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)

Experimental studies have suggested an important role for abnormal lipid metabolism as an integral factor in modulating progressive renal damage. Dietary induced hypercholesterolemia induced relatively modest glomerular injury. However, in the presence of reduced nephron population or in the presence of underlying renal diseases, such as diabetes, nephrotic syndrome, and hypertension, nephron injury can be markedly exaggerated. These experimental results suggest that an important interaction may occur between renal disease and the occurrence of abnormalities of lipid metabolism. Additional support for the role of lipids in progressive renal injury can be obtained from studies in which pharmacological interventions reduced circulating lipids and this led to decreased glomerular damage. The mechanisms whereby lipids may amplify glomerular injury are not completely understood but may include an interaction with macrophages, alteration in vascular and mesangial functions, changes in production of mediator substances or alterations in membrane fluidity. Local glomerular modification of lipoproteins could also occur and contribute to the development of glomerular pathologic changes. Clinically, few data are available that provide insights into the potential role of renal-related lipid abnormalities in the progression of human renal disease.
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PMID:Hyperlipidemia and progressive renal disease. 204 70

Altogether, a growing amount of clinical and experimental data suggests that lipids may be important in the development and progression of chronic renal injury. Abundant clinical data have demonstrated that hyperlipidemia is associated with diabetes, decreased renal function, and the nephrotic syndrome. Although clinical correlations between plasma lipid levels and renal dysfunction do not prove a cause-and-effect relationship, potentially injurious lipid abnormalities are invariably present in those patients most likely to progress to end-stage renal disease. In several animal models, pharmacologic treatment of lipid abnormalities has been shown to ameliorate renal disease. Moreover, experimental data suggest that lipid-induced alterations in a number of immune and nonimmune mechanisms could explain the association between lipids and renal injury. A better understanding of these alterations and mechanisms may ultimately lead to more effective treatment of patients with chronic progressive renal disease.
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PMID:The role of lipid abnormalities in the pathogenesis of chronic, progressive renal disease. 206 7

Investigation of renal biopsy specimens from 488 patients with diabetic glomerulosclerosis (DGS) of varying severity revealed the following: 1) The severity of DGS increases with the duration of the diabetes. 2) As the severity of DGS increases, it is complicated with increasing frequency by exudative changes, which correspond in detail to hyperperfusion lesions described in the literature. 3) As the severity of DGS increases, the severity of arteriolosclerosis and the incidence of nephrotic syndrome increase significantly. 4) The 5- and 10-year renal survival rates are highest for those diabetic patients in whom the tubules and renal cortical interstitium are of normal appearance. These survival rates are diminished if any of the following are present at the time of biopsy: a) interstitial fibrosis; b) hyperperfusion lesions; c) nephrotic syndrome; d) elevation of the serum creatinine concentration to more than 1.3 mg%. 5) No significant correlation was found between renal survival rate and age, sex, or type of diabetes. 6) The inflammation of the renal interstitium seen in diabetes does not differ from that seen in chronic glomerulonephritis. Monocytes, macrophages, T lymphocytes, fibroblasts and fibrocytes play the major role in this inflammation. This inflammatory process is considered to represent not pyelonephritis, but rather an auto-immune process. In other words, it is proposed that the diabetic kidney fails not only as a result of non-specific glomerular lesions (hyperperfusion lesions) but also because of non-specific tubulointerstitial changes, whereas diabetic glomerulosclerosis alone does not lead to chronic renal failure.
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PMID:The pathogenesis of chronic renal failure in diabetic nephropathy. Investigation of 488 cases of diabetic glomerulosclerosis. 206 8

