Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A child developed steroid-responsive nephrotic syndrome at the age of 3 years. 6 years later, he developed insulin-dependent diabetes mellitus. At this time renal biopsy disclosed minimal-change disease. After multiple relapses requiring cyclophosphamide or repeated courses of steroid therapy, a second renal biopsy, 5 years after the first, revealed early diabetic changes with associated exudative lesions. The nephrotic syndrome remains responsive to steroids and cyclophosphamide, and the patient maintains an increased glomerular filtration rate and normal blood pressure 3.5 years afterwards. His HLA typing showed DR4 and DR7. Since DR4 and DR7 are associated with diabetes and minimal-change disease, respectively, we speculate that he could carry the genetic predisposition for the development of both diseases.
Nephron 1987
PMID:Steroid-responsive relapsing nephrotic syndrome associated with early diabetic glomerulopathy in a child. 360 Sep 16

To elucidate the nature of the abnormality of elastin metabolism in arteriosclerosis, we determined the elastase-type activity in the human radial artery of patients with chronic renal failure due to glomerular disease and diabetes. Elastase-type activity was determined by HPLC analysis of the hydrolyzed products of succinyl-trialanine-4-nitroanilide, a sensitive synthetic substrate for elastase. Three kinds of hydrolyzed products, (L-Ala)2-NA, L-Ala-NA and NA, were found after incubation of the substrate with human radial artery in the presence of amastatin (an inhibitor of aminopeptidases). We assumed the activity that liberates NA to be an elastase-type activity because purified human aorta elastase liberates NA from the substrate. The pH optima of the human artery and rat aorta activities were 6.0 and 6.8, respectively. The elastase activity in human radial artery and rat aorta was inhibited by diisopropyl phosphofluoridate, a serine protease inhibitor, and by elastatinal, an elastase inhibitor. The elastase-type activity in the radial artery of patients with chronic renal failure was significantly lower than that of the control group, and the decrease was especially marked in the patients with juvenile onset diabetes. These results suggest that the elastin metabolism is abnormal in the radial artery in diseases that tend to cause atherosclerosis.
Nephron 1986
PMID:Elastase-type activity in human radial artery in patients with chronic renal failure. 363 13

Renal biopsies were obtained from 164 patients with diabetes mellitus. Their histological changes were evaluated together with clinical findings and prognosis. In 36 patients, various types of glomerulonephritis were complicated: mesangial proliferative glomerulonephritis (17 patients), membranous glomerulonephritis (8), endocapillary proliferative glomerulonephritis (5), membranoproliferative glomerulonephritis (4) and minimal change nephrotic syndrome (2). Superimposed glomerulonephritis was suspected in diabetic patients with a short history of less than 5 years, persistent proteinuria, occasional hematuria and no retinopathy. They may, however, produce little effects on the long-term prognosis of diabetic patients except membranoproliferative glomerulonephritis.
Nephron 1986
PMID:Glomerulonephritis in diabetic patients and its effect on the prognosis. 370 65

It is proposed that stiffened red cells can interfere with normal microvascular and glomerular function. In diabetics intrinsic stiffening of red cells is intensified during poor metabolic control when plasma osmolarity is increased. Hypoxia, acidosis, catecholamines and other changes in red cell environment also increase red cell stiffness. Exercise proteinuria may help to identify individuals with the greatest intrinsic stiffening of red cells which appears to be due to the disposition of spectrin molecules rather than to changes in the lipid bilayer. Stiffened red cells may impede blood flow in the microcirculation and stimulate an autoregulated vasodilation which increases perfusion pressure, enhancing transudation. In the absence of vasodilation, stasis will lead to vascular occlusion and localised ischaemic necrosis. If diabetic microangiopathy is caused by abnormal haemorheology then the possibility exists that the complications of diabetes might be alleviated or prevented by agents which enhance red cell flexibility and improve blood rheology.
Nephron 1985
PMID:Intrinsic stiffening of red blood cells as the fundamental cause of diabetic nephropathy and microangiopathy: a new hypothesis. 388 63

Peritoneal permeability to proteins was measured in diabetic and non-diabetic continuous ambulatory peritoneal dialysis patients during peritonitis and control periods. Clearances of albumin, transferrin, IgG, C3 and alpha 2-macroglobulin appeared to decrease as molecular weight increased. This relationship could be described by a power curve fit. The decrease was more than could be explained by differences in free diffusion only, indicating a size-selective barrier in the peritoneum. For all measured proteins clearances were higher in the diabetic patients. This may reflect a generally increased permeability due to their microangiopathy. The largest increase in protein loss and protein clearances was found during peritonitis. Our results do not suggest increased local production of any of the investigated proteins during the inflammation. Therefore, an increase in either peritoneal permeability or effective surface area or both is the most likely explanation. It is concluded in this study that peritoneal protein clearances are dependent on their molecular weight and that they are proportionally increased in patients with diabetes and during peritonitis.
Nephron 1986
PMID:Peritoneal permeability to proteins in diabetic and non-diabetic continuous ambulatory peritoneal dialysis patients. 394 51

