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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinicopathologic studies of four patients with juvenile diabetes mellitus and renal disease demonstrated the pathogenetic variability of nephropathy in diabetic patients. Only in one patient was the clinical nephropathy associated with the typical diabetic glomerulosclerosis. Another patient had steroid responsive nephrotic syndrome superimposed on minimal diabetic glomerulosclerosis. A third patient had steroid resistant nephrotic syndrome associated with mild diabetic glomerulosclerosis and with later appearance of Grave's disease. The fourth patient, in addition to moderate diabetic glomerulosclerosis had prominent tubulointerstitial nephritis, the latter probably being responsible for the rapidly declining renal function. The poor prognosis associated with diabetic nephropathy warrants a careful search for other potentially treatable causes of nephropathy in patients with juvenile diabetes mellitus.
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PMID:Etiologic variability of nephropathy in juvenile diabetes mellitus. 58 80

Spontaneous diabetes mellitus, observed in a colony of guinea pigs, parallels in many ways the syndrome known as juvenile diabetes mellitus in man: elevated blood glucose levels; reproductive dysfunction in the female; degranulation and severe cytoplasmic vacuolation of beta cells, severe fatty degeneration of acinar cells, and hyperplasia of the islets of the pancreas; and a high frequency of abnormal pancreatic secretions. Islet-cell necrosis and insulinitis usually seen in viral infections was not observed. Microangiopathy, another characteristic of juvenile diabetes mellitus in man was demonstrated as a significant increase in the thickness of the basal membranes in peripheral capillaries. A glomerular lesion encountered in some of the diabetic guinea pigs was shown to be similar to the glomerular sclerosis seen in human diabetics. Although a definitive etiologic agent was not identified, the disease was clearly contagious in origin.
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PMID:The guinea pig as an animal model of diabetes mellitus. 59 30

The case history and the autopsy findings of a 44-year-old women who died shortly after her flight to Khartoum (Sudan) in a hospital is presented. The clinical diagnosis in Africa was "shock caused by gastroenteritis". The body was embalmed thoroughly and brought back to Germany. The autopsy was performed just prior to the cremation (according to "section 3 Abs. 2 Nr. 2 Feuerbestattungsgesetz"). Morphological findings (nodular glomerulosclerosis and glycogen nephrosis with Armanni-Ebstein-cells) and postmortem biochemical analyses of vitreous humour led to the diagnosis of a hyperglycaemic coma. The fatal course might have been prevented by sufficient health information to the patient (who suffered from type 1 diabetes); the diagnostic errors in the hospital could have easily been avoided by careful anamnesis and diagnostic procedures.
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PMID:[Fatality in diabetic coma during foreign travel]. 128 47

Lytic changes to the mesangium and subendothelial area in diabetic glomerulosclerosis were studied by electron microscopy with an emphasis on the mechanism of nodule formation. Renal biopsy specimens were obtained from 30 diabetics (11 males, 19 females; 27 NIDDM, 3 IDDM; mean age, 52.2 years) with renal involvement. Evaluations were made of the glomerular lesions, particularly the ultra-structural findings contributing to nodule formation, mainly by electron microscopy. Varying degrees of lytic change, such as a loose and edematous mesangial matrix, widening of the subendothelial space, followed by endothelial detachment, and destruction of anchor points, were observed in close association with progression of the diffuse lesions. Plasma proteins were found to infiltrate into the widened subendothelial space. Mesangial cells also protruded into the same space and encroached around the whole capillary wall. The interposed mesangial cells were occasionally separated from the basement membrane. Monocytes identified from their ultrastructure were frequently present noticed in the lytic areas, suggesting a reaction to lytic changes. These processes may occur repeatedly with direct expansion of the mesangial matrix, subsequently revealing a nodular appearance.
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PMID:Early mesangiolysis and monocyte influx observed in diabetic glomerulosclerosis: relation to nodule formation. 203 30

