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

Coincidence of chronic renal failure and diabetes mellitus brings with it serious therapeutic problems, especially in dietetic treatment. It is not possible to wish to do justice to all the therapeutic principles of the text books to the same extent. The condition of renal failure with its demands takes precedence in all cases. But if the renal disease has not yet led to a perceptible retention of normal urinary constituents in the serum, no specific dietary measures are necessary. In these cases, the diabetic diet is proceded with in the usual manner.
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PMID:[Dietetic therapy of diabetes and renal insufficiency (author's transl)]. 40 67

The uptake of 45Ca was measured in slices of kidney cortex from normal rats, streptozotocin-diabetic rats, and streptozotocin-diabetic rats treated early and late with insulin. Insulin therapy was performed such that blood glucose levels were controlled in half the treated diabetic animals but not in the others. Considerably earlier than evidence of nephropathy (i.e., proteinuria and increased BUN levels) in streptozotocin-diabetic rats, there was a significant decrease in active uptake of calcium by the kidney. Insulin therapy, begun immediately upon diagnosis of diabetes, maintained normal calcium transport even when blood glucose levels were not controlled. On the other hand, insulin therapy, begun 1 mo after diabetes was confirmed but before evidence of nephropathy, did not restore calcium transport to normal whether or not blood glucose was controlled. We conclude that this biochemical mechanism, which possibly may be implicated in the pathophysiology of diabetic nephropathy, is clearly influenced by duration of insulin deficiency and not by the degree in hyperglycemia.
Diabetes 1979 Dec
PMID:Effectiveness of insulin therapy on altered renal calcium transport in diabetic rats. 51 Aug 5

This review concerns the present state of accomplishments in the study of SEM of human and experimental renal disease. Critical techniques of specimen preparation reviewed include perfusion fixation, razor tissue sectioning, alcohol cryofracture, microtome sectioning of paraffin or styrene embedded tissue, ultraplaning with glass knives of hard carbowax embedded tissues and glomerular isolation. Gold-palladium coating and heavy metal impregnation with osmium, uranium, and silver are discussed. A compendium of SEM observations of human glomerular, vascular and tubular disease is presented. Techniques for SEM of experimental renal disease are reviewed. These include latex vascular injection, freeze drying, x-ray microanalysis and use of backscattered electron imaging. Experimental models previously investigated by SEM are puromycin aminonucleoside nephrosis, daunomycin nephrosis, and N,N1-Diacetylbenzedine glomerulopathy, nephrotoxic serum nephritis, and protamine perfusion glomerulopathy. Reviewed are acute tubular necrosis caused either by angiotensin, hypotension, norepinephrine, glycerol, mercury, and unilateral renal artery occlusion, also potassium depletion nephropathy, alloxan diabetes and diphenylamine-induced polycystic disease.
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PMID:SEM of human and experimental renal disease. 52 33

The efficacy of correlating the L/S ratio in the amniotic fluid with fetal lung maturity has been substantiated in normal pregnancies. In gestations complicated by fetomaternal diseases, however, the assay is less reliable. This study involves 555 pregnancies in which there was a significant maternal, fetal, or placental disorder. The L/S ratio was related to fetal respiratory maturity as measured by Dubowitz criteria and the occurrence of RDS. The results show that pre-eclampsia, chronic hypertension, diabetes (Class D, E, F), significant cardiovascular disease, severe hemoglobinopathies, various congenital anomalies, chronic placental insufficiency, and prolonged ruptured membranes accelerated the L/S ration. Conversely, mild diabetes (Class B, C), intrinsic renal disease, hepatitis, collagen disease, hydrops fetalis, syphilis, and toxoplasmosis were associated with a delay in the L/S ratio. A significant increase in erroneous responses was noted in these patients when the L/S ratio was correlated to infant maturity and to the incidence of RDS. Possible mechanisms for these findings are discussed.
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PMID:The lecithin/sphingomyelin ratio in cases associated with fetomaternal disease. 57 73

A report is given on ten (seven female, three male) diabetis with uncommonly long duration of the disease. Diabetes had become manifest at an early age (mostly childhood) and, then, had continued for a period of fifty to sixty-one years. Eight patients suffer from retinopathy, two are free from it. Only three cases show nephropathy of moderate development and inconspicuous progression. Coronary sclerosis, peripheral sclerosis, and neuropathy recede with time. There is a surprising discrepancy of findings concerning retinopathy - on the one hand: simple retinopathy tending to spontaneous regression; on the other hand: malignant proliferating retinopathy. Uncommon also is the tarrying behaviour of nephropathy.
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PMID:[Retinopathy and angiopathy in diabetes of fifty to sixty years duration (author's transl)]. 59 66

The changes in plasma renin activity (PRA) and plasma aldosterone concentration (PA) in response to dietary sodium restriction and upright posture were evaluated in 7 patients with juvenile-type, insulin-dependent, uncomplicated diabetes mellitus and in 5 healthy volunteers. All patients had normal blood pressure, 24-hour urine protein excretion and endogenous creatinine clearance. Renal sodium conservation and concentrating ability were grossly normal and 5 patients so tested, had normal renal acidification. PRA and PA were normal in every subject suggesting that abnormalities of the renin-aldosterone axis are late complications of diabetes mellitus usually associated with hypertension and nephropathy or neuropathy.
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PMID:Renin-aldosterone responsiveness in uncomplicated juvenile-type diabetes mellitus. 64 May 77

