Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A microemulsion formulation of cyclosporin (Neoral) has been developed to overcome the problems of poor and variable absorption of cyclosporin. Neoral is a potent immunosuppressive agent that is highly bound in the plasma. It has been proposed that low-density lipoprotein (LDL) delivers cyclosporin (CsA) to T-lymphocytes via the LDL receptor pathway, where it produces its therapeutic effects. Herein, we report a case of minimal change nephrotic syndrome with type 2 diabetes mellitus treated by Neoral and fluvastatin. A 65-year-old male with a 10-year history of type 2 diabetes mellitus suddenly developed nephrotic syndrome. The potential causative drugs, such as NSAIDs and antibiotics, had not been administered. The laboratory findings were as follows: proteinuria 23 g/day, serum albumin 1.9 g/dl, total cholesterol 629 mg/dl, LDL-Cho 1,930 mg/dl. Renal biopsy was normal on light microscopy, and immunofluorescence demonstrated no staining. Due to the risk of deterioration of diabetes by administering prednisolone, he was given Neoral at 2.0 mg/kg/day. He was also given fluvastatin (40 mg/day) for hyperlipidemia after the renal biopsy. At four weeks after the start of Neoral and fluvastatin, his nephrosis continued, but his LDL-Cho and total cholesterol decreased. At six weeks after treatment, proteinuria gradually reduced. At eight weeks after treatment, the proteinuria had disappeared. Nephrotic syndrome is often associated with abnormal lipid metabolism, and many patients with nephrotic syndrome show high levels of LDL-Cho. It has been reported recently that LDL apheresis is effective against nephrotic syndrome. However, in the present case, it can be speculated that the improvement of hyperlipidemia by fluvastatin probably augmented the effect of Neoral, presumably through the increased cellular uptake of Neoral. This suggests that fluvastatin may be considered as the treatment of choice for the disturbed lipoprotein profile in patients with nephrotic syndrome.
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PMID:[Complete remission of minimal change nephrotic syndrome with type 2 diabetes mellitus treated by microemulsion formulation of cyclosporin and fluvastatin]. 1197 50

"The death rates at ages over 40 in Japan were analyzed using Japanese Vital Statistics for 1947-1988. Secular changes in the death rate and the age-specific death rate were analyzed according to sex and major causes of death. Twelve major causes of death were as follows: (1) malignant neoplasms, (2) heart disease, (3) cerebrovascular disease, (4) pneumonia and bronchitis, (5) accidents and adverse effects, (6) senility without mention of psychosis, (7) suicide, (8) chronic liver disease and cirrhosis, (9) nephritis, nephrotic syndrome and nephrosis, (10) hypertensive disease, (11) diabetes mellitus and (12) mental disorders.... The mean age at death increased 50 years [over] the last 38 years." (SUMMARY IN ENG)
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PMID:[[Mortality in the elderly population aged over 40 in Japan, 1947-1988]]. 1228 12

SEVERAL MECHANISMS: The progression in renal failure first implies hemodynamic mechanisms and among which angiotensin II has a central role, but also an increase in proteinuria and the induction of many inflammatory and mitogenic mediators that enhance fibrosis (TGF-beta), an effect stimulating the thrombotic mechanism. Among these factors of progression in renal failure, hypertension and proteinuria are the two major factors. Proteinuria is "nephrotoxic" and leads to glomerular and tubulo-interstitial lesions. THE ROLE OF ANGIOTENSIN-CONVERTING ENZYME INHIBITORS: Angiotensin-converting enzyme inhibitors (ACE) affect the different mechanisms that lead to glomerulosclerosis: antihypertensive effect, with the normalisation of blood pressure having demonstrated its determining role in the production of nephrosis in various epidemiological studies; hemodynamic effect with a decrease in glomerular capillary pressure, in the filtration fraction, and inhibition of the bradykinin deterioration; antiproteinuric effect superior to that of other anti-hypertensive drugs (excepting angiotensin II-receptor antagonists). Two indications ACE inhibitors have demonstrated their efficacy in slowing the progression of renal failure in two large pathological fields: diabetic nephropathy in which this effect is demonstrated in type I diabetes, although the results are not as obvious in type II diabetes in which the nephropathy is multi-factor. The recent French and American recommendations are that ACE inhibitors should be used in first intention in diabetic nephropathies and aimed at tight blood pressure control; non-diabetic nephropathies Two pivotal studies have demonstrated the efficacy of ACE inhibitors in nephropathies whatever their type. These data have led to propose ACE inhibitors in first intention in patients exhibiting chronic nephropathies, whether hypertensive or not THE COMBINATION WITH OTHER HYPERTENSIVE DRUGS: Calcium channel blockers have a beneficial trophic effect in renoprotection and can be combined with ACE inhibitors, particularly in the case of diabetic nephropathies. ACE inhibitors and angiotensin II-receptor antagonists have comparable effect on hemodynamics and glomerulosclerosis factors. Clinically, the decrease in proteinuria is identical. Endothelin antagonists have also been studied in renoprotection and appear to have a beneficial effect when combined with ACE inhibitors. GLOBALLY: ACE inhibitors remain the only treatment with demonstrated long-term efficacy in the progression of chronic renal failure. However, the concept of renoprotection needs to be widened to all the factors implied in the progression of chronic renal failure, and ACE inhibitors only represent one aspect of treatment. The role of angiotensin II-receptor antagonists, alone or combined, is clearly promising.
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PMID:[The effect of angiotensin-converting enzyme inhibitors on the progression of chronic renal failure]. 1246 54

