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Query: UMLS:C0011854 (type 1 diabetes)
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There are two types of diabetes mellitus. Type I, insulin-dependent diabetes (IDDM), which becomes manifest before the age of 40, is the result of an absolute deficiency of insulin. Type II, the non-insulin-dependent diabetes (NIDDM), develops in the elderly and is caused by a relative insulin deficiency. Patients with type-I diabetes are prone to the development of ketoacidosis, while type II causes hyperglycaemic, hyperosmolar, nonketotic coma. Apart from these acute metabolic alterations, the long-term complications of diabetes are of concern to the anaesthesiologist. Hypertension, coronary artery disease, renal insufficiency and autonomic neuropathy are common and can result in myocardial ischaemia, cardiovascular instability and gastroparesis, with an increased risk of aspiration. Limited movement of the atlanto-occipital joint can cause difficult intubation. To avoid perioperative metabolic catastrophy, blood glucose concentration should be kept between 6.7 and 10 mmol.l-1 (120-180 mg.dl-1). Hypoglycaemia can result in neurological damage, whereas hyperglycaemia causes impaired wound healing and susceptibility to infections and worsens ischaemic damage to the myocardium and brain. Perioperative diabetes management depends on the severity of the surgical procedure and the type of diabetes. All type-I diabetics, whatever operation being performed, need insulin. The intravenous route is recommended as it allows better adjustment. After determination of the fasting blood glucose level, insulin is given at a dosage of 0.5-1 U.h-1 (at gluc < 11.1 mmol.l-1), 1.5-2 U.h-1 (at gluc 11.1-16.7 mmol.l-1) or 3 U.h-1 (at gluc > 16.7 mmol.l-1). In addition, 5-10 g glucose.h-1 is given. In type-II diabetes the oral antidiabetic drug is withheld. During minor surgery the blood glucose concentration is monitored frequently, and if necessary insulin (with gluc > 13.9 mmol.l-1) or glucose is given. In most cases of major surgery insulin therapy will be necessary. Administration should follow the guidelines listed for type-I diabetes. Whether the intravenous or the subcutaneous route is used for insulin, repeated glucose determinations are mandatory. If ketoacidosis develops the volume depletion is treated with normal saline. For hyperglycaemia and acidosis insulin (3-6 U.h-1) with 10-20 mmol.h-1 potassium phosphate is given. Bicarbonate is only indicated when the serum pH is lower than 7.1. It must be borne in mind that perioperative management of diabetes does not end with postanaesthesia care.
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PMID:[Anesthesia and diabetes mellitus]. 804 63

We investigated both sodium-lithium countertransport (Na-Li CT) and ouabain-sensitive sodium transport (Na pump) of erythrocytes in healthy subjects (group A), patients with non-insulin-dependent diabetes (NIDDM) without nephropathy (group B), patients in the proteinuric stage (group C), and those in the renal insufficiency stage (group D). Erythrocytes from all four groups had a similar initial water and ionic content and were loaded with similar degrees of Li and Na for efflux studies. There were no significant differences in erythrocyte Na-Li CT or Na pump among the four groups. However, the maximal rate of Na-Li CT was significantly higher in a group of subjects with essential hypertension when compared with groups A, B and C, consistent with the view that there is a genetic marker for essential hypertension. Ouabain-insensitive Na efflux (Na leak) of erythrocytes was found to be significantly higher in group D than in groups A or B. Also, a significant positive correlation existed between Na leak and urine protein levels of the subjects studied. Our results thus indicate that in contrast with insulin-dependent diabetic patients (IDDM) where an elevated Na-Li CT is observed, with diabetic nephropathy, Na-Li CT in NIDDM is apparently not associated with nephropathy; rather the ouabain-insensitive Na efflux appears to be correlated with the stages of nephropathy in NIDDM. The association suggests that the rate of ouabain-insensitive Na efflux may provide an index for assessing the degree of nephropathy in NIDDM patients.
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PMID:Abnormalities of sodium transport in non-insulin-dependent diabetes: association with renal disease. 810 99

