A re-evaluation of diabetic glomerulo-sclerosis 50 years after the discovery of insulin

Bloodworth, J. M. B.

doi:10.1016/s0046-8177(78)80029-x

Cited by 63 publications

(38 citation statements)

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“…Because in our study proliferated intramembranous cells forming enmeshed or reticular structures were relatively immature according to their morphological characteristics and accompanied by the basement membrane-like structure, it is thought that they are derived from local mesenchymal cells. Bloodworth (1978) regarded proliferated cells as mesangial cells, but in the present study these proliferated cells could not be identified clearly as endothelial or mesangial cells by their morphological characteristics at least in the early stage. Therefore, we instead used the term "intramembranous cells" defined as the cells enclosed by the glomerular basement membrane.…”

Section: Discussioncontrasting

confidence: 80%

“…It was unclear, however, whether the cell proliferation is found or not in the early stage of nodular lesion formation. Bloodworth (1978) demonstrated transition phases between the large open microaneurysms completely filled with red blood cells and the mature Kimmelstiel-Wilson nodule, and presented that the proliferating mesangial cells push laterally into the microaneurysm which initially is quite cellular and contains fine fibers or fibrils and osminophilic granular deposits between the cells. The features of this lesion seems to correspond to those of the enmeshed or reticular structure in this study.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, axially accumulated cells without facing blood stream may acquire more characters of mesangial cells, while peripherally situated cells lining recanalized blood spaces may become to have more endothelial natures. Bloodworth (1978) regarded the cell proliferations showing the reticular structure as the organization of microaneurysm and considered that some unknown injury or stimulus causes disruption of anchor points. On the other hand, Saito et al (1988) regarded the reticular structure as the result of mesangiolysis, probably due to glomerular ischemia caused by arteriolosclerosis.…”

Section: Discussionmentioning

confidence: 99%

“…Bloodworth (1978) postulated that large Kimmelstiel-Wilson nodules are formed by the organization of the glomerulocapillary microaneurysms caused by disruption of so-called "anchor points". Saito et al (1988) suggested the concept of "mesangiolysis" as a developmental process of nodular lesions without microaneurysm formation, in which loosening and dissociation of the mesangial matrix…”

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confidence: 99%

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Disorganization process in the development of diabetic nodular glomerulosclerosis.

Shioi

Fujimoto

1989

Tohoku J. Exp. Med.

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In order to clarify the mode of development of the diabetic nodular glomerulosclerosis, 38 kidney specimens of autopsied and biopsied diabetic cases were studied light and electron microscopically including serial sections. Disorganization process occurred chiefly at the capillary region of glomeruli. Early change of this process was proliferation of intramembranous cells following histolysis in the glomerular loop and it was characterized by transformation of the glomerular loop into enmeshed or reticular structure, that is, disorganization of the glomerular architecture. In the subsequent stage intercellular matrix production and hyalinization accompanied by axial crowding of proliferated intramembranous cells and peripheral recanalization of blood spaces were clarified. And in the later stage axially crowded intramembranous cells decreased in number and the matrix was increased and hyalinized, resulting in the formation of the axial hyaline nodule. The distribution of this process was focal and segmental, lesions of various stages coexisted, and it was suggested that glomerular lesions may spread all over the kidney by recurrence of this process. This process was quite similar to those seen in disorganization process of glomerulonephritis. But another characteristic changes were the presence of foam cells, intra-and intercellular deposition of lipid droplets, and increased matrix formation. diabetic nodular glomerulosclerosis ; disorganization ; recurrence ; lobular glomerulonephritis Diabetic nodular glomerulosclerosis, which was first described by Kimmelstiel and Wilson (1936), is thought to be the most characteristic lesion in diabetic nephropathy.In the recent decades it has been proposed that lytic changes in glomerular loops may play an important role in the morphogenesis of this lesion. Bloodworth (1978) postulated that large Kimmelstiel-Wilson nodules are formed by the organization of the glomerulocapillary microaneurysms caused by disruption of so-called "anchor points". Saito et al. (1988) suggested the concept of "mesangiolysis" as a developmental process of nodular lesions without microaneurysm formation, in which loosening and dissociation of the mesangial matrix

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Section: Discussioncontrasting

confidence: 80%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Disorganization process in the development of diabetic nodular glomerulosclerosis.

