Background: Clinical remission is frequent in cats with well-controlled diabetes mellitus, but few studies explored predictors of this phenomenon.Hypothesis: Data retrieved from medical records at admission might be valuable to identify likelihood of remission and its duration in diabetic cats.Animals: Ninety cats with newly diagnosed diabetes, followed-up until death or remission. Methods: Retrospective cohort study. Data were collected from records at admission, including history, signalment, physical examination, haematology, and biochemical profile, and the occurrence and duration of remission, defined as normoglycemia without insulin for !4 weeks. Predictors of remission were studied with univariate and multivariate logistic regression. Factors associated with remission duration were analyzed with Kaplan-Meier and Cox proportional hazard models.Results: Forty-five (50%) cats achieved remission, after a median time of 48 days (range: 8-216). By study end, median remission duration was 114 days (range: 30-3,370) in cats that died and 151 days (range: 28-1,180) in alive cats. Remission was more likely with higher age (OR: 1.23, 95% CI: 1.04-1.46; P 5 .01) and less likely with increased serum cholesterol (OR: 0.36, 95% CI: 0.11-0.87; P 5 .04). Remission was longer with higher body weight (HR: 0.65, 95% CI: 0.42-0.99; P 5 .04) and shorter with higher blood glucose (HR: 1.01, 95% CI: 1.00-1.02; P 5 .02).Conclusions and Clinical Importance: Age, body weight, cholesterol, and glucose levels are suggested for prediction of remission or its duration in diabetic cats. Older cats developing diabetes may have a better outcome, possibly suggesting a slower disease progression.
Cats with newly diagnosed diabetes mellitus had a fair to good prognosis. High serum creatinine concentration at diagnosis was associated with a poor outcome, likely because of the adverse effects of renal dysfunction. Ketoacidosis apparently was not associated with decreased survival time, suggesting that this complication should not necessarily be regarded as unfavorable.
The continuous glucose monitoring system allows generation of detailed glucose curves via measurement of glucose concentration in interstitial fluid. The conventional site for sensor placement in diabetic cats is the subcutaneous tissue of the lateral chest wall. The aim of this study was to investigate the feasibility and accuracy of sensors placed in the lateral chest wall and in two alternative sites -the dorsal neck and lateral knee fold -of diabetic cats. Initialisation was successful in 15/20 lateral chest wall sensors, 9/10 neck sensors and 3/10 knee fold sensors. Compared with the reference portable blood glucose meter, 0.8% of measurements from lateral chest wall sensors, 0.7% from knee fold sensors and 0% from neck sensors would have resulted in erroneous treatment. This preliminary study suggests that dorsal neck placement may be superior to lateral chest wall and lateral knee fold; however, further investigation with a larger number of cases would be required to confirm this finding.
BackgroundCats with diabetes mellitus can have subclinical pancreatitis but prospective studies to confirm this are lacking. Metabolic control of diabetic cats with pancreatitis is difficult.HypothesisSubclinical pancreatitis occurs in diabetic cats at the time diabetes is diagnosed or might develop during the follow‐up period, hampering diabetic remission.AnimalsThirty cats with newly diagnosed diabetes without clinical signs of pancreatitis on admission.MethodsProspective study. On admission and 2 and 6 months later, serum Spec fPL and DGGR‐lipase were measured and the pancreas underwent ultrasonographic examination. Pancreatitis was suspected if serum markers were increased or ≥2 ultrasonographic abnormalities were detected. Cats were treated with insulin glargine and diabetic remission was defined as euglycemia ≥4 weeks after discontinuation of insulin. Nonparametric statistical tests were used for analysis.ResultsSubclinical pancreatitis at the time of diagnosis was suspected in 33, 50, and 31% of cats based on Spec fPL, DGGR‐lipase and ultrasonography, respectively; and in 60% when diagnostic criteria were combined. During the follow‐up period, suspected pancreatitis developed in additional 17–30% cats. Only 1 cat had transient clinical signs compatible with pancreatitis. Seventeen of the 30 cats (57%) achieved remission. Frequency of abnormal Spec fPL and DGGR‐lipase and abnormal ultrasonographic findings did not differ in cats achieving remission and those who did not. Cats achieving remission had significantly lower Spec fPL at 2 months (P < .001).Conclusions and Clinical ImportanceBased on laboratory and ultrasonographic measurements, many cats with diabetes might have pancreatitis, although without clinical signs. Cats with high Spec fPL might have a reduced chance of diabetic remission; however, this topic needs further studies in large cohorts of diabetic cats.
Aim: A decrease in glomerular heparan sulfate (HS) proteoglycan (PG), without apparent decrease in HSPG core protein expression, has been reported to occur in diabetic nephropathy (DN). In most studies however, agrin, the major HSPG core protein in the glomerular basement membrane, has not been studied. This prompted us to study the glomerular expression of agrin in parallel to the expression of HS-glycosaminoglycans (GAG) in biopsies of patients with DN. Furthermore, the influence of glucose on agrin production in cultured podocytes and the expression of agrin in fetal kidneys was investigated. Methods: Cryostat sections of renal biopsies from patients with DN (n = 8) and healthy controls (HC, n = 8), were stained for agrin and HS-GAG. Sections of fetal kidneys were double stained for agrin and CD35 or CD31. Stainings were performed by indirect immunofluorescence (IIF). The production of agrin by cultured human podocytes was tested by ELISA and IIF. Results: The expression of agrin, detected by AS46, was significantly reduced in biopsies from patients with DN compared to HC (p < 0.01). Similar findings were observed when monoclonal antibody JM72 was used (p < 0.05). In addition, a significant reduction in the glomerular expression of HS-GAG was detected with JM403 in these patients (p < 0.01). Agrin is expressed in cultured podocytes, the expression hereof was reduced when the cells were cultured in the presence of 25 mM D-glucose (p < 0.01). In biopsies of human fetal kidneys, glomerular expression of agrin coincided with the expression of CD31. In early stages of glomerular differentiation there was a strong staining for agrin and CD31 while CD35 was only slightly positive. Conclusions: Our data argue against a selective dysregulation in HSPG sulfation in DN, but suggest a pivotal role for hyperglycemia in the downregulation of agrin core protein production.
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