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)

Nephrotic syndrome developed in a 45-year-old white woman who had insulin-dependent diabetes mellitus. Following diuretic therapy and intravenous infusions of albumin, painful induration developed in the thighs and abdomen. A biopsy of the affected subcutaneous tissue demonstrated interstitial deposition of calcium. In this case of calcifying panniculitis, the conditions for calciphylaxis appear to have been present.
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PMID:Calcifying panniculitis associated with renal failure. A case of Selye's calciphylaxis in man. 707 8

We determined antibody titers to Endostreptosin (ESS), a recently described protein antigen in the cytoplasm and the plasma membrane of Group A streptococci in 286 normals of different age groups and in 34 children and 19 adults who had or had had at one time a nephrotic syndrome due to idiopathic nephrosis. Antistreptolysin O titers were also determined in 33 of the idiopathic nephrotics. Similarly, antibody titers to Streptozyme were determined in 21 patients with idiopathic nephrosis and 61 normals with a similar age distribution. Severe depression of these antibody titers was found in almost all patients with this disease not only during the presence of a nephrotic syndrome but for long periods up to 20 years following an episode of a nephrotic syndrome when the patients were in complete remission. Patients with a nephrotic syndrome due to chronic glomerulonephritis (5), S.L.E. (4), membranous nephropathy (5), diabetes mellitus (1) or amyloidosis (1) did not show abnormally low values for antibodies to Endostreptosin, Streptolysin O or Streptozyme. High-dose steroid medication as such for prolonged periods of time does not depress Endostreptosin or Streptolysin O antibody titers below the expected mean, as demonstrated in 15 patients with S.L.E.
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PMID:Depression of endostreptosin, streptolysin O and streptozyme antibodies in patients with idiopathic nephrosis with and without a nephrotic syndrome. 724 25

Type V hyperlipoproteinemia is an unusual entity in children. Only 6 cases have been described so far to our knowledge. Authors present a 9 year old male that came for diagnosis of a hepatosplenomegaly. There was no evidence of abdominal pain, xanthomas or pancreatitis. Secondary disorders such as uncontrolled insulinopenic diabetes mellitus, glycogen storage disease, administration of estrogen compounds, nephrotic syndrome or uremia, and dysglobulinemias were excluded. His father presented the same lipoprotein pattern suggesting a dominant mode of inheritance. The administration of heparin showed a good response of serum proteinlipase.
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PMID:[Primary hyperlipoproteinemia in childhood (author's transl)]. 728 88

The present study described 3 patients with idiopathic membranous glomerulonephritis associated with diabetes mellitus. Clinical characteristics of the 3 patients contrasted with diabetic glomerulosclerosis in the following manner: absence of diabetic retinopathy and neuropathy, and presence of nephrotic syndrome associated with relatively short duration of diabetes mellitus. Renal histology showed the characteristic changes of membranous glomerulonephritis along with those of diabetic glomerulosclerosis. Immunofluorescent studies demonstrated a granular pattern of IgG and C3 deposits along the glomerular capillary wall. Electron microscopic study also demonstrated thickening of glomerular basement membrane and increase of mesangial matrix as well as the presence of electron-dense deposits primarily in the subepithelial and mesangial areas.
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PMID:Idiopathic membranous glomerulonephritis associated with diabetes mellitus: light, immunofluorescence and electron microscopic study. 730 Oct 1

A graded sieving procedure was used to isolate glomeruli and tubules from renal cortex of men of premature age up to 80 years and of 4 patients suffering from Zellweger syndrome, congenital nephrotic syndrome, polycystic renal disease or diabetes mellitus. Glomerular and tubular basement membranes (GBM and TBM, respectively) were obtained with a detergent procedure. Purity of basement membrane preparations was controlled with light and electron microscopy and by estimating total phosphorus content. Amino acid and carbohydrate composition of the basement membranes were determined and statistically evaluated. Comparison of GBM and TBM from the same kidneys showed at all ages that GBM contains more 3-hydroxyproline, neuraminic acids and mannose. These differences may contribute to the different immunogenic properties of the two basement membranes reported in the literature. Significant changes with age in the chemical composition were found, suggesting that the proportion of collagenous peptide moieties increases and that of noncollagenous peptide moieties decreases with age in both GBM and TBM. In addition, the hydroxylation grade of proline and lysine increases significantly with age reaching an adult level for GBM after 4-6 months of age and for TBM at late childhood. The age-related changes in basement membrane composition may influence functional properties of these extracellular renal structures. The chemical composition of GBM and/or TBM of the 4 patients showed some differences in comparison to control preparations from persons with ages approximating that of the patients.
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PMID:Variations in chemical composition of human glomerular and tubular basement membranes with age and disease. 732 36

Three adults with diabetes mellitus and nephrotic syndrome of recent onset underwent renal biopsies because of certain unusual clinical features. Despite heavy proteinuria, one patient had no evidence of diabetic retinopathy, one had preservation of normal renal function, while the third had sudden onset of renal failure. Microscopic examination of renal biopsy material disclosed pure membranous nephropathy in one, membranous nephropathy and nodular glomerulosclerosis in two. Because of significant differences in the natural history of these two glomerulopathies and the possible beneficial effects of steroid therapy in membranous nephropathy, we suggest that renal biopsies be performed in diabetic patients having persistent hematuria, sudden onset of renal failure, massive proteinuria without azotemia, retinopathy, or other evidence of microvascular disease, to uncover superimposed and treatable disorders that may influence the course of renal disease.
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PMID:Idiopathic membranous glomerulonephritis in diabetic patients: report of three cases and review of the literature. 739 88

