Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was designed to compare changes in lipid status following organ transplantation between type I diabetes mellitus (DM-I) patients receiving combined pancreas-kidney transplantation (PKT) with those receiving kidney transplantation alone (KTA). A retrospective chart review was used to identify pre- and posttransplantation fasting total cholesterol (TC) and triglycerides (TG) in three groups: DM-I patients receiving KTA (DM:KTA; n = 14), DM-I patients receiving PKT (DM:PKT; n = 20), and kidney transplant recipients without DM (NDM; n = 16). The groups were matched for age, gender, weight, duration of dialysis, smoking history, and duration of diabetes mellitus. Linear regression was used to analyze differences in lipid trends over time (up to 24 months posttransplantation) and the effects of prednisone dose, cyclosporine dose, and serum creatinine. Preoperative TC was significantly lower in the DM:KTA group (P < 0.05) compared with DM:PKT or NDM. There were no significant differences in preoperative TG between the three groups. TC and TG decreased over time only in DM:PKT (P = 0.0112, P = 0.0278, respectively). TC increased and TG was unchanged over time in DM:KTA (P = 0.0003, P = 0.1103, respectively). Neither TC nor TG changed over time in NDM. Trends of TC and TG for DM:PKT were significantly different from DM:KTA (P < 0.01 for both). Trend of TC for NDM was also significantly different from DM:PKT (P = 0.0061). Prednisone dose was significantly related to TC in DM:KTA and NDM (P < 0.01) while cyclosporine dose was significantly related to TC for DM:KTA only (P = 0.0013) in the presence of time. None of the variables tested (prednisone dose, cyclosporine dose, and serum creatinine) significantly affected TG in the presence of time. In summary, TC and TG decreased over time only in DM:PKT. In contrast, TC increased while TG was unchanged in DM:KTA over the same interval (0-24 months). If these trends continue, the beneficial change in lipids in the DM:PKT group may translate into a net improvement in atherosclerosis-mediated events for diabetic patients with chronic renal failure who receive PKT compared with those who do not.
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PMID:Lipid status after combined pancreas-kidney transplantation and kidney transplantation alone in type I diabetes mellitus. 146 93

Simultaneous transplantation of the pancreas is an option for diabetic patients undergoing kidney transplantation to attempt to halt progression of diabetic complications, but the additional risk imposed by the procedure is unclear. Our aim was to determine the morbidity attributable to pancreas transplantation during simultaneous pancreas and kidney transplantation. We compared the first posttransplant year of 18 consecutive recipients of combined pancreas and kidney transplantation to 18 consecutive recipients of kidney transplantation alone. All patients received cadaver donor allografts between 1986 and 1989, and had type I diabetes mellitus with chronic renal failure. There were no differences in patient survival (94% both groups) or satisfactory renal allograft function (89% pancreas/kidney group, 83% kidney group) up to 18 months after transplantation. Eighty-eight percent of pancreas allografts were functioning satisfactorily at 18 months. There was a mean (+/- SD) of 1.5 +/- 1.0 acute rejection episodes per patient for the pancreas/kidney group compared to 0.8 +/- 6 for the kidney-only group (P less than 0.02). Cytomegalovirus infection and wound complications were each encountered more often after pancreas/kidney transplantation than kidney transplantation alone, and together with rejection accounted for a difference in days of hospitalization during the first year (71 +/- 34 vs. 27 +/- 13, P less than 0.001). We conclude that simultaneous pancreas transplantation during cadaver donor kidney transplantation accounted for more frequent rejection episodes, CMV infections, and wound complications. These complications resulted in more hospitalization for patients undergoing simultaneous pancreas/kidney transplantation than kidney transplantation alone.
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PMID:Morbidity of pancreas transplantation during cadaveric renal transplantation. 184 52

Osteocalcin, non-collagenous vitamin K dependent bone protein is as a biochemical indicator of osteoblastic activity and metabolic turnover in bone, valuable in the diagnosis of several diseases and in investigations of the dynamics of osseous changes (processes) during treatment of osteopathies. Elevated osteocalcin levels are normal in childhood and adolescence. In the diurnal rhythm the peak is recorded in the early hours. Pathologically elevated values are associated with primary hyperparathyroidism, Paget's disease, chronic renal failure, acromegaly and some malignities. A rise in women during the early postmenopausal period signalizes an enhanced metabolic turnover of bone in those women who are candidates of postmenopausal osteoporosis. Low levels are as a rule recorded in advanced age, in nanism, hypoparathyroidism, type 1 diabetes, rheumatoid arthritis, vitamin D deficiency, vitamin K deficiency, hypercorticalism and glucocorticoid treatment.
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PMID:[Osteocalcin]. 227 72

