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Query: UMLS:C0020473 (hyperlipidemia)
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The precise pathogenesis of human diabetic kidney disease and the factors responsible for the susceptibility to it remain to be established. However, there is now evidence that renal disease clusters in families and that genetic factors are of central importance in determining liability. A predisposition to arterial hypertension has been suggested as playing a contributory role in the development of kidney disease. Genetically controlled hypertrophic processes may be implicated in the susceptibility to arterial wall damage and glomerular injury in diabetes. This suggestion derives from the observation that the fibroblasts of patients with diabetic nephropathy show a higher Na+/H+ antiport activity and a greater 3H-thymidine incorporation into DNA than fibroblasts of diabetic patients without nephropathy. The first sign of renal damage is the appearance of microalbuminuria and of a small elevation in arterial pressure, changes associated with significant mesangial expansion. Microalbuminuria is associated with abnormalities of lipoprotein profiles possibly as a consequence of insulin-resistance-induced hyperinsulinemia. It could be postulated that the environmental changes brought about by diabetes lead in susceptible individuals to increased systemic and intraglomerular pressure on the one hand and mesangial expansion on the other. These two processes would cause proteinuria and glomerulosclerosis. Lipid abnormalities would further aggravate the renal histological damage and, in combination with hypertension, contribute to the accelerated atherosclerosis typical of patients with diabetic kidney disease. A vicious circle would thus be triggered of reduction in renal function, more hypertension, more proteinuria, more glomerular obsolence, more hyperlipidemia and eventually end-stage renal failure or premature cardiovascular death.
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PMID:Mechanisms of diabetic renal and cardiovascular disease. 207 90

A prospective study of 150 diabetic patients was undertaken with the aim of determining the factors associated with the development of foot ulcerations. Seventy five patients had foot ulceration and 75 had no foot lesions. Peripheral (78.7%) and autonomic (38.7%) neuropathy were more commonly found in the "ulcer" group, as were vascular insufficiency (49.3%) and hyperlipidaemia (60%). Renal failure (9.3%) and ketoacidosis (20%) were also commoner in patients with foot ulceration. Most, if not all, of the aetiological factors are related to prolonged uncontrolled hyperglycaemia.
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PMID:Aetiology of diabetic foot ulceration. 207 69

The overall cardiovascular mortality in patients with chronic renal failure is about 30 per cent of which 10 per cent is attributed to myocardial infarction. This prevalence led some workers to propose a hypothesis of "accelerated atherosclerosis" due to the hyperlipidaemia observed in 30 to 70 per cent of patients. However, the concept of accelerated atherosclerosis, which was based essentially on clinical studies, has been questioned. Pericardial effusion is a common complication of chronic renal failure and has been reported in over 62 per cent of patients in echocardiographic studies. There are many causes and symptoms are often mild; systematic echocardiographic examination of patients with renal failure undergoing haemodialysis has shown 32 per cent of pericardial effusions to be asymptomatic. There are two potential complications: cardiac tamponade and, lesser frequently, constrictive pericarditis. Cardiac failure is a common cause of death in patients undergoing long-term dialysis. The myocardial histological appearances are those of fibrosis, the etiology of which is not fully understood although the dialysis membranes and hypotensive episodes occurring during haemodialysis have been thought to play a role. Left ventricular hypertrophy and fibrosis may give rise to ventricular arrhythmias which could explain some of the cases of sudden death observed in patients with renal failure and often wrongly attributed to ischemic heart disease. Another form of myocardial disease which is observed later is characterised by an alteration of systolic function with left ventricular dilatation and hypokinesia and increased end diastolic pressures without an increase in left ventricular wall thickness. Valvular heart disease may also result from renal failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[So-called uremic heart diseases]. 210 35

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

Fifty-two patients with terminal renal failure (TRF) placed on elective hemodialysis were examined for serum lipids and red blood cell membranes with the aid of chromatographic separation of lipids in thin-layer silica gel on Silufol plates followed by densitometry. Spectrocytophotometry was employed to study red blood cell distribution on the basis of the content of lipoproteins in TRF patients. Fluidity of the lipid bilayer of the red blood cell membrane was measured on Hitachi spectrofluorimeter according to the degree of eximerization of fluorescent pyrene. Dyslipidemia manifested itself as hyperlipidemia, hypertriglyceridemia, hypercholesterolemia and hyperphosphatidylcholinemia. The lipid profile of the red blood cell membranes was found to be deranged, which was evidenced by the reduced content of lipoproteins, total phospholipids, triglycerides, and cholesterol esters. In addition, there was a significant rise in the content of free cholesterol, lysolecithin and phosphatidyl ethanolamine. Impairment of lipid exchange between blood serum and the red blood cell membrane in TRF patients is under discussion. The changes in the lipid spectrum of the red blood cell membranes mirror their morphofunctional failure, supported by derangement of fluidity of the lipid bilayer of the red blood cell membrane. Both increase of viscosity of the lipid bilayer of the red blood cell membrane caused by a high level of cholesterol in the membrane and changes in the cholesterol/phospholipid ratio and reduction of the lipid bilayer viscosity related to the rise of the content of membrane lysolecithin in part of TRF patients were discovered. Hemodialysis influenced the lipid content of blood serum, producing no effect on the lipid spectrum of the red blood cells membrane.
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PMID:[Disordered lipid metabolism and the morphofunctional instability of the erythrocyte membranes in patients with terminal kidney failure]. 221 35