Pseudomonas aeruginosa bacteremia has the highest mortality among Gram-negative infections. We studied its clinical and epidemiological patterns in order to achieve an early and accurate diagnosis and treatment. We prospectively studied 211 cases of P. aeruginosa bacteremia admitted to our hospital from 1991 to 1998. All patients had at least one positive blood culture for P. aeruginosa and clinical symptoms of bacteremia. The prognosis of the underlying disease, past illnesses, foci location, initial clinical status, type of bacteremia, complications, and the type of antibiotic treatment were analyzed. Clinical and microbiological controls were carried out at baseline, at the end of the treatment period, and 1 month later. Of the 211 cases, 73% were men with a mean age of 56.5 years. Overall, 45.5% were hospitalized in the ICU, 28% in the surgical ward, and 26% in the medical service, with a mean length of stay of 40.4 days. As risk factors we identified a length of stay more than 14 days (76.7%), previous manipulations (87.6%), and surgery (44.5%). A total of 43.1% had had an infection in the last 6 weeks, and 46.4% were treated with antibiotics, usually broad-spectrum antibiotics without activity against P. aeruginosa. The most frequent underlying diseases were neoplasia (25.5%), postsurgical cardiopathy (24.1%), nephrosis (22.7%), chronic obstructive pulmonary disease (17.5%) and diabetes (13.2%). The most frequent foci were pulmonary (29.3%), urinary (21.8%), and undetermined (38.3%). The mortality rate was 27.9% and was considered related to P. aeruginosa bacteremia in 76.2% of the cases. The antibiotic treatment was considered adequate in 89% of the cases. It was concluded that knowledge of the clinical and epidemiological factors of patients with P. aeruginosa bacteremia may help to optimize its management and to reduce its morbidity and mortality.
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PMID:[Pseudomonas aeruginosa bacteremia: clinical and epidemiological patterns and treatment]. 1258 42

The important problem of the fate of glycogen-accumulating clear cells in glycogen nephrosis is still unsettled. In this study, we examine whether apoptosis plays a relevant role in the development of diabetic glycogen nephrosis and explore the involvement of the Fas/Fas-L system and the activation of the caspase cascade. Diabetes was induced in rats by streptozotocin injection. Glycogen-accumulating clear cells were identified in renal tissues of hyperglycemic rats. They were found to be concentrated in the thick ascending limbs and distal tubules. Large cellular glycogen accumulations were confirmed by biochemical assays and enzyme-gold cytochemistry. Clear cells displayed apoptotic features such as Annexin V binding, nuclear TUNEL (terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling), and the simultaneous occurrence of Fas, Annexin V, and TUNEL positivity. Western blot analysis demonstrated enhanced expression of Fas receptor/ligand and the activation of the caspase cascade in these cells because cleaved forms of the caspase-3, -8, and -9 were detected. Furthermore, active caspase-3 was located in nuclei by immunoelectron microscopy. Our results indicate that epithelial cells in thick ascending limbs and distal tubules that develop glycogen nephrosis in response to hyperglycemia undergo Fas/Fas-L mediated cell death. Thus, apoptosis could be playing a significant role in renal epithelial cell deletion during diabetes.
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PMID:Apoptosis of tubular epithelial cells in glycogen nephrosis during diabetes. 1286 Oct 46

