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

Diabetic donors are still reluctantly accepted as potential organ donors because of supposed poor graft function caused by diabetic lesions. The results of transplantation of six kidneys from three donors with insulin dependent diabetes mellitus are reported. All three donors had a normal creatinine clearance and absence of proteinuria. Renal biopsies were taken. Five grafts are still functioning, six months to two years after transplantation with a mean creatinine clearance of 69ml/min (range 51-95). Three of five biopsies taken six months after transplantation showed marked decrease of the diabetic lesions. On the basis of these findings it seems justified to accept kidneys from diabetic donors for transplantation.
Proc Eur Dial Transplant Assoc Eur Ren Assoc 1985
PMID:Results of transplantation of kidneys from diabetic donors. 388 78

To evaluate the role of renal haemodynamic factors in the pathophysiology of diabetic nephropathy, we determined by radionuclear techniques glomerular filtration rate (GFR) and renal plasma flow (RPF) in 18 patients affected by insulin dependent diabetes mellitus (IDDM) in good metabolic control, with normal blood pressure and plasma creatinine. GFR and RPF measured in the same patients after ten months correlated with proteinuria and duration of diabetes. Our finding of a significant correlation between the decline of RPF and duration of diabetes may support the haemodynamic hypothesis of progression of diabetic nephropathy.
Proc Eur Dial Transplant Assoc Eur Ren Assoc 1985
PMID:Radionuclear determination of glomerular filtration rate and renal plasma flow to detect early decrease of renal function in insulin dependent diabetes. 399 57

Renal responses to low-dose infusion of angiotensin II (ANGII, 1.25 and 2.5 ng.kg-1 min-1) were examined in 15 patients with type 1 diabetes and in 10 control subjects after pretreatment with lithium carbonate (750 mg, 20 mmol). Mean arterial pressure rose during ANGII infusion in both groups. The renal haemodynamic response to angiotensin II was not abnormal in the diabetic patients. Absolute proximal reabsorption of sodium was increased at baseline in the diabetic group, and fell during ANGII. Fractional lithium excretion was reduced in the diabetic patients at baseline (P < 0.05), and the fall in fractional lithium excretion during ANGII was less than in the control group (P = 0.012). In the diabetic group correlations existed between glycated haemoglobin and baseline glomerular filtration rate (P < 0.05), baseline fractional lithium excretion (P = 0.03), and the fall in fractional lithium excretion during angiotensin II infusion (P = 0.013). There was no correlation between glycated haemoglobin and absolute lithium clearance. Some indices of sodium reabsorption by the proximal renal tubule in diabetic patients correlate with prevailing chronic glycaemic control, largely reflecting changes in glomerular filtration rate. Reduced fractional proximal tubular responsiveness to exogenous angiotensin II is consistent with a role for endogenous angiotensin II as one mediator of increased tubular reabsorption of sodium in type 1 diabetes, but the data does not exclude alternative mechanisms.
Nephrol Dial Transplant 1994
PMID:Renal tubular responses to low-dose infusion of angiotensin II in type 1 diabetes mellitus; relation to chronic glycaemic control. 781 87

Urinary enzymes were determined in a controlled study including 28 type I diabetes mellitus patients. Fifteen patients had persistent microalbuminuria and were compared to 13 normoalbuminuric patients with comparable age and sex distribution. All patients had normal renal function as measured by serum creatinine. Human intestinal alkaline phosphatase (hIAP), a specific marker of the proximal tubular S3 segment, was elevated in the urine of microalbuminuric patients while human tissue non-specific alkaline phosphatase (hTNAP), indicating effects mainly at the S1-S2 segments, was not. Urinary hIAP was correlated with serum glycated haemoglobin. These results suggest that tubular alterations are present at an early stage of diabetic nephropathy, especially at the S3 segment, and that hIAP may have promise as an early marker.
Nephrol Dial Transplant 1994
PMID:Human urinary intestinal alkaline phosphatase as an indicator of S3-segment-specific alterations in incipient diabetic nephropathy. 808 50