A 34-year-old woman who had type I diabetes mellitus for 22 years and chronic renal failure for 2 years underwent a combined kidney and pancreas transplantation. Her uremia and insulin-dependence disappeared thereafter. However, she suddenly developed acute respiratory distress and died 22 days after the surgery. Diffuse pulmonary microemboli composed of necrotic tissue debris, fat cells, and muscle fragments were found. The source of the emboli was apparently a localized liquefying hematoma with necrotic muscle and fat in the left retroperitoneal space. Although such an occurrence seems to be extremely rare, the present case demonstrates that a liquefying hematoma with necrotic tissue in a confined space may indeed give rise to fatal pulmonary microembolism.
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PMID:Diffuse fatal pulmonary microembolism of retroperitoneal extravascular origin. 258 56

It is well known that 30 to 50% of patients with Type I Diabetes develop nephropathy and that chronic renal failure, it's final pathway, is the main cause of death. Assessment of urinary albumin becomes an essential tool for identifying the population at risk of developing nephropathy, to study its physiopathologic mechanisms and to evaluate the response to therapeutic trials. The present article is a preliminary report on the study of urinary albumin excretion rate (AER) in a pediatric population with Type I Diabetes and its relation to teh duration of the disease. A RIA technique with double antibody was developed for albumin assessment, with a displacement range of 1 to 300 ng/tube. Urine samples were collected during short periods with water load as suggested by Mogensen. Thirty nine children (30 patients and 9 controls) free of renal disease and with normal blood pressure were studied. Patients were divided according to duration of the disease in: Group I: less than 5 years, Group II: 5 to 10 years and Group III: more than 10 years. Results (mean +/- SD) in micrograms/min/1.73 m2 were: Control Group (n = 9) 4.30 +/- 2.53, GI: (n = 12) 10.44 +/- 9.47, GII (n = 10) 8.03 +/- 7.27 and GIII (n = 8) 8.56 +/- 4.26. The mean value of the Control Group (+3 SD) 12 micrograms/min/1.73 m2, was considered as the upper normal limit. Thus, 16.6%, 40%, and 12.5% of children in Groups I, II and III had microalbuminuria.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Diabetic nephropathy in children: study using the amount of urinary albumin]. 263 Aug 69

Urinary enzyme excretion and proteinuria were studied in 316 children with different underlying diseases. Activities on N-acetyl-beta-D-glucosaminidase and alanine aminopeptidase decreased progressively with age in the urine of 66 healthy prematures, newborns, infants or children. In 51 children with nephrotic syndrome, tubulopathies or chronic renal failure, excretion of NAG and AAP rose 3 to 30 fold. Contrary to molecular weight dependent protein analysis, determination of enzymuria did not allow to differentiate between glomerular and tubular disorders. After renal transplantation, 31 out of 52 children had a pathological enzymuria. NAG and AAP were more frequently elevated during treatment with cyclosporine A (21/29), than with azathioprine (10/23). The influence of nephrotoxic drugs upon enzymuria was documented in 14 children with cystic fibrosis or septicaemia treated with tobramycin. Activities of NAG and AAP rose transiently, whereas proteinuria remained almost unchanged. Only three out of 45 children receiving nonsteroidal antiinflammatory drug therapy for juvenile rheumatoid arthritis or spondylarthritis showed a pathological increase in enzymuria. Mean urinary NAG and AAP excretion in 154 children with insulin dependent diabetes mellitus were not different from controls and were unrelated to either duration of disease or HbA1 concentration. The determinations of urinary enzymes as non-invasive tests of renal integrity in medicine and toxicology provide a very sensitive indicator of renal damage. The assays of NAG and AAP have proven to be most valuable; however, due to a lack of specificity for the type and origin of renal dysfunction, these urinary enzyme assays are most useful when carried out in conjunction with electrophoretic analyses of proteinuria.
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PMID:[Enzymuria and kidney diseases in childhood]. 288 Nov 98

