scott@vtx-cpd.com
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Replying to Emma Hunter 19/09/2022 - 15:29
Welcome Emma!
So pleased to have you on board and good to hear you are enjoying the course!
Scott 🙂
Replying to Felipe M. 15/09/2022 - 21:38
Felipe!
Thank you so much for joining us. It is such an honor to have you be involved with the course.
Scott 🙂
Replying to Mary S. 16/09/2022 - 09:35
Hello Mary.
Sorry you were not able to attend. We will make the recording available and it will be displayed like the other lessons.
We will do this ASAP and let you know when it is ready.
Scott 🙂
Replying to sara h. 15/09/2022 - 21:18
Really lovely to meet you!
Thank you so much to everyone for your brilliant contribution!
Scott 🙂
Replying to Emma Holt 14/09/2022 - 15:40
Good questions!
The following is helpful treatment wise:
”Parenteral amino acid supplementation is the treatment of choice for improving skin lesions in animals with an underlying hepatopathy (Hnilica, 2011). 10% crystalline amino acid solution, or 3% amino electrolyte solution, both at a dose of 25mL/kg intravenously are administered over eight hours. This treatment is repeated every seven to 10 days with improvement in skin lesions to be expected within one to three weeks. A less effective alternative (Hnilica, 2011) is oral supplementation with three to six raw egg yolks per day together with zinc and essential fatty acid supplementation”.
I will look in to where the amino acids are sourced from. As far as I remember you can use the amino acid portion of TPN bags.
Will get back to you.
Scott 🙂
Replying to Amy Arbuthnott 12/09/2022 - 17:59
I know… poor puppy!
Interesting case though.
Scott 🙂
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 Andrea Scott 12/09/2022 - 20:55
Brilliant!
We will know where to direct all of our bacteria related questions!
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 Victoria Rubasinska 13/09/2022 - 10:56
Hey.
I do think this is possibly most relevant at initial catheter placement. This is a good opportunity to get some blood and this is something we have been doing more routinely. I am also less sure about doing it when the IV line has been in and had fluids etc. going in. I suppose it is good to know it is an option in really tricky cases.
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 scott@vtx-cpd.com 12/09/2022 - 17:46
All great questions Kelly!!!!
There are indeed live Q&A sessions which are recorded to watch back. Would be lovely to see you live if you can make it!
Regarding the coagulation and proteinuria. Again, not straightforward. Because emboli may be difficult to detect, the prevalence of thromboembolism in dogs with glomerular disease may be higher than indicated. The risk of thromboembolism is highest in dogs with nephrotic-range proteinuria and hypoalbuminemia. Pulmonary thromboembolism is most common, but emboli may also lodge in other arteries (e.g., mesenteric, renal, iliac, brachial, coronary) or the portal vein. Although urinary loss of antithrombin (AT) has gained the most attention in veterinary medicine, the pathogenesis of the hypercoagulable state is multifactorial. AT is a serine protease inhibitor that modulates fibrin generation; heparin catalyzes these reactions. AT (65,000 Daltons) is similar in charge and size to albumin (69,000 Daltons); serum AT activity closely correlates with the serum albumin concentration. Prior studies have suggested that this close correlation can be used to predict thromboembolism when the serum albumin concentration is <2 g/dL, when serum AT III activity would be expected to be less than 75% of normal. Albumin binds to arachidonic acid, which, if unbound, would stimulate platelet aggregation through the generation of prostaglandins (i.e., thromboxane B2); hypoalbuminemia is associated with increased platelet aggregation. Hypercholesterolemia contributes to platelet hypersensitivity by influencing membrane-associated enzyme and receptor activity through alteration of the membrane composition. The role of platelet hypersensitivity in the development of hypercoagulability may be enhanced by thrombocytosis, which occurs in many animals with glomerular disease. Increased fibrinogen concentrations (i.e., above 300 mg/dL), which are often present in patients with NS, lead to increased fibrin complex formation and platelet hyperaggregation. The risk of thromboembolism may be further enhanced by increased concentrations of alpha2 macroglobulin; alpha2 antiplasmin; procoagulant cytokines; coagulation factors V, VII, VIII, and X; increased plasma viscosity and interstitial pressure; decreased plasma plasminogen concentrations; decreased plasma volume and blood flow; endothelial injury; and infections.
I hope that helps.
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 🙂
Just a wee note to say that the wonderful Helen has been a guest on our podcast:
Do check it out!
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:
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.
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