scott@vtx-cpd.com

Replying to Victoria Rubasinska 10/09/2022 - 21:15

Hello Victoria.

Thank you so much for your brilliant questions. I have popped your questions below and then my thoughts under each part:

1 – Molly – I know her ALP wasn’t so high and you didn’t feel it was necessary to do investigation into Cushing’s. However she did have an abdominal scan so did you check adrenal size anyway?

It is really important that the decision to investigate Cushing’s is based on a really strong clinical suspicion. Also, I would never perform endocrine testing (ACTH stim/LDDST) in patients with significant co-morbidities. We did indeed check the adrenal gland size during the scan and they were normal in this case.

2 – Ace – sorry a little more random but I was wondering if the PU could have been related to the fact it was an E. coli infection possibly causing a toxaemia like in a pyometra?

This is indeed a possibility! The other reasons that patients with liver disease are PUPD are alterations in cortisol metabolism, reductions in urea (effecting renal concentrating ability) and PUPD related to hepatic encephalopathy.

And you mentioned a few topics that you might post some extra information on
– bile acid stimulation tests (that is all I wrote on my notes so I can’t remember why)

I have popped on a post about this.

– a reticulate count papter

I have popped on a post about this.

– and the current thoughts on whether to use ACEi or Telmisartan for proteinuria —I’ve had a case recently that I had a similar dilemma with and we opted to try an ACEi initially.

This is a great questions. There are a few papers now that suggest telmisartan may well be more effective than ACE inhibitors at treating proteinuria. I have popped one example below. ACE inhibitors are still very effective. The biggest issue with using telmisartan is the availability of licenced products and dosing in dogs being very expensive when using the available products:

Enter site

It makes treatment very expensive in dogs. In short, both are reasonable options and sometimes you need to use both in combination. ACE inhibitors are probably still a reasonable first line in dogs.

Hope that helps.

Scott 🙂

Efficacy of telmisartan for the treatment of persistent renal proteinuria in dogs: A double-masked, randomized clinical trial

Abstract
Background: Information regarding efficacy of the angiotensin II receptor blocker, telmisartan, for treatment of proteinuria in dogs is limited.

Objective: To evaluate the antiproteinuric efficacy of telmisartan, as compared to enalapril, in dogs with chronic kidney disease and persistent, renal proteinuria.

Animals: Thirty-nine client-owned dogs with chronic kidney disease and urinary protein-to-creatinine ratio (UPC) > 0.5 (if azotemic) or ≥ 1.0 (if nonazotemic).

Methods: In this prospective, randomized, double-masked clinical trial, dogs were block randomized, according to presence or absence of azotemia and systemic arterial hypertension, to receive telmisartan (1.0 mg/kg PO q24h), or enalapril (0.5 mg/kg PO q12h), and followed for 120 days. Up-titration of study drug dosage on days 30 and 60, and addition of the other study drug at day 90, were performed if UPC > 0.5 was noted at these visits. Percentage change in UPC relative to baseline was calculated for all time points. Data are presented as median (range).

Results: Thirty-nine (20 telmisartan-treated, 19 enalapril-treated) dogs were included. At day 30, percentage change in UPC was greater for telmisartan-treated (-65% [-95% to 104%]) vs enalapril-treated (-35% [-74% to 87%]) dogs (P = .002). Among dogs persistently proteinuric at earlier visits, telmisartan remained superior to enalapril at days 60 (P = .02) and 90 (P = .02). No difference in percentage change in UPC between study groups was observed at day 120, when combination therapy was allowed. Combination therapy resulted in relevant azotemia in 4/13 (31%) dogs.

Conclusions and clinical importance: Telmisartan might be a suitable first-line therapy for dogs with renal proteinuria.

Replying to Kathryn B. 08/09/2022 - 20:44

Thank you so much for sharing this.

Scott 🙂

Replying to Mariska H. 07/09/2022 - 02:56

Hello.

Thank you so much for these brilliant questions. I have posted your questions below and then popped my thoughts underneath:

1. Is there a benefit of performing in-house sediment exams to look for bacteria/neutrophils (if very easy to miss wbc etc)? Would you just do it to look for crystals? I perform it with every urinalysis but always wonder if I am doing it correctly/wasting my time and should just send it off for cytology. Do you do it with every urinalysis?

This is a great question. I suppose it comes down to why you are doing the urine analysis. In some cases the most important information is the USG and the rest is less helpful. I think in any case where you suspect UTI or crystals/stones it would be important. However, struvite, amorphous phosphate and oxalate crystals are commonly seen in urine of healthy animals. Urate, cysteine, or large quantities of calcium oxalate crystals are usually abnormal. If you get any other abnormalities on your initial dipstick, I would also do sediment exam. If you get blood or protein on dipstick I would also do a sediment exam.

