Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
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Diabetic nephropathy, which represents a major form of chronic kidney disease (CKD), is a leading cause of end-stage renal disease worldwide, and is also a risk factor for cardiovascular disease (CVD). Patients with diabetes and CKD have poorer outcomes after myocardial infarction. The underlying pathogenic mechanism that links diabetic nephropathy to a high risk of CVD remains unclear. In addition to traditional risk factors, including hypertension, hyperglycemia, and dyslipidemia, identification of novel modifiable risk factors is important in preventing CVD in people with diabetes. Inflammation/oxidative stress are known to be associated with an increased risk for CVD in patients with diabetic nephropathy. Moreover, homocysteine, advanced glycation end products, asymmetric dimethylarginine, and anemia may play a role in the development and progression of atherosclerosis in patients with diabetic nephropathy. This review summarizes the epidemiologic evidence, molecular mechanisms responsible for the increased risk for CVD in patients with diabetic nephropathy, and therapeutic intervention for diabetic nephropathy as evidenced by large-scale clinical trials.
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PMID:Cardiovascular disease in patients with diabetic nephropathy. 1878 60

The inflammatory variant of aortic aneurysms has 3 unique features: marked thickening of the aneurysm wall, fibrosis of the adjacent retroperitoneum, and rigid adherence of the adjacent structures to the anterior aneurysm wall. Abdominal tenderness with or without a pulsatile abdominal mass is the most common finding, although it is present in only about 33% of patients. Systemic symptoms, such as fever, malaise, and weight loss, are reported in about 20% to 50% of patients. A contrast-enhanced computed tomography scan, magnetic resonance imaging, and a transesophageal echocardiogram are among the best modalities to evaluate for inflammatory thoracoabdominal aneurysm, but a transthoracic echocardiogram can frequently be very suggestive. Medical treatment options include corticosteroids or other anti-inflammatory and immunosuppressive therapies. Surgical intervention usually consists of a transperitoneal approach with infrarenal aortic clamping. This case review describes a 64-year-old woman with a history of hypertension and dyslipidemia who presented with anemia, lower back pain, and a recent 30-pound weight loss.
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PMID:Inflammatory aneurysm of the thoracoabdominal aorta with associated dissection. 1895 81

The principal causes of morbidity and mortality in children with chronic renal failure on maintenance hemodialysis are cardiovascular complications. Recently, it has been suggested that oxidative stress, chronic inflammation and malnutrition are risk factors for cardiovascular disease. However, to date, biomarkers of oxidative stress have not been well studied in children. The aim of this study was to investigate the relationship between oxidative stress and cardiovascular risk factors in children on hemodialysis therapy. Twenty-eight hemodialysis patients (13 females, 15 males; mean age 15.1 +/- 2.5 years) and 20 healthy children (13 females, seven males; mean age 14.3 +/- 2.7 years) were included in the study. Levels of antibodies to oxidized low-density lipoprotein (oLABs), high sensitivity C-reactive protein (hs-CRP), albumin, prealbumin, transferrin, and ferritin were measured. Antibodies to oxidized low-density lipoprotein (LDL) in hemodialysis patients were lower than those in the controls (P < 0.05). The patients with lower oLAB titers had higher levels of hs-CRP and ratio of erythropoietin to hematocrit (EPO/Htc), and lower levels of albumin, prealbumin, apolipoprotein A-1 (ApoA(1)), and high-density lipoprotein (P < 0.05). Antibodies to oxidized LDL in hemodialysis patients with dyslipidemia were lower than those of patients with normal lipid profile (P < 0,05). This study showed that children treated by hemodialysis are exposed to oxidative stress and chronic inflammation. We suggest that oLAB levels are decreased in children on hemodialysis as a result of severe oxidative stress and that these antibodies are related to inflammation, anemia, malnutrition and dyslipidemia.
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PMID:Oxidative stress in children on hemodialysis: value of autoantibodies against oxidized low-density lipoprotein. 1895 4

The natural history of most chronic kidney diseases (CKD) indicates that glomerular filtration gradually declines over time, progressing to more advanced stages of kidney failure. Since the publication of the first studies by the Modification of Diet in Renal Disease (MDRD) Study Group, numerous factors have been identified that can accelerate this progression. Some are dependent on the etiology, but other are common to all and may accelerate progression of kidney disease: Non-modifiable progression factors for CKD: - Etiology of kidney disease - Degree of initial kidney function - Gender - Age - Ethnicity/Other genetic factors - Birth weight Modifiable progression factors for CKD: - Proteinuria - High blood pressure - Poor glycemic control in diabetes - Smoking - Obesity - Metabolic syndrome/Insulin resistance - Dyslipidemia - Anemia - Metabolic factors (Ca/P, uric acid) - Use of nephrotoxic drugs. Therapeutic intervention on these factors has shown that it reduce the rate of progression of CKD (Strength of Recommendation A).There is no clear evidence that correction of these factors slows CKD (Strength of Recommendation C), although it has been shown to have a beneficial effect on cardiovascular risk at other levels.
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PMID:[Progression factors for chronic kidney disease. Secondary prevention]. 1901 33

