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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The effects of a high cholesterol diet on urinary albumin excretion were examined in spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats over 36 weeks. 2. Cholesterol feeding resulted in an increase in total-cholesterol and a decrease in HDL-cholesterol without influencing triglyceride levels in both strains. 3. Urinary albumin excretion was significantly elevated in cholesterol-fed SHR and WKY rats. 4. These results suggest that hyperlipidaemia may be important in acceleration of experimental nephropathy.
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PMID:Hyperlipidaemia increases albuminuria in hypertensive and normotensive rats. 234 Jun 46

The effect of exercise on the progression of experimental renal disease was studied in adriamycin (ADR)-treated rats, a model of sclerosing glomerulonephritis with nephrotic syndrome. Two hours of daily swimming exercise was carried out for 20 weeks in ADR-treated male Lewis rats fed with either an ad libitum intake of regular chow (group 1) or a restricted amount of food (group 3), which was equal to the amount of food freely ingested by ADR-treated rats not undergoing swimming exercise (group 2). Group 3 resulted in a significantly lower serum creatinine, higher inulin clearance and lower glomerular sclerosis index compared to group 2. The progress of renal dysfunction did not differ significantly between group 1 and group 2. Hyperlipidemia, especially, hypertriglyceridemia was significantly lower in the exercise groups than in the sedentary group. Among all the rats, inulin clearance was inversely correlated with either cholesterol (r = 0.560, p less than 0.01) or triglyceride (r = 0.423, p less than 0.05) and the glomerular sclerosis index correlated positively with cholesterol (r = 0.599, p less than 0.005). Systolic blood pressure was 10 mm Hg lower in group 3 than in group 2 and the difference was significant. It is concluded that swimming exercise with a relative restriction of food intake can improve hyperlipidemia and prevent progressive renal dysfunction in ADR-induced nephritic rats.
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PMID:Effect of swimming exercise on the progress of renal dysfunction in rat with focal glomerulosclerosis. 237 Sep 32

In the last few years, remarkable advances have been made in the understanding of lipoprotein metabolism in the pathogenesis of renal disease in animal models and in vitro cell culture. Central to this work is the problem of the progression of renal disease in humans. This review recapitulates the theory (Lancet 1982; II: 1309-1312) that the progression of disease depends in part on the damage inflicted on the glomerulus by lipoproteins. The glomerular environment of high or low pressure, basement membrane damage, and destruction or damage of the mesangial and epithelial cells permits the filtration of protein, the consequence of which is hyperlipidemia. Whatever the therapeutic measures employed, if proteinuria persists, hyperlipidemia will follow. This suggest that lipoprotein toxicity may contribute to the final common path of renal damage in progressive renal disease. "Lipoprotein toxicity" in arteries is called atherosclerosis, but this term ignores the complexity of the glomerulus and the possible tubular damage that might be caused by filtered lipoprotein. It is clear there is insufficient knowledge of the metabolism of the damaged kidney to confidently attribute the pathology of progression of disease to any single process.
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PMID:Glomerular structures and lipids in progressive renal disease. 248 39

Progressive deterioration in renal function frequently occurs in the absence of the original cause of injury. During the past decade, intense investigations into the factors responsible for progressive nephron destruction have demonstrated that hemodynamic stresses and metabolic and coagulation abnormalities participate in glomerular injury. Hyperlipidemia is a common abnormality in renal disease and is frequently aggravated by protein-uria. Experimentally, therapy with the lipid-lowering agents clofibric acid or lovastatin reduced circulating lipids, particularly cholesterol, decreased proteinuria, and prevented glomerular damage in normotensive and hypertensive models of progressive renal disease. These beneficial effects occurred independently of changes in systemic blood pressure or glomerular injury, supporting the notion that cholesterol or its accompanying changes, or both, were central in lipid modulation of glomerulosclerosis. Clinically, lipid abnormalities are common in patients with renal disease, and atherosclerotic cardiovascular disease is the most frequent cause of death in these patients. Although the role of lipids in atherosclerotic disease has been well established, whether a similar effect of lipids occurs in the microvasculature of the kidney is unknown. Whether therapeutic approaches directed at reducing hyperlipidemia in patients with renal disease will provide a measure of renal protection, as has been seen in experimental models of renal disease, is also unknown.
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PMID:Therapeutic implications of lipid-lowering agents in the progression of renal disease. 248 40

To better understand the pathogenesis of focal and segmental glomerular hyalinosis and sclerosis (FSGHS), a variety of animal models have been developed--mainly in rats--that allow a comprehensive study of all variables involved, such as hemodynamic, genetic, and metabolic factors. In this article, we briefly review the role of lipids in the pathogenesis of FSGHS and provide evidence that "atherosclerosis of the glomerular mesangium" contributes to the ultimate histopathologic lesion of FSGHS in susceptible rat strains. Observations in a FSGHS-resistant strain revealed several characteristic features that may protect these rats against chronic renal disease such as high nephron numbers, glomerular visceral epithelial cells with a remarkable resistance to toxic injury, minimal sequestration of serum proteins and cholesterol from the circulation into the mesangium, and a remarkable lipoprotein profile in normal as well as nephrotic states with a very low cholesterol content of the very-low-density and low-density lipoprotein fractions. Recent clinicopathologic studies also indicate a correlation between hyperlipidemia and the progression of renal disease. The concept of lipid-mediated glomerular injury warrants further study.
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PMID:Genetic differences in susceptibility to glomerular sclerosis: a role for lipids? 248 43

