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

The best definition of risk factors for renal injury, irrespective of the aetiological agent, comes from observations in patients with acute renal failure. From such observations, two subdivisions have evolved, i.e., acute insults and host risk factors. Acute renal insults include: hypertension, sepsis, use of nephrotoxic drugs (e.g., aminoglycoside antibiotics and contrast media), haemoglobinuria or myoglobinuria, liver disease and extracellular volume depletion. Host risk factors include: advanced age, hypertension, gout and hyperuricaemia, diabetes mellitus, chronic renal failure and use of diuretics. Furthermore, the mechanism of acute renal injury can be correlated with different risk factors: for a tubular toxic agent, acting either directly on the cells or haemodynamically, a dose-dependency is characteristic; while for immunologically mediated injury, genetic predisposition is more important. The identification of risk factors for chronic toxic injury is confounded by the possibilities of multiple episodes of subclinical renal injury, the distinct possibility that a major component of the ageing process may be a loss of renal reserve, and a progressive body burden, of, e.g., cadmium, which may deplete intrinsic protective mechanisms. However, clinically relevant risk factors can alert the clinician to exercise additional caution when prescribing medications that are potentially nephrotoxic. Such factors include dehydration, pre-existing renal disease, age, co-existing diseases that cause renal ischaemia, gender, concomitantly administered drugs, and electrolyte abnormalities.
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PMID:Risk factors for toxic nephropathies. 265 33

Circadian rhythms of insulin needs and action are a frequently discussed issue that is both of considerable physiological interest and of clinical importance in case of insulin substitution in type 1 diabetes. Basally, insulin is released in a pulsatile fashion which seemingly is erratic but at close analysis displays 'free-running' cyclical rhythmicity of 8-30 min duration that possibly guarantees optimal insulin action. This basal mode of insulin secretion is subject to a multitude of endogenous control systems that act on the B-cell both in a stimulatory (e.g., beta-agonists, glucagon as well as glucose and amino acids) and an inhibitory fashion (e.g., alpha-agonists, somatostatin). Since impairment of target cell sensitivity to insulin action and hyperglycemia may be caused by the stress hormones, cortisol, epinephrine and growth hormone included, with in part intrinsic rhythmicity, as well as by dehydration and by prolonged insulin withdrawal, a secondary feed-back signal on insulin release may easily be induced by rising blood glucose levels. In that modulators of insulin release and action are themselves secreted in a circadian fashion they tend to secondarily imprint the mode of insulin release. Therefore, any difference between a daily maximum and minimum in plasma insulin concentration besides its free-running short-term rhythmicity has to be regarded as a composite secondary circadian rhythm. It is in particular due to variable secondary early-morning and late-afternoon insulin resistance.
Diabetes Res Clin Pract 1989 May 15
PMID:Circadian rhythms of insulin needs and actions. 266 58

