scott@vtx-cpd.com
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Replying to Talia C. 17/12/2024 - 06:45
Dear Talia,
Thank you for continuing to share your thoughts on Joplin’s case. Reflecting on the initial presentation, I think it’s important to go back to the starting point of why this dog was investigated in the first place. As far as I can see, Joplin initially presented asymptomatically, with incidental increases in liver enzymes prompting further investigation. Given this, even if she were in an early stage of Cushing’s disease, I feel there aren’t enough clinical signs at this time to justify starting treatment.
The current major concerns appear to be the adrenal gland changes and how best to monitor those moving forward. I think you are absolutely sensible to continue supporting the liver and gallbladder with ursodeoxycholic acid and SAM-e-type products, as these address the specific changes seen on ultrasound.
When it comes to adrenal gland changes, the primary goal is to determine functionality. While the LDDS test results lean toward a diagnosis of Cushing’s, I believe the overall findings remain equivocal. At this stage, it may be prudent to repeat the abdominal ultrasound in about three months to monitor for progression of the adrenal nodules. The key risk to watch for is the potential extension of the adrenal mass and invasion into surrounding structures, including the caudal vena cava.
In terms of further testing, you could consider urine normetanephrine/metanephrine analysis for pheochromocytoma, but as you noted, this is a costly option. Instead, serial blood pressure measurements would be a more cost-effective and practical approach for monitoring. Regularly tracking Joplin’s clinical signs and biochemical parameters will also help guide future decision-making.
I agree that testing 17-hydroxyprogesterone may not be particularly helpful at this stage. For now, repeating the scan and reassessing in three months feels like the most logical next step. This will allow you to observe any changes in clinical signs or adrenal size, at which point further diagnostic testing or treatment decisions can be revisited.
In summary, I wouldn’t pursue treatment for Cushing’s at this time, as the evidence remains inconclusive. I would focus on monitoring Joplin with regular reassessments and supporting her liver and gallbladder health, as you are already doing. Please don’t hesitate to reach out if there are any updates or additional questions as this case evolves.
Best regards,
Scott 🙂
Replying to Talia C. 17/12/2024 - 07:04
Hi Talia,
I completely agree that urine cultures in these cases can be tricky. I wouldn’t recommend routinely culturing these patients every time. Instead, my decision to reculture would usually depend on clinical signs and the presence of comorbidities. For example, in asymptomatic patients with conditions like chronic kidney disease or diabetes, I might consider reculturing, but there’s certainly a lot of debate around this.
Unless the patient is systemically unwell or showing specific symptoms that warrant further investigation, I don’t think routine reculturing is necessary. I’d focus more on clinical indicators and ongoing monitoring strategies like creatinine, SAA, and ultrasound, which you’re already doing. This targeted approach helps balance the need for thorough care with cost considerations and avoids unnecessary interventions.
Best,
Scott 🙂
Replying to Steph Sorrell 21/12/2024 - 17:12
Thank you Steph.
Have a wonderful Christmas!
Scott 🙂
Replying to Georgina F. 21/12/2024 - 08:44
So interesting!
Thank you for sharing… I am off to educate myself!
Scott 🙂
Replying to Talia C. 17/12/2024 - 07:13
Dear Talia,
Thank you for the update!
Yes, I typically monitor the urine specific gravity and water intake over 3-5 days during a desmopressin trial. Ideally, you’d check USG first thing in the morning, as this is when urine concentration should be at its peak if the dog is responding. Monitoring water intake simultaneously is key, as a clear reduction in polydipsia, along with increased USG, would strongly support central diabetes insipidus. If there’s minimal or no response in either, it would point more toward nephrogenic diabetes insipidus or primary polydipsia.
Given that she is now in heat, you’re absolutely right to keep this in mind, as hormonal fluctuations can potentially influence renal water handling. Your recent CDI case with the pituitary mass is really interesting!
Let me know how the DDAVP trial progresses in this current case.
Best regards,
Scott 🙂
Replying to Talia C. 17/12/2024 - 07:17
Dear Talia,
Urine protein dipstick tests are more sensitive for detecting albumin than globulin, which is important to keep in mind when interpreting results. Dipstick results must always be evaluated in the context of urine specific gravity (USG) and pH. In concentrated urine, such as with a USG of 1.050 or higher, or in the presence of a high pH, even a “2+” result may not be clinically significant due to the higher risk of false positives. Conversely, in dilute urine, particularly with a USG of 1.015 or lower, even a “1+” result becomes more concerning and may indicate clinically significant proteinuria.