This study examines the association between education and mortality from specific causes of death based on mortality records for 1996 and 1997, and 1996 population census data from the Region of Madrid (Spain). Poisson regression models were used to estimate the percentage increase in mortality associated with 1 year less education. The percentage increases in mortality from stomach cancer, lung, bladder and liver cancers, for aids, chronic obstructive pulmonary disease, pneumonia and influenza, and chronic liver disease and cirrhosis were higher in men than in women, whereas the percentage increases in mortality from colon cancer, diabetes mellitus, ischemic heart disease and nephritis, nephrosis and nephrotic syndrome were higher in women. The results found for some causes of death--lung cancer, ischemic heart disease, diabetes mellitus and chronic obstructive pulmonary disease--reflect the variations by educational level in the prevalence of lifestyle-related risk factors in men and women. Various hypotheses have been suggested for other causes of death, but it is not known why the magnitude of the association between education and mortality from some causes of death differs between men and women. Future studies of this subject may provide some clues as to the underlying mechanisms of this association.
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PMID:The size of educational differences in mortality from specific causes of death in men and women. 1288 84

After the intravenous injection of heparin the plasma concentration of non-esterified fatty acids rises in normal subjects and in patients with nephrosis or diabetes but not in patients with portal cirrhosis.
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PMID:Nmn-esterified fatty acids and lipoprotein lipase activity in patients with cirrhosis of the liver. 1387 81

Intravenous immunoglobulin infusion induces acute renal failure via a mechanism of osmotic nephrosis. Most reported cases are related to the use of sucrose-based intravenous immunoglobulin. Maltose-based intravenous immunoglobulin is thought to be a safer alternative and have a lower risk of renal toxicity than sucrose-based preparations. Maltase, but not sucrase, is present in the brush border of proximal convoluted renal tubules, where the maltose is metabolised. We report a case of maltose-based intravenous immunoglobulin-induced acute renal failure in an elderly diabetic woman. In this case, the risk factors included advanced age, hypovolaemia, sepsis, diabetes mellitus, and the high infusion rate of the intravenous immunoglobulin. Maltase is readily inhibited by hyperglycaemia; therefore, poor glycaemic control may predispose patients to develop acute renal failure even with the better-tolerated maltose-based intravenous immunoglobulin.
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PMID:Acute renal failure related to intravenous immunoglobulin infusion in an elderly woman. 1568 16

Acute renal failure (ARF) is a rare complication of the use of intravenous immunoglobulins (IVIg) with an estimated incidence lower than 1 %. It is related to acute tubulo-interstitial nephropathy due to to the occurrence of osmotic nephrosis mainly in the proximal tubule. The recovery of renal function usually occurs within ten days. The risk factors for the occurrence of ARF during the use of IVIg are: age > 65 years, preexisting renal failure (creatinine clearance < 60 ml/min), diabetes, dose, hypovolemia, the concomitant use of other nephro-toxic agents (contrast media agents, etc.). IVIg related ARF has been reported mainly with saccharose-containing IVIg but also with maltose and glucose-containing IVIg. However, no definite conclusion can be drawn concerning the role of the stabilising agent in the genesis of ARF due to the larger use of saccharose-containing IVIG compared to other IVIG and the absence of controlled trials comparing various types of IVIg. Clinicians must be aware that ARF may occur with all types of IVIg. In patients with at least one risk factor for ARF, diuretics should be discontinued, an hydration using saline solutions should be started and the concomitant administration of other nephrotoxic drugs be avoided. Clinicians should use the minimal required dose of IVIg and slow the flow of perfusion (1-2 ml/kg/h).
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PMID:[Intravenous immunoglobulins and acute renal failure: mechanism and prevention]. 1776 31

Two hundred and seven albino rats were injected subcutaneously with alloxan in doses varying from 140 to 200 mg. per cent per kilo of body weight. Fifty-nine animals which developed hyperglycemia (blood sugar levels above 150 mg. per cent) were observed for periods from 5 days to 32 weeks. Postmortem examination of the kidneys of these diabetic animals revealed glycogen deposition in the loops of Henle and convoluted tubules in 26 rats or 44 per cent. Glycogen could not be demonstrated in the glomeruli. Within the time limits of this experiment (32 weeks) no intercapillary glomerulosclerosis was observed. The following facts were revealed regarding glycogen nephrosis in alloxan diabetes: (a) Its appearance in the kidneys of the diabetic rats depended solely upon the terminal blood sugar levels of these animals. A value of 350 mg. per cent was the critical level, above which glycogen nephrosis was almost invariably demonstrable. With terminal levels below 300 mg. per cent no glycogen nephrosis was found. (b) No relationship existed between the postmortem finding of glycogen nephrosis and the initial blood sugar level, or the maximum height of the hyperglycemia attained by individual rats. (c) The results suggest that glycogen nephrosis is a reversible lesion.
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PMID:STUDIES ON GLYCOGEN NEPHROSIS IN ALLOXAN-TREATED DIABETIC RATS. 1987 22


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