Gene/Protein Disease Symptom Drug Enzyme Compound
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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuronopathic Gaucher disease can present as a continuum of clinical findings, including somatic symptoms of anemia, thrombocytopenia, hepatosplenomegaly, and bone disease as well as neurologic sequelae. There is a spectrum of neurologic symptoms ranging from oculomotor apraxia to severe convulsions. The heterozygosity of phenotypes makes it difficult to predict the disease course. We describe an 8-year-old male with neuronopathic type III Gaucher disease who developed bladder dysfunction and was unable to completely void. He also presented with hypertension and acute renal insufficiency, most likely secondary to urinary retention. A complete evaluation was done for causes of urinary retention and bladder dysfunction. A renal bladder ultrasound demonstrated marked hydroureteronephrosis. There was no clinical evidence of infection and cystoscopy revealed no anatomic obstruction. In addition, MRI showed no spinal abnormalities. His bladder dysfunction was managed operatively by creating a catheterizable stoma, using his appendix, to empty his bladder, and surgical findings were consistent with neurogenic bladder. He continues to be managed for his Gaucher disease and neurogenic bladder by genetics, nephrology and urology. This is the first clinical report of neurogenic bladder dysfunction in neuronopathic Gaucher disease.
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PMID:Neurogenic bladder dysfunction presenting as urinary retention in neuronopathic Gaucher disease. 2466 77

Children and adolescents with chronic kidney disease (CKD) are at high risk for cardiovascular morbidity and mortality. This review provides a comprehensive overview of the possible risk factors for early atherosclerosis in children with CKD. Endothelial dysfunction, a precursor of atherosclerosis, starts early in renal disease, as indicated by increased carotid artery intima media thickness, carotid arterial wall stiffness, impaired flow mediated dilatation, and coronary artery calcification, which are frequently present in children with CKD. Many risk factors for atherosclerosis, such as hypertension, dyslipidemia, renal bone disease, hyperhomocysteinemia, and uremia-related cardiovascular risk factors are associated with CKD. All of these risk factors are modifiable and optimal clinical management can delay or prevent cardiovascular disease. Another strategy to decrease the risk of premature cardiac disease and death in children with CKD is to slow the progression of renal disease.
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PMID:Pediatric CKD and cardiovascular disease. 2472 Apr 58

Diabetes is the most important risk factors for chronic kidney disease (CKD). The risk of CKD attributable to diabetes continues to rise worldwide. Diabetic patients with CKD need complicated treatment for their metabolic disorders as well as for related comorbidities. They have to treat, often intensively, hypertension, dyslipidaemia, bone disease, anaemia, and frequently established cardiovascular disease. The treatment of hypoglycaemia in diabetic persons with CKD must tie their individual goals of glycaemia (usually less tight glycaemic control) and knowledge on the pharmacokinetics and pharmacodynamics of drugs available to a person with kidney disease. The problem is complicated from the fact that in many efficacy studies patients with CKD are excluded so data of safety and efficacy for these patients are missing. This results in fear of use by lack of evidence. Metformin is globally accepted as the first choice in practically all therapeutic algorithms for diabetic subjects. The advantages of metformin are low risk of hypoglycaemia, modest weight loss, effectiveness and low cost. Data of UKPDS indicate that treatment based on metformin results in less total as well cardiovascular mortality. Metformin remains the drug of choice for patients with diabetes and CKD provided that their estimate Glomerular Filtration Rate (eGFR) remains above 30 mL/min per square meter. For diabetic patients with eGFR between 30-60 mL/min per square meter more frequent monitoring of renal function and dose reduction of metformin is needed. The use of sulfonylureas, glinides and insulin carry a higher risk of hypoglycemia in these patients and must be very careful. Lower doses and slower titration of the dose is needed. Is better to avoid sulfonylureas with active hepatic metabolites, which are renally excreted. Very useful drugs for this group of patients emerge dipeptidyl peptidase 4 inhibitors. These drugs do not cