Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Elevated serum levels of the atherogenic and thrombogenic lipoprotein (a) (Lp(a)) have been recognized as a feature of the nephrotic syndrome associated hyperlipidaemia. To examine a possible relationship between serum Lp(a) concentration and proteinuria, serum albumin, or blood pressure, we studied nine patients with nephrotic-range proteinuria both at baseline and after various forms of antihypertensive and antiproteinuric treatment. In fixed order, patients received conventional antihypertensive treatment (either alpha-methyldopa or clonidine), subsequently ACE-inhibition therapy (lisinopril), ACE inhibition combined with an NSAID (indomethacin), and finally NSAID plus conventional antihypertensive therapy. Measurements were performed at the end of each 2-month study period. When compared to controls (n = 29), proteinuric patients before treatment showed increased levels of total cholesterol, very-low and low-density lipoprotein (VLDL+LDL) cholesterol, triglycerides and apolipoprotein B (apoB), while high-density lipoprotein (HDL) HDL cholesterol was lower. Lp(a) was significantly higher in patients (107 (95% CI: 55-208) mg/l) as compared to controls (25 (13-49) mg/l, P < 0.01). Conventional antihypertensive treatment did not reduce proteinuria, while Lp(a) remained unaffected. ACE-inhibitor treatment lowered proteinuria, raised serum albumin, while La(a) tended to fall (-11 +/- 8%). Addition of an NSAID induced a further fall in proteinuria and a rise in serum albumin. Lp(a) now fell by 40 +/- 5% from baseline values (P < 0.01). Both serum total, HDL and VLDL+LDL cholesterol fell significantly. Finally, during subsequent single therapy with NSAID most parameters, including proteinuria and Lp(a), returned towards values obtained during single therapy with ACE inhibiton.(ABSTRACT TRUNCATED AT 250 WORDS)
Nephrol Dial Transplant 1994
PMID:Symptomatic antiproteinuric treatment decreases serum lipoprotein (a) concentration in patients with glomerular proteinuria. 805 29

Low-density lipoprotein apheresis (LDL-A) was performed for nine episodes of steroid-resistant nephrotic syndrome in eight patients. The clinical and immunohistological findings were analysed retrospectively. Six of the patients had focal glomerular sclerosis (FGS), one had minimal-change nephrotic syndrome (MCNS), and one had membranous nephropathy (MN) with FGS. The LDL-A treatment, carried out 2-13 times (mean 7.33 +/- 4.05) for one nephrotic episode, at average intervals of 3-16 days (mean: 8.5 +/- 5.1 days) and combined with steroid pulse therapy and the administration of an antihyperlipidaemic agent in some cases, led to rapid amelioration of hyperlipidaemia. In six nephrotic episodes (5 patients) more than 50% reduction of proteinuria occurred (less than 3.5 g/day) (response-group). A significant elevation of serum albumin (more than 3.0 g/dl) was obtained in five of these episodes. The other three patients were resistant (resistant-group). The number of and intervals between LDL-A treatments in the response group (5 +/- 2.8 times and 5.8 +/- 4.1 days) were significantly less than those in the resistant-group (12.0 +/- 0.8 times and 13.2 +/- 1.8 days) (P < 0.05). After LDL-A, significant reductions were observed in the serum total cholesterol (T-CHO), phospholipid (PL), triglyceride (TG), free-CHO (F-CHO), and beta-lipoprotein (beta-lipo) (P < 0.05). HDL-cholesterol (HDL-C) increased somewhat after LDL-A. Further, Ccr was elevated in all nephrotic episodes, except in one patient who manifested renal failure after 6 months.(ABSTRACT TRUNCATED AT 250 WORDS)
Nephrol Dial Transplant 1994
PMID:Does LDL-apheresis in steroid-resistant nephrotic syndrome affect prognosis? 805 31

Increased incidence of cardiovascular morbidity and mortality has been observed in continuous ambulatory peritoneal dialysis (CAPD) patients. Hyperlipemia is an important etiologic factor in the pathogenesis of coronary artery disease. Lovastatin has been shown to effectively lower both the serum total cholesterol and triglyceride levels, the most common abnormalities in these patients. In a retrospective study we assessed the lipid-lowering effects of lovastatin (20 mg/day) in 8 CAPD patients whose serum cholesterol and/or triglycerides remained greater than 240 mg/dL, despite a low cholesterol diet. At 6 months of lovastatin therapy, moderate reductions in total cholesterol and triglyceride levels were observed in 2 patients. Although 20 mg/day of lovastatin were well tolerated, the treatment was not universally effective in lowering the serum cholesterol and triglyceride levels.
Adv Perit Dial 1993
PMID:Lipid-lowering effects of lovastatin in CAPD patients. 810 45

