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)

Isolated rat renal glomeruli incorporate radioactive sulfate into glycosaminoglycans, which are integral components of the glomerular basement membrane. Cellulose acetate electrophoresis and specific enzymatic sensitivities of glycosaminoglycans prepared after pronase digestion of purified glomerular basement membrane indicate the presence of heparan sulfate. We examined the effect of experimental diabetes on the incorporation of [(35)S]-sulfate into glycosaminoglycans deposited into newly synthesized glomerular basement membrane in vitro. Basement membranes were purified from glomeruli isolated from normal and streptozotocin-diabetic rats after incubation for 2 hr with radiolabeled sulfate and then were subjected to pronase digestion for isolation of the glycosaminoglycans. [(35)S] incorporation into basement membrane glycosaminoglycans was significantly decreased in glomeruli from diabetic animals. The addition of insulin (100 micron U/ml) in vitro did not affect [(35)S] incorporation into glycosaminoglycans of the glomerular basement membranes in normal or diabetic glomeruli. High glucose concentration (5 vs. 20 mM) was without effect in short-term incubations of glomeruli from normal animals. The results indicate that experimental diabetes influences [(35)S] sulfate incorporation into glomerular basement membrane glycosaminoglycans and suggest that decreased heparan sulfate production and/or sulfation may contribute to the increased permeability of the glomerular basement membrane in diabetes.
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PMID:[(35)S]sulfate incorporation into glomerular basement membrane glycosaminoglycans is decreased in experimental diabetes. 702 93

Our objective was to determine whether patients with chronic renal failure requiring maintenance hemodialysis retain intrinsic renal function longer when using reprocessed polysulfone (PS) membrane hemodialyzers or single-use cellulose acetate (CA) membrane hemodialyzers. Fifty consecutive patients with residual renal function (urea clearance > 2.0 mL/min) using PS dialyzers were compared with a retrospective, disease- and time-matched population of patients using CA dialyzers. Endogenous urea clearance was measured every 3 months in all patients with remaining residual function. Other data collected included age, sex, cause of chronic renal failure, use of angiotensin-converting enzyme inhibitors or calcium channel blockers, and hemodynamic stability during hemodialysis. All patients were observed for at least 6 months while using a single type of dialyzer. Study end points included loss of residual renal function (urea clearance < 1.0 mL/min), death, transplant, transfer to peritoneal dialysis, or change of dialyzer. The PS and CA groups of patients were well matched for sex, age, initial renal clearance, predialysis blood pressure, and hemodynamic stability during hemodialysis. The PS patients had a higher delivered Kt/V (1.34 +/- 0.30 [mean +/- SD]) than the CA patients (1.06 +/- 0.20). The PS group had a higher average urea clearance than the CA group after 4 to 9 months of dialysis (2.8 +/- 2.6 mL/min v 1.7 +/- 1.6 mL/min, respectively), after 10 to 15 months of chronic dialysis (2.0 +/- 2.4 mL/min v 1.1 +/- 1.5 mL/min, respectively), and after 16 to 21 months of dialysis (1.3 +/- 1.9 mL/min v 0.5 +/- 1.1 mL/min, respectively; all P < 0.03, t-test). After 22 to 24 months of dialysis, the difference between the two groups was not significant. When comparing patients with identical causes of chronic renal failure, there were no differences between the PS and CA groups for those with diabetes mellitus, tubulointerstitial disease, or polycystic disease. Patients with parenchymal renal disease (glomerulonephritis or nephrosclerosis) had markedly better retention of intrinsic renal function with PS than with CA dialyzers (all P < 0.01). Kaplan-Meier analysis for retention of intrinsic renal function showed that PS patients with parenchymal renal disease had a mean of 23 months before loss of intrinsic renal function, whereas for CA patients the mean was 11 months before loss of intrinsic renal function (P = 0.0005). Cellulose acetate patients lost renal function at an average rate of 0.27 +/- 0.22 mL/min/mo, whereas for PS patients the rate was 0.14 +/- 0.56 mL/min/mo (P = 0.06, rank sum). CA patients with parenchymal renal disease lost renal function at a rate of 0.29 +/- 0.22 mL/min/mo, whereas for PS patients the rate was 0.0 +/- 0.8 mL/min/mo (P = 0.004, rank sum). Age, sex, and the use of either angiotensin-converting enzyme inhibitors or calcium channel blockers did not have an effect on the loss of intrinsic renal function. Patients with nondiabetic parenchymal renal disease receiving chronic hemodialysis with hydrogen peroxide/peroxyacetic acid-reprocessed PS dialyzers and a higher Kt/V lose residual renal function at a slower rate than disease-matched patients using single-use CA dialyzers. Our findings provide further evidence that the choice of dialyzer membrane may have an effect on intrinsic renal function.
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PMID:Improved preservation of residual renal function in chronic hemodialysis patients using polysulfone dialyzers. 910 48

Glycated haemoglobin (HbA1c) measured by high performance liquid chromatography (HPLC) in a 20 year old female with insulin dependent diabetes mellitus was consistently within the normal range although her daily blood glucose values were > 11.1 mmol/l. HbA1c measured by immunoagglutination and fructosamine was elevated and correlated with the patient's blood glucose values. The HPLC chromatogram showed an additional peak at HbA0. Electrophoresis of haemoglobin on citrate agar gel revealed an abnormal haemoglobin anodal of HbS. Cellulose acetate electrophoresis and isoelectric focusing demonstrated an additional haemoglobin migrating close to HbA2. Amino acid analysis and DNA sequencing revealed an alpha 30 (B11) Glu-->Lys replacement, that is, haemoglobin O Padova. Investigations of two family members without diabetes revealed the same rare haemoglobin variant. This case showed that this silent haemoglobin mutation caused an additional peak and falsely low HbA1c values when measured by HPLC, the gold standard for this evaluation.
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PMID:Haemoglobin O Padova and falsely low haemoglobin A1c in a patient with type I diabetes. 921 29