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

Renal venous thrombosis, a clotting process that originates in the venous radicles and progresses into the main renal vein and vena cava, predominantly affects newborn infants. It may be manifest in one or both kidneys and follow maternal diabetes, diarrhea and dehydration, congenital heart disease, acute blood loss, sepsis, asphyxia, and shock. The most common signs include gross hematuria, enlarged palpable kidneys, and thrombocytopenia. Evaluation should include ultrasonography of the kidneys (demonstrating renal enlargement with disruption of the normal echo pattern), computed tomography, and renal isotope scanning. The initial treatment is supportive. Surgical intervention is not indicated in the acute phase except in the rare instance of bilateral disease. Anticoagulant therapy is still controversial. Late sequelae include impairment of renal function, shrunken hypoplastic kidney, arterial hypertension, and tubular defects.
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PMID:Renal venous thrombosis in children: changes in management. 635 1

Risk factors for nephrotoxicity in patients treated with aminoglycosides were determined from the case records of 214 patients in two prospective, randomized clinical trials of gentamicin and tobramycin. Nephrotoxicity, defined as a 50% or greater fall in calculated creatinine clearance, developed in 30 patients (14.1%). Patients with nephrotoxicity had higher initial calculated creatinine clearances, were more often women, and were more likely to have liver disease. Using stepwise discriminant analysis, these factors were selected with the initial 1-hour post-dose aminoglycoside level, patient age, and shock. An equation was generated that was accurate in discriminating between patients with and without nephrotoxicity when validated in an independent population. Factors that did not add significantly to the equation were diabetes, dehydration, serum bicarbonate, bacteremia, urinary tract infection, gentamicin or tobramycin use, duration of therapy, total aminoglycoside dose, or the use of clindamycin, furosemide, or cephalothin.
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PMID:Risk factors for nephrotoxicity in patients treated with aminoglycosides. 636 8

The deterioration of glucose tolerance and insulin resistance observed in states of hypertonic dehydration are commonly ascribed to a concomitant increase in circulating insulin counterregulatory hormones. To examine the effect of hyperosmolality per se on carbohydrate metabolism, tissue sensitivity to insulin was assessed by means of the euglycemic insulin clamp technique and simultaneous 3H-3-glucose kinetic analysis. Eight healthy volunteers participated in three protocols: (1) In the hyperosmolal study, serum osmolality was raised from 280 +/- 1 to 302 +/- 1 mosm/kg by a primed continuous infusion of hypertonic mannitol. Following 2 h of hypertonicity, a euglycemic insulin clamp study was performed. The plasma insulin concentration was acutely raised and maintained at 147 +/- 20 microU/ml, while plasma glucose was maintained at basal levels; (2) In the control insulin clamp study, isotonic sodium chloride was infused instead of mannitol. No significant change in serum osmolality was observed during the control study; (3) To examine the effect of mannitol per se on insulin-mediated glucose metabolism, isotonic mannitol was infused in a third study to raise the plasma mannitol level to a similar extent as observed during the infusion of hypertonic mannitol. The serum tonicity did not change during the isotonic mannitol infusion. Insulin-mediated glucose utilization (M) was 6.69 +/- 0.51 mg/kg X min in the control study and decreased to 5.84 +/- 0.40 mg/kg X min following the exposure to hyperosmolality (P less than 0.05).2+ +/- 0.60 versus 4.30 +/- 0.43 mg/kg X min per microU/ml X 100).(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1983 Nov
PMID:Impairment of insulin-mediated glucose metabolism by hyperosmolality in man. 641 9

