Causes & Risk Factors
Causes are often difficult to determine since the structural and functional endpoint of irreversible nephron damage is the same. Renal diseases that have been associated with the development of CKD in cats include amyloidosis, glomerulonephritis, primary tubulointerstitial disease, ascending urinary tract infections (bacterial pyelonephritis), nephrolithiasis, polycystic kidney disease, feline infectious peritonitis, and neoplasia.
Typical gross appearance of chronic kidney disease. Note the irregular borders and "lumpy-bumpy" surface.
Pathophysiology
Nephron damage associated with CKD is usually irreversible and can be progressive (stage I and early stage II CKD may not be progressive, but later stage II to IV is almost always progressive). Renal failure results when three quarters or more of the nephrons of both kidneys are not functioning. Whether the underlying CKD primarily affects glomeruli, tubules, interstitial tissue, or renal vasculature, irreversible damage to any portion of the nephron renders the entire nephron nonfunctional. Healing of irreversibly damaged nephrons occurs by replacement fibrosis.
Progressive diseases that destroy nephrons at a slow rate allow intact nephrons to undergo compensatory hypertrophy which can delay the onset of renal failure. When renal failure finally occurs, the nephron hypertrophy can no longer maintain adequate renal function and < 25% of the original nephrons are functional.
The pathophysiology of CKD can be considered at both the organ and systemic level. At the level of the kidney, the fundamental pathology of CKD is loss of nephrons and decreased glomerular filtration. Reduced glomerular filtration results in increased plasma concentrations of substances that are normally eliminated from the body by renal excretion (eg, creatinine, urea nitrogen, and phosphorus). In addition to excretion of metabolic wastes and maintenance of fluid and electrolyte balance, the kidneys also function as endocrine organs and catabolize several peptide hormones. Thus, hormonal disturbances also play a role in the pathogenesis of CKD. Examples include decreased production of erythropoietin, which contributes to the nonregenerative anemia of CKD, decreased metabolism, and excretion of parathyroid hormone and gastrin, which contribute to osteodystrophy and gastritis, respectively.
Finally, part of the pathophysiology of CKD is brought about by compensatory mechanisms. For example, osteodystrophy occurs secondary to hyperparathyroidism, which develops in an attempt to maintain normal plasma calcium and phosphorous concentrations. Similarly, the individual glomerular filtration rate of intact nephrons increases in CKD in an attempt to maintain adequate renal function; however, proteinuria and glomerulosclerosis may be consequences or "trade-offs" of this hyperfiltration.
Signs
History. Dependent on the stage of CKD (see Table 1). History is often unremarkable in stage I and early stage II. In later stage II and beyond, history may include anorexia, weight loss, vomiting, polydipsia, and polyuria.
Physical examination. Dependent on the stage of CKD (see Table 1). Physical exam may be normal in stage I and early stage II. In later stage II and beyond, findings may include dehydration; poor body condition; uremic breath; oral ulcers; and small, firm, irregularly-shaped kidneys. Hypertensive retinopathy is possible.
Pain Index
In general, the kidneys of cats with CKD are not painful (exceptions may include lymphosarcoma causing renal swelling and the presence of nephroliths or ascending infections). Gastrointestinal irritation can result in mild to moderate pain; oral ulcers may be quite painful.
Diagnosis
