Granulomatous Myocarditis Caused by Candida Spp Infection in a Spontaneously Diabetic Torii Rat.

Background: Myocarditis refers to myocardial inflammation with necrosis caused by non-infectious of infectious agents such as bacteria, fungi, or drugs. Candida is known to cause myocarditis in healthy and immunocompromised individuals. Diabetes mellitus causes chronic hyperglycemia due to impaired secretion or hypofunction of insulin, induces a compromised state, and increases the risk of contracting various infections. Objective: We report a case of granulomatous myocarditis caused by Candida in a Spontaneously Diabetic Torii rat, a non-obese diabetic model. Case report: A male SDT rat, 61 weeks of age, was housed in conventional environment. The rat was provided a commercial diet and tap water ad libitum. The heart was sampled and prepared the specimen of hematoxylin-and-eosin-, Sirius-red-, Giemsa-, Grocott-stain. Histologically, formation of large granulation tissue was observed in the left ventricular wall. A center of the foci showed necrosis. Moreover, inflammatory cells infiltration and fibrous component were increased surrounding the foci and between myocardial cells. A Grocott and Giemsa staining-positive cell masses occasionally appearing in the foci were considered to be Candida because of their characteristic form. Conclusion: The development and progression of myocarditis were potentially related to a diabetes-induced compromised state.

Effects of salt supplementation in uninephrectomized KK-Ay mice: Examining the potential of a diabetic kidney disease model.

Diabetic kidney disease (DKD) is the leading cause of end-stage renal disease (ESRD). Although current therapeutic strategies for DKD, including sodium-glucose cotransporter-2 inhibitors and mineralocorticoid receptor antagonists, have shown some degree of efficacy, they have failed to completely halt the progression of DKD to ESRD owing to the complexity of DKD pathogenesis. Elucidating the pathophysiological mechanism of DKD is essential for the development of novel therapeutic strategies. In this study, we investigated the pathophysiological characteristics of uninephrectomized (UNx) KK-Ay mice and examined the effects of salt supplementation on the acceleration of renal injury in these mice. UNx KK-Ay mice exhibited pathophysiological renal abnormalities with glomerular and tubulointerstitial fibrosis. Additionally, salt supplementation exacerbated renal injury, particularly tubular injury. These results suggest that UNx KK-Ay mice are useful models for advanced DKD and that salt exacerbates tubular damage in DKD.

Effects of excessive sodium chloride loading in the spontaneously diabetic torii (SDT) fatty rats, a preclinical model of type 2 diabetes mellitus.

Type 2 diabetes mellitus represents an international health concern with its growing number of patients worldwide. At the same time, excessive salt consumption is also seen as a major cause of diseases such as hypertension and may expedite renal complications in diabetic patients. In this study, we investigated the effects of excessive sodium chloride supplementation on the kidney of the Spontaneously Diabetic Torii-Leprfa (SDT fatty) rat, an obese type 2 diabetes model. Male and female SDT fatty rats and normal Sprague-Dawley (SD) rats at 5 weeks of age were loaded with 0.3% sodium chloride (NaCl) in drinking water for 13 weeks. Blood serum and urinary parameters were observed throughout the experiment and kidney samples were examined in histopathological and genetical analyses. Significant changes on the body weight, blood pressure, urine volume, creatinine clearance, blood urea nitrogen (BUN), relative gene expressions of tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), monocyte chemotactic protein-1 (MCP-1) and transforming growth factor-ß (TGF-ß) were observed in the salt-loaded male SDT fatty rats. Urinary L-type fatty acid-binding protein (L-FABP) and albumin levels were higher observed in the salt-loaded male SDT fatty rats throughout the period, but urinary albumin levels in the female SDT fatty rats remain unchanged. In the kidney, slight Armani-Ebstein changes, tubular degeneration, hyaline cast, and inflammatory cell infiltration were observed in female SDT fatty rats while the levels of some changes were higher in the salt-loaded group. The kidney of the salt-loaded male SDT fatty rats demonstrated a higher degree of lesions compared to the female group and the male unloaded group. Histopathological changes in salt-loaded SDT fatty rats show that excessive salt consumption may act as a diabetic pathology exacerbation factor, but the pathology may be influenced by gender difference. Urinary L-FABP levels may act as a useful biomarker to detect slight tubular damages in the kidney. Excessive salt loading was shown to exacerbate the renal injury in SDT fatty rats.