Hyperglycaemic hyperosmolar non-ketotic syndrome (HHNS) is a life-threatening complication of uncontrolled diabetes mellitus. This syndrome is characterised by severe hyperglycaemia, a marked increase in serum osmolality, and clinical evidence of dehydration without significant accumulation of ketoacids. HHNS is typically observed in elderly patients with non-insulin-dependent diabetes mellitus, although it may rarely be a complication in younger patients with insulin-dependent diabetes, or those without diabetes following severe burns, parenteral hyperalimentation, peritoneal dialysis, or haemodialysis. Patients receiving certain drugs including diuretics, corticosteroids, beta-blockers, phenytoin, and diazoxide are at increased risk of developing this syndrome. Patients usually present with a prolonged phase of osmotic diuresis leading to severe depletion of both the intracellular and extracellular fluid volumes. Losses of water exceed those of sodium, resulting in hypertonic dehydration. Therefore, correction of the syndrome will ultimately require administration of hypotonic fluids. Patients presenting with HHNS also have significant depletion of potassium and other electrolytes that will need to be replaced. The principal goal at the outset of therapy must be restoration of the intravascular volume to assure adequate perfusion of vital organs. It remains controversial whether 0.9% or 0.45% NaCl should be the initial fluid infused intravenously. We prefer to administer 0.9% NaCl until the vital signs have stabilised and then substitute 0.45% NaCl. 10 to 15 units of regular human insulin should be injected as a bolus, followed by a continuous infusion of approximately 0.1 U/kg/h. Once the blood glucose approaches 13.9 to 16.7 mmol/L (250 to 300) mg/dl, 5% dextrose should be added to the intravenous fluids and the rate of insulin infusion reduced. Following recovery many patients presenting with HHNS will not require long term insulin therapy and can be managed effectively with diet or oral agents. Precipitating causes of HHNS must be identified and treated simultaneously with correction of the metabolic abnormalities. Appropriate management of precipitating illnesses will limit the high mortality associated with HHNS. This review discusses the current state of knowledge concerning the pathogenesis of HHNS, the clinical features of the disorder, and a systematic approach to treatment.
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PMID:Treatment of hyperglycaemic hyperosmolar non-ketotic syndrome. 268 Apr 38

The ultrastructure of the hypothalamo-neurohypophysial system of rats was examined 8 weeks after streptozotocin-induction of type I diabetes. These studies provided evidence for numerous neuronal alterations to the hypothalamo-neurohypophysial system in streptozotocin-diabetic rats. Changes were observed in the somata, dendrites and axons of both the supraoptic and paraventricular nuclei as well as in axon profiles in the neurohypophysis. Many of these changes suggest an increased activity of the hypothalamo-neurohypophysial complex, with increased synthesis of neurohypophysial hormones in the hypothalamus together with depletion of neurosecretory granules in axons in the neurohypophysis. Some degenerative changes, however, were also observed. It is proposed that chronic dehydration and hypoxia in diabetes may contribute to the ultrastructural reorganization of the hypothalamo-neurohypophysial complex in streptozotocin-diabetic rats.
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PMID:The hypothalamo-neurohypophysial system in streptozotocin-diabetic rats. Ultrastructural evidence for neuronal alterations in the supraoptic and paraventricular nuclei and in the neurohypophysis. 279 83

A baby boy with transient neonatal diabetes mellitus presenting with hyperglycaemia, glycosuria, and dehydration without ketonuria on the second day of life is reported. C-peptide levels were measured to aid in the assessment of insulin treatment. Very low levels were found for the first 5 months of life (less than 0.06 nmol/l). Thereafter insulin treatment was discontinued and the baby thrived showing normal growth and development at age 2 1/2 years.
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PMID:C-peptide levels in transient neonatal diabetes. 295 Nov 42

Although some previous studies have suggested that insulin-dependent diabetes mellitus (IDDM) is a heterogeneous condition with variant forms being associated with HLA-DR types, the evidence, thus far, is conflicting. To address this issue, we have examined the presenting characteristics of a consecutive admission series of 200 newly diagnosed cases of IDDM from the Children's Hospital of Pittsburgh. Because HLA-DR frequencies vary by race, data are presented only for the 172 white cases with complete HLA-DR typing. HLA-DR3 was found more frequently among male cases and DR4 among female cases (P less than 0.005). Generally, patients with DR4 presented with a severer clinical picture, being more likely to have impaired consciousness and significant dehydration. In addition, patients with DR4 were more likely to be acidotic, ketotic, and to more frequently report a recent viral infection. This latter finding was supported by a greater frequency of antibodies to Coxsackie-B viruses in the DR4 cases at presentation. These results therefore suggest that there is considerable heterogeneity in IDDM, at least in presenting characteristics, according to HLA-DR type.
Diabetes 1985 Dec
PMID:HLA heterogeneity of insulin-dependent diabetes mellitus at diagnosis. The Pittsburgh IDDM study. 299 11

