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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The renal function in a group of diabetic children (n=29;age;4-17 yr; IDDM duration: 1,5-13 yr) was studied with a 3 year interval. At the first evaluation glomerular filtration rate (GFR) as assessed by inulin clearance was significantly increased compared to control values (167 +/- 32 vs. 124 +/- 18 ml/min/1.73 m2; pl less than 0.01). Eighteen out of 29 children exhibited a glomerular hyperfiltration (GFR greater than 160). Three years later mean GFR was identical (169 +/- 25 ml/min/1.73 m2) and 16 children were hyperfiltrating. Among them, 11 have had a persisting glomerular hyperfiltration over the 3-year period. Renal plasma flow (RPF) was positively correlated to GFR (r=0.7; p less than 0.01) and remained elevated at both evaluations (794 +/- 163 and 812 +/- 157 ml/min/1.73 m2, p greater than 0.01 vs, control values). When the children were separated into 3 groups according to IDDM duration no significant differences were observed in the results for GFR and RPF, Mean urinary albumin excretion was comparable at the 3-year interval, and not significantly different from the control values (5.2 +/- 3.7 and 8.2 +/- 6.6 respectively vs. 8.65 +/- 4 microgram/min). None of the children demonstrated a persistent microalbuminuria. This study reveals a high proportion of diabetic children with a persisting glomerular hyperfiltration, without any other symptom of incipiens nephropathy, If elevated GFR plays an important role in the development of diabetic nephropathy, this study emphasizes the value of regular evaluation of renal function in diabetic children.
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PMID:Persisting glomerular hyperfiltration in short-term diabetic children without microalbuminuria. 259 78

Diabetic renal disease is a major source of morbidity and mortality in Pima Indians. Excess mortality in NIDDM occurs principally in those with proteinuria regardless of whether death is due to cardiovascular or renal disease. Diabetes duration is a strong predictor of diabetic renal disease. Additional predictors include blood pressure, severity of diabetes, and, most likely, genetic or shared environmental determinants. The incidence rate of diabetic renal disease in Pima Indians with NIDDM is similar to that reported for subjects with IDDM with equivalent durations of diabetes. These observations suggest that clinical proteinuria and renal failure may occur in patients with NIDDM just as frequently as in those with IDDM. This finding has important implications and suggests that the variations in the frequency and age of onset of NIDDM among different populations and ethnic groups may be primarily responsible for the apparent variations in the frequency of ESRD associated with diabetes in different populations. Furthermore, diabetic renal disease appears to account for virtually all of the excess mortality associated with diabetes among Pima Indians and may perhaps do so in other populations. Improved survival of persons with NIDDM, an increasing incidence of this disease, and a relatively early age of onset in many populations could lead to a dramatic increase in the incidence of ESRD in the future. On the other hand, if diabetic renal disease and its consequences could be prevented, a profound improvement in the longevity and quality of life of those afflicted with diabetes might be possible.
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PMID:Diabetic renal disease in Pima Indians. 260 4

Fig. 5 provides a summary of the natural history of diabetic nephropathy in IDDM patients. The figure also includes the possibilities of intervention in the various stages of diabetic nephropathy. GFR values in normals are shown by the hatched area in the upper part of the figure. The lower part shows development of albuminuria. The level 20-200 micrograms/min is the microalbuminuric range. At present it is not possible to predict a malignant course either from the parental history (1), or from the prediabetic course (2). Neither at clinical diagnosis of diabetes, can complications be predicted (3). The figure shows a typical course in a patient developing diabetes at the age of 14 years. The patient showed poor metabolic control as indicated by the high level of GFR (greater than 150 ml/min) (4) and the increasing albumin excretion rate (4). At the age of 22 years the patient developed microalbuminuria (5) and later clinical nephropathy at age 30 years, typically after 16 years of diabetes. Blood pressure rises, and GFR starts to decline during incipient diabetic nephropathy with increasing microalbuminuria (greater than 70 micrograms/min) (5) (6), and end-stage renal failure reached at the age of 40 years,--if intervention is not undertaken. Intervention is possible as follows: A) hyperfiltration may be reduced by non-glycemic intervention such as a moderate reduction of protein intake, treatment with aldose reductase inhibitors (work in progress) or acute administration of a somatostatin analogue.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of blood pressure intervention on renal function in insulin-dependent diabetes. 261 18

