Chronic kidney disease can be treated if it is detected early, but as the disease progresses, it becomes impossible to recover. Finally, renal replacement therapy such as transplantation or dialysis should be used. Ultrasonography is used to diagnose kidney cancer, inflammatory disease, nodular disease, and chronic kidney disease. It is used to identify information about degree of inflammation using information such as kidney size, internal echo characteristics. Currently, the degree of disease in the clinic uses the value of glomerular filtration rate. However, even in ultrasound, changes in the degree of inflammation and disease can be observed. In this study, we used ultrasound images to quantify the changes in brightness, size, cortex, and subclinical changes of the kidney with progression of the disease, and compared them with the glomerular filtration rate used in clinical practice . In 105 cases, we performed 35 cases of normal kidney, 35 cases of early kidney disease, and 35 cases of terminal kidney. The brightness of the cortex of the image was obtained and the difference in brightness between the cortex and the proximal portion was obtained by the slope. The graph of the portion which was not smooth due to the ultrasonic characteristics was used as the function regrass. The size reduction was obtained from the original data. The results were as follows: It was proportional to the glomerular filtration rate. It is considered that the algorithm can be applied to the disease if the algorithm study continues.

This is the case report of a 58-year-old man who developed acute severe hypoglycemia after a spinal block. He had a history of injecting insulin combined with 50% dextrose for hyperkalemia control. After the spinal block, he presented with hypo-glycemic symptoms and went into convulsions. Following injection of midazolam and 10 ml of 50% dextrose, his mental state returned to alert. We recommend careful monitoring of blood sugar level of chronic kidney disease patients who under-go neuraxial block.

A 72-year-old woman with diabetic chronic kidney disease visited the authors’ hospital with fever, dysuria, and left flank pain. She did not complain of typical angina upon her admission, however, given the presence of a new-onset left-bundle branch block, elevated cardiac enzymes, and documented E. coli septicemia, coronary angiography and percutaneous coro-nary interventions were performed for the mid-left anterior descending artery and the mid-to distal-right coronary artery. We should keep in mind that urosepsis in patients with diabetic chronic kidney disease, who are at high risk of cardiovascular disease, can be associated with painless acute myocardial Infarction.

The activation of protooncogenes or the inactivation of their gene products may be a specific and effective functional study for human neoplasia. To examine this possibility, we have used the tetracycline regulatory system to generate transgenic mice that conditionally express the HccR-2 protooncogene in vivo. The new human cervical cancer protooncogene (HccR-2) was detected from cervical cancer cell line. To elucidate its biological functions, we generated transgenic mice that expressed the HccR-2 gene. The sustained expression of the HccR-2 transgene culminated chronic neutrophilic leukemia (CNL). CNL is a rare chronic myeloproliferative disorder that presents as a sustained, mature neutrophilic leukocytosis with few or no circulating immature granulocytes, the absence of peripheral blood monocytosis, basophilia, or eosinophilia, and infiltration of neutrophils at the liver, spleen and kidney. Mice expressing the HccR-2 and tetracycline-transactivating protein (tTa) transgene were found to have altered myeloid development that was characterized by increased percentages of mature neutrophil and band form neutrophil in the peripheral blood, liver and spleen. Activation of the transgene causes CNL. In our model, expression of HccR-2 transgene mice was similar in many respects to the human CNL. This model will be valuable not only for investigating the biological properties of the HccR-2 and other protooncogenes in vivo but also for analyzing the mechanism involved in the progression of CNL.