2. What is your technique to get a good diagnostic sediment slide?

This is a really good guide for sediment preparation:

https://www.bristol.ac.uk/media-library/sites/vetscience/documents/clinical-skills/Urine%20Sediment%20Preparation.pdf

3. With incontinent dogs – when would you consider looking for a UTI? I recently had a dog on stiboesterol for 5 years from another vet, owner said had been licking vulva for 5 (?!) years. I treated for UTI and she came off the pills. I felt so bad for the poor dog. So now when I am newly diagnosing an incontinent dog I always worry that they have a UTI primarily or as well as being incontinent.

Good question. I think it depends a bit on the reason for the incontinence. In most cases I would look when there are signs of a UTI. I tend to not look for infection unless they are showing signs of stranguria, dysuria or pollakiuria. Some of these clinical signs will cross over between UTI and incontinence. It would not be unreasonable to culture the urine of dogs in the initial phases of an incontinence work up.

4. Molly has Na:k ratio 27. What makes you not test for addissons? Simply because no clinical signs?

Indeed. I think we have to be careful with the Na:K ratio. It can be low for other reasons. I would only worry about Addison’s if there were other compatible signs.

5. Could you briefly go through the changes you would expect to see on bloods etc and pathway to diagnose pyelonephritis (temp?) and AKI (not anuric) please? I feel like these are the two I struggle with in practice.

Urinalysis not only is instrumental in the diagnosis of pyelonephritis, but it will also provide valuable information on possible comorbidities. In turn, this determines the need for additional diagnostic tests and is an important element for guiding the treatment plan. Sampling method, sample volume, and macroscopic evaluation should be noted, and will help with interpretation of final result. A routine urine examination generally includes refractometer determination of specific gravity and dipstick analysis for presence of at least glucose (combined with ketones) in view of predisposing factors.

Microscopic examination will help distinguish haematuria from haemo- (myo-) globinuria and could hold clues to help with localization (casts, different epithelial cells) and underlying disease (e.g., crystals, infection). Examination of stained, air-dried sediment can allow identification of white blood cells and potential causal agents (ranging from bacteria, yeasts, and fungal components to parasite ova). The magnitude of presumed renal proteinuria, which is measured by means of a urinary protein-to-creatinine ratio, is best assessed after urinary tract inflammation is addressed.

Assessing the haematocrit has no diagnostic value for pyelonephritis itself, but it can have an impact on patient management in view of suspected comorbidities, or when findings during physical examination were suggestive of either anaemia or erythrocytosis. Similarly, patients with pyelonephritis can display abnormal white blood cell counts ranging from leukopenia to (predominantly neutrophilic) leukocytosis. If characterized by a left shift, leukocytosis also can be indicative of secondary bacteraemia.

Whether cause or consequence, abnormal renal function is a common feature of pyelonephritis reflected not only in urinary abnormalities but also through serum electrolyte disturbances and possible development of azotaemia if both kidneys are involved. For those patients that show other comorbidities, a much wider range of parameters can become of interest; for example, in cases with glucosuria, plasma glucose levels will also be of interest.

I hope that helps!

Scott 🙂

Replying to Elaine K. 08/09/2022 - 10:03

Hello Elaine.

Welcome to the course. Great to have you onboard!!! Please let me know if you have any questions.

Scott 🙂

Replying to Josep B. 06/09/2022 - 10:01

Hello Josep.

So excited that you are part of our course. Neurology is such a challenging area for most of us and I am sure you will make the management of the neurological patient that little bit easier!

Scott 🙂

Replying to Lori D. 06/09/2022 - 13:15

Lori!

Really excited that you are joining us. I hope the course can help get you back in to the swing of the cats and dogs! Sounds like you have had a really interesting career. I am sure you could teach us a few things!

Let me know if you have any questions at any time.

Scott 🙂

Replying to Nicholas K. 05/09/2022 - 14:59

Hey Nick.

Hope you are well. Thank you so much for your great questions. Regarding Molly/CKD cases. I think it does vary with these cases as far as how often you need to run bloods. The are two main scenarios:

1. Not that often! There is a lot about these patients that will not change. Once they have been diagnosed with CKD, the renal parameters are not suddenly going to dramatically reduce with diet etc. I think I would be generally monitoring these patients every 3-6 months depending on clinical signs. Monitoring with bloods/urine is important as there are changes that can be acted on. If the patient becomes proteinuric, that can be treated. If the patient becomes hyperphosphataemic, that can be treated. If the patient becomes anaemia, that can be treated. Does that make sense?

2. Much more often! If the patient presents more acutely with renal disease, I would monitor bloods more. It is important to remember that patients with acute or acute on chronic renal problems might get better with initial fluid therapy, but they might also never go back to ‘normal’.

Regarding treatment with the PUPD patient while you are investigating. I would warn the owner from the start that the PUPD may be a persistent issue until you get right to the bottom of the problem. I would reassure them many of the DDX are not life threatening. There is no rush to diagnose Cushing’s disease! Most of the more serious issues would become evident more quickly. I would offer symptomatic treatment if needed (maropitant for vomiting/nausea).

Does that answer your question? I hope it helps.

Scott 🙂

• This reply was modified 2 years, 10 months ago by scott@vtx-cpd.com.