Ureteral obstructions (UOs) are most typically caused by calculi (in around 80 percent of cases), with a smaller proportion caused by ureteral strictures (around 20 percent of cases). In cats, more than 92 percent of these calculi are calcium oxalate stones and the remaining 8 percent are calcium phosphate, magnesium ammonium phosphate (struvite) or dried solidified blood (DSB)/inflammatory debris calculi (eg purulent material associated with pyelonephritis).
There does not appear to be any gender predisposition to ureteral calculi in cats but the DSH and DLH are the most commonly affected breeds. Most cats tend to be middleaged to older at the time of presentation but this condition can be seen at any age so this should not preclude screening of younger cats with a suspicion of UO.
UO leads to a rapid build-up of uraemic toxins and progressive renal damage. The presence of azotaemia depends on the contralateral kidney function, the number of ureters affected and the severity and duration of the obstruction. UO can result in life-threatening azotaemia, especially if a bilateral obstruction (as in around 15 percent of cases) is present or if the cat has concurrent pre-existing renal insufficiency (seen in 70 to 95 percent). UO is a challenging disorder requiring knowledge of the condition, an index of suspicion to assess for UO and often highly sophisticated therapeutic aids and specialist surgical/interventional skills to manage the condition.
Most cats with UO present for medical care with advanced disease; however, a significant proportion of cats may only show subtle clinical signs in the early stages of unilateral obstruction/partial obstruction which may go undetected. The mechanical obstruction is aggravated by secondary local inflammation and spasm. Local ureteral damage (eg stricture or rupture) is a potential complication of UO but increased intra-ureteral hydraulic pressure and decreased
renal blood flow are more common consequences. The increased hydraulic pressure results in increased pressure within the renal tubules and Bowman’s space causing direct nephron damage and a precipitous decline in GFR.
If the contralateral renal function is preserved, clinical signs, if present, are pain-related and often overlooked, thus the episode may go unnoticed. If the obstruction is dynamic, it may also resolve spontaneously. The progressive damage to the obstructed kidney is determined by the severity of obstruction (partial vs complete) and the chronicity of this obstruction.
Limited work has been performed assessing the timing of renal insult in cats but this has been more extensively reviewed in dogs. If the canine kidney is completely obstructed, renal blood flow decreases to 40 percent of normal within 24 hours and to 20 percent of normal by two weeks. As a result, GFR permanently declines by 54 percent after 14 days and by 100 percent after 40 days, indicating the need for urgent intervention in patients with complete UO. It is also worth noting that the canine models above had no evidence of pre-existing renal disease and hence we can conclude that a worse outcome would be expected in feline patients with complete UO.
In contrast, partial UO appears to result in less severe nephron destruction and in one dog model, GFR returned to normal with intervention after a partial obstruction had been present for four weeks. Many feline patients present with suspected chronic partial UO and it may be questioned if intervention is required if the cat is “coping” with the partial obstruction. The above models indicate that improvement in renal function is possible even after chronic partial obstructions are identified, hence treatment should be pursued in these patients.
“Big kidney-little kidney syndrome”
If a unilateral obstruction resolves (the cat may not even be presented to the practice due to subtle signs), the affected kidney may have residual damage or normal function. If a complete UO does not resolve, renal fibrosis of the ipsilateral kidney and compensatory hypertrophy of the contralateral kidney occurs.
This results in the finding of “big kidney-little kidney syndrome”, which can be detected on abdominal palpation. At this stage of the disease process, cats may be free of uraemic signs as the compensatory hypertrophy allows steady state renal function, and hence a degree of suspicion is again very important if the “big kidney-little kidney syndrome” is to be detected (with or without azotaemia, these cats need to be investigated urgently). Prompt intervention will reduce the degree of nephron damage.
An acute uraemia will develop following obstruction of the hypertrophied kidney. The severity of the clinical signs depends on the degree of UO and the function of the contralateral kidney. Unfortunately, this is the stage that many cats typically present in practice and this can easily be diagnosed as “simple” chronic kidney disease (CKD) and treatment implemented for that alone (acute on chronic kidney injury).
If only one ureter is obstructed and the cat is azotaemic, this is a clear indication of reduced function in the contralateral kidney, but again, these cats are often diagnosed as CKD and the ureteric obstruction can be missed at this crucial early phase. Therefore, if a cat presents with acute onset azotaemia or apparent rapid progression of preexisting CKD, possible ureteral obstruction should be urgently investigated.