Chronic uremia caused by diabetic glomerulopathy accounts for about 25 percent of new patients treated by maintenance hemodialysis. At the onset of glucose intolerance, insulin dependent diabetics have larger than normal kidneys, with a markedly increased glomerular filtration rate. During the subsequent 15 to 20 years of insulin use, glomerulosclerosis progresses silently, until a clinically overt nephrotic syndrome becomes evident. Thereafter, the clinical manifestations of nephropathy appear rapidly with an exponential decline in creatinine clearance to less than 5 ml/min within one to five years. Putting together a life plan for a nephrotic and azotemic diabetic involves awareness, and coordinated management of not only renal but extrarenal vasculopathic complications of diabetes, especially proliferative retinopathy. Carefully made preparations for hemodialysis and/or renal transplantation with increase changes for at least a short-term favorable outcome, which can now be anticipated in a growing proportion of patients.
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PMID:Uremia in diabetics: the prognosis improves. 745 92

We report here two cases of mixed cryoglobulinemia showing renal involvement associated with hepatitis C virus (HCV) infection. The subjects were 62- and 63-year-old males. Both patients presented with purpura on the legs, which was diagnosed as allergic vasculitis by skin biopsy. Case 1 followed a clinical course of progressive nephrotic syndrome with mild hematuria. He also had diabetes mellitus and hypertension. In contrast, case 2 showed only mild hematuria without proteinuria at the time of the renal biopsy. Both cases had immunological disarrangements, such as severe hypocomplimentemia and seropositive rheumatic factor. Recently, it was reported that patients with type II mixed cryoglobulinemia had HCV seropositivity, and revealed membranoproliferative glomerulonephritis. These facts strongly suggested that renal lesions are the result of direct damage mediated by cryoglobulinemia and an activated complement pathway through an immune complex mechanism related to HCV.
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PMID:[Glomerular lesion in patients with type II mixed cryoglobulinemia having antibodies to hepatitis C virus]. 747 12

It has recently been suggested that immunotactoid glomerulopathy be separated from much more common fibrillary glomerulonephritis by ultrastructural features of highly organized immune deposits containing tubules of more than 30 nm in diameter. We report and discuss the results of a light, immunofluorescence and electron microscopic study of a needle renal biopsy from a 75-year-old, non-insulin dependant diabetic female presented with nephrotic syndrome, hypertension and a progressive renal failure. A unique coexistence of nodular glomerulosclerosis, as traditionally ascribed to diabetes with a peculiar type of immunotactoid glomerulopathy was confirmed by the exclusion of amyloidosis, monoclonal gammopathies, systemic autoimmune diseases and cryoglobulinemia. Mesangial, scattered subepithelial and segmentally prominent subendothelial immune deposits were found highly organized in mostly parallel arrays of 40 to 91 nm thick tubules. The average thickness of 67 nm exceeds the average diameter of tubules in all other 11 published cases of immunotactoid glomerulopathy to date. By immunofluorescence, predominantly capillary wall, thick, ribbon-like glomerular deposits contained IgG, IgM, kappa and lambda light chains of equal intensity, C3, C4 and fibrin related antigens. Mild to moderate glomerular cell proliferation associated with nodular sclerosis has been assumed to be causally related to immunotactoid deposits.
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PMID:Immunotactoid glomerulopathy with unusually thick extracellular microtubules and nodular glomerulosclerosis in a diabetic patient. 747 81

During the past decade, experimental and clinical evidence has indicated an important role for the renin-angiotensin system in the progressive destruction of nephrons in a wide variety of chronic renal diseases. Studies have indicated that in the subtotally nephrectomized rat model of progressive glomerulosclerosis, in experimental diabetes mellitus, in the chronic phase of puromycin aminonucleoside-induced nephrotic syndrome and in Heymann's nephritis, angiotensin-converting enzyme (ACE) inhibitors dramatically preserve both nephron structure and function. Clinical studies have similarly noted that chronic administration of ACE inhibitors inhibits progression of renal failure in type I diabetes and type II diabetes as well as primary glomerulopathies, sickle cell nephropathy, systemic lupus erythematosis, chronic pyelonephritis and adult polycystic kidney disease. Current evidence suggests that the beneficial effect of ACE inhibitors is primarily due to inhibition of angiotensin II production, and there is strong suggestive evidence for increases in local intrarenal activation of the renin-angiotensin system in these conditions. In obstructive uropathy, activation of the renin-angiotensin system has also been shown to be an important aspect of the early functional changes and may be of importance in the subsequent generation of interstitial fibrosis. In the obstructed kidney, renin and angiotensinogen production increase and type I angiotensin receptors decrease. Inhibitors of angiotensin II production and angiotensin II action partially reverse the vasoconstriction and the reduced renal blood flow, and abolish the changes in expression of AT1 MRNA induced by obstruction. Studies suggest that the angiotensin-mediated increases in tubulointerstitial fibrosis may be mediated by increased production of transforming growth factor-beta.
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PMID:Angiotensin II-mediated renal injury. 756 81


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