Nephrologists should promote the detection of CKD in heart disease patients. The evaluation should include estimation of GFR and detection of microalbuminuria in a recently voided urine sample by the albumin:creatinine ratio. Any patient with stage 3 or 4 CKD and rapid deterioration of GFR should be evaluated by the nephrologist. - Patients with CKD have a high risk of cardiovascular (CV) complications and heart disease patients have a high incidence of CKD and progression is also more rapid (Strength of Recommendation B). The most likely pathophysiological hypothesis is endothelial damage. - The CV risk profile should be established in each patient followed by adequate compliance with control goals for common CV risk factors: smoking, obesity, sedentarism, hypertension, dyslipidemia. Early treatment of anemia and bone mineral disease as CV risk factors requires special mention (Strength of Recommendation B). - Management of these patients will be based on individualization of treatment, close systematic follow-up, and integration between care levels: Specialized care (nephrologists and cardiologists) and primary care. - The cardiorenal syndrome (CRS) is a condition in which both organs are simultaneously affected and their deleterious effects are reinforced in a feedback cycle, with accelerated progression of renal and myocardial damage. Because of its prognostic value, treatment of HF takes precedence over CKD. Most studies on cardiovascular risk and on HF exclude patients with stage 4-5 CKD. We thus do not have sufficient strong evidence and recommendations are based on the extrapolation of data from studies with normal GFR or milder grades of CKD, and on the empirical use of certain treatments. - ARBs and ACEIs are the mainstays of treatment of HF with systolic and diastolic dysfunction, and have been shown to reduce mortality in studies in the general population (Strength of Recommendation A). The may also slow progression of CKD, especially in diabetics. Dual renin-angiotensin blockade with the combined use of lower doses of both drugs has shown promising results for control of CKD progression, but there are no data to recommend its use for control of HF in advanced stages of CKD (stage 4-5) (Strength of Recommendation C). - In these stages of CKD, only loop diuretics have sufficient potency. The therapeutic dose range should be achieved. Lowdose thiazides achieve diuretic synergy. The use of spironolactone and eplerenone has shown benefits in patients with AMI and HF with an ejection fraction < 40% without advanced CKD. They should always be used with strict control of GFR and K+. No benefit has been shown for the use of <<dopamine in diuretic doses>> (may even be harmful) or continuous infusion of furosemide (Strength of Recommendation B). The use of beta-blockers should be increased in these patients. - Treatment-refractory heart failure in the context of stage 3 CKD could be amenable to ultrafiltration techniques. Continuous ambulatory PD could be an alternative treatment to maintain hemodynamic equilibrium while also allowing pharmacological treatments to be prescribed that would not be feasible without dialysis and could even improve myocardial and kidney function (Strength of Recommendation C).
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PMID:[Cardiorenal syndrome]. 1901 35

Familial hypertriglyceridemia (FHTG) is an uncommon primary (genetic) dyslipidemia. FHTG is characterized by moderately elevated serum triglycerides, usually in the absence of significant hypercholesterolemia and rarely manifests in childhood. We report an eight-month-old boy incidentally diagnosed as a case of FHTG due to lipemic serum (patient was admitted for malaria with anemia). He had elevated serum triglycerides with normal serum cholesterol, but had no symptoms related to the primary disorder (FHTG).
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PMID:Familial hypertriglyceridemia. 1905 57

Successful kidney transplantation leads to restoration of renal function. Some metabolic disorders from chronic renal failure may persist and new metabolic abnormalities can develop (obesity, diabetes, hypertension, bone disease, and anemia). Additionally, influence of immunosuppressive drugs (corticosteroids, cyclosporine A, tacrolimus, and rapamycin) may aggravate the course of diabetes, hypertension, and dyslipidemia. Nutritional management of renal transplantation is divided into the pretransplant period, transplant surgery, and early and late posttransplant period. Patients in the pretransplant period in dialysis treatment may develop protein-energy malnutrition and negative nitrogen balance, with loss of lean body mass and fat deposits. Nutritional management in the early posttransplant period with a functioning kidney graft necessitates fluid and electrolyte balance control with protein intake of 1,2/kg BW/day and 30-35 kcal/kg BW/day. In a nonfunctioning kidney graft, dialysis treatment continues and the therapeutic dose of immunosuppressive drugs must be reduced. The principal objective in the late posttransplant period is the maintenance of optimal nutritional status. Nutrition is important in managing obesity, insulin resistance, diabetes, hyperlipidemia, and hypertension. Other posttransplant conditions for which diet and/or nutritional supplements may be beneficial include hypomagnesemia, hypophosphatemia, hyperuricemia, hyperkalemia, hyperhomocysteinemia, chronic renal allograft failure, renal anemia, and renal bone disease.
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PMID:Nutritional consequences of renal transplantation. 1912 81

