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)

Intravenous glucose tolerance tests (30 g, 5 min, constant rate) were performed in 8 IDDM patients and in 8 controls. The consequences of the osmotic pressure, induced by glucose, were investigated. Serum choline esterase was used as an endogenous marker of serum dilution. Five minutes after the end of infusion plasma glucose was raised by 182 +/- 12 mg.dl-1 in patients and by 189 +/- 6 mg.dl-1 in controls. Choline esterase values decreased by 6.6 +/- 0.8% and 6.3 +/- 1.0% respectively, P less than 0.01 each. Calculated water shifts into the extracellular space were 924 +/- 112 ml and 882 +/- 140 ml respectively. Fifteen minutes after the end of infusion glucose decreased by 32 +/- 1 mg.dl-1 in IDDM patients and by 57 +/- 2 mg-1 in controls. Serum choline esterase recovered by 2.6 +/- 0.2% and 2.7 +/- 0.2% respectively, P less than 0.01 each, indicating comparable water correction in spite of the slower fall of glucose in IDDM patients. Water correction was more rapid than glucose fall. Diuresis (46 +/- 4 ml versus 42 +/- 3 ml) or cellular uptake of serum solutes (electrolytes, amino acids, urea, creatinine) could not explain this. It is hypothesized that accumulation of free intracellular glucose reduces the osmotic gradient and facilitates cellular water re-uptake.
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PMID:Osmotic stress due to changes in plasma glucose and its regulation in IDDM patients. 152 25

A 71-year-old man with type I diabetes mellitus was admitted to the hospital for the treatment of osteomyelitis of the left great toe secondary to methicillin-resistant Staphylococcus aureus. The patient was enrolled in an investigational protocol and was treated with teicoplanin 1200 mg/day. Following 40 days of treatment, the patient developed both markedly elevated serum creatinine and blood urea nitrogen. Urine analysis also showed the presence of protein. The eosinophils were markedly elevated in the blood. The patient was subsequently diagnosed with a probable drug-induced acute interstitial nephritis. Treatment with furosemide and hemodialysis over the next two weeks failed to produce improvement in renal function. The patient was referred for long-term dialysis. The data presented in this report suggest the possible relationship of teicoplanin and the development of renal failure in this patient. Periodic monitoring of renal function and follow-up are probably warranted in patients receiving long-term teicoplanin therapy.
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PMID:Teicoplanin nephrotoxicity: first case report. 153 25

The objective of this study was to examine the relationship between blood pressure, albumin excretion, and renal function in patients with type I diabetes mellitus. The study design was as follows: nonselected consecutive patients with type I diabetes mellitus were divided into three groups by level of albumin excretion rate (AER): less than 20 micrograms/min, 20 to 200 micrograms/min, and greater than 200 micrograms/min. The setting for the study was an outpatient diabetic clinic in a tertiary referral center. There were 166 patients studied: 53% men, 47% women, 86% white, 17% treated for hypertension. Seventy-six percent had an AER less than 20 micrograms/min, 18% had an AER of 20 to 200 micrograms/min, and 6% had an AER of greater than 200 micrograms/min. Glycosylated hemoglobin did not differ between groups. AER was increased with age and disease duration (P less than 0.005 by analysis of variance) after 10 yr of disease. Serum creatinine (P less than 0.005) and systolic (P less than 0.005) and diastolic (P less than 0.01) blood pressures were also increased with AER. Serum creatinine and blood pressure were found to be increased in parallel after 10 yr of disease, but both remained within the normal range overall. A comparison of individual blood pressures in patients not taking antihypertensive drugs (N = 138) with age-related blood pressures of nondiabetic subjects revealed increased systolic and diastolic blood pressures at all ages. Group comparison demonstrated a significant link between increased AER and serum creatinine (declining renal function) and increased blood pressure after a latent period of 10 yr. Blood pressure appears to be increased from the earliest age in diabetes compared with healthy populations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of disease duration and hypertension in albumin excretion of type I diabetes mellitus. 161 Sep 79