Hyperlipidaemia is common after renal transplantation, and because of its association with atherosclerosis, interest has increased in the use of lipid-lowering drugs in transplant patients. Dietary approaches have not been consistently successful, and multiple pharmacotherapy and drug interactions have led to difficulties in establishing lipid-lowering drug regimes. The statins reduce plasma cholesterol by inhibiting the rate-limiting step in cholesterol synthesis, and although some side-effects have been reported in their use after transplantation, the efficacy and safety of low doses has not been formally established. A randomized single-blind placebo crossover study designed to determine the safety and effectiveness of simvastatin in a single daily 5-mg evening dose was therefore conducted in 26 stable renal transplant patients, 14 of whom were receiving cyclosporin A. The results demonstrated no difference between total cholesterol levels in the baseline simvastatin and placebo periods: 7.97 +/- 1.2 and 7.59 +/- 1.5 mmol/l respectively. After 8 weeks of simvastatin, the total cholesterol declined significantly to 6.72 +/- 0.87 mmol/l (P < 0.001). A significant difference was found when the placebo and simvastatin cholesterol levels were compared at 4 and 8 weeks (P < 0.01). LDL cholesterol decreased from 4.74 +/- 0.87 to 3.78 +/- 0.78 mmol/l after 8 weeks on simvastatin (P < 0.001), and apo B fell from 142 +/- 31 to 112 +/- 22 mg/dl (P < 0.001). The difference in LDL cholesterol and apo B after 8 weeks of simvastatin when compared with the corresponding values on placebo was also significant (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Nephrol Dial Transplant 1993
PMID:Low-dose simvastatin is safe in hyperlipidaemic renal transplant patients. 839 49

A functioning kidney transplant provides the uraemic diabetic patient a greater survival with greater rehabilitation than does either CAPD or maintenance haemodialysis. There are no reports, however, of prospective controlled studies of dialysis versus kidney transplantation in diabetic patients whose therapy was assigned randomly. For the minority ( < 10%) of diabetic ESRD patients who have insulin-dependent diabetes mellitus (IDDM), serious consideration should be devoted to performance of a combined pancreas and kidney transplant to cure diabetes. No matter which ESRD therapy has been elected, optimal rehabilitation in diabetic ESRD patients requires that effort be devoted to recognition and management of co-morbid conditions. Uraemia therapy, whether CAPD, haemodialysis or a kidney transplant should be individualized to the patient's specific medical and family circumstances. Attention to control of hypertension and hyperlipidaemia may slow the course of macrovascular disease, particularly of the coronary arteries, which threatens long-term survival of diabetic kidney recipients. Pretransplant cardiac evaluation is mandatory to identify and correct silent coronary artery disease that may be severe and life threatening. Survival is continuously improving in treating ESRD in diabetes by dialytic therapy, renal transplantation, and in IDDM, by combined pancreas and kidney transplantation. This inexorable progress in therapy reflects multiple small advances in understanding of the pathogenesis of extrarenal micro- and macrovasculopathy in an inexorable disease, coupled with safer immunosuppression.
Nephrol Dial Transplant 1995
PMID:Management choices in diabetic end-stage renal disease. 857 82

Several rat models of polycystic kidney disease (PKD) have been published. The only rat model of autosomal dominant polycystic kidney disease currently used is the so-called Hannover rat (Han:SPRD cy/+). This model is characterized by a slow progression of uraemia, proteinuria and hyperlipidaemia. Histological changes clearly resemble those seen is human PKD. The localization of Na+/K(+)-ATPase correlating with the phenotype of the cysts--basal in moderately expanded and apical in highly expanded cysts--suggests that the mislocation of the Na+/K(+)-ATPase is involved in the mechanism of cyst expansion rather than formation, and a consequence of cell dedifferentiation rather than an initial event. Of note is a considerable gender difference in disease severity. Disease anticipation or genetic imprinting does not occur. In addition to gender, a number of interventions influence the progression rate: acceleration is noted after unilateral nephrectomy, the induction of acidosis, chloride feeding or an increased protein intake; slowing down of the course occurs after the induction of alkalosis and castration, and after treatment with lovastatin and methylprednisolone. Thus the Han:SPRD cy/+ rat represents the only well-documented rat model of autosomal dominant PKD resembling a number of features of the human disease.
Nephrol Dial Transplant 1996
PMID:Rat models of autosomal dominant polycystic kidney disease. 904 28

