When blood results don’t match up what do you do? Ask our amazing specialists on the VetCT App for the answers!
But first let's see what you would do in this curious case:Phoenix, an 11yo ME Alaskan Malamute, presented for marked polyuria and polydipsia, but was otherwise reported to be clinically well, and his exam was unremarkable. His primary care veterinarian contacted VetCT to discuss some confusing biochemistry results.His story had begun several months earlier, after an at home dosing error of his longer term NSAID prescription for spinal pain. At this time he had developed gastrointestinal signs, and an acute kidney injury (AKI) and this was successfully managed with supportive care and normalisation of his creatinine was documented prior to discharge. An ACTH stimulation test had also been performed at that time to ensure hypoadrenocorticism was not a cause.Despite remaining clinically very well, his owner felt that water consumption was persistently increased since discharge and he had returned for further evaluation.Biochemistry results obtained at this more recent presentation showed azotaemia (magnitude consistent with IRIS Stage II CKD). Urine was found to be isosthenuric (USG 1.011), with an unremarkable sediment examination, a negative urine culture and a UPC of 0.1. However symmetric dimethylarginine (SDMA) concentration was within the normal reference range, which was an unexpected result leading to the case discussion.
- What do you know about SDMA and how it compares to measurement of creatinine?
- How would you interpret these results?
- What would your diagnostic and management recommendations be?
SDMA is an endogenous byproduct of protein metabolism that is excreted by the kidneys. It is generally considered a more sensitive marker of glomerular filtration rate than creatinine, increasing as early as 25% renal functional loss, with reliable increases usually seen at 40% loss. SDMA is also generally considered to be less affected by extra-renal factors such as body condition / lean mass, age and concurrent disease. SDMA is found to be increased in both acute and chronic kidney disease, but is not able to differentiate between these.
The finding of an increased creatinine, with a normal SDMA is unusual, but can occur with severe haemolysis resulting in a reduced SDMA, biologic and assay variability resulting in fluctuations at the upper end of the normal range, as well as in well compensated CKD patients.
In Phoenix’s case, progression to CKD following an AKI was still suspected as the most likely cause of presentation despite the disparate results, and given the combination of azotaemia, with isosthenuria and exclusion of other contributing factors. We discussed that it might be wise to further evaluate the abdomen with ultrasound to review the kidneys, and the prostate to further exclude pyelonephritis as a cause of both azotaemia and PU/PD, as well as to look for evidence of more chronic renal change.
Where disparate results are obtained, serial monitoring, assessment of urine concentrating ability and exclusion of other causes as discussed for this case can help clarify the situation.
Otherwise, discussion for Phoenix surrounded monitoring and management of probable CKD according to IRIS guidelines with the view of repeating a renal profile in 4 weeks to assess stability of the azotaemia, together with monitoring blood pressure, and repeating the UPC. A change to Phoenix’s pain protocol was also discussed such that NSAIDs were removed as a risk factor for ongoing renal injury.
The following article reviews current evidence for SDMA, and guidance on the clinical application for creatinine and SDMA, including the renal and non-renal influences that might affect interpretation.