Urinary transferrin excretion was measured by radioimmunoassay in 74 children with Type 1 diabetes mellitus and in 40 normal children, and compared with urinary excretion of albumin, alpha-1-microglobulin, and N-acetyl-beta-D-glucosaminidase. Urinary transferrin excretion was significantly elevated in diabetic (median (range) 186 (18-1671) mg mol-creatinine-1) compared with normal (85 (27-668) mg mol-creatinine-1) children (p less than 0.001). Seventeen diabetic children had transferrin excretion above the 95th centile for normal children. In contrast there was no significant increase in urinary albumin excretion in the diabetic children although 8 had urinary albumin excretion which exceeded the 95th centile for normal children (6 of these 8 patients having coexistent urinary hyperexcretion of transferrin). Urinary transferrin excretion correlated significantly with urinary albumin excretion in both normal (rs = 0.62, p less than 0.001) and diabetic (rs = 0.61, p less than 0.001) children. The indices of proximal renal tubular function (urinary excretion of alpha-1-microglobulin and N-acetyl-beta-D-glucosaminidase) correlated significantly with transferrin excretion in both diabetic (rs = 0.43 and rs = 0.41, p less than 0.001) and normal (rs = 0.40, p less than 0.02 and rs = 0.53, p less than 0.001) children, but not with albumin excretion (rs = 0.20, p greater than 0.05 and rs = 0.22, p greater than 0.05). In addition urinary transferrin excretion significantly correlated with urinary glucose concentration (rs = 0.34, p less than 0.007) in Type 1 diabetic children. The discrepancy in urinary excretion of transferrin and albumin may reflect impaired proximal renal tubular reabsorption of transferrin and/or altered glomerular basement membrane selectivity for the two proteins.
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PMID:Increased urinary excretion of transferrin in children with type 1 diabetes mellitus. 168 49

Glomerular and tubular microproteinuria precede the development of overt nephropathy in Type 1 diabetes mellitus. However, in Type 2 diabetes urinary protein excretion and its relationship to diabetic nephropathy has not been clearly characterized. Twenty consecutive, newly diagnosed patients with Type 2 diabetes, whose urine was Albustix-negative and sterile on culture, were studied. Two timed overnight urine samples were collected at diagnosis, and after 2 months and 2 years, and excretion rates of albumin, alpha-1-microglobulin and N-acetyl-beta-D-glucosaminidase were calculated. HbA1c fell from 12.1 +/- 2.4% at diagnosis to 9.5 +/- 1.5% at 2 months and 9.6 +/- 2.2% at 2 years. Albumin excretion rate fell marginally from 6.5 (2.1-242.5) micrograms min-1 at diagnosis to 5.5 (1.7-274.0) micrograms min-1 at 2 months (p less than 0.05) rising again to 6.1 (1.9-201.7) micrograms min-1 at 2 years. alpha-1-Microglobulin excretion rate fell from 13.5 (3.6-59.9) micrograms min-1 at diagnosis to 8.4 (2.9-16.1) micrograms min-1 at 2 months and 8.8 (1.8-54.1) micrograms min-1 at 2 years (both p less than 0.05). Albumin excretion rate was found to correlate significantly with creatinine clearance at diagnosis (rs = 0.61, p less than 0.005), though not subsequently. In contrast, excretion rates of alpha-1-microglobulin and N-acetyl-beta-D-glucosaminidase correlated with HbA1c (rs = 0.68 and 0.66, respectively, p less than 0.005 at diagnosis and rs = 0.57 and 0.53, p less than 0.05 subsequently in both cases).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Microproteinuria in type 2 diabetes mellitus from diagnosis. 169 21

The short-term effects of prostaglandin synthesis inhibition (PGSI; single dose 500 mg of naproxen) on renal function were studied in six women (age: 21.9 +/- 2.4 yrs) with insulin dependent diabetes mellitus (IDDM) of 14.3 +/- 2.8 yrs' duration, and in nine age- and sex-matched controls. The diabetics had no overt signs of nephropathy (Albustix neg, normal serum creatinine, and blood pressure). The clearance of inulin (CIn) and PAH; the filtration fraction (FF); and the excretion of Na, albumin and PGE2 were studied under water diuresis on two separate mornings, first without and then with PGSI. With PGSI all individuals has lower PGE2 excretion. The CIn and FF were significantly (p less than 0.05) higher in the diabetics than in the controls both without (129.4 +/- 23.9 ml/min/1.73 m 2 and 23.4 +/- 2.8% vs. 107.6 +/- 10.3 and 19.7 +/- 1.6) and with (133.7 +/- 29.4 and 22.6 +/- 2.1, vs. 106.8 +/- 10.3 and 20.1 +/- 1.5) PGSI. The diuresis and Na excretion were significantly lower with PGSI, than without, in both groups. The albumin excretion was significantly higher in the diabetics under both conditions (29.9 +/- 16.6 and 34.2 +/- 19.9 micrograms/min/100 ml GFR, vs. 14.5 +/- 10.6 and 12.9 +/- 8.3 in controls). We conclude that the hyperfiltration in this stage of IDDM does not appear to be PG dependent, and that PGSI does not give any immediate effects on the albumin excretion.
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PMID:Renal functional effects of prostaglandin synthesis inhibition in patients with insulin-dependent diabetes mellitus of long duration without nephropathy. 179 42