The parathyroid gland responsiveness to hypocalcemia induced by short-term calcium-free hemodialysis in patients with insulin-dependent diabetes mellitus was investigated in comparison with 10 nondiabetic uremic patients and compared with test results from the autonomic nervous system. Diabetic patients had lower C-terminal parathyroid hormone (cPTH) levels before hemodialysis than uremic control patients and showed a significantly smaller increase in cPTH during hypocalcemia. The neurological tests revealed severe disturbances of the autonomic functions in the diabetic group. In conclusion, the disturbances observed in the parathyroid secretory pattern are probably caused by gland dysfunction; it is hypothesized that the defective autonomic nervous system has an additional effect on the development of this hormonal dysfunction.
Nephron 1986
PMID:Diminished parathyroid gland responsiveness to hypocalcemia in diabetic patients with uremia. 396 Feb 40

Disturbances of peripheral and autonomic nervous system function were evaluated in 37 normal subjects, in 52 patients with non diabetic chronic renal insufficiency (25 predialysis patients, 27 dialysis patients), and in 21 patients with diabetic chronic renal failure (10 predialysis patients, 11 dialysis patients). In nondiabetic patients, the predialysis group showed abnormal test results indicating parasympathetic lesions, in dialysis patients these derangements were nearly normalized. In predialysis diabetic patients, the autonomic alterations were much more extensive, corresponding to alterations of electroneurographical findings; in addition to parasympathetic lesions, sympathetic disturbances were seen. In contrast to the nondiabetic groups, in dialysis patients a deterioration of autonomic lesions was observed. In conclusion, these data indicate that deranged autonomic functions are common in uremia; they improve in dialysis patients with nondiabetic renal failure in contrast to diabetic patients; in this group the autonomic functions worsen in dialysis patients as a function of duration of diabetes and hemodialysis.
Nephron 1985
PMID:Autonomic neuropathy in chronic renal insufficiency. Comparative analysis of diabetic and nondiabetic patients. 403 42

The clinical features of 88 patients who developed carpal tunnel syndrome (CTS) in association with end stage renal failure and chronic hemodialysis were studied (11 original cases and 77 collected from the literature). Hemodialysis-associated CTS was found to have a 2 to 1 male predominance, to occur more often in angioaccess-bearing (86%) than in unoperated arms (48%) (p = 0.005), and to require surgical release of the median nerve in most of the cases (86%). The analysis of 48 of these patients revealed two patterns of presentation. Patients with the 'early pattern' (41.6%) developed CTS within 1 year of commencing hemodialysis; diabetes mellitus and/or severe polyneuropathy were present in at least 40%. In contrast, patients with the 'late pattern' (58.4%) developed symptoms after at least 1 year on hemodialysis; diabetes mellitus and/or polyneuropathy were present in less than 10%. CTS should be considered in any hemodialysis patient with upper extremity neurological symptoms; early diagnosis and treatment will prevent loss of hand function.
Nephron 1985
PMID:Hemodialysis-associated carpal tunnel syndrome. A clinical review. 403 44

In order to investigate the influence of diabetes mellitus on immune complex-mediated nephritis , we produced Heymann nephritis in streptozotocin-induced diabetic rats (DM-HN group) in which the clinical course for 24 weeks and histological changes were examined. Nondiabetic rats with Heymann nephritis (HN group) and diabetic rats (DM group) were also examined as controls. The degree of proteinuria, hypoproteinemia, hyperlipidemia and anemia were more pronounced and the mortality rate was higher in the DM-HN group than in the HN group or in the DM group. Histologically, larger and more subepithelial or intramembranous electron-dense deposits as well as a more markedly thickened glomerular basement membrane (GBM) were observed in the DM-HN group than in the HN group. In conclusion, the nephrotic manifestations and histological changes in the GBM in Heymann nephritis were augmented by the association with diabetes mellitus.
Nephron 1984
PMID:Autologous immune complex nephritis in streptozotocin-induced diabetic rats. 623 73

Collagenolytic activity of rat kidneys with streptozotocin diabetes was estimated by means of a biological collagenase assay and compared to healthy controls. Collagenolytic activity was found significantly decreased in rat kidneys with diabetes correlating with blood glucose levels (r = -0.82, p less than 0.001). Elevated blood glucose levels seem to be responsible for the inhibition. This is supported by our experiment of incubating bacterial collagenase with several carbohydrates as glucose, galactose and saccharose: glucose and galactose significantly inhibited the collagenolytic activity, while saccharose failed to inhibit the enzymatic reaction. The interpretation of the results is that glucose is able to bind to the enzyme as Schiff base, which could be shown by tritiated sodium borohydride reduction of the Schiff base formed between collagenase and glucose. Another support of the hypothesis is that blocking of the amino group of lysine at the active site either by glucose or trifluoroacetylation of collagenase is reducing the collagenolytic activity. The biological significance could be the decreased catabolism of collageneous material of the extracellular matrix, as, e.g., the glomerular basement membrane, which was reported in a previous publication.
Nephron 1982
PMID:Reduced collagenolytic activity of rat kidneys with steptozotocin diabetes. 628 20


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