Cats with ureteral obstructions can present with varying signs ranging from no or very subtle signs (inappetance and lethargy) to signs associated with severe azotaemia and pain
Cats with ureteral obstructions can present with varying signs ranging from no or very subtle signs (inappetance and lethargy) to signs associated with severe azotaemia and pain. The pain associated with ureteral obstruction is the result of direct ureteral stimulation at the site of obstruction and stretch of the collecting system and the renal capsule.
Clinical signs are usually non-specific, including inappetance and lethargy, but may progress to more marked signs on development of azotaemia and uraemic signs such as vomiting, polyuria (PU) and polydipsia (PD), weight loss, haematuria and renal pain. With complete bilateral obstruction, more advanced signs of acute kidney injury (eg oliguria/ anuria, bradycardia, vomiting, severe depression/obtundation) will be seen. Abdominal palpation may reveal renal/ abdominal pain and asymmetric kidneys – this should ring alarm bells for a possible ureteric obstruction, especially if one kidney is small and irregular and the other is large and painful. If renal pain is detected, this should prompt investigation for a ureteric obstruction as many cats may present with only vague clinical signs and unremarkable blood results.
Diagnosis of partial and complete ureteric obstructions
Physical examination findings
Abdominal palpation may reveal signs of abdominal or renal pain. Findings of the “big kidney-little kidney syndrome” should also prompt investigation. Detection of pyrexia may be associated with pain but may also be indicative of pyelonephritis.
Blood and urine tests
Serum biochemistry in affected cats can range from being completely unremarkable (for example in unilateral ureteric obstruction with normal function of the contralateral kidney) through to changes consistent with severe CKD or acute kidney injury (eg severe azotaemia, hyperphosphataemia, hyperkalaemia and anaemia of chronic disease). USG is often less than 1.035 and pyuria, proteinuria and crystalluria may also be detected.
Urine culture should be performed in all cases, as pyelonephritis can be an exacerbating problem and a UTI is found in approximately 30 percent of cats with ureteric obstruction. It should be noted that more than 75 percent of cats are azotaemic with a unilateral obstruction, indicating contralateral renal insufficiency.
Radiography and ultrasound
The combination of abdominal radiography and ultrasound has been demonstrated to be the most sensitive, readily available diagnostic tool for detection of ureterolithiasis in general practice. More advanced techniques such as intravenous pyelography, antegrade pyelography and computed tomography (CT-IVP) have been found to be inconsistent in diagnosis of UO and may offer very little additional clinical information. The use of intravenous contrast agents and additional anaesthesia should also be questioned in these renally compromised patients.
The retroperitoneal space should be carefully scrutinised for any mineral opacities (Figure 1). Ureteroliths can be obscured by gas in the gastrointestinal tract during ultrasound assessment, hence the combination of ultrasound with radiography increases the sensitivity of detecting UO. Renal size and shape should also be assessed together with the renal pelvic area for nephroliths (commonly found with ureteroliths). Plain abdominal radiographs can readily be performed in practice and are crucial for reaching an early diagnosis of ureterolithiasis allowing intervention at the earliest possible stage with the aim of preventing further nephron damage. An enema is highly recommended prior to performance of radiography to ensure ureteroliths are not obscured by faecal material.
DSB calculi, strictures (found in 20 percent of cats with UO) or inflammatory debris obstructing the ureter (eg pyelonephritis) may not be observed on plain radiographs. Abdominal ultrasound is a sensitive imaging modality for detection of hydronephrosis and/or hydroureter and can be valuable in cases where ureteroliths are not observed on plain radiographs. Hydronephrosis (Figure 2) is usually readily detectable on renal ultrasound; however, detection of hydroureter (Figures 3 and 4) can be more challenging and is dependent on the quality of the ultrasound machine/probe and the skill of the veterinarian performing the procedure.
Renal pelvic mineralisation may also be noted during ultrasound examination (Figure 5) and radiography (Figure 1). Dilation of the ureter and/or renal pelvis is usually apparent on ultrasonography within three to four days of obstruction. Although there is significant discussion of renal pelvic size as an indicator of UO, the presence of renal pelvic dilation (more than 1.5 to 2mm) with concurrent hydroureter raises concern for UO until proven otherwise. Observation of the above with a ureteric obstruction (stone, DSB, inflammatory debris) is of course diagnostic and should prompt immediate intervention to decompress the renal pelvis and allow return of renal function.
It is possible that no structural obstruction will be observed despite a very strong suspicion for UO. This is usually due to either a ureteric stricture or DSB calculi that do not shadow on ultrasound or are not radiopaque on radiographs. In this instance, antegrade pyelography may be helpful to more clearly define the ureteric obstruction; however, the clinician should also consider if this will provide any additional benefit to the patient in terms of management (if there is a strong index of suspicion of UO).