Neopterin is specifically produced by interferon-activated macrophages, and it may be considered a marker of cellular immunity. In 40 newly diagnosed and 38 longer standing type 1 (insulin-dependent) diabetics the relationship between urinary neopterin levels and islet cell antibodies (ICA) was investigated. Raised urinary neopterin levels were found in 30 ICA positive (mean +/- SD: 729.8 +/- 602.1 mumol/mol creatinine, p = 0.0001) and 10 ICA negative (433.4 +/- 191.2 mumol/mol creatinine, p = 0.0005) diabetics at onset of disease compared with age-matched control subjects (118.1 +/- 33.2 mumol/mol creatinine). No significant difference in urinary neopterin levels was observed between diabetic groups. After the first stages of disease (greater than 5 months from onset), a significant difference (p = 0.0002) in urinary neopterin excretion was found between longer standing ICA positive patients and controls, but not between ICA negative diabetics and controls. In longer standing diabetics, neopterin levels were significantly higher in ICA positive patients than in ICA negative patients (544.6 +/- 341.3 versus 201.7 +/- 180 mumol/mol creatinine, p = 0.0002). No correlation between newly diagnosed or longer standing patients and HbA1c levels was found. Our results suggest that increased neopterin excretion in type 1 diabetes seems to be a sensitive indicator for the activation of cell-mediated immunity even when ICA are undetectable.
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PMID:Relationship between urinary neopterin excretion and islet cell antibodies in type 1 (insulin-dependent) diabetes. 181 78

To determine the effectiveness of dietary protein restriction on proteinuria in patients with non-insulin dependent diabetes (NIDDM), 14 diabetic patients with overt nephropathy were placed on either a low protein diet (N = 7) or conventional protein diet (N = 7) for one month. After the study period, daily urinary protein excretion rates decreased significantly, from 3.2 +/- 0.4 to 1.9 +/- 0.4 g/day, and serum albumin levels increased from 3.3 +/- 0.2 to 3.7 +/- 0.5 g/dl only in the low protein diet group, without any significant changes in either serum creatinine levels or creatinine clearance. These findings suggest that dietary protein restriction has a beneficial role in the treatment of NIDDM patients with overt nephropathy.
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PMID:Effect of dietary protein restriction on proteinuria in non-insulin-dependent diabetic patients with nephropathy. 182 Apr 50

Fifty patients with Type 1 diabetes mellitus were observed over 6 years. Serum and urinary N-acetyl-beta-glucosaminidase (NAG) activity, and albuminuria were measured in groups of patients subdivided according to ophthalmological findings. Significantly higher mean serum NAG activity was found at the beginning of the study in patients who later developed diabetic retinopathy in comparison with those who did not (geometric mean (2SD range) 19.7 (12.4-31.2) vs 14.4 (9.5-22.7) U l-1, p less than 0.01). Urinary NAG activity was significantly higher in all groups of diabetic patients than in healthy control subjects (p less than 0.05). A significant increase in albumin:creatinine ratio during the study was found in patients with newly developed diabetic retinopathy compared with patients who did not (at 6 years 1.33 (0.40-4.43) vs 0.75 (0.24-2.31) g mol-1, p less than 0.01). No differences in either biochemical variable were found between hypertensive and normotensive diabetic patients at the end of the study. The results suggest that both serum NAG activity and albuminuria may serve as early functional indicators of diabetic retinopathy.
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PMID:A six-year follow-up of the relationship between N-acetyl-beta-glucosaminidase and albuminuria in relation to retinopathy. 183 8

An open, randomized, cross-over study was undertaken to assess the effects of lisinopril and nifedipine on albumin excretion, renal haemodynamics and segmental tubular reabsorption in overt diabetic nephropathy. The study consisted of a 4-week run-in period, a 3-week active treatment period, a 4-week wash-out period and a second 3-week active treatment period. Twelve patients with type 1 diabetes with albuminuria, mild to moderate hypertension and a serum creatinine level of less than 200 mumol l-1 were included. Lisinopril reduced albumin excretion from 1343 +/- 337 micrograms min-1 to 879 +/- 299 micrograms min-1 (P less than 0.01), whereas nifedipine was without effect, 1436 +/- 336 micrograms min-1 vs. 1319 +/- 342 micrograms min-1. Glomerular filtration rate (GFR) was unchanged by either drug. Both drugs increased effective renal plasma flow (ERPF) by about 20%. No differences between the drugs were observed with regard to their effect on renal haemodynamic parameters. By contrast, nifedipine exerted an inhibitory effect on several proximal tubular transport markers, whereas lisinopril was without effect. The different actions on tubular transport mechanisms exerted by lisinopril and nifedipine may contribute to the observed effect on albumin excretion.
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PMID:Contrasting effects of lisinopril and nifedipine on albuminuria and tubular transport functions in insulin dependent diabetics with nephropathy. 184 21


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