When dipstick-detected proteinuria is identified, further quantitative analysis with a urine protein-to-creatinine ratio (UPC) is recommended. This is particularly important if proteinuria persists, such as with “++” or “+++” readings, which should always be repeated. Any “+” result in urine with a USG less than 1.012 warrants additional assessment with UPC. Additionally, if globulinuria is suspected or if there is a high urine pH, confirmation via UPC becomes necessary as the dipstick may not provide an accurate representation. It is also important to note that USG alone does not accurately predict significant proteinuria.
It is essential to place results in the context of USG and pH, as these factors influence the significance of the findings. Dilute urine with even mild proteinuria, as well as persistent “++” or higher readings, should prompt further evaluation with UPC.
I hope that helps!
Scott 🙂
Replying to Talia C. 17/12/2024 - 07:26
I must admit… I was slightly uncertain about the Chia seeds in such a young cat.
Doing well so far, but I will keep you posted.
Scott 🙂
Replying to Talia C. 10/12/2024 - 06:42
Dear Talia,
Thank you for sharing this challenging and case. The lack of Pu/Pd and the relatively high urine specific gravity (USG) do make the diagnosis of hyperadrenocorticism (HAC) less clear-cut, especially since Pu/Pd is a hallmark feature in the majority of Cushing’s cases. However, the presence of clinical signs such as polyphagia, alopecia, and a pot-bellied abdomen, coupled with the adrenal nodules and elevated alkaline phosphatase (ALP), certainly raises the suspicion for HAC.
The low-dose dexamethasone suppression (LDDS) test results, while supportive of HAC, do carry a risk of false positives, especially in dogs without classic clinical signs. This makes it even more important to interpret these results within the broader clinical context. While the urinary cortisol-to-creatinine ratio (UCCR) was elevated, it is worth noting that UCCR has a lower specificity for HAC, and the high USG (1.041) further challenges the diagnosis, as lower USG is often expected in Cushingoid dogs due to impaired concentrating ability.
Given these nuances, the Cushing’s Risk Predictor Tool published by the Royal Veterinary College (RVC) could be a valuable next step. This tool integrates multiple clinical and laboratory findings to provide a percentage likelihood of HAC, and it may help refine the diagnostic certainty in this case. The adrenal nodules, while consistent with HAC, could also represent incidental age-related changes, functional changes secondary to another condition, or even a different type of neoplasia.
Blood pressure monitoring is another key consideration here, as adrenal changes and HAC can predispose dogs to systemic hypertension. While the systolic blood pressure (SBP) of 155 mmHg is mildly elevated, stress could be a factor, so I’d recommend repeat measurements to confirm whether intervention is necessary.
Overall, while the LDDS test suggests HAC, the absence of Pu/Pd, high USG, and the nuanced clinical picture raise the possibility of a false positive. If you remain uncertain, it would not be unreasonable to hold off on starting treatment for HAC immediately and instead continue monitoring clinical signs and rechecking key parameters. Using the RVC’s predictive tool could provide additional clarity in this decision-making process.
This is undoubtedly a tricky case, and your cautious approach is well justified. Please let me know if you’d like to discuss further or explore additional diagnostic or management strategies.
Best regards,
Scott 🙂
Replying to Lara Brunori 09/12/2024 - 10:58
Hi Lara,
Thanks for sharing this case! Starting Denamarin as a hepatoprotective measure was a reasonable step, especially considering the potential for xylitol-induced liver injury. I would have done the same thing in this situation.
Please keep me updated on how Oasis is doing! I’d be curious to hear if the ALT normalized or if there were any further developments.
All the best,
Scott 🙂
Replying to Rosie Marshall 11/12/2024 - 20:35
Hello Rosie!
Lurking encouraged and supported here at VTX!
You’re absolutely right that omeprazole can reduce gastric acid secretion, potentially impairing calcium absorption over time. This is particularly relevant in humans with conditions like osteoporosis.
