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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lewis rats were treated with streptozotocin to induce hyperglycemia and glycosuria (400-600 mg/dl). Transplantation of approximately 1,000 dissociated islets obtained from collagenase-treated pancreases from 4 donors will promptly correct induced diabetes. Functional survival of islet allografts is related to genetic disparity between donor and recipient strains. In the closely matched Fisher-to-Lewis combination, islets functioned for a mean of 4.2+/-1 days while in the AgB-incompatible Wistar/Furth-to-Lewis combination, islets functioned for a mean of only 2.1+/-0.5 days. Treatment of recipients with antithymocyte globulin (ATG) for 3 days extended islet survival to a mean of 11.8 +/- 1.9 days in the Wistar/Furth-to-Lewis combination and to as long as 184+/-87.5 days in the Fischer-to-Lewis combination. ATG may have a role in trials of clinical islet transplants.
Nephron 1978
PMID:Effect of antithymocyte globulin on islet of Langerhans transplantation. 10 12

In a group of 48 patients with a renal cadaveric allograft 38 acute rejection episodes were treated by increasing the daily prednisolone doses to 300 mg the first day, 200 mg the second day and 100 mg the third day, gradually tapering down over a matter of weeks. In a second group of 48 patients 39 acute rejections were treated by 1 g of methylprednisolone intravenously on alternate days with a maximum of four injections. Rejection treatment was successful in 26 of 38 in the first group (68%) and in 30 of 38 in the second group (76%). Complications such as gastrointestinal bleeding, aseptic necrosis and diabetes were more frequent in the first series.
Nephron 1976
PMID:High intravenous doses of methylprednisolone for acute cadaveric renal allograft rejection. 76 73

Changes in renal function and structure are frequently observed in patients with diabetes mellitus. In the early phases of the disease, alterations in glomerular filtration rate, renal plasma flow, glomerular permeability and tubular capacity for glucose reabsorption occur. In the late stages of juvenile onset diabetes, renal failure is a common cause of death. For this reason, increasing attention is being paid to the possibility of long-term dialysis and renal transplantation in these patients. The kidneys play an important role in regulating insulin metabolism. The renal arteriovenous difference is approximately 30-45% and a linear relationship exists between the arterial insulin level and the renal arteriovenous concentration difference. The renal extraction of insulin is 200 ml/min in man, and it is estimated that 6-8 U are removed and degraded by the kidney in 24 h. The quantity of insulin in urine is small. However, its clearance is relatively constant over a wide range of serum concentrations and is 0.15-0.5 ml/min. The mean basal insulin excretion is 3.6 muU/mg creatinine, and a fourfold rise occurs following a glucose load. The urinary insulin values in neonates, children and patients with diabetes and renal failure are reviewed. In diabetic patients, progressive renal disease is accompanied by decreasing insulin requirements. In contrast, nondiabetic patients who develop renal failure frequently show abnormalities in carbohydrate metabolism, the commonest of which is a pseudodiabetic state.
Nephron 1975
PMID:Insulin and the kidney. 110 Oct 90

A 66-year-old white man presented with severe chronic renal failure. He had no past or present symptomatic glucose intolerance nor a family history of diabetes mellitus. Several fasting plasma glucose determinations, hemoglobin Alc and an oral glucose tolerance test were normal. Funduscopic ophthalmoscopy and retinal fluorescein angiography did not demonstrate diabetic retinopathy. The kidney biopsy showed nodular diabetic nephropathy, with increased mesangial matrix, thickened glomerular basement membrane, and afferent and efferent glomerular arteriolar hyalinization. The diagnosis of nodular diabetic nephropathy was made in this patient in the absence of past or present or familial evidence of diabetes mellitus.
Nephron 1992
PMID:Nodular diabetic glomerulosclerosis without diabetes mellitus. 143 40

Lipids, apoproteins and associated enzyme activities in type 2 diabetic end-stage renal disease (ESRD) were compared with that in nondiabetic ESRD and normal controls. Of the 40 uremic patients with non-insulin-dependent diabetes mellitus, 20 patients were receiving stable continuous hemodialysis treatment (CHT). Of the 39 patients with nondiabetic ESRD, 21 were undergoing CHT. Patients with nondiabetic ESRD exhibited elevated levels of serum triglyceride and a marked reduction in high-density-lipoprotein (HDL) cholesterol. Concentrations of serum apolipoprotein (Apo) C-3 were higher than in controls, whereas mean levels of serum Apo E were lower. The concentrations of serum Apo A-1 and Apo A-2 decreased with diminished lecithin: cholesterol acyltransferase activity. Lipoprotein lipase activity decreased in undialysed patients, and hepatic triglyceride lipase activity decreased significantly throughout the observation. Patients with diabetic ESRD exhibited elevated serum Apo B and normal serum Apo E levels, besides the lipid and Apo abnormalities observed in nondiabetic ESRD. Moreover, a prominent reduction in serum Apo A-1 was found in dialysed diabetic patients. The Apo B/Apo A-1 ratio was significantly higher in diabetic ESRD than in nondiabetic patients undergoing CHT. These results indicate that lipid abnormalities are accelerated in diabetic ESRD and may constitute a serious risk for the development of atherosclerosis.
Nephron 1992
PMID:Comparison of lipids, apoproteins and associated enzyme activities between diabetic and nondiabetic end-stage renal disease. 150 37