There have been only a few investigations that have considered renal disease or any disturbance of renal function in the calculation of risk in cardiac surgery. Risks of cardiac surgery have to be considered for renal disease without direct connection to heart disease (e.g., infections of the kidney and of the urinary tract, primary and secondary glomerulonephritis, parenchymal renal disease, and impaired renal function of unknown origin), as well as in renal disease with concomitant influence on heart and kidney (e.g., infective endocarditis, arterial hypertension, systemic disease of heart and kidney such as with diabetes mellitus, disturbance of kidney function or electrolyte balance due to heart failure). In most cases, the problem is solved by therapeutic intervention and postponement of cardiac surgery. A limited or negative operative indication is found with untreatable infection of the kidney or urinary tract, with untreatable nephrotic syndrome, in advanced renal disease with heart transplantation, as well as in case of severe arterial hypertension with possible organ complications, and in advanced diabetes mellitus with ESRD and multiorgan involvement. After cardiac surgery, acute renal failure represents a critically important complication. Primary therapeutic procedures must include prophylaxis of hemodynamic unstable situations, as well as prophylaxis of infectious complications. Cardiac surgery in dialysis patients and post-transplant patients is basically possible and only has a slightly increased risk compared to patients with normal renal function. Seventy-seven dialysis patients were operated (49 aorto-coronary bypass operations, 19 single-valve and multiple-valve replacements, five patients with valve replacement and aorto-coronary bypass, and four other cardiac surgical operations). Only in valve replacement, was mortality significantly higher than in renal healthy persons, the main causes of death being cerebrovascular complications and septicemia.
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PMID:[Extracardiac risk factors in heart surgery--the kidney]. 208 10

Capgras' syndrome, one form of the delusional misidentification syndromes, is described. Three patients with the syndrome are reported. The first had a right cerebral infarction, the second had nephrotic syndrome secondary to severe pre-eclampsia in the puerperium, and the third had uncontrolled diabetes mellitus with dementia. Evidence is reviewed regarding an organic aetiology for Capgras' syndrome. We conclude that, when the syndrome is present, a thorough search for organic disorder should be made.
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PMID:Capgras' syndrome with organic disorders. 208 56

Kidney biopsy (KB) is controversial in the elderly because it is generally felt that the risks exceed the potential therapeutic benefits. In this review of our personal experience and the literature reports, we discuss the risks of this diagnostic procedure and its use in the four main circumstances of patient referral. On the one hand, KB does not seem to be more hazardous in the elderly, provided that it is not performed in patients in poor condition or with atrophic kidneys or suspected vascular lesions. On the other hand, KB is clearly useful in a number of elderly patients either to assess the diagnosis of a systemic disease involving the kidney or to select the appropriate treatment. 1. In patients with non nephrotic proteinuria, KB should be performed if the proteinuria is associated with extra-renal signs suggestive of systemic disease or with deterioration of renal function. 2. Nephrotic syndrome without evidence of amyloidosis and diabetes, should lead to KB to identify patients with minimal change disease (MCD) requiring steroid treatment. Indeed, MCD can rarely be suspected on clinical grounds as the resulting nephrotic syndrome is rarely "pure" at this age. 3. In acute renal failure, KB seems to be essential and urgent in patients with rapidly progressive glomerulonephritis and in those with renal failure of dubious origin to select the most appropriate treatment according to the etiology and the type of renal lesions (sclerotic or "active"). 4. KB is useless and hazardous in chronic renal failure, except in case of unexplained rapid worsening of renal function in patients with previously moderate renal failure.
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PMID:[For or against renal biopsy after 65 years]. 209 Sep 64

Nephrotic syndrome has been reported in obesity; its precise incidence in obese patients without diabetes mellitus and/or arterial hypertension is however unknown. Thirty-two obese subjects without complications were therefore assessed before and after weight loss, together with 18 healthy control subjects. Overnight albumin excretion rate (AER) was assessed using a RIA method (H. Albumin-Kit, Sclavo). Glomerular filtration rate (GFR) was also evaluated in 10 obese subjects using Cr51 before and after weight loss. AER was found to be higher, although the difference was not statistically significant, in obese subjects compared to controls, but was significantly reduced after weight loss (p = 0.05). GFR also showed a non-significant tendency to decrease following loss of weight. Systolic and diastolic blood pressures were significantly decreased following weight loss (p less than 0.01 and p less than 0.025 respectively). In conclusion, although it is not possible to confirm the presence of true nephropathy in uncomplicated obesity, the latter can facilitate the onset of hemodynamic-type mechanisms which, in the presence of diabetes mellitus or arterial hypertension, may lead to the appearance of the nephrotic syndrome.
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PMID:[Possible correlations between protein-loosing nephropathy and obesity]. 209 54