Chronic renal disease is a progressive process. Implicated factors include abnormalities of the clotting cascade, altered prostaglandin metabolism, increased dietary protein intake, and abnormalities of lipoprotein metabolism. Several animal models have associated increased serum concentrations of cholesterol and triglycerides with progressive decline in renal function. The mechanism(s) of lipid-associated renal injury are unknown but may relate to lipid uptake by glomerular mesangial cells, hyperviscosity secondary to the hyperlipidemia, and a direct effect of the lipids on the glomerular basement membrane. Patients with chronic renal disease have well recognized increases in serum lipid concentrations. Whether lowering these concentrations will delay or prevent progressive renal failure or renal histologic abnormalities is unknown, but studies are underway to evaluate the effect of lipid-lowering agents in patients at risk for chronic progressive renal disease.
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PMID:Lipoprotein abnormalities in the progression of renal disease. 222 43

Little notice has been paid in the surgical literature to problems with psychoeffective lithium, which by interfering with adenylate cyclase affects thyroid and parathyroid function, causing hypercalcemia, hyperparathyroidism, and hypothyroidism. Seven patients with lithiumogenic hyperparathyroidism occurring after years of lithium therapy underwent treatment and manifested osteoporosis (n = 2), hypertension (n = 2), nephrolithiasis (n = 1), coma (n = 1), rising hypercalcemia (n = 1), goitrous myxedema (n = 4), nephrogenic diabetes insipidus (n = 2), renal failure (n = 2), and hyperlipidemia (n = 1). Disease-directed parathyroidectomy (without morbidity) was curative. Unique laboratory findings included normal serum phosphorus and reduced urinary calcium and cyclic adenosine monophosphate values. Three separate cases of thyroid carcinoma after long-term lithium therapy were also treated, being preceded by myxedema (n = 2) and concurrent with hyperparathyroidism (n = 1). There has been only one previous report of lithium-associated thyroid carcinoma. All patients taking lithium should undergo surveillance for thyroid and parathyroid dysfunction and neoplasia, and appropriate surgical and medical treatment should be considered in each situation. Although hyperparathyroidism may be reversible with lithium discontinuance, such therapy may be obligatory for patient well-being, thus dictating parathyroidectomy.
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PMID:Lithiumogenic disorders of the thyroid and parathyroid glands as surgical disease. 224 24

Two patients with severe hyperlipidemia receiving long-term hemodialysis were classified as type III hyperlipoproteinemic subjects. They are homozygous for apolipoprotein E2 and have an elevated VLDL-cholesterol/plasma-triglyceride ratio. The dyslipoproteinemia was severely aggravated by the renal failure, but careful treatment with bezafibrate was able to effectively lower elevated serum lipids. Accurate diagnosis of lipid abnormalities in patients with chronic renal failure seems to be necessary to plan appropriate therapeutic interventions and to lower the risk for accelerated atherosclerosis.
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PMID:Severe type III hyperlipoproteinemia in two patients maintained on chronic hemodialysis. 231 34

Hyperlipidemia is usually present in patients with the nephrotic syndrome. The most common lipid abnormality is hypercholesterolemia, although as the disorder progresses, hypertriglyceridemia may develop. Elevated plasma lipids have two potential vascular consequences, namely, atherosclerosis and progression of renal failure. Neither of these complications has been proven with certainty, but there is growing evidence to indicate that both may be long-term consequences of the nephrotic syndrome. Therefore, effective therapy of hyperlipidemia, particularly elevated cholesterol levels, is needed as a protection against these complications. Since nephrotic hypercholesterolemia frequently is severe, dietary therapy, although a valuable adjunct, will not normalize cholesterol levels in most nephrotic patients. Thus, if effective serum cholesterol lowering is to be achieved, drug therapy will be required. Bile acid-binding resins have been shown to lower cholesterol levels in nephrotic patients, but the decline in cholesterol concentrations is usually insufficient to produce a marked reduction in coronary risk. Nicotinic acid theoretically should be useful for treatment of nephrotic hyperlipidemia, but it has not been adequately tested. The new drugs that inhibit cholesterol synthesis, e.g., lovastatin, appear to be highly promising for treating elevations of both serum cholesterol and triglycerides in the nephrotic syndrome. However, testing of these drugs in this condition has been limited, and the possibility of significant side effects in an appreciable portion of patients has not been ruled out. Of particular concern is the development of severe myopathy that can produce myoglobinuria and acute renal failure. This side effect is relatively rare in patients without the nephrotic syndrome, but its prevalence in the latter condition has not been determined. The fibric acids will lower triglyceride levels in nephrotic patients, but they are not effective in lowering cholesterol levels; consequently, they probably have little role in the treatment of nephrotic hypercholesterolemia. Finally, the drug probucol will lower cholesterol levels in nephrotic patients, although not to desirable levels; still, probucol could prove useful in combination with other cholesterol-lowering drugs.
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PMID:Rationale and management of hyperlipidemia of the nephrotic syndrome. 248 42

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


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