Shioi

Fujimoto

1989

Tohoku J. Exp. Med.

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“…In the kidneys, the microvascular alterations, i.e. glomerulosclerosis (GS), were graded according to the following scheme [19]: slightly diffuse GS (1); moderately diffuse and <50% nodular GS (2); severely diffuse and moderate GS with>10% hyalinosis (3); and severe GS with over 50% hyalinosis (4). Comparison of the graded vascular changes of the pancreas and kidney revealed close correlation between 1 + pancreatic microangiopathy and GS (1) and (2), and 2 + microangiopathy and GS (3) and (4) (r = 0.73).…”

Section: Methodsmentioning

confidence: 99%

Residual insulin positivity and pancreatic atrophy in relation to duration of chronic Type 1 (insulin-dependent) diabetes mellitus and microangiopathy

1987

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Summary.The relationship of residual insulin positivity in chronic Type I (insulin-dependent) diabetes and atrophy of the exocrine pancreas to duration of diabetes, age at onset and microangiopathy was studied in 26 patients (disease duration 2 to 54 years, mean 26 years). Islets containing insulin cells were found in 13/26 pancreata. In 5/13 pancreata insulin positive cells were detected in only one lobule, while in 8/13 insulin positivity was multifocal. All patients with diabetes duration less than 11 years had residual insulin cells; whereas, the rate of insulin positivity was near 40% with diabetes duration of more than 11 and 21 years, respectively. Survival of insulin cells was not clearly related to age at onset. HLA-DR expression on insulin cells was seen in one case. lnsulitis was lacking. Pancreatic volume determined in 18 patients ranged from 14-110ml (age adjusted mean 56.3 ml) and was significantly less than that of control subjects (age adjusted, mean 89.9 ml, p < 0.0001). Computerized morphometry of the exocrine pancreas revealed severe acinat atrophy due to a reduction in size of acinar cells. Acinar atrophy correlated neither with the degree of insulin positivity, disease duration nor severity of microangiopathy. The findings suggest that in about 40% of patients with Type 1 diabetes a small population of insulin cells may escape autoimmune destruction, irrespective of disease duration or age at onset. Though exocrine atrophy and insulin deficiency are associated, the variable extent of pancreatic atrophy could not to be related to such factors as amount of surviving insulin cells, duration of diabetes or microangiopathy.Key words: Chronic Type 1 (insulin-dependent) diabetes, residual insulin cells, exocrine atrophy, HLA-DR expression, diabetic microangiopathy.Loss of insulin cells characterises the islet lesions in patients with Type 1 (insulin-dependent) diabetes mellitus [1][2][3][4]. This loss, however, need not to be complete, since B cells, though severely reduced, have been demonstrated even in patients with a diabetes duration up to 37 years [1,3], The mechanisms which may protect some insulin cells from destruction by the autoimmune process underlying Type I diabetes are largely unkrlown.Another finding that characterises the pancreas in chronic Type 1 diabetes is a reduction in weight and volume [3,[5][6][7][8]. The pancreatic atrophy is attributed to the lacking trophic effect of insulin on the acinar cells [2,3,[9][10][11][12][13]. The extent of the exocrine atrophy, however, appears to vary considerably from patient to patient and has not yet been related to the remaining insulin positivity in the pancreas, to diabetes duration or to the degree of microangiopathy. * Presented in part at the 22 nd EASD meeting in Rome, 1986 ** Present address: Department of Pathology, Free University of Brussels, BelgiumThe aim of the present study was to investigate the degree and distribution of residual insulin positivity in the pancreas of patients with long-standing Type 1 diabetes by immunocyt...

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The History of Diabetes Mellitus

Tattersall

2016

Textbook of Diabetes

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A re-evaluation of diabetic glomerulo-sclerosis 50 years after the discovery of insulin

Cited by 63 publications

References 3 publications

Disorganization process in the development of diabetic nodular glomerulosclerosis.

Disorganization process in the development of diabetic nodular glomerulosclerosis.

Residual insulin positivity and pancreatic atrophy in relation to duration of chronic Type 1 (insulin-dependent) diabetes mellitus and microangiopathy

The History of Diabetes Mellitus

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