The clinical course of 24 patients with insulin-requiring diabetes mellitus who had received total parenteral nutrition (TPN) was retrospectively analyzed. Routine nutritional assessment disclosed significant depression of anthropometric indices and secretory protein levels in patients with chronic renal failure complicating juvenile onset diabetes mellitus (JODM). Biochemical complications including hypo- or hyperglycemia were significantly more frequent (p less than 0.001) in JODM than in maturity-onset diabetes and found to a lesser degree in patients with renal failure. The catheter infection rate was substantially higher (17%) than usually encountered in TPN therapy. Positive nitrogen balance was achieved in the majority of patients with an average 84% and 92% of estimated protein and caloric requirements being provided. Close monitoring and a protocol of infusion plus supplemental subcutaneous regular insulin was useful in providing adequate TPN safely to these high-risk patients.
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PMID:Total parenteral nutrition in patients with insulin-requiring diabetes mellitus. 308 5

In 1982-3, 35 children from the West Midlands developed the haemolytic-uraemic syndrome. This was a higher incidence than expected and included an epidemic localised to the Wolverhampton area in July 1983 which comprised 11 cases in two weeks. Twenty three children were treated with dialysis, of whom three died. Six patients developed chronic renal failure, four of them from Wolverhampton. Extrarenal manifestations included neurological sequelae in four, two of whom also developed insulin dependent diabetes mellitus and chronic renal failure. Cardiomyopathy occurred in one child, who also had chronic renal failure. The outcome of these 35 patients was not predictable from prognostic criteria derived from previous experience in Britain. This, together with the high prevalence of extrarenal disease and the geographical localisation of the 1983 outbreak, suggested an aetiological agent new to the region. Faeces from 10 patients were examined for verotoxin producing Escherichia coli, and positive strains of serotype O157.H7 were found in three patients during the Wolverhampton outbreak.
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PMID:Haemolytic-uraemic syndrome: clinical experience of an outbreak in the West Midlands. 308 99

Mitochondrial dysfunctions of the muscle in diabetic amyotrophy and of the liver in diabetic fatty liver have been reported. We investigated mitochondrial gene mutations in three cases: (1) a patient with diabetic amyotrophy in the muscles of the lower extremities, and neuropathy; (2) 5 diabetics with myoatrophy, diabetic nephropathy, and chronic renal failure; and (3) an IDDM patient with a diabetic fatty liver. We identified a 5778-bp deletion (8214-13991) in mitochondrial DNA from the muscle and liver biopsy specimens by the primer shift PCR and PCR-direct sequence methods. It is speculated that 5778-bp deletion is due to homogeneous recombination in the 7-bp repeat sequence of TCCTAGA flanking the region deleted in the mitochondrial DNA. Determination of respiratory chain enzyme activities in fresh muscle mitochondria demonstrated the defect in complex I activity. The deletion covers areas coding ND3, ND4, ND4L, and ND5 in complex I. The 5778-bp deletion might cause a defect in mitochondrial oxidative phosphorylation and contribute to the pathogenesis of diabetic amyotrophy, myoatrophy with diabetic nephropathy, and chronic renal failure, as well as diabetic fatty liver in IDDM.
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PMID:A new mitochondrial DNA deletion associated with diabetic amyotrophy, diabetic myoatrophy and diabetic fatty liver. 760 16

The development of kidney disease in diabetes mellitus can be viewed as a two-stage process: (1) the development of proteinuria, and (2) its progression to chronic renal failure. Determinants of the latter were examined in 439 IDDM patients who had nephropathy and participated in the Diabetic Retinopathy Study. Using serum creatinine levels obtained during the follow-up period to assess the rate of loss of renal function, we found that only one-third of these patients experienced a rapid loss of function, while the others had slowly declining or unchanging renal function despite the presence of proteinuria and severe diabetic retinopathy. Among the many baseline variables examined, only elevated cholesterol and elevated systemic blood pressure were predictors of a rapid loss of renal function. Patients with this rapid loss of renal function also had the highest risk of death due to cardiovascular causes, as well as all causes. Once again, hypercholesterolemia was the major predictor of these deaths. In conclusion, efforts should be undertaken early to identify patients who are rapidly losing renal function so that interventions to modify systemic blood pressure and hypercholesterolemia may prevent or postpone the development of renal failure and death in patients with IDDM.
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PMID:Hypercholesterolemia--a determinant of renal function loss and deaths in IDDM patients with nephropathy. 815 81


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