The pathogenesis of diabetic nephropathy relative to the changes in the glomerular extracellular matrices was investigated. Renal tissues from 10 diabetic patients were immunostained with antibodies directed against heparan sulfate proteoglycans (HS-PGs), laminin, type IV collagen and fibronectin. Seven patients were nephrotic and had advanced glomerulosclerosis with nodular lesion, while the other 3 had no renal manifestations or minor glomerular tissue alterations. Controls included kidneys removed from patients with renal tumors and specimens obtained by renal biopsy from patients with IgA nephropathy. Relationships among proteinuria, intensity of fluorescence and glomerular changes were studied. In diabetes 3 patients with minor glomerular lesions were found to have no changes in various components of extracellular matrices. A marked reduction in the intensity of staining with anti-HS-PG antibodies was observed in renal specimens from patients with nodular glomerulosclerosis and proteinuria, while a mild decrease in the intensity of fluorescence was observed in tissues stained with antilaminin antibodies. An increase compared to normal control sample findings in type IV collagen and fibronectin was observed in the mesangium of sclerosing glomeruli. No loss of HS-PG was observed in patients with IgA nephropathy. These results indicate that glomerular extracellular matrix HS-PG is lost in association with diabetic nephropathy; this loss results in alteration of the charge-selective properties of glomerular capillaries. This alteration may, in part, be the cause of the proteinuria associated with diabetic nephropathy.
Nephron 1992
PMID:Heparan sulfate proteoglycans are lost in patients with diabetic nephropathy. 150 38

Serum uric acid has been described as being increased in the prediabetic stage of diabetes mellitus and as being decreased in overt diabetes. In this study we compared the serum uric acid levels of patients with insulin-dependent diabetes mellitus (IDDM) to those of controls matched for sex, age and ethnic origin. Also the correlation between serum uric acid levels and the fractional excretion of uric acid in IDDM patients was investigated, as well as the correlation between glycosuria and the fractional excretion of uric acid. The mean serum uric acid was lower in IDDM patients than in normal controls (4.0 +/- 1.3 vs. 4.3 +/- 1.3 mg/100 ml; p less than 0.03), mainly due to significantly lower levels in male and Ashkenazi IDDM patients, as compared to their respective controls. The fractional excretion of uric acid was found to be elevated in IDDM patients: 13.0 +/- 8.6% (mean +/- SD). A significant negative correlation was found between serum uric acid levels and the fractional excretion of uric acid in IDDM patients (p less than 0.001), although not when the males were examined separately. We found no correlation between the fractional excretion of uric acid and the degree of glycosuria in IDDM patients. In addition, the prevalence of hypouricemia (serum uric acid less than 2.5 mg%) was the same in IDDM patients and controls.
Nephron 1992
PMID:Urine uric acid excretion in patients with insulin-dependent diabetes mellitus. 155 96

Two patients with diabetes mellitus had persistent hypouricemia due to increased urate clearance; the degree of the apparent renal hypouricemia with uricosuria was quite mild. At the onset of diabetes, their serum urate levels were normal. Even after good diabetes control in both cases, hypouricemia continued. Based on the pharmacological evaluation in both patients, pyrazinamide administration could partially decrease urate clearance, however, suppression by pyrazinamide was less than in normal subjects, and probenecid increased urate clearance. These results suggest that the present cases had a renal abnormality affecting tubular presecretory reabsorption of urate, which might be due to diabetes mellitus.
Nephron 1992
PMID:Two cases of persistent hypouricemia associated with diabetes mellitus. 163 May 45

This double-blind cross-over study was performed to investigate whether the lipoproteins in plasma were different on furosemide (Lasix Retard) and thiazide (hydrochlorthiazide) treatment in patients suffering from type II diabetes. Twenty-four patients were randomly allocated to either furosemide-hydrochlorthiazide (LR-HCT) or HCT-LR treatment. The treatment period was 12 months: 6 months on each sequence. After inclusion, the patients were seen every second month. Laboratory data were recorded at each visit. The only significant treatment effect was observed for high-density-lipoprotein3 cholesterol concentration (HDL3 cholesterol concentration), which was higher when patients were on furosemide therapy (p less than 0.05). We conclude from the present study that blood-glucose HbA1c, and the concentration of lipoproteins connected to development of atherosclerosis is unaffected whether type II diabetes patients are treated with HCT or furosemide.
 ...
PMID:Lipoproteins and diuretics in type II diabetes. 183 Mar 13

We investigated the urinary albumin excretion and renal hemodynamics of normotensive nonobese patients with impaired glucose tolerance (IGT) and non-insulin-dependent diabetes mellitus (NIDDM) in an early microalbuminuric stage (defined by albuminuria less than 30 mg/day). In comparison with normal subjects, a significant increase in urinary albumin excretion was observed already in the IGT stage [U-albumin/U-creatinine: NL (20 subjects), 5.3 +/- 1.7 mg/g Cr; IGT (23 subjects), 11.9 +/- 6.7 mg/g Cr; DM (20 subjects), 12.8 +/- 5.7 mg/g Cr]. A 3-week diet therapy combined with physical exercise prescribed for 53 normotensive non-obese mild NIDDM patients resulted in improvement in glucose tolerance, concomitant with lowered systemic blood pressure and a decrease in urinary albumin excretion (SBP: 128.4 +/- 13.0 to 106.4 +/- 10.2 mm Hg, p less than 0.01; DBP: 78.2 +/- 10.8 to 66.0 +/- 8.0 mm Hg, p less than 0.01; U-albumin: 19.4 +/- 10.3 to 10.1 +/- 9.1 mg/day, p less than 0.01). However, glomerular filtration rate, renal plasma flow, filtration fraction and urinary beta 2-microglobulin excretion remained unchanged. From these results, we hypothesized that focal glomerular hyperperfusion increases urinary albumin excretion in patients with early NIDDM.
Nephron 1991
PMID:Urinary albumin excretion in patients with non-insulin-dependent diabetes mellitus in an early microalbuminuric stage. 185 79


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