A longitudinal study for six months was conducted to demonstrate the influence of enalapril therapy on microalbuminuria in a group of patients with IDDM without arterial hypertension. An evaluation was also considered of its possible activity on other biochemical parameters, particularly plasma lipid levels. Thirty-four patients with IDDM were selected, with a mean age of 26.1 +/- 7.2 years and a mean clinical course of 11.8 +/- 5.6 years. Arterial blood pressure (ABP) was confirmed lower than 140/85 mmHg in all cases. Patients were administered 5 mg/day of enalapril and if a decrease in microalbuminuria higher than 25% was not achieved at the end of the first month of therapy, the dose was doubled (10 mg/day). No significant differences were found in ABP and in HbA1c throughout the study period. Albumin excretion in the initial period was 125.1 +/- 79.28 mg/24 h, at one month in the follow-up 47.6 +/- 44.1 mg/24 h, at three months 23.8 +/- 18.1 mg/24 h, and at the end of the 6th month 15.33 +/- 6.9 mg/24 h, all differences being significant. Renal function parameters and Na+ and K+ measurements remained unchanged for the follow-up period. No significant changes were detected for lipid and lipoprotein values for the length of the study. We conclude that therapy with enalapril in insulin-dependent diabetic patients without hypertension has an important effect on microalbuminuria during the first month of therapy; a stabilization in the normal range was reached in the third and sixth months of follow-up. No changes in arterial blood pressure nor in renal function were observed. Plasma lipid values were in the normal range throughout the study. Therefore, treatment for microalbuminuria with the ACEI assayed was efficient, in absence of arterial hypertension and irrespective of the metabolic control obtained. Future long-term studies are needed to evaluate the possible delay in the emergence of renal insufficiency.
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PMID:[Effect of enalapril on microalbuminuria and lipid profile of normotensive type I diabetes mellitus patients]. 876 69

The prevalence of abnormally elevated albumin excretion rate (> 30 mg/24 h) is approximately 40% in insulin-dependent (IDDM) and non-insulin-dependent (NIDDM) diabetic patients. Diabetes has become the leading cause of end-stage renal failure in the US, Japan and Europe. Approximately 90% of the direct and indirect cost of caring for diabetic patients are spent on the complications of diabetes. Identification of patients at high risk of developing diabetic nephropathy is possible by screening for microalbuminuria (30-300 mg/24 h). Elevated urinary albumin excretion rate indicates a substantially increased mortality risk in diabetic patients. Randomised controlled trials in normotensive IDDM and NIDDM patients with persistent microalbuminuria indicate that ACE inhibitors diminish urinary albumin excretion rate, postpone it and may even prevent progression to clinical overt nephropathy. These findings indicate that screening and intervention programs are likely to have life saving effects and lead to considerable economic savings. Systemic blood pressure elevation to a hypertensive level is an early and frequent phenomenon in diabetic nephropathy. Furthermore, nocturnal blood pressure elevation (non-dippers) occurs more frequently in patients with nephropathy. Systemic blood pressure elevation and to a lesser degree albuminuria accelerate the progression of diabetic nephropathy. Effective blood pressure reduction with non-ACE-inhibitors and/or ACE-inhibitors frequently in combination with diuretics: (a) reduces albuminuria; (b) delays the progression of nephropathy; (c) postpones renal insufficiency; and (d) improves survival in IDDM and NIDDM patients with diabetic nephropathy. A specific renal protective effect of ACE-inhibitors in diabetic nephropathy has been demonstrated in IDDM patients with moderately reduced kidney function (s-creatinine > 133 mumol/l) while the data conflict with NIDDM patients. Antihypertensive treatment for diabetic nephropathy simultaneously extends life and saves money. Finally, reduced risk of fatal and non-fatal cardiovascular events have been demonstrated when diabetic patients with isolated systolic hypertension are treated with blood pressure lowering agents. Absolute risk reduction with active treatment compared to placebo was twice as great for the diabetic versus non-diabetic patients (101/1000 versus 51/1000 randomised participants at the 5-year follow-up), reflecting the higher risk of diabetic patients. In conclusion, early detection and aggressive treatment of arterial hypertension with ACE-inhibitors, long acting calcium antagonist and low dose diuretics as first line drugs are highly warranted in diabetic patients with or without diabetic renal disease.
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PMID:Is antihypertensive treatment the same for NIDDM and IDDM patients? 964 59