End Stage Renal Disease (ESRD) is a common consequence of diabetic nephropathy (DN). DN is the major cause of death in patients with IDDM, accounting for greater than 40% of deaths with this form of diabetes. There is no clearly documented therapeutic technique that will prevent or reverse progressive renal damage in IDDM. While pancreatic transplantation and "cure" of diabetes in experimental animals may be associated with some histological reversal of renal pathology, this has not been documented in humans. Most studies agree that once diabetic renal disease is present (as documented by proteinuria), progression is inevitable, albeit the rate of progression may be altered by different therapeutic methods. There is considerable hope that "tight metabolic control" will prevent the initial damage that leads to DN and ESRD, but evidence remains inconclusive. There is some evidence that careful monitoring for microalbuminuria will allow for very early detection of damage and alterations in therapy. Our studies have documented a decrease in both morbidity and mortality in IDDM in patients who have been competitive athletes, suggesting that promotion of physical fitness may be a valuable means of delaying progression of renal disease while control of BP delays progression. Early detection and aggressive therapy is recommended. Some studies utilizing diets low in sodium and/or protein appear beneficial but more studies are needed before pediatric application.
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PMID:Can management strategies alter the course of diabetic nephropathy? 263 85

Many areas of information in the epidemiology of diabetic nephropathy are lacking, but multiple studies designed specifically to answer these questions are currently being conducted. In the next 5-10 years, our current understanding of the epidemiology of diabetic nephropathy may either be confirmed or discredited. In the meantime, clinicians should use the data available to make decisions about treatment and should focus on the modifiable factors of glucose and blood pressure control in both IDDM and NIDDM, especially in patients with low-level albuminuria or clinical proteinuria.
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PMID:The epidemiology of diabetic nephropathy. 268 17

Approximately one third of patients with IDDM develop end-stage renal disease. About the same percentage, though not of certainty the same patients, have elevated GFRs and plasma flow rates early in their disease and probably have elevated capillary pressure. Arterial hypertension in the setting of this pattern of renal vasodilation may be particularly predisposing to glomerular injury. Treatment of established diabetic nephropathy with good antihypertensive control can dramatically reduce the rate of progression of the disease. However, blood pressure control should be targeted to near normal ranges, that is, mean arterial pressures less than 100 mmHg and preferably lower. Some agents may be particularly beneficial in slowing the progression of the disease, but even standard agents have very important effects.
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PMID:Antihypertensive therapy in diabetes. 273 23

Of 1088 consecutive Ethiopian diabetic patients registered over 9 years 80 (7.4%) were diagnosed at or before age 15 years. There were 48 girls and 32 boys, with mean age of onset of 10.1 years. Diabetes had been present 10 years or less in 62, 11 to 20 years in 15, and more than 20 years in only 2. Twenty-two were rural, 27 had poverty certificates. Twenty-three have known diabetic relatives. The original mode of presentation could not be verified in 16, 7 presented in ketoacidosis, 5 were diagnosed by a diabetic relative, and the rest presented with the rapid onset of classical symptoms. To date, 43 have been ketoacidotic at least once. No pancreatic calcification was seen in 34 abdominal radiographs. Three of 6 newly diagnosed patients tested had islet cell surface antibodies. Three cases, initially suggestive of 'tropical malnutrition diabetes', evolved into typical type 1 diabetes. Serious complicating illnesses were tuberculosis (6), bacterial endocarditis (1) and rhinocerebral mucormycosis (1). Six patients have had metabolic cataracts. Ten patients (12%) have died, 4 of ketoacidosis and 4 of diabetic nephropathy. Childhood diabetes mellitus in Ethiopians is clinically very similar to type 1 diabetes elsewhere.
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PMID:Childhood diabetes mellitus in Ethiopians. 295 Nov 86

