scott@vtx-cpd.com

Replying to Amy Arbuthnott 12/09/2022 - 18:05

Hey.

We generally use standard microscope cleaning wipes, nothing fancy. As far as a more comprehensive clean, you normally would have to send them away.

Scott 🙂

Replying to Victoria Rubasinska 13/09/2022 - 10:49

That is why it stuck out to me!

I am surprised it is the first report like this!

Scott 🙂

Replying to Andrea Scott 11/09/2022 - 20:09

Andrea!

Lovely to hear from you! How interesting, what was you masters in?

Scott 🙂

Replying to Kelly M. 11/09/2022 - 21:29

Hello Kelly.

I hope you are well. The pathophysiology of post obstructive diuresis is quite complicated and not fully understood. There is evidence that POD is partially caused by downregulation of aquaporin-2 (AQP2). Aquaporins (AQP) are active water carriers that are mainly responsible for the transport of water in the renal medullary collecting duct (MCD), and this downregulation is probably caused by temporary resistance against the antidiuretic hormone arginine vasopressin (AVP). POD could be considered a form of acquired nephrogenic diabetes insipidus. The pathophysiology of AVP resistance is complex and includes the release of atrial natriuretic peptide (ANP) induced by atrial stretch due to hypervolaemia as well as an obstruction-induced increase in cyclooxygenase-2 in the kidney, which leads to the elevated production of prostaglandin E2 (PGE2), and to the impairment of the cyclic adenosine monophospate-regulated expression of AQP and urea transporters (UT) located in the MCD. Changes in intrarenal haemodynamics due to obstruction apparently play an important role, as do increases in nitric oxide and catecholamines. Whether a change in blood pH also has a direct effect on the expression of AQP in the mammalian MCD has not yet been researched. However, there is evidence that AQP in certain plants reacts to changes in the intracellular pH. Besides, acidaemia has recently been suggested to worsen brain oedema by playing a role in AQP1 downregulation. Thus, acidaemia might causally contribute to the pathogenesis of POD by its suspected effect on the translocation of AQP2 to the apical membrane of the MCD. Of the other circulating factors that have often been discussed to play a part in the pathogenesis of POD, particular emphasis has been set for sodium and BUN. Owing to the impaired ability of the obstructed kidney to reabsorb sodium, natriuresis has often been found to occur simultaneously with diuresis in POD.

I hope that helps!

Scott 🙂

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:

https://semintra.co.uk/

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 🙂