A case of acute intestinal vascular necrosis in a 19-year-old user of oral contraceptives (OCs) is described, and hypotheses explaining the digestive complications of synthetic estrogens are reviewed. The patient had originally presented with a violent gastric pain that subsequently spread to the entire abdomen. An abrupt worsening of her condition involved cardiovascular collapse associated with a peritoneal syndrome, vomiting and dehydration, and hyperleukocytosis. Emergency opening of the peritoneum was followed by evacuation of a large quantity of fetid gas and alimentary debris, and observation of a completely necrosed stomach. A careful lavage of the entire intestinal cavity led to temporary improvement, but it became clear during an attempt at gastrectomy that further treatment would be unavailing and the patient died shortly thereafter. Estrogens were believed to be responsible for the digestive necrosis because it occurred in a young woman who had used an estrogen-rich OC for 3 years and who smoked; a hapatic biopsy confirmed the diagnosis. No traces of other risk factors such as hypertension, hyperlipidemia, diabetes, neoplasia, or obesity were observed. Recent publications indicate that OCs are responsible for a certain number of digestive problems, which may include acceleration of intestinal transit, severe diarrhea, rectorrhagia, ischemic or ulcerative colitis, intestinal infarct which is usually localized, and hepatocellular problems ranging from moderate hepatic insufficiency to malignant tumor and Budd-Chiari syndrome. OCs do not modify hemodynamic regimes, but they may cause elevation of fibrinogen and thrombin, diminution of antithrombin III acitivty, increased platelet adhesivity, and decreased fibrinolysis leading to hypercoagulability. These modifications in hemostasis occur in all OC users and are not statistically correlated with occurence of thrombotic accidents. OCs are probably responsible for parietal vascular lesions; experimental injection of synthetic estrogens is associated with both arterial and venous lesions. The most characteristic anomaly is at the level of the intima, with proliferation of smooth muscle cells and increased conjunctive tissue fibers associated with proliferation of the media or the endothelium. The absence of lipid deposits, the simultaneous appearance of arterial and venous lesions, and other evidence argues against and atheromatous origin of parietal lesions. A significant correlation has been found between high levels of anti-synthetic ethinyl estradiol antibodies and the presence of vascular lesions. It is hypothesized that these circulating immune complexes penetrate the vascular walls of OC users and produce lesions, which may depend on factors such as smoking.
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PMID:[Digestive complications of oral contraceptives: a case of extensive digestive necrosis in a young woman]. 647 54

Direct measurement of plasma AVP and indirect assessment of antidiuretic activity during standard dehydration tests were made in 21 polyuric and polydipsic patients to establish the efficacy of each method in determining the cause of polyuria. Patients with acquired nephrogenic diabetes insipidus (e.g. diabetes mellitus, renal failure, hypercalcaemia) were excluded from the study. Cranial diabetes insipidus was diagnosed by plasma AVP responses to osmotic stimulation during infusion of hypertonic 5% saline which were subnormal in 13 patients, 4 of whom had undetectable plasma AVP and 3 who had reduced but osmoregulated AVP release. Standard water deprivation tests confirmed cranial diabetes insipidus in all but 2 patients who were diagnosed as partial nephrogenic diabetes insipidus. The remaining 8 patients had normal, osmoregulated AVP secretion; the cause of their polyuria was determined by their renal response to desmopressin. Two patients had nephrogenic diabetes insipidus and 6 had primary polydipsia. The majority of polyuric patients could be accurately diagnosed by carefully performed dehydration tests. We suggest that direct measurements of plasma AVP during osmotic stimulation are only necessary to distinguish mild forms of cranial from nephrogenic diabetes, or to define precisely the characteristics of AVP secretion.
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PMID:A comparison of diagnostic methods to differentiate diabetes insipidus from primary polyuria: a review of 21 patients. 665 43

The effect of weight loss produced by gastric exclusion on the metabolism of previously morbidly obese persons was examined. A standardized gastric exclusion procedure was performed in 150 morbidly obese patients during a 6 year period. These patients were followed for from 6 to 60 months (mean 27.8 months). The mean excess weight loss was 75 percent and was maintained from 2 to 5 years. A small but significant decrease was noted during the first 3 to 6 postoperative months in the parameters of protein metabolism examined. Although this may reflect mild depletion in protein stores, of greater importance was the demonstration that these parameters spontaneously corrected themselves by 12 months. Mild abnormalities in serum electrolyte concentrations were noted in the postoperative period. They appeared to be related to dehydration, were not clinically significant, and also resolved spontaneously. Clinically significant abnormalities in divalent ions were absent. Significant and sustained reductions in blood pressure, fasting glucose concentration, serum triglyceride values, and uric acid and hepatic enzyme concentrations were demonstrated in the entire population. A small and non-sustained decrease in cholesterol was seen. Hypertension was eliminated in 96 percent of the affected subpopulation, diabetes in 100 percent, gout in 100 percent, hyperlipidemia in 92 percent, and improved hepatic function was found in 95 percent. These changes should reduce the overall morbidity and mortality of the patient population in the future.
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PMID:Prospective metabolic evaluation of 150 consecutive patients who underwent gastric exclusion. 671 48

