scott@vtx-cpd.com

Replying to Anna M. 13/05/2025 - 09:31

Hi Anna,

The connection between hypothyroidism and fructosamine lies in how thyroid hormone levels influence protein metabolism, particularly albumin turnover. Fructosamine reflects the average blood glucose over the preceding two to three weeks by measuring the degree of glycation of circulating proteins, especially albumin. In hypothyroid dogs, there is a reduction in protein turnover, including albumin, which can result in artificially elevated fructosamine levels that do not accurately reflect glycaemic control. This can make it appear as though a diabetic dog is poorly regulated when, in fact, glucose levels may be acceptable.

So in dogs with concurrent hypothyroidism and diabetes, fructosamine may overestimate average blood glucose, particularly if the hypothyroidism is not well controlled. For monitoring these patients, I generally recommend placing greater emphasis on home blood glucose curves or using continuous glucose monitoring if available, as these provide real-time data that are not influenced by protein metabolism. It’s also important to ensure that the hypothyroidism is well managed and that T4 levels are within the therapeutic range before placing much weight on fructosamine values. If fructosamine is used, it should be interpreted cautiously and in the context of clinical signs, body weight trends, and serial blood glucose data, rather than in isolation.

I hope this helps clarify the connection, and I’d be happy to discuss further if helpful. Let me know how you are getting on with the course.

Best regards,

Scott 🙂

Replying to Jane Sedgewick 06/05/2025 - 16:46

Hi Jane,

Great question! t’s something many of us are wrestling with as SDMA becomes a routine part of senior wellness panels. I completely agree, identifying early kidney changes is only worthwhile if we know what to do with that information, and the evidence on early intervention, particularly before azotaemia, is still catching up. IRIS Stage 1 CKD is now formally recognized and includes patients with persistent renal changes like proteinuria or elevated SDMA in the absence of azotaemia. While we don’t yet have large prospective studies showing that intervention in these cases extends lifespan, there is growing support for the idea that earlier detection allows us to modify risk factors and potentially slow progression. Interventions might include addressing proteinuria with ACE inhibitors or ARBs even before creatinine rises, ensuring optimal hydration (especially in older or low body condition dogs), and, in selected cases, adjusting diet to moderate phosphorus and protein intake, though timing of dietary change is still a debated topic.

That said, in real-world clinical practice, I rarely find myself asking for SDMA unless it’s already included in a panel. Most of the dogs I see already have obvious disease, and if they’re azotemic, then SDMA really adds little, its value as an early biomarker becomes moot.

But for earlier-stage cases, especially the older dog who “seems well” but turns up with a borderline USG and mildly elevated SDMA, it does prompt more thoughtful discussion. Ideally, I think SDMA is most useful when paired with urine findings and muscle condition score as part of a broader screening protocol. A persistently elevated SDMA across timepoints, particularly in the presence of proteinuria or low USG, is much more convincing than a single raised value. That layered context helps distinguish signal from noise and guides whether to start more frequent monitoring, recommend dietary changes, or even consider ACE inhibition pre-emptively.

Are you seeing more cases now where SDMA is elevated in isolation? How are you deciding when to act and when to wait?

I hope you are having a lovely weekend.

Scott 🙂

Replying to Yvonne McGrotty 10/05/2025 - 16:40

I consider Britney to be a legend too… she is still in her 40’s!

Scott 🙂

Replying to Jane Sedgewick 06/05/2025 - 20:07

Hey Jane.

I am really pleased you enjoyed the session. Yvonne is a bit of a legend!

I will make sure she sees this.

Scott 🙂

Replying to Kerida Shook 06/05/2025 - 00:23

Hi Keri,

Thanks so much for your thoughts. There were definitely some interesting features on these radiographs, and you picked up on several areas that also caught our attention.

The final radiology report describes a multifocal, bilaterally symmetric, moderate-to-severe unstructured interstitial to alveolar pulmonary pattern, particularly cranioventrally and caudodorsally, with border effacement of pulmonary vasculature and mild vessel dilation. There was no mention of mineralization or calcification within the lung fields, though I agree that there are regions that could give that impression, especially where patterns coalesce.

The stomach contents are described as containing a moderate amount of gas and a small amount of heterogeneous soft tissue opaque material, considered to be normal ingesta. No concerns were raised regarding obstruction or abnormal foreign material.

With regard to the kidneys, the report notes a few pinpoint, irregularly shaped mineral foci in the region of the right renal pelvis and mildly undulating renal cortical margins bilaterally, which could indicate chronic cortical infarcts. There is no mention of overall renal enlargement, though I agree that the contour changes are noticeable.

The radiologist’s interpretation favors left-sided congestive heart failure secondary to cardiomyopathy as the most likely cause for the pulmonary pattern, with other differentials including pneumonitis (such as from asbestos exposure), pneumonia, acute lung injury, or pulmonary hemorrhage. Vitamin D toxicity and fungal disease were not specifically discussed, but I agree those are valid considerations given the pattern and your impression of possible mineralization.

Blood work has been submitted and we’re waiting on results. Depending on what that shows, a BAL could still be helpful if cardiogenic causes are ruled out or if there’s a non-resolving component. For now, we’re prioritizing echocardiography to clarify the cardiac silhouette and vascular findings.

And yes, standing strong and still very much not the 51st state! Thanks again for engaging with the case, and I’ll let you know what the next steps reveal.

Best,

Scott

Replying to Alison M. 05/05/2025 - 21:02

Hi Alison,

Thanks so much for your comment. I’m really glad you found the session helpful.

You’re certainly not alone in checking BP at diagnosis but not always following up. It’s a common challenge in busy practice, especially when the initial reading is normal and the cat appears clinically stable. That said, we do recommend regular blood pressure monitoring for all hyperthyroid cats, regardless of treatment path, and that includes those who undergo definitive treatment like radioactive iodine or surgery.

Even after successful treatment, some cats can remain at risk for developing hypertension later on, particularly if there’s underlying renal disease or if they were borderline hypertensive to begin with. I typically suggest checking BP at each recheck visit during the initial treatment phase (for example, every 2 to 4 weeks if on methimazole) and then every 3 to 6 months long term once they’re stable. For cats who have had I-131 or thyroidectomy, I still aim for 3 to 6 monthly BP checks, at least for the first year, then tailored based on the individual.

Hope that helps, and great to hear you’re thinking of incorporating this more routinely.

Best,

Scott

Replying to Liz Bode 05/05/2025 - 19:45

Welcome Liz!

Fancy seeing you here!

Scott 🙂