The performed studies covered 28 patients with nephrotic syndrome and 10 healthy individuals. The oral glucose tolerance test in 20 patients with nephrotic syndrome revealed glycemic values within the norm, and features of defective tolerance to glucose or diabetes in 8 subjects. Hyperglucagonemia was recorded in all the patients with increased glycemic values in the oral glucose tolerance test. It was found that hyperglucagonemia appeared in 70% of studied patients with normal glucose tolerance. All the groups of patients with nephrotic syndrome disclosed a decrease in glucagonemia, observed in normal subjects, in the course of oral glucose tolerance test as well as slower disappearance of glucagon from the circulatory system, which may be of certain significance in the occurrence of hyperglucagonemia. It has been ascertained that hyperglucagonemia may be one of the factors having influence upon a higher incidence rate of glucose tolerance abnormalities than in general population; can have a share in intensified catabolic processes, and also counteracts the effects of increased tissue absorption of glucose in patients with nephrotic syndrome. There has been a lower stimulating action of exogenic glucagon on insulin secretion in patients with nephrotic syndrome and hyperglucagonemia as compared to patients with normoglucagonemia and to healthy subjects.
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PMID:[Glucagon secretion in patients with nephrotic syndrome in primary glomerulonephritis during the period of renal efficiency]. 209 3

Acquired hyperlipidemia (secondary dyslipoproteinemias) results from underlying disorders that lead to alterations in plasma lipid and lipoprotein metabolism. Secondary dyslipoproteinemias may mimic primary forms of hyperlipidemia and can have similar consequences. They may result in increased predisposition to premature atherosclerosis or, when associated with marked hypertriglyceridemia, may lead to the development of pancreatitis and other features of the chylomicronemia syndrome. Diabetes mellitus and use of drugs such as diuretics, beta blockers, and estrogens are commonly encountered causes of secondary dyslipoproteinemia. Other conditions leading to acquired hyperlipidemia include hypothyroidism, renal failure, nephrotic syndrome, alcohol usage, and some rare endocrine and metabolic disorders. When secondary and familial forms of hypertriglyceridemia coexist, triglyceride removal mechanisms may be saturated and marked hypertriglyceridemia with fasting chylomicronemia might ensue. Treatment of the underlying condition, when possible, or discontinuation of the offending drugs usually leads to an improvement in the hyperlipidemia. Specific lipid-lowering therapy may be required in certain circumstances.
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PMID:Acquired hyperlipidemia (secondary dyslipoproteinemias). 219 73

1H-NMR spectra of 60 human urine specimens were recorded without pretreatment by a JEOL FX 90 Q spectrometer operating at 89.55 MHz. The signals of the methyl protons of creatinine (3.04 +/- 0.02 ppm) were observed in all spot fasting morning urine samples collected from 7 healthy persons, 10 patients with nephrotic syndrome and 43 patients with diabetes mellitus. The concentrations of creatinine measured by NMR spectroscopy (Y) and the chemical assay based on the Jaffe reaction (X), over the range of 19-190 mg/dl, were compared by the least-squares linear regression analysis (Y = 6.7799 + 0.6717 X). The mean urinary creatinine concentration by NMR spectroscopy appeared to be lower than that obtained by the Jaffe reaction at the normal and high normal levels. In the urine of 20 diabetic patients with an average blood glucose of 251.30 +/- 50.26 (SD) mg/dl typical spectra of the multiple large signals of glucose protons at position from 3.13 +/- 0.04 to 4.04 +/- 0.12 (SD) ppm were shown. Moreover, some urinary metabolites and amino acids spectra were occasionally detected at one time.
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PMID:Identification of urinary metabolites and quantitative measurement of creatinine by a proton nuclear magnetic resonance spectrometry. 226 55


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