Diabetic nephropathy (DN) appears in about 30% of patients with type 1 diabetes (D1) and 15 to 60% of patients with type 2 diabetes (D2). It is preceded by microalbuminuria. Microalbuminuria is defined as an albumin excretion rate between 30 and 300 mg/24 h (on a 24-hour urine collection) or between 20 and 200 micrograms/min (on an overnight collection) in at least two out of three consecutive collections made within a 6-month period. Alternative screening techniques use either dipstick (Micral-Test II) or the albumin to creatinine ratio on an early morning urine sample (30-300 mg/g creatinine). Once persistent microalbuminuria is confirmed, 80% of type 1 diabetic patients and 20 to 50% of type 2 diabetic patients will progress to DN. In D2, microalbuminuria also represents a powerful predictor of early mortality from cardiovascular disease. Macroalbuminuria (AER > 300 mg/24 h, corresponding to a total protein excretion > 500 mg/24 h) will eventually lead to a end-stage renal insufficiency within 10 to 20 years. In D2, numerous patients will die from cardiovascular disease before reaching end-stage renal failure. Angiotensin-converting enzyme inhibitors can slow down the evolution toward DN when prescribed when microalbuminuria appears. Screening for microalbuminuria should therefore be a part of the annual clinical assessment in every diabetic patient.
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PMID:[How I evaluate...diabetic nephropathy. First part: micro- and macroalbuminuria]. 981 Feb 12

Amadori-glycated albumin in diabetic nephropathy: Pathophysiologic connections. Nonenzymatic glycation of proteins represents a major mechanism by which hyperglycemia leads to diabetic renal disease. Recent research has shown that Amadori-modified albumin, the principal glycated protein in plasma, elicits pathobiologic effects in cultured renal cells that are identical to those of high ambient glucose. When added to the incubation media of glomerular mesangial and endothelial cells, glycated albumin stimulates protein kinase C (PKC) activity, increases transforming growth factor-beta (TGF-beta) bioactivity, and induces gene overexpression and enhanced production of extracellular matrix proteins. These cellular events, whereby PKC-mediated TGF-beta activation leads to increased matrix expression, are inextricably linked, and they form the central tenets of a pathophysiologic connection between glycated proteins and diabetic nephropathy. In vivo studies further corroborate the role of glycated proteins in the pathogenesis of diabetic nephropathy. Reduction or neutralization of glycated albumin in the db/db mouse model of type 2 diabetes significantly ameliorates the proteinuria, renal insufficiency, mesangial expansion, and overexpression of matrix proteins. In human type 1 diabetes, the plasma-glycated albumin concentration is independently associated with the presence of nephropathy. Abrogating the biologic effects of increased glycated albumin has novel therapeutic potential in the management of renal complications in diabetes.
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PMID:Amadori-glycated albumin in diabetic nephropathy: pathophysiologic connections. 1099 89

In patients with chronic renal failure, three kinds of treatments can slow the progression of renal insufficiency: optimal control of blood pressure; use of converting enzyme inhibitors; low-protein diet. The MDRD study strongly suggests that blood pressure should not be higher than 130/85 mmHg in patients with chronic renal failure, and than 125/75 mmHg in patients with chronic renal failure and proteinuria above 1 g/d. Converting enzyme inhibitors have been shown to be beneficial to patients with IDDM and either microalbuminuria or overt diabetic nephropathy and to patients with chronic renal failure and proteinuria above 1 g/d. A diet containing less than 1 g/kg/d of proteins should be prescribed to patients with chronic renal failure, and this protein content should be lowered to 0.75 g/kg/d (or to 0.60 g/kg/j in some cases) when creatinine clearance falls below 25 mL/min.
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PMID:[How to slow the progression of chronic renal insufficiency]. 1135 1