Creatinine clearance decreases with age by 1 ml/min/year after 40 years of age, although serum creatinine remains constant because of reduction of muscle mass. Reduction of water intake may occur in the elderly because of a reduced sensation of thirst; this is associated with a tendency to lose water with urine. The capacity to respond to sodium load is impaired in aged kidneys, thereby leading to ECV expansion and hypertension. But there is also, in the elderly, a reduced capacity for retaining sodium (FENa is higher than in young subjects), making old subjects sensitive to salt depletion and ECV contraction. Hypernatraemia (Nas > 150 mmol/l) is not infrequent in the elderly (1%) and is usually due to water deficiency (old subjects should be forced to drink), and rarely to iatrogenic excess of sodium. It is the abrupt occurrence of severe hypernatraemia that causes neurological symptoms due to dehydration and brain shrinking, which may lead to cerebral haemorrhage and death. Hyponatraemia (Nas < 130 mmol/l) is frequent among the elderly (7-11%) and is mainly due to water overload, which is usually iatrogenic. Hypovolaemic hyponatraemia occurs when salt depletion causes ECV contraction > 10%, and is due to water retention in an attempt to normalize ECV. Hypervolaemic hyponatraemia is due to ADH hypersecretion because of a decrease in 'effective' circulating blood volume. 'Pseudohyponatraemia' may occur because of hyperlipidaemia or hyperproteinaemia. It is the abrupt occurrence of severe hyponatraemia that causes neurological symptoms (water intoxication), secondary to the oedomatous swelling of the brain within the skull. While rapidly occurring hyponatraemia may be lethal, slowly occurring hyponatraemia is usually asymptomatic. Rapid correction of hyponatraemia may cause cerebral dehydration and 'osmotic demyelination syndrome' ('central pontine myelinosis'). Decrease (e.g. by diuretics) or increase (e.g. by ACE-inhibitors, non-steroidal anti-inflammatory drugs, beta-blockers) or serum potassium may occur in the elderly. Diuretics should be used with caution in elderly subjects to avoid salt depletion, hypotension and renal function impairment.
Nephrol Dial Transplant 1996
PMID:Some sodium, potassium and water changes in the elderly and their treatment. 905 29

The progressively growing number of patients with end-stage renal failure (ESRF) associated with diabetes mellitus and requiring renal replacement therapy (RRT) stimulated both nephrologists and diabetologists to investigate the mechanisms linking hyperglycaemia to diabetic renal failure and to set up measures to prevent the onset and slow the progression of diabetic nephropathy. Over the last few decades, a large number of studies have investigated both the incidence of diabetic nephropathy and the relationship between metabolic control and the development of diabetic nephropathy. Chronologically, the first type of diabetes and diabetic nephropathy to be studied was type I, and it is only in recent years that metabolic control has been proven to be a contributor to the development of nephropathy in such patients. Recently, the DCCT demonstrated that metabolic control in the prealbuminuric phase was effective in reducing the incidence of microalbuminuria, even if it was unable to reduce the incidence of overt proteinuria in patients with type I diabetes and established proteinuria. On the other hand, in type II diabetes, the number of studies demonstrating a favourable effect of metabolic control on onset and progression of diabetic nephropathy is only slightly greater than those that failed to show a favourable effect. This feature may suggest that in type II patients, genetic and ethnic differences, nutritional aspects, lifestyle and other confounding factors may play a relevant role in the course of the disease. However, the trials performed and the retrospective analyses generally agree that glycated haemoglobin two standard deviations greater than the mean is related to a worsening in progression of diabetic nephropathy and to an enhanced risk of other complications. In general, a glycated haemoglobin < or =8% seems advisable. Moreover, in both type I and type II, greater emphasis should be placed on the major risk factors such as hypertension, smoking habits and hyperlipidaemia.
Nephrol Dial Transplant 1998
PMID:The effect of metabolic control on development and progression of diabetic nephropathy. 987 Apr 24

Most patients receiving renal replacement therapy have cardiovascular disease. The most frequent conditions are left ventricular hypertrophy and coronary artery disease. Hemodialysis is associated with a characteristic spectrum of acute complications (such as hypotension, sudden death) that can be explained by typical dialysis-induced effects on the heart. With continuous peritoneal dialysis (CAPD) some of the cardiovascular complications are ameliorated owing to slow ultrafiltration and absence of an arteriovenous fistula. CAPD might be concluded to be the preferable option in patients with cardiovascular disease, but a few disadvantages, such as hyperlipidemia and hyperinsulinemia, also exist. Nurses also play an important role in the therapeutic success and outcomes of these patients.
Perit Dial Int 1999
PMID:Continuous ambulatory peritoneal dialysis in high-risk patients: patients with cardiovascular diseases--role of the nurse. 1040 72

Plasma concentrations of lipoprotein (a) [Lp(a)] are increased in patients on renal replacement therapy. Lipoprotein (a) is increasingly being recognized as an independent cardiovascular risk factor. In an effort to explore the mechanism for elevation of Lp(a) in patients on dialysis we have performed turnover studies of Lp(a) with radioactive iodine. Lp(a) was isolated from 1 patient on hemodialysis (HD) and 1 patient on continuous ambulatory peritoneal dialysis (CAPD); the protein was labeled with 125I and returned to each patient. Lipoprotein (a) was subsequently isolated from the patients over a 15-day period and the decay of the specific radioactivity of Lp(a) was used to determine the fractional catabolic rate (FCR), which was 0.27 (pool/day) for the HD patient and 0.28 (pool/day) for the CAPD patient. These rates are indistinguishable from those measured in 4 patients with hypercholesterolemia (0.29, SEM = 0.01) and in 4 other familial hypercholesterolemic patients (0.29, SEM = 0.02) studied previously using the same method by Knight et al. (7). We found no difference in the FCR of patients on dialysis when compared to patients with hyperlipidemia and normal renal function. Increased plasma concentration of Lp(a) in our patients on renal replacement therapy is not due to decreased catabolism, but is caused by increased synthesis.
Adv Perit Dial 1998
PMID:Mechanism for elevated plasma lipoprotein(a) concentrations in patients on dialysis: turnover studies. 1064 29


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