To examine the interaction between angiotensin II (ANGII) and dopamine in type 1 diabetes mellitus, urinary dopamine excretion was examined during ANGII infusion in 15 diabetic patients and 10 control subjects after pretreatment with lithium 750 mg and placebo. The antinatriuretic response and the urinary dopamine response to ANGII did not differ within or between the two groups on each study day. No correlation was observed between the decrements in urinary sodium excretion and urinary dopamine output during ANGII infusion in either group. The effect of insulin on urinary dopamine excretion was studied separately in seven non-diabetic subjects; sodium and potassium retention occurred during a hyperinsulinaemic euglycaemic clamp, but urinary dopamine did not change. The data suggest that the relationship between urinary sodium excretion and tubular dopamine synthesis remains normal in early type 1 diabetes mellitus both at baseline and during the antinatriuresis induced by angiotensin II. The cause of the reduction in urinary dopamine during ANGII infusion is unclear, but is probably not mediated directly by changes in proximal tubular sodium transport.
Nephrol Dial Transplant 1993
PMID:Urinary dopamine response to angiotensin II is not abnormal in type 1 (insulin-dependent) diabetes mellitus. 838 32

Alterations in the fibrinolytic system have been demonstrated in noninsulin-dependent diabetic patients (NIDDM) but not in insulin-dependent diabetic patients (IDDM). Since the activity of the fibrinolytic system can affect the turnover of extracellular matrix and therefore theoretically can affect the peritoneal transport, we tried to determine if there was a difference in the performance of the peritoneal equilibration test (PET) between IDDM and NIDDM patients receiving peritoneal dialysis (PD). The PET data from 11 IDDM patients (2 female, 9 male) and 13 NIDDM patients (3 female, 10 male) were reviewed. These two groups of patients were matched in gender, duration of end-stage renal disease, PD, and hypertension, blood pressure, degree of uremia, weekly KT/V, and body surface area. The IDDM patients (41.4 +/- 13.9 years) were younger than the NIDDM patients (58.8 +/- 7.1 years, p = 0.0026). There were no differences in hematocrit and serum chemistry profile including glucose and albumin between the two groups. Our data showed that there was no difference in PET performance between IDDM and NIDDM patients.
Adv Perit Dial 1995
PMID:Peritoneal transport in type I (insulin-dependent) and type II (noninsulin-dependent) diabetic peritoneal dialysis patients. 853 39

As angiotensin-converting enzyme inhibition is accompanied by a marked decrease in glomerular protein loss, the hypothesis was tested that an increase of the glomerular transcapillary hydraulic pressure difference by exogenous angiotensin II would increase microalbuminuria in patients with insulin (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM). Acute effects of increasing doses of angiotensin II (1, 3 and 6 ng/kg/min) were studied on mean arterial pressure (MAP), glomerular filtration rate (GFR), effective renal plasma flow (ERPF), filtration fraction (FF), total renal vascular resistance (TRVR), and urinary albumin excretion rate (UAER) in 11 IDDM and 11 NIDDM microalbuminuric patients. Angiotensin II infusion changed MAP from 100 +/- 3 mmHg at baseline to 105 +/- 3, 111 +/- 3, and 116 +/- 3 mmHg (P < 0.001), ERPF from 542 +/- 29 to 478 +/- 24, 429 +/- 23, and 382 +/- 19 ml/min (P < 0.001), FF from 20.2 +/- 0.06 to 23.1 +/- 0.7, 27.1 +/- 1.1, and 29.8 +/- 1.2% (P < 0.001), and TRVR from 9454 +/- 809 to 11,158 +/- 930, 13,310 +/- 1206, and 15,538 +/- 1362 dyne s cm-5 (P < 0.001). GFR and UAER, however, did not change significantly. Therefore, during angiotensin II infusion ERPF decreased, while FF and TRVR increased. As UAER and GFR remained unchanged, the presumed rise in intraglomerular capillary pressure by exogenous angiotensin II did not increase UAER. We suggest that during manipulation of the renin-angiotensin system, as in other renal diseases with proteinuria, factors other than glomerular transcapillary hydraulic pressure determine the degree of urinary albumin loss in microalbuminuric IDDM and NIDDM patients.
Nephrol Dial Transplant 1997 Feb
PMID:Urinary albumin excretion rate during angiotensin II infusion in microalbuminuric patients with insulin and non-insulin-dependent diabetes mellitus. 913 45