Forty per cent of all Danish insulin-dependent diabetic (IDDM) patients survive for at least 40 years after diagnosis. In an attempt to identify factors influencing the probability of surviving for 40 years or more, we followed all IDDM patients diagnosed before 1943 and admitted to the Steno Memorial Hospital. Patients surviving greater than or equal to 40 years were compared with patients dying within 35 years of diabetes diagnosis. Patients dying within 35 years were characterized by male preponderance (p less than 0.01), poor metabolic control (p less than 0.05), and by less frequent attendance at a specialized care unit (p less than 0.0001). Death due to uraemia/diabetic nephropathy was also characterized by male preponderance, poor metabolic control, and few contacts with a specialized care unit but in patients dying from cardiovascular disease (CVD), no effect of sex was found, indicating that the protection from CVD found in the female non-diabetic population is absent in IDDM patients. We conclude that long-term survival with IDDM may be determined by factors susceptible to intervention such as metabolic regulation and patient attitude to their disease.
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PMID:The natural history of insulin-dependent diabetes in Denmark: 2. Long-term survival--who and why. 295 21

This report reviews data regarding diabetic nephropathy and proliferative retinopathy (PR) that were derived from three inception cohorts of insulin dependent diabetics (IDDM) under the age of 21 years at the onset of diabetes mellitus in the index years 1939, 1949, and 1959. Nephropathy occurred in only a subsegment of this population and was age dependent rather than dependent on the duration of diabetes. It occurred earlier and was more aggressive in those with poorer control of the diabetes. The cumulative incidence of nephropathy decreased significantly between 1939 and the 1949 and 1959 cohorts. Possible reasons for this decline are discussed. Similarities and differences between the occurrence of nephropathy and PR are reviewed. The findings suggest that different etiologic factors are involved in the pathogenesis of these two microvascular complications.
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PMID:Diabetic nephropathy: natural history and declining incidence in diabetic children. 297 59

Hyperfiltration is a very characteristic feature in insulin-dependent diabetes. Hyperfiltration is to some extent associated with long-term glycemic control but the correlation is not very strong. Long-term hyperfiltration may play a role in the genesis of late diabetic nephropathy, but it is difficult to distinguish effects of hyperfiltration per se from effects of poor metabolic control. Long-term hyperfiltration without diabetes does not produce nephropathy. It is hypothesized that IDDM patients who do not show considerable hyperfiltration in spite of poor metabolic control may be those who are to some extent protected against late diabetic nephropathy, but other mechanisms may also be involved in the renal protection of these patients, who survive long-term diabetes without nephropathy. On the other hand, those with poor metabolic control combined with hyperfiltration are likely to develop nephropathy. In addition, it is suggested that the metabolic aberrations in diabetes, with the subsequent changes in the biochemistry of the glomerular wall, are permissive and absolutely required for the development of diabetic nephropathy. Of note, diabetic glomerulopathy in NIDDM occurs without significant hyperfiltration and extreme hyperfiltration in the one-kidney-model (without diabetes) does not produce nephropathy. Nonglycemic modalities of intervention, resulting in reduced hyperfiltration, e.g., low-protein diet or administration of somatostatin analogues, deserves interest as new potential ways of preventing or postponing diabetic nephropathy. Also intervention with aldose-reductase inhibitors may be an important therapeutic modality for those patients in whom good metabolic control is not obtainable. It is now well-established that antihypertensive treatment, including ACE-inhibition, reduces rate of decline in GFR in patients with already established nephropathy. In addition, protein excretion is diminished in IDDM patients with incipient diabetic nephropathy by antihypertensive treatment where GFR is well-preserved during treatment. No data are available for NIDDM.
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PMID:Comparative renal pathophysiology relevant to IDDM and NIDDM patients. 306 56


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