Plasma aldosterone (PA) and plasma renin activity (PRA) were determined in 44 diabetics, of whom nine were normotensive but not nephropathic (group 1), 10 were hypertensive but not nephropathic (group 2), and 25 were hypertensive and nephropathic (group 3); they were kept in balance on a diet composed of 10 to 20 mEq. of sodium (Na) and 100 mEq. of potassium (K). Supine PA in group 1 was 38 +/- 7 ng. per deciliter, whereas in normals it was 24 +/- 2 ng. per deciliter (P less than 0.05); beyond that, neither supine nor upright PA or PRA differed significantly from normal in groups 1 and 2. By contrast, in group 3, supine PA was 13 +/- 1 ng. per deciliter and PRA 2.0 +/- 0.2 ng./ml. and upright PA was 39 +/- 7 ng. per deciliter and PRA 3.8 +/- 0.5 ng./ml., all significantly lower than those in the other groups (P less than 0.01). Nine patients, one in group 1 and eight in group 3, had low supine and upright PA and PRA; four had hyperkalemia. An additional nine patients in group 3 had low upright PA, with normal or low PRA; two had hyperkalemia. Of the 18 patients with low upright PA, K correlated with glucose (R = 0.46, P less than 0.05). These results suggest (1) the renin-aldosterone system generally responds normally in diabetics without nephropathy but responds subnormally when nephropathy is present, (2) hyporeninemic hypoaldosteronism is frequent in diabetics with nephropathy but may occur in the absence of clinical nephropathy, and (3) hyperkalemia in some diabetic patients may be secondary to hypoaldosteronemia and hyperglycemia.
Diabetes 1978 Jul
PMID:Aldosterone responsiveness in patients with diabetes mellitus. 65 19

The natural history of patients with glucose intolerance was observed in 334 patients during a period of 18 years. Glucose tolerance testing (100 g orally) was characterized by measurement of induced insulin secretion. Diabetic complications of retinopathy, sensory neuropathy, and renal disease developed only in the group of patients in whom the induced serum insulin peak fell below 60 mu U/ml. Preservation of an insulin secretory reserve that permitted serum insulin peaks of 60 muU/ml or greater was not associated with development of these complications or symptoms of insulin deficiency despite the presence of an equal degree of fasting hyperglycemia and glucose intolerance. A critical amount of insulin secretory reserve distinguishes between two qualitatively distinct clinical syndromes: true diabetes mellitus (the development of signs and symptoms of insulin deficiency) and the syndrome of pure resistance to insulin (signs and symptoms of hyperglycemia in the setting of adequate or excessive insulin secretion, frequently with obesity, but without diabetic complication).
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PMID:Insulin secretion in the diagnosis of adult-onset diabetes mellitus. 67 27

Using clearances of microaggregated iodinated human serum albumin in a serial 'stress test,' defective phagocytosis by the Kupffer cells has been demonstrated in diabetic patients with K.W. nephropathy and proliferative retinopathy. This indicates a disturbance of phagocytic cell function that has implications for the cellular pathology of microangiopathy. The effect is not due to uremia, but could be due to T3 deficiency or lipid deposition. In hypothyroidism, there is defective RES phagocytosis, and alcoholics with hyperlipidemia can have impaired clearances. Hence, patients with advanced diabetes, hypothyroidism, and some alcoholics are at risk from infection.
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PMID:Reticuloendothelial cell dysfunction in diabetes and hyperlipidemia. 69 80

We studied the prevalence and the risk factor among the patients of gout in Mexico. Research was conducted in the National Institute of Cardiology and in our private practice. Prevalence of hiperuricemia and gout in the Institute of Cardiology was of 1% (970 out of nearly 100,000 patients). We divided those cases of two subgroups: Reumatology patients (333) and Cardiovascular patients (529). In the first group primary gout was (96.3), and (50.32% in the second. Risk factor was quite different too: nephropathy 9.9%, lithiasis 9.3%, pyelonephritis 2.7%, cardioangiosclerosis 12.9%, aortosclerosis 6.6%, coronary insufficiency 6.3%, myocardial infarction 0.9%, arterial hypertension 24.6% obesity 56.1% and diabetes 9.9% in the Reumatology group; in the Cardiovascular one, nephropathy 14.3%, lithiasis 12.2%, pyelonephritis 7.1%, cardioangiosclerosis 62.7%, aortosclerosis 31.7%, coronary insufficiency 24.9%, myocardial infarction 29%, arterial hypertension 51%, obesity 54.8% and diabetes 20.4%. Among the private practice patients prevalence was of 10.1% (961). In an early age (39 years) in men and a later one for women (53 years). Other characteristics of epidemiology and risk factor are: primary gout 89%, atherosclerosis 5%, coronary disease 4.6%, lithiasis 4.7%, nephropathy 2%, pyelonephritis 1%, obesity 43%, and diabetes 4.6%. In an small group of patients of our private practice we made an exhaustive study of risk factor and the metabolic disorder of lipids. We found the following frequency: 9.3 of nephropathy, 31.2% of lithiasis, 18.7% of pyelonephritis, 68.9% of cardioangiosclerosis, 46.8% de coronary insufficiency, 9.3% of myocardial infarction, 68.7% of arterial hypertension, 68.7% of obesity and 18.7% of diabetes. In the lipid profile we found an increase in triglicerids and prebeta lipoprotein. We have amply discussed the relation between hiperuricemia and pathology considered as a risk factor from the genetic point of view as well as the metabolic and circumstancial aspect. From all that we concluded that risk is multifactorial.
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PMID:[Various epidemiological aspects of hyperuricemia and gout in Mexico: incidence and the cardiovascular risk factor]. 72 44


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