Upper tract uroliths have been relatively rare in cats until the last ten years. Many are asymptomatic and are discovered when lower urinary tract stones are creating clinical signs, or when abdominal radiographs or ultrasound are performed for other reasons. However, nephroliths and ureteroliths are being found more frequently in cats presented for acute or chronic renal failure, and present unique challenges to the feline practitioner. Most dramatically, ureteroliths, virtually unreported before 1990, became the most common cause of acute azotemia in cats in this decade. Ureteral obstruction is now a common challenge for practitioners, internists and surgeons in veterinary medicine.

Most (> 70%) upper urinary tract uroliths in cats are now calcium oxalate in composition. Small, multiple stones are common, usually found in both kidneys and/or ureters. Small ureteroliths appear to migrate over time in cats; it is unknown how many cats have passed and voided smaller uroliths prior to detection of upper tract uroliths. Approximately 15% of cats with upper tract uroliths had concurrent lower tract uroliths in one retrospective analysis. Purebred cats, including Siamese, Persians, Burmese and Himalayans, appear to be at increased risk for formation of nephroliths. Upper tract urolithiasis usually affects middle-aged to older cats, although some young (<6 years of age) cats are being presented now with severely compromised urinary tracts, presumably due to previous or long-standing stone disease.

Table 1. Causes of ureteral obstruction

Uroliths and other material are moved down the ureter by passive flow and ureteral peristalsis. In dogs, the ureteral lumen is fairly distensible and can accommodate 2 – 3 mm uroliths easily. The canine ureteral also distends significantly with fluid diuresis. In cats, however the normal ureteral lumen is tiny (0.4 mm) and fairly unforgiving. Although some cats can pass 1 -2 mm obstructions, many are obstructed with the tiniest of stones.

With obstruction, progression varies depending on age, species, degree of obstruction, and whether obstruction is unilateral or bilateral. In general, complete outflow obstruction raises ureteral pressure, which is then transmitted to the proximal tubules and affects renal filtration forces and blood flow. Blood flow and glomerular capillary hydrostatic pressure actually increase initially, features that usually increase the driving force for glomerular filtration, however these increases are soon offset and exceeded by the high opposing pressure in the tubules. Because of this, the net hydrostatic pressure gradient across the glomerular capillaries decreases, resulting in a decline in filtration (decreased GFR). Later (after 5-24 hours), intratubular pressures decline, but glomerular capillary pressures decline faster, so GFR stays significantly decreased (> 50%).

Renal function can deteriorate by 70 – 80% within 2 weeks. Partial obstruction can be expected to have less effect on renal blood flow and GFR. Reversibility depends predominantly on duration of obstruction, but also is affected by severity of obstruction and function of the contralateral kidney. In dogs, complete reversibility may be obtained if the obstruction is removed within 4 – 7 days; reversibility declines to approximately 30% by 4 weeks and 0% by 6 – 8 weeks of complete obstruction. With long term obstruction, histological changes include interstitial fibrosis and tubular basement membrane thickening, signs of irreversible renal damage. In the obstructed ureter, distension is accompanied by smooth muscular hypertrophy, and eventual fibrosis. With this in mind, treatment decisions often need to be made quickly to protect renal function.