Contrast nephropathy is an adverse alteration in renal function induced by intravascular contrast media. Most cases involve transient asymptomatic episodes; yet a significant number involve oliguria and/or permanent renal damage. The incidence of contrast nephropathy in the general hospitalized population is about 5%, and is associated with preexisting renal insufficiency and diabetes mellitus. The incidence in patients with normal renal function is significantly lower - 0.6% following IVP and 2% following angiography. Angiography carries risks inherent to the technical problems of the procedure itself. Preexisting renal insufficiency is the most significant predisposing condition of contrast nephrotoxicity. As many as two-thirds of patients with chronic renal failure may experience an acute deterioration in renal function following exposure. Most of these episodes are transient and benign. Diabetic patients with preexisting renal insufficiency are at an even greater risk; about 75% of such patients will experience renal complications. The risk is even higher in JODM patients with severe renal disease; there is an over 90% incidence of nephrotoxicity with as many as half sustaining permanent renal damage. Adequate hydration does not appear to reduce the incidence of contrast nephropathy in susceptible patients, but it may reduce the likelihood of oliguria and permanent damage. In multiple myeloma the risk of contrast-induced renal failure is low, and probably involves a different pathogenesis than seen in other cases of contrast nephropathy. The incidence in myeloma patients is probably increased in the presence of dehydration and renal insufficiency. Peripheral vascular disease, hypertension, old age and large and repeated doses of contrast may increase the risk in susceptible patients. Prevention of contrast nephropathy must start with identification of patients at risk. In patients with preexisting renal insufficiency, and especially diabetic patients with preexisting renal insufficiency, the anticipated benefit should outweigh the potential risk of exposure to contrast media.
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PMID:Contrast nephropathy. 675 74

It has been generally accepted that acidosis results in hyperkalemia because of shifts of potassium from the intracellular to the extracellular compartment. There is ample clinical and experimental evidence, however, to support the conclusion that uncomplicated organic acidemias do not produce hyperkalemia. In acidosis associated with mineral acids (respiratory acidosis, end-stage uremic acidosis, NH4Cl-or CaCl2-induced acidosis), acidemia per se, results in predictable increases in serum potassium concentration. In acidosis associated with nonmineral organic acids (diabetic and alcoholic acidosis, lactic acidosis, methanol and the less common forms of organic acidemias secondary to methylmalonic and isovaleric acids, and ethylene glycol, paraldehyde and salicylate intoxications), serum potassium concentration usually remains within the normal range in uncomplicated cases. A number of factors, however, may be responsible for hyperkalemia in some of these patients other than the acidemia per se. These include dehydration and renal hypoperfusion, preexisting renal disease, hypercatabolism, diabetes mellitus, hypoaldosteronism, the status of potassium balance, and therapy. The mechanism(s) of this differing effect of mineral and organic acidemias on transmembrane movement of potassium remains undefined. The prevalent hypothesis, however, favors the free penetrance of the organic anion into cells without creating a gradient for the hydrogen ions and, thus, obviating the efflux of intracellular potassium. The importance of the presence of hyperkalemia in clinical states of organic acidemias is obvious. A search for the complicating factors reviewed above should be undertaken since organic acidemias per se, should not be expected to be accompanied by elevations of serum potassium concentration. Moreover, the classical teaching that the absence of hyperkalemia during severe acidosis is indicative of severe potassium deficiency, may not be universally valid in patients with uncomplicated organic acidemias.
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PMID:Serum potassium concentration in acidemic states. 679 Oct 40

Clinical and biochemical findings, obtained in 76 diabetic children aged 3 to 15 years, were analyzed. Osmolarity of the plasma and plasmic components (electrolytes, glucose and urine) as well as blood antidiuretic activity (ADA) were studied. Osmolarity and plasmic ADA indices increased and water-electrolyte balance deteriorated as metabolic disorders developed. No exact linear correlation between osmolarity and the blood ADA indices was observed in diabetes decompensation. A high blood ADA level is considered to be a manifestation of the pronounced organism dehydration. It was shown that blood coagulation, accumulation of active osmotic substances in the blood, i.e. glucose, urine and other products of the disordered metabolism, as well as a decrease in renal glomerular filtration cause the hyperosmolaric syndrome in diabetic children.
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PMID:[Osmotic homeostasis and blood antidiuretic activity in diabetes mellitus in children]. 686 50

A case of transient diabetes "mellitus" in a newborn infant with secondary hypertonic dehydration is presented. Authors review the problematical ethiology of this rare disease and a commentary is made on the adequate control of their case with continuous endovenous infusion of insulin.
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PMID:[Transient neonatal diabetes (author's transl)]. 699 39


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