Much recent work has focused on the progressive nature of renal injury, and hemodynamic alterations have been implicated in the pathogenesis of the predominant lesion, focal glomerulosclerosis. Despite the well-documented atherogenic toxicity of lipids in cardiovascular morbidity, little is known about lipid-associated renal injury. However, lipids are toxic to endothelium, and the glomerulus is a vascular bundle. Several authors participating in this symposium have presented evidence for an association between hyperlipidemia and glomerulosclerosis in animal models. This association is particularly significant given the expanded therapeutic armamentarium now available to treat hyperlipidemia. In fact, glomerular injury may be moderated by pharmacologic treatment of hyperlipidemia in a rat renal ablation model. Very little evidence exists, however, for a similar association in human renal disease. We have, in the course of clinical practice, made certain observations in renal biopsy specimens that may for the first time link atherogenesis and lipid deposition to human glomerular injury.
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PMID:Similarities between glomerular sclerosis and atherosclerosis in human renal biopsy specimens: a role for lipoprotein glomerulopathy. 248 45

Disordered lipid metabolism is believed to play an important role in accelerating the progression of chronic renal disease toward uremia. We examine this hypothetic role of lipids in a large population of patients on long-term dietary protein restriction. In our experience, there is no conclusive evidence that lipids may accelerate the progression of functional deterioration in patients with reduced renal function. Hyperlipidemia seems to be only one among the many factors affecting the prognosis of primary renal disease. Dietary protein restriction is effective in maintaining normal or only slightly elevated serum lipid levels in patients with early renal failure. Moreover, patients with renal failure maintained on this diet, which provides an elevated ratio of polyunsaturated to saturated fatty acids, have a more favorable lipid composition of erythrocyte membrane (low percentage of saturated fatty acids and high percentage of polyunsaturated fatty acids) when compared with patients on an unrestricted diet.
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PMID:Serum lipids in patients with chronic renal failure on long-term, protein-restricted diets. 248 48

The metabolic disturbances in glucose-6-phosphatase deficiency (von Gierke's disease) are the consequence of hypoglycemia, occurring mostly during the night. Continuous provision of glucose is the aim of every recently introduced treatment procedure. We studied the influence of continuous ambulatory peritoneal dialysis (CAPD) on the metabolic disturbances in a 42-year-old female patient with von Gierke's disease and end-stage renal disease. During six months of CAPD, there were no dialysis-related complications. The metabolic acidosis didn't worsen: arterial bicarbonate and lactate were not changed. Mean glycemia was 118.6 +/- 14.4 mg%. Total lipemia, cholesterol and triglycerides were not different from those before CAPD, despite the fact that all hypolipidaemic drugs were stopped. Three different exchange procedures were compared during the night: no dialysis, one exchange with a 2 L solution without buffer containing glucose 15 g/L and containing glucose 42.5 g/L. The results show that the 4.25% glucose solution prevents hypoglycaemia, and diminishes the increase in lactate and pyruvate concentration. Intraperitoneal glucose normalizes the plasma free fatty acid concentration. A very important result is the disappearance of hypo-insulinism. We conclude that, from a clinical point of view, CAPD is a well-tolerated treatment in von Gierke's disease. The limited results provide some evidence that the use of a 4.25% glucose solution as an overnight exchange, instead of the usual 1.5% solution, can prevent at least partly the glycogenolysis and consequently the metabolic disturbances of von Gierke's disease.
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PMID:Continuous ambulatory peritoneal dialysis (CAPD) in a patient with glucose-6-phosphatase deficiency. 248 95

Renal disease from a variety of causes often progresses to end-stage renal failure. The progression may be caused by factors accompanying, but not initiating, renal injury. These factors include glomerular hyperfiltration, glomerular hypertension, systemic hypertension, and hyperlipidemia. Studies, primarily in animals, indicate that causative factors may be altered by control of systemic hypertension, dietary protein restriction, administration of angiotensin-converting enzyme inhibitors or calcium channel blockers, and plasma lipid control. Whether such interventions will significantly alter progressive renal disease in humans is, as yet, uncertain.
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PMID:Can progression of renal disease be prevented? 266 51

Abnormalities of Zn metabolism are well documented in patients with chronic renal disease, especially those with nephrotic disease and uremia. The causes of Zn deficiency in kidney disease are not clear. Decreased dietary Zn intake and intestinal absorption, increased endogenous Zn secretion, and increased urinary Zn excretion (as in the nephrotic syndrome and in renal transplant recipients) all may contribute to altered Zn metabolism. Zn depletion may account for decreased taste, sexual and gonadal dysfunction, hyperprolactinemia, glucose intolerance, hyperlipidemia, growth retardation in children, neuropathy, anemia, abnormalities of neutrophil and lymphocyte function, and delayed wound healing. The benefit of pharmacologic doses of Zn, in the treatment of such manifestations, requires further evaluation under controlled conditions. Before use of Zn routinely for therapeutic purposes in uremic subjects, the cause(s) of abnormal Zn metabolism should be identified.
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PMID:Zinc in kidney disease. 267 56


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