BACKGROUND Diabetic nephropathy is the most common cause of end-stage renal disease and it has various pathologic features. We investigated the clinicopathologic differences between the histologic classes of diabetic nephropathy. METHODS A total of 46 patients with diabetic nephropathy were evaluated. Morphologically, the renal lesions were divided into three categories: class 1, diffuse or nodular glomerulosclerosis: class 2, vascular change without evidence of glomerulosclerosis: and class 3, non-diabetic renal disease superimposed on diabetic glomerulosclerosis.
We evaluated the laboratory findings and the histologic findings, including mesangial expansion, interstitial fibrosis and inflammation, arteriolar hyalinosis and tubular atrophy. RESULTS The proportion of each class was 32 cases (70%), 4 cases (9%) and 10 cases (21%), respectively. The clinical and laboratory data showed no significant difference among the classes. For the groups of class 1, the group with nodular sclerosis showed a higher serum creatinine level than did the diffuse group (p=0.003). IgA nephropathy was the most common non-diabetic renal disease superimposed on diabetic glomerulosclerosis in our study. CONCLUSIONS The patients with nodular glomerulosclerosis presented with a more progressed clinicopathological features than did the patients with class 1 diffuse glomerulosclerosis. We also found 21% of all the patients with diabetic nephropathy had superimposed non-diabetic renal disease in a Korean population.
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Lymphocytic hypophysitis is an autoimmune disorder of the pituitary gland which usually occurs in a woman in the postpartum period. Diabetes insipidus is not a major clinical feature of this disorder. We report a case of a 22-year-old man with lymphocytic hypophysitis which presented with diabetes insipidus and also involved his cavernous sinus. This represents the seventh reported and the youngest case of a man with lymphocytic hypophysitis. A comparative study of all six male patients is also presented. We suggest diabetes insipidus should be added to the spectrum of clinical manifestations of this disorder.
To investigate the relationship between insulin response and morphometric changes of the mitochondria of pancreatic beta-cell, this study was performed using hyperglycemia and streptozotocin as oxidative stresses.
Adult and neonatal rats were used. Intravenous glucose tolerance test (IVGTT) and morphologic examination of pancreas using immunohistochemical stain, in situ end-labeling method and electron microscopic study were performed. Various mitochondrial parameters were measured by image analyzer. Immunohistochemical stain revealed a markedly reduced islet size and decreased number of beta-cells and the increased number of non-beta-cell in adult and neonatoal streptozotocin group, and the appearance of insulin positive cells throughout the exocrine parenchyma in neonatal streptozotocin group.
Three days after injection of streptozotocin in adult streptozotocin group, TUNEL stain showed increased apoptotic cells in islets. Ultrastructurally, beta-cells in adult streptozotocin group showed increase in number and size of mitochondria, and disruption of mitochondrial structures.
Hyperglycemic group and neonatal streptozotocin group showed preserved mitochondrial ultrastructure. Ultrastructural morphometric study revealed increase in size and number of mitochondria and decrease in mitochondrial contour index in adult streptozotocin-treated rats, which suggested mitochondrial degeneration. Hyperglycemic group showed mild increase in size of mitochondria.
Increased number of mitochondria was also observed in neonatal streptozotocin group. IVGTT revealed marked decrease in insulin response in adult streptozotocin group, and non-insulin-dependent diabetes mellitus pattern in glucose and insulin response in neonatal streptozotocin group.
Hyperglycemic group showed a glucose and insulin response similar to control group.
The above results suggest that a severe oxidative injury may cause degeneration and disruption of mitochondria of pancreatic beta-cell, and may be associated with substantial apoptotic cell death. The changes in the morphology and the number of mitochondria may result from streptozotocin treatment within neonatal period and hyperglycemia treatment, which may be associated with changes in insulin response.
In this study the effect of insulin and aminoguanidine on the expression of iNOS and the development of insulitis in the multiple low dose streptozotocin (SZ) induced diabetic (LDSD) mice was evaluated. Eighty mice (Charles-River CD-1 mice) were divided into four groups. Group I received SZ for five days.
Group II received SZ for five days and was followed by insulin treatment. Group III received SZ for five days and was followed by aminoguanidine treatment. Group IV was normal control group. The blood glucose level and body weight were measured weekly. On the 35th day, pancreat ic sections were observed to evaluate the frequency and the severity of insulitis in addition to the immunohistochemical expression of iNOS in the pancreatic islets. Blood glucose levels of group IV were significantly lower than other experimental groups on the 21st, 28th, and 35th day. The difference in blood glucose levels was not statistically significant. Incidence of the insulitis was lower in group II than in groups I and III. The severity of insulitis correlated with the increase in blood glucose level only in group II.
The expression of iNOS was more pronounced in group I than in groups II and III.
Aminoguanidine did not inhibit development of the insulitis but decreased expression of iNOS in the pancreatic islets. Therefore it is speculated that iNOS production is one of the factors and other pathogenetic mechanisms might be involved in the development of insulitis.
Diabetic mastopathy is a clinicopathologic entity which was first described as a dense fibrous breast mass in insulin-dependent diabetes mellitus. The purpose of this article was to document diabetic mastopathy histologically which had been diagnosed as fibrocystic disease and to avoid unnecessary surgical procedures in breast mass simulating malignancy in diabetic patients. We examined eight excisional breast biopsies from seven patients. Three diabetic patients with type I insulin-dependent diabetes mellitus presented with bilateral (2 patients) or unilateral (1 patient) rapidly growing palpable breast masses. Four patients with type II noninsulin-dependent diabetes mellitus presented with bilateral (2 patients) or unilateral breast mass (1 patient). One patient had no symptoms. All of them had late complications of diabetes mellitus such as nephropathy, neuropathy and retinopathy. Mammographic findings such as ill- defined mass density and asymmetric increased density suggested malignancy. However, all of them had been diagnosed as fibrocystic disease. On review, the most consistent pathologic finding was keloid-like stromal fibrosis. Others were ductitis or ductulitis, thickening of basement membrane of ducts or ductules, mononuclear perivasculitis and lobulitis. Six of eight breast satisfied all five criteria for diabetic mastopathy.