Recently evidence has accumulated that diabetic nephropathy clusters in families, both in insulin-dependent (IDDM) and non-insulin-dependent (NIDDM) diabetic patients. Furthermore, hypertension and cardiovascular accidents are found more frequently in families of NIDDM with diabetic nephropathy. Some observations in offspring of NIDDM patients with diabetic nephropathy point to high urinary albumin excretion and slightly greater blood pressure values, both within the normal range compared to offspring of patients without diabetic nephropathy. Further follow-up is required to assess whether these findings are indicative of a possible genetic predisposition to diabetic nephropathy.
Nephrol Dial Transplant 1997
PMID:Risk factors for development of diabetic nephropathy: a review. 926 95

Insulin-dependent diabetes mellitus (IDDM) develops predominantly in children and young adults, but may appear in all age groups. The incidence of IDDM differs greatly among populations, with Finland and Sardinia showing the greatest incidence rates (approximately 30-35% of cases annually per 100000 children up to age 14 years) and oriental populations showing the lowest rates. IDDM is diagnosed more frequently in the winter months. The major genetic susceptibility to IDDM is linked to the HLA complex on chromosome 6. These genetic backgrounds interact with environmental factors (possibly certain viruses, foods and climate) to initiate the immune-mediated process that leads to beta-cell destruction. Non-insulin dependent diabetes (NIDDM) is the most common form of diabetes. The prevalence of NIDDM varies enormously from population to population. The greatest rates have been found in Pima Indians. The major environmental factors identified as contributing to this form of diabetes are obesity and reduced physical activity. NIDDM shows strong familial aggregation in all populations and is clearly the result of an interaction between genetic susceptibility and environmental factors. Before NIDDM develops, insulin concentrations are high for the degree of glycaemia and of obesity, reflecting the presence of insulin resistance. As insulin resistance worsens, glucose levels increase, with the appearance of glucose intolerance and, finally, of NIDDM, when insulin response cannot compensate for insulin resistance.
Nephrol Dial Transplant 1998
PMID:The epidemiology of diabetes mellitus. 987 Apr 17

Thirty-two patients with diabetes mellitus (22 IDDM and 10 NIDDM, 21 males and 11 females, age 44+/-11.8 years) were followed for 5.2+/-3.8 years after the onset of chronic renal failure, with the aim of evaluating the effect of low protein diets on the rate of decline of the residual renal function. During the 1.8+/-1.6 year follow-up period on free or uncontrolled low protein diet the mean rate of decline of creatinine clearance was 0.9+/-0.6 ml/min/month, significantly greater than that observed during 3.7+/-3.1 years on low or very low protein diets. The reduction of protein intake was followed by a significant decrease in daily urinary protein loss. A better glycaemic control was obtained on the low protein diet, and the daily insulin requirement decreased. The anthropometry, as well as the serum concentrations of rapid turnover proteins, did not change, in spite of the low or very low protein dietary supply for a long duration. The values of mean arterial pressure were quite similar during the follow-up period on free or uncontrolled low protein diet and during the study period on the low protein diet. A good compliance with reduced dietary intake (as demonstrated by the measurement of the daily urea excretion) was obtained in a large number of patients. In conclusion, our study confirms the protective effect on the residual renal function of low protein diets in IDDM and NIDDM patients with chronic renal failure due to diabetic nephropathy, in the absence of any sign of protein malnutrition.
Nephrol Dial Transplant 1998
PMID:Dietary treatment of diabetic nephropathy with chronic renal failure. 987 Apr 26


<< Previous 1 2 3 Next >>