Title: 2015 ACVIM Forum Research Abstract Program Document date: 2015_5_27
ID: 3pnuj5ru_635
Snippet: Caloric intakes were similar between diets (P = 0.83). In the table, superscripts indicate significant differences between diets (Scheffe adjustment for test multiplicity). The kidneys play an important role in magnesium homeostasis and the renal handling of magnesium is highly adaptable, and when renal function declines significantly, increase in serum magnesium is detected. However, hypomagnesemia is also common in chronic kidney disease (CKD) .....
Document: Caloric intakes were similar between diets (P = 0.83). In the table, superscripts indicate significant differences between diets (Scheffe adjustment for test multiplicity). The kidneys play an important role in magnesium homeostasis and the renal handling of magnesium is highly adaptable, and when renal function declines significantly, increase in serum magnesium is detected. However, hypomagnesemia is also common in chronic kidney disease (CKD) in human, and it has been associated with the development of vascular calcification and the poor clinical outcomes. Most of studies of serum magnesium concentrations in veterinary medicine were related to a few diseases such as feline and canine diabetes mellitus, canine parvoviral enteritis, and protein-losing enteropathy in dogs, but so far, there is no data in dogs with CKD. The goal of this study was to evaluate the serum total magnesium in dogs with chronic kidney disease in stages 2 and 3 (IRIS). Sixteen CKD dogs were included in the study (stage 2, n = 6; stage 3, n = 10), and they were followed-up for two to 12 months, and the measurements of serum total magnesium (kit MG3880, Randox) were performed monthly. Serum total magnesium was also measured in 10 clinically normal dogs (mean AE SD; 2.24 AE 0.31 mg/dL); the normal range considered for this study was from 1.93 to 2.55 mg/dL. Mean of serum magnesium concentrations in CKD dogs stage 2 and stage 3 were 2.32 mg/dL (SEM AE 0.10) and 2.40 mg/dL (AE 0.07), respectively. Hypermagnesemia (>2.55 mg/ dL) was detected in all dogs in stage 2 (6 out of 6) and in 8 out of 10 (80%) dogs in stage 3, and it was noticed at some point of the follow-up, and usually it was associated with the highest level of serum creatinine. Hypomagnesemia (<1.93 mg/dL) was detected in 5 out of 6 dogs (83%) in stage 2 and in all dogs (100%) in stage 3 at some point, and usually it was detected in the beginning of the follow-up. No correlation was observed between serum magnesium and serum urea, creatinine, ionized calcium, total calcium, bicarbonate and phosphorus. In conclusion, magnesium may be considered as an indicator or a marker of progression of CKD in dogs, since the impairment of renal function may result in hypermagnesemia, as it has been observed in humans with CKD. In other hand, it has been well proven that in humans and rats, hypomagnesemia is associated with faster deterioration of kidney function and vascular calcification. The role of magnesium in dogs with CKD has not been investigated yet, and its clinical importance could be underestimated. Thus, additional studies are needed for the better understanding of magnesium in the pathophysiology of mineral metabolism in dogs with chronic kidney disease. To prospectively evaluate the perioperative outcome of cats with benign ureteral obstructions undergoing ureteral stenting with a secondary goal of comparing to similar cases undergoing ureterotomies.
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