There are several reports of glomerulonephritis (GN) in diabetics or patients with diabetic glomerulosclerosis. Cases of rapidly progressive GN where crescentic histologic changes are superimposed on diabetic glomerulosclerosis are very unusual. We report the case of a patient with type I diabetes mellitus, who developed rapidly progressive renal insufficiency. Renal biopsy disclosed anti-glomerular basement membrane nephritis superimposed on classical diabetic glomerulosclerosis.
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PMID:Anti-GBM nephritis complicating diabetic nephropathy. 1193 33

Many clinicians are uncomfortable about using angiotensin-converting enzyme (ACE) inhibitors or angiotensin II type 1 receptor blockers (AT(1)-blockers) to treat patients with renal disease because of concerns about increasing serum creatinine levels. However, the benefits of these medications, particularly their efficacy in slowing the progression of renal disease, outweigh such concerns. ACE inhibitors are effective in patients with type 1 diabetes and renal disease, as well as in those with nondiabetic renal disease and proteinuria >0.5 g/d. AT(1)-blockers slow the progression of diabetic nephropathy in patients with type 2 diabetes. Although these classes of medications should not be used in patients with severe renal insufficiency (e.g., glomerular filtration rate <20 mL/min), they may be beneficial in patients with mild-to-moderate renal insufficiency. Nonetheless, caution should be exercised in those with a glomerular filtration rate <30 mL/min, and serum creatinine and potassium levels should be checked approximately 1 week after starting treatment. There is also evidence suggesting that these medications lead to greater reductions in blood pressure and proteinuria when used in combination than when alone. The purpose of this paper is to review the mechanisms of action of these two classes of medication, as well as the experimental and clinical evidence that they slow the progression of renal disease.
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PMID:Comparative effects of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers on blood pressure and the kidney. 1275 83

Kidney involvement in diabetes mellitus has negative impact on the outcomes of disease. Strong relationship between progressive diabetic kidney disease and the development of other diabetic complications was found by many investigators. In order to evaluate the dynamics of diabetic nephropathy in type I diabetes mellitus during 6-year period and its relationship with other diabetes mellitus complications and control of glycemia and hypertension, in 2002 we reviewed ambulatory case records of patients, who were followed by endocrinologists and who were investigated by us in 1996. During 6-year period, 5.1% from 156 pts. died and all of them had diabetic nephropathy; 26.9% of pts. moved to general practitioners and never visited endocrinologists again. Only 105 pts. remained under follow-up by endocrinologists. Their mean age 37.6+/-1.3 yrs. Out of all patients, 54% were males and 46% females. Mean diabetes mellitus duration was 19.5+/-0.9 yrs. Control of glycaemia was poor and insufficient in 2/3 of pts. HbA(1C) wasn't checked in 68.9% of pts. Control of arterial hypertension became better, but not sufficiently. During 6-year period persistent proteinuria developed in 12.1% of pts., who had no or transient proteinuria <0.5 g/l in 1996. Persistent proteinuria developed 19.9+/-1.8 yrs. after the diabetes mellitus onset and correlated with hypertension and renal insufficiency. Higher level of proteinuria was associated with worse control of glycemia. Progression of diabetic retinopathy and neuropathy over 6 yrs. were more expressed than in diabetic nephropathy. On average retinopathy developed after 14+/-1.8 yrs. after the diabetes mellitus onset, neuropathy--17.8+/-2.2 yrs., renal failure--21.1+/-2.8 yrs., heart failure--22.9+/-1.9 yrs. and arterial hypertension--12.1+/-1.3 yrs. The prevalence and time of incipient diabetic nephropathy appearance remained unknown because the test for microalbuminuria was not available in the primary health care centres.
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PMID:[Dynamics of diabetic nephropathy and other complications of type I diabetes mellitus in the period of 1996-2002 (data from 2 Kaunas outpatient polyclinics)]. 1276 21


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