The chronic complications of diabetes are thought to be caused by an interaction between hyperglycemia or other metabolic consequences of insulin deficiency and other poorly defined independent genetic or environmental factors. Several important biochemical sequelae to hyperglycemia are discussed. Macrovascular disease appears to be primarily age-related in diabetic patients. The clinical course, manifestations, and management of diabetic complications are significantly altered when they appear against a background of the degenerative changes of aging, greatly complicating diagnosis and management. In elderly patients, the acute complications of diabetes--ketoacidosis and hyperosmolar dehydration--often occur in the context of chronic complications that greatly compound their management and increase their morbidity and mortality.
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PMID:Acute and chronic complications of diabetes mellitus in older patients. 301 Jul 19

A patient who developed hyperosmolar, hyperglycemic, nonketotic coma (HHNC) while receiving home total parenteral nutrient (TPN) therapy is described, and the etiology, clinical features, and treatment of HHNC are reviewed. A 51-year-old black man diagnosed as having Dukes' stage D signet-cell carcinoma of the rectum was discharged on home TPN therapy after a prolonged hospital course and the persistence of a gastrointestinal fistula. Seventeen days after discharge, the patient developed polyuria, became febrile, and lost mental acuity. Upon hospitalization, the patient's physical condition and laboratory values were consistent with the diagnosis of HHNC. The patient was treated with intravenous fluids and small quantities of insulin. The patient's home records indicated that he had lost large volumes of fluid through his fistula, resulting in a net negative fluid balance. The patient's records also indicated that he had had mild glycosuria with a normal urine output at home. This normal urine output despite a body-fluid deficit could be explained by osmotic diuresis related to either glucose or urea. Hypotonic fluid loss resulting from fistula output and osmotic diuresis may have led to this patient's hypertonic state and critical illness. The patient died on hospital day 11 as a result of widely disseminated cancer. HHNC arises most often as a complication of non-insulin-dependent diabetes. It is also a major complication resulting from hypertonicity related to glucose intolerance or other conditions that can occur in patients receiving TPN therapy. The underlying cause of the hyperosmolar state appears to be dehydration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hyperosmolar, hyperglycemic, nonketotic coma in a patient receiving home total parenteral nutrient therapy. 310 54

Aldose reductase [aldehyde reductase 2; alditol:NAD(P)+ 1-oxidoreductase, EC 1.1.1.21] catalyzes conversion of glucose to sorbitol. Although its activity is implicated in the progression of ocular and neurological complications of diabetes, the normal function of the enzyme in most cells is unknown. Both aldose reductase activity and substantial levels of sorbitol were previously reported in renal inner medullary cells. In this tissue, the extracellular NaCl concentration normally is high and varies considerably depending on the urine concentration. We report here on a line of renal medullary cells in which medium that is high in NaCl greatly increases both aldose reductase activity and intracellular sorbitol. In these tissue culture cells (and presumably also in the renal inner medulla), the intracellular sorbitol helps balance the osmotic pressure of elevated extracellular NaCl and thus prevents cellular dehydration.
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PMID:Induction of aldose reductase and sorbitol in renal inner medullary cells by elevated extracellular NaCl. 310 2

Hyperosmolar nonketotic diabetic coma (HHNC) is a syndrome of acute decompensation of diabetes mellitus, occurring mainly in the elderly and characterized by marked hyperglycemia, hyperosmolarity, severe dehydration, occasional neurological signs, obtunded sensorium, and absence of ketonemia or acidosis. The mortality is high. Early aggressive therapy with large amounts of normal or half normal saline, insulin, and potassium is of prime importance. Since associated diseases cause most fatalities the importance of managing these problems effectively cannot be overemphasized. Complications of therapy can be congestive heart failure secondary to excessive fluid administration, hypoglycemia if too much insulin is given, and hypokalemia if potassium is inadequately replaced.
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PMID:Hyperosmolar nonketotic diabetic coma: diagnosis and management. 331 90


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