In cases of renal secondary hyperparathyroidism, where calcium metabolism is already disrupted, this is worth considering, though the clinical significance in veterinary patients isn’t fully understood. That said, I’d generally reserve omeprazole for clear indications, such as confirmed or suspected gastrointestinal ulceration (e.g., melena or hematemesis). For CKD patients with secondary hyperparathyroidism but no GI symptoms, it’s probably better to avoid unnecessary interventions that might further complicate calcium-phosphorus balance.
Scott 🙂
Hi Sam,
This is a really interesting case! If possible, it would be fantastic if you could share more of the blood results, particularly the full biochemistry and haematology panels. Do you have any radiographs of the bones, especially the long bones, as these might provide additional insights?
Regarding the anaemia, it would be helpful to know more about the red blood cell indices, including the MCV, MCHC, and RDW, to assess for potential iron deficiency. Was a blood smear performed, and were there any morphological abnormalities observed, such as hypochromasia or microcytosis, which could support a diagnosis of iron deficiency anaemia? Additionally, do you have the ionized calcium results?
Given the stage of kidney disease and the increased risk of gastrointestinal bleeding in such cases, I’d agree that balancing interventions is critical. If gastrointestinal blood loss is suspected, an abdominal ultrasound to rule out any GI pathology could be beneficial. Alternatively, fecal occult blood testing may help confirm GI bleeding.
For phosphate binders, aluminium hydroxide could also be considered.
The anaemia itself is fascinating, as CKD-associated anaemia is typically non-regenerative. Interestingly, Varenzin™-CA1 (molidustat oral suspension) is the first and only FDA conditionally approved option for the treatment of non-regenerative anaemia in cats with chronic kidney disease (CKD). While I haven’t used this product myself, and it’s not yet available in the UK (or on many other markets due to regulatory processes), it has generated some interesting initial feedback.
In practice, I still routinely use darbepoetin in these cases as it remains a reliable option. If iron deficiency is confirmed or suspected, addressing it before considering erythropoiesis-stimulating agents (e.g., darbepoetin) would be ideal. Supplementation with parenteral iron (e.g., iron dextran) might be beneficial if needed.
Looking forward to more details if you’re able to provide them, I’d love to delve deeper into this case!
Best regards,
Scott 🙂
Replying to Talia C. 04/12/2024 - 19:58
Hi Talia,
You’ve raised some excellent points and highlighted the key challenges in this case, particularly Siichba’s young age and the uncertainty around the stone composition. I’ll share what we’ve done so far and my evolving thoughts.
I agree that simply extending the antibiotic course without addressing the calculi as a nidus of infection is unlikely to fully resolve the issue. While Clavaseptin has good coverage, I’ve transitioned Siichba to a fluoroquinolone to improve penetration into the urinary tract and stones, particularly given the persistent E. coli infection. This choice will be reassessed pending final culture sensitivities.
Determining the stone composition has indeed been challenging. The association between E. coli and struvites makes it tempting to focus on dissolution, but without definitive analysis, we’re balancing probabilities. Given Siichba’s young age and the likelihood of struvite stones in young cats, I’ve started a dissolution diet (feline c/d). This will continue for two weeks, after which I plan to transition to feline i/d to ensure nutritional adequacy for a growing kitten while supporting urinary health. We’re monitoring urine pH to assess dietary impact, and if calcium oxalate becomes a stronger suspicion, I may consider potassium citrate to alkalinize the urine.
To manage the marginally elevated ionized calcium, I introduced 1 gram of soaked chia seeds daily into Siichba’s diet. I hoped this would help reduce calcium availability and minimize calcium precipitation in the urine. It’s a bit of an outside-the-box approach, and I’d love your thoughts on whether this was the right move! If the urinalysis confirms acidic urine with calcium oxalate, I might pivot to other strategies like citrate supplementation.
Hydronephrosis and partial obstruction of the left kidney are concerning, and I completely agree that quick action is essential to preserve renal function. While Siichba’s bloodwork doesn’t yet show signs of renal insufficiency, I’ve implemented close monitoring with serial ultrasounds and bloodwork to track progression. If the obstruction worsens, a ureteral stent or SUB will likely be our next steps.
To manage pain and improve comfort, I’ve started buprenorphine and Prazosin to help relax the ureteral smooth muscle and encourage stone passage. Siichba is also on IV fluids to maintain hydration and dilute urine, reducing the risk of further stone aggregation.