Cardiovascular disease (CVD) is the main cause of death in peritoneal dialysis (PD) patients, a situation that can be explained by a combination of traditional and nontraditional risk factors for CVD in these patients. Glucose and insulin homeostasis are altered in chronic kidney disease (CKD) patients even in the early stages of CKD, leading to insulin resistance by various pathways. Several factors have been implicated in the pathogenesis of insulin resistance, including anemia, dyslipidemia, uremia, malnutrition, excess of parathyroid hormone, vitamin D deficiency, metabolic acidosis, and increase in plasma free fatty acids and proinflammatory cytokines. Insulin resistance and dyslipidemia are observed and increase with the progression of CKD, playing an important role in the pathogenesis of hypertension and atherosclerosis. Particularly in PD patients, exposure to glucose from dialysis fluid accentuates the foregoing metabolic abnormalities. In conclusion, insulin resistance and altered glucose metabolism are frequently observed in CKD, and although dialysis partly corrects those disturbances, the use of glucose PD solutions intensifies a series of harmful metabolic consequences. New therapeutic measures aimed at reducing metabolic disorders are urgently needed and perhaps will improve PD patient survival.
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PMID:Insulin resistance and glucose homeostasis in peritoneal dialysis. 1927 Feb 4

Middle molecules can be defined as compounds with a molecular weight (MW) above 500 Da. An even broader definition includes those molecules that do not cross the membranes of standard low-flux dialyzers, not only because of molecular weight, but also because of protein binding and/or multicompartmental behavior. Recently, several of these middle molecules have been linked to the increased tendency of uremic patients to develop inflammation, malnutrition, and atheromatosis. Other toxic actions can also be attributed to the middle molecules. In the present publication we will consider whether improved removal of middle molecules by large pore membranes has an impact on clinical conditions related to the uremic syndrome. The clinical benefits of large pore membranes are reduction of uremia-related amyloidosis; maintenance of residual renal function; and reduction of inflammation, malnutrition, anemia, dyslipidemia, and mortality. It is concluded that middle molecules play a role in uremic toxicity and especially in the processes related to inflammation, atherogenesis, and malnutrition. Their removal seems to be related to a better outcome, although better biocompatibility of membranes might be a confounding factor.
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PMID:Back to the future: middle molecules, high flux membranes, and optimal dialysis. 1937 41

A 31-year-old man with no significant medical history presented with a 5-day history of progressive left upper quadrant abdominal pain. Physical examination revealed a tender guarded abdomen, no icterus, and bilateral corneal "arcus senilis"-like changes. Laboratory workup showed a mild normocytic, normochromic anemia; and target cells were seen in the peripheral blood smear. Serum was turbid; and the lipid profile showed elevated total cholesterol, low high-density lipoprotein cholesterol, and elevated triglycerides. Urinalysis revealed nephrotic range proteinuria with microhematuria. An abdominal computed tomographic scan demonstrated a homogeneously enlarged spleen. The patient was discharged after symptomatic treatment to be followed as an ambulatory patient. Several days later, he returned with severe left upper quadrant pain and was admitted to the surgical service for further evaluation. A splenectomy was performed for a suspected splenic lymphoma. Upon gross examination, spleen was moderately enlarged, weighing 780 g. Sectioning revealed a beefy red cut surface without gross lesions. Wright-Giemsa-stained touch imprints showed many sea-blue histiocytes. A renal biopsy was also performed, demonstrating focal segmental glomerular sclerosis and mesangial expansion with extramembranous and intramembranous deposition of lipids. In the absence of hematologic malignancy and in light of the abnormal lipid profile, a disorder of lipid metabolism was suspected. Histologic and ultrastructural findings in the kidney and spleen raised the likelihood of lecithin-cholesterol acyltransferase (LCAT) deficiency, which was confirmed by the markedly decreased serum LCAT activity and serum LCAT mass. We describe a case with the triad of splenomegaly with sea-blue histiocytes, nephropathy, and dyslipidemia in a patient with LCAT deficiency.
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PMID:Splenomegaly with sea-blue histiocytosis, dyslipidemia, and nephropathy in a patient with lecithin-cholesterol acyltransferase deficiency: a clinicopathologic correlation. 1959 52


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