the cause, distribution, or severity
of the lesions and importantly nothing about the level of renal function that exists. Chronic kidney disease (CKD) can be
caused by diseases/disorders that affect any portion of the nephron, including the glomerulus, the tubule, the vascular supply,
and surrounding interstitium. Early detection of CKD, prior to the onset of renal azotemia and chronic renal failure (CRF),
should facilitate appropriate intervention that could stabilize renal function or at least slow its progressive decline.
Early Detection of CKD
Most acquired (vs hereditary or familial) canine and feline CKD and CRF occurs in middle to older aged patients. An annual
health examination, that includes a complete blood count, serum biochemistry profile, and urinalysis, is one of the best ways
to detect declining renal function. Special attention should be paid to decreases in appetite, body weight, packed cell volume,
and urine specific gravity. Conversely, increases in serum urea nitrogen, creatinine, and phosphorus, or urinary excretion
of protein or albumin may indicate the onset of renal disease. Although each of these parameters alone is relatively nonspecific
for CKD, when they are considered as a group, their value increases. Plotting the inverse of the serum creatinine concentration
vs time can demonstrate a decrease in renal excretory function; the steeper the slope, the more rapid the functional decline.
Developing data flow charts is a excellent way to keep track of changes in body weight and clinicopathologic values. Longitudinal
assessment of serum creatinine for example can indicate declining renal function even when values remain in the normal range.
A serum creatinine concentration of 1.2 mg/dl may be overlooked on a single biochemistry profile, however if previous results
showed a serum creatinine concentration of 0.6 mg/dl, ≥ 50% loss of renal excretory function may have occurred. It's important
to keep in mind that hydration status and muscle mass can influence serum creatinine concentrations; concurrent assessment
of urine specific gravity and body condition will aid in the interpretation of serum creatinine concentrations. Dogs and
cats may also become more susceptible to bacterial urinary tract infections as their ability to concentrate urine decreases
and the antibacterial properties of their urine decreases. If any of the above parameters suggest the possibility of renal
disease, an ultrasound examination may be indicated to evaluate kidney tissue architecture. Pyelonephritis, renoliths, and
renal cortical fibrosis can be demonstrated by ultrasound. Percutaneous or ultrasound-guided renal biopsy can also be utilized
to confirm or further define renal cortical disease in selected cases.
Table.Clinicopathologic findings that may be associated with early renal disease in dogs and cats
Importance of Proteinuria as a Marker of Early CKD
Persistent proteinuria with an inactive urine sediment has long been a recognized clinicopathologic hallmark of CKD in dogs
and more recently in cats. Beyond this diagnostic marker utility, the potential for proteinuria to be associated with the
progression of CKD has also been recognized in dogs and cats. The implication that proteinuria may be a mediator of renal
disease progression has stimulated a discussion about what level of protein in the urine is normal. Development of species
specific albumin ELISA technology that enables detection of low concentrations of canine and feline albuminuria has helped
drive this reevaluation process.