While the ultrasound findings are detailed, I’m still considering a contrast-enhanced CT to better visualize the ureteral anatomy and obstruction.
I’ll keep you posted on Siichba’s progress, and I completely agree that a discussion on ureteral calculi and stents would be a fantastic topic. Thank you for your input, and I’d love to hear your thoughts on some of the management choices, particularly the use of chia seeds.
Best,
Scott 😊
Really interesting!
I thought this was something only rabbits got!
Scott 🙂
Replying to Lara Brunori 02/12/2024 - 13:38
Hi Lara,
Thank you for your kind reply and for following up!
You’re absolutely right that Hill’s i/d isn’t typically marketed for urinary health specifically. It does have some urinary benefits because of its S+OX Shield™, which is designed to promote a urinary environment that reduces the risk of struvite and calcium oxalate crystal formation. While it’s not as focused as diets like c/d or s/d, its nutritional profile (moderate magnesium and phosphorus levels) and acidifying properties make it a good option, particularly for growing kittens who need a complete and balanced diet.
Latest Cystocentesis Results
We’ve received the results of the latest urine analysis, which show:Amber colour, slightly cloudy appearance
Specific gravity: 1.032 (well concentrated)
pH: 5.0 (acidic)
Protein: 1 g/L
Blood: +4 with TNTC RBCs
WBC: 0-3/HPF
Bacteria: Negative
Transitional cells: Few present
Crystals: None detected
It’s great news that the bacteria have cleared, so no further antibiotics are needed at this stage. However, the persistent haematuria and transitional cells are something we’ll continue to monitor closely.On another note, are you still working at Vets Now? Congratulations on passing your boards, such a fantastic achievement.
I’ll keep you updated as we progress, and please let me know if you have any further thoughts or questions about the case.
All the best,
Scott
Replying to Talia C. 02/12/2024 - 08:55
Dear Talia,
Thank you for sharing this case. Pyelonephritis can be such a diagnostic puzzle? The combination of fever, weight loss, and reduced appetite alongside the initial ultrasound findings and positive E. coli culture certainly pointed toward pyelonephritis as the likely culprit. Starting enrofloxacin was a solid choice, and her clinical response after the two-week course was really encouraging. That said, I agree with your instincts—it might’ve been better to extend the course to 4–6 weeks, given the nature of renal infections and their tendency to hang around if not completely eradicated. These infections like to play the long game!
At the three-month follow-up, I think you did the right thing by repeating the ultrasound and urine culture. Even though she’s clinically well now, the residual urine culture positivity raises the question of whether we’re dealing with asymptomatic bacteriuria (ASB) or some lingering infection. The ultrasound findings of mild pelvic dilation and increased cortical echogenicity could well be residual scarring from the earlier infection. It’s always a bit tricky to interpret those changes—renal pelvic dilation can be non-specific, and chronic changes don’t necessarily mean ongoing infection. But I would agree it’s worth keeping an eye on.
Now, about the current culture result showing E. coli in her urine. In a cat who’s bright, eating, and symptom-free, I’d lean toward considering this as ASB rather than an active infection. Studies suggest treating ASB isn’t always beneficial and can even encourage resistance. That said, if she starts showing any clinical signs—lethargy, dysuria, or even subtle changes like hiding more—I’d definitely revisit the idea of treating her with a longer antibiotic course, ideally guided by sensitivity testing.
When it comes to further management, here’s what I’d suggest: No immediate antibiotics. Since she’s well in herself and there are no systemic signs, we can probably leave the E. coli alone for now. Just keep monitoring her closely. Recheck urine culture in 2–3 months. If it’s still positive but she remains symptom-free, I’d still hold off on antibiotics unless her bloodwork (e.g., creatinine, SAA) or clinical signs change. Routine follow-ups. Periodic ultrasounds and blood checks will help keep tabs on her kidney function and detect any recurrence early. It’s also a good opportunity to discuss any subtle behaviour changes with her owner.
I’d be slightly cautious about relying on enrofloxacin for future treatment in this girl if she does need antibiotics again. There have been occasional reports of retinal toxicity in cats on enrofloxacin, especially at higher doses, so it might be worth considering alternatives like marbofloxacin or cefpodoxime instead. It’s a small risk, but I’d rather play it safe when we have options.
Let me know how she gets on or if you’d like to chat through anything further!
Warm regards,
Scott 🙂
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