Nephron loss is a common progression of a diverse range of kidney diseases. Recent experimental models of chronic renal disease have suggested that hemodynamic and nonhemodynamic mechanisms play key roles in progressive renal injury. Extensive renal ablation in the rat was followed by development of altered glomerular hemodynamics. Albuminuria and histologic damage leading to focal glomerulosclerosis were preceded by the development of increased glomerular pressures and were prevented by interventions such as severe dietary protein restriction and angiotensin-converting enzyme (ACE) inhibitor therapy. Both experimental interventions ameliorated glomerular hypertension. It was therefore concluded that these interventions ameliorated injury by glomerular hemodynamic effect. Similar findings were obtained in a rat model of type I diabetes mellitus induced by streptozotocin in which glomerular hemodynamic factors appeared important to the development of progressive renal disease. Recent studies have suggested that nonhemodynamic factors have important roles in the progression of glomerular injury. For example, although the predominant effects of ACE inhibitor therapy appear to be hemodynamically mediated, data are emerging which suggest that these agents may also influence growth/proliferation of glomerular cells. Because hyperplasia/hypertrophy may influence glomerular susceptibility to injury, this may also be a potential mechanism whereby ACE inhibitor therapy influences glomerular damage. In addition, a variety of studies have suggested that hyperlipidemia, which is frequent accompaniment of glomerular disease, is an important modulator of glomerular injury independent of glomerular hemodynamic effects. Coagulation factors, calcium phosphorus balance, as well as the genetic susceptibility of the glomerulus to injury, all appear to contribute to progressive nephron destruction.
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PMID:Renal protective effects of angiotensin-converting enzyme inhibition. 218 11

At present the pathogenesis of diabetic nephropathy remains unresolved. Clearly lack of insulin, with its associated disorders of carbohydrate, protein, and/or lipid metabolism, initiates the process which eventually leads to the characteristic histologic picture of diabetic nephropathy. The disturbance in cellular metabolism per se could directly injure the kidney by altering the energy needs of the cell or by leading to the accumulation of cellular toxins (ie, polyols) or by causing the deficiency of key cellular metabolites (ie, myoinositol). Elevation of the plasma glucose concentration enhances the glycosylation of proteins, which in turn can lead to glomerular basement membrane thickening, loss of charge selectivity, and direct cellular damage. The multiple disturbances in intermediary metabolism are associated with increased levels of and/or enhanced sensitivity to a variety of growth factors, including IGF-I and angiotensin, and this could lead to glomerular hypertrophy. An increase in the filtered load and subsequent reabsorption of electrolytes and metabolites also could contribute to renal hypertrophy. In all animal models of nephropathy, including diabetes, glomerular hypertrophy has been shown to be the best correlate of glomerular sclerosis, proteinuria, and progressive renal deterioration. The potential mechanisms by which glomerular hypertrophy can lead to renal histologic damage were discussed previously. By increasing the luminal diameter, glomerular hypertrophy also would be expected to augment wall tension and thereby increase intraglomerular pressure. Derangements in cellular metabolism or altered sensitivity to angiotensin also can directly elevate the intraglomerular pressure and lead to structural renal damage. In this schema, elevated intraglomerular pressure is but one of many pathogenic factors that contribute to the development of diabetic glomerulopathy and albuminuria. The precise role of increased glomerular pressure in the evolution of diabetic nephropathy remains uncertain at present. In rats, severe diabetic nephropathy can occur without an increase in Pgc, while in humans, hyperfiltration does not appear to be a predictor of proteinuria and renal dysfunction. Lastly, it is likely that a variety of other factors, including the coagulation system, plasma/cell lipid levels, prostaglandins, etc, also play a role in the pathogenesis of diabetic nephropathy. According to the outline presented in Figure 1, it is unlikely that any single factor will be sufficient to explain the development of diabetic glomerulosclerosis. Ultimately, the origin of diabetic nephropathy in IDDM must be traced to insulin lack, with its associated derangements in cellular metabolism. Therefore, the importance of tight glucose control should not be underemphasized.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hyperfiltration and diabetic nephropathy: is it the beginning? Or is it the end? 219 Feb 80

Insulin-dependent diabetes mellitus (IDDM) results from the destruction of pancreatic beta cells. Viruses have been suggested as one of the possible causes. The evidence for viruses comes largely from experiments in animals, but several studies in humans also point to viruses as a trigger of this disease in some cases. Encephalomyocarditis (EMC) virus, Mengovirus (2T), and Coxsackie B4 virus infect and destroy pancreatic beta cells when inoculated into mice. This results in hypoinsulinemia and hyperglycemia. The development of EMC virus-induced diabetes is dependent on the genetic background of the host and genetic makeup of the virus. Animals with diabetes for several months show some long-term complications, including glomerulosclerosis, ocular changes, and decreased bone formation and mineralization in addition to acute metabolic changes. EMC virus-induced diabetes can be prevented by a live-attenuated vaccine. The capacity of Coxsackie B4 virus to induce diabetes is also influenced by the genetic background of the host. However, Mengovirus-induced diabetes is not dependent on the genetic background of the host. In contrast to the EMC, Mengo, and Coxsackie B4 viruses, reovirus type 1 seems to be somehow associated with an autoimmune response producing a diabetes-like syndrome in suckling mice. This virus produces an autoimmune polyendocrinopathy that results in very mild and transient glucose intolerance. Several common human viruses including mumps, Coxsackie B3 and B4 viruses, and reovirus type 3 can infect human beta cells in culture and destroy them. A variant of Coxsackie B4 virus has been isolated from the pancreas of a child who died of acute-onset IDDM.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Perspectives on the role of viruses in insulin-dependent diabetes. 299 65

The time course of the blood level of C-peptide was studied in 20 patients with insulin dependent diabetes mellitus in the course of 1 year after human fetal pancreatic islet cell allotransplantation. All the recipients suffered from a labile type of diabetes complicated by polyneuropathy, glomerulosclerosis and progressive retinopathy. C-peptide concentration was determined by a radioimmunoassay using Behring-Werke AE kits (FRG). The recipient were divided into 3 groups with relation to the preoperative level of C-peptidemia (with a low level 0.17 +/- 0.06 ng/ml, a mean level 0.9 +/- 0.11 ng/ml and a high level 3.07 +/- 0.24 ng/ml). One-two days before cell culture allotransplantation the mean concentration of C-peptide was 0.3 +/- 0.02 ng/ml. One-two weeks after transplantation it rose up to 0.89 +/- 0.11 ng/ml (p less than 0.01), by the end of the 1st month it reached 2.85 +/- 0.54 ng/ml, in 2-3 months it was lowered up to 1.98 +/- 0.21 ng/ml and remained at this level in the next months decreasing up to 1.4 +/- 0.36 ng/ml and approximated the preoperative levels by the end of the year. The same time course was noted in all 3 groups irrespective of the preoperative levels and differed in quantitative indices only. Stabilization of a course of disease, normalization of some biochemical indices, disappearance or weakening of a degree of concomitant symptoms and a decrease in an exogenous dose of insulin were noted.
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PMID:[Changes in the C-peptide concentration in the blood of patients with diabetes mellitus after the transplantation of cultures of pancreatic islet cells]. 314 6

A retrospective study was done on 109 diabetic patients who had renal biopsies during 1974-1984 to determine factors identifying nondiabetic renal disease in patients with diabetes mellitus presenting with renal dysfunction. Six of 49 (12%) patients with type I and 17 of 60 (28%) with type II diabetes mellitus had other renal diseases, with or without diabetic glomerulosclerosis. Multivariate predictors of other renal disease in type I diabetes mellitus were duration less than 5 years (p less than 0.001), absence of proteinuria (p less than 0.001), and absence of neuropathy (p less than 0.05). In type II diabetes mellitus these were late age of onset (p less than 0.001), absence of neuropathy (p less than 0.05), and Caucasian race (p less than 0.005). Some patients with other diseases appeared to respond to therapy directed at their nondiabetic glomerulosclerosis disease. We emphasize the need to distinguish between the subgroup of diabetic patients with nondiabetic renal disease from the majority who have diabetic glomerulosclerosis alone. The latter group should be spared the discomforts, risks, and costs of a renal biopsy.
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PMID:Clinical identification of nondiabetic renal disease in diabetic patients with type I and type II disease presenting with renal dysfunction. 323 94

In 42 patients with insulin dependent diabetes mellitus of average and grave forms with preserved glomerular renal function without signs of dehydration and hypovolemia renal function was investigated by maximum osmotic urine concentration (on dry food for 36 h) which was assessed on the basis of maximum osmolarity of urine and renal capacity for osmotic dilution of urine (on the 2nd hour after water load per os, 20 ml per 1 kg of body mass) assessed on the basis of the clearance of osmotically free water from 100 ml of the glomerular filtrate. Disorder of function of osmotic urine concentration revealed in 1/4 th of the patients, was moderate; it was most frequent in complication of disease with diabetic glomerulosclerosis, less frequent in diabetic angiopathies and was absent in patients without vascular lesion. Disorder of the capacity of the kidneys for osmotic urine dilution was revealed in 50% of the patients, it was probably of functional nature and was mainly associated with raised permeability of nephron distal segments for water.
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PMID:[Osmoregulatory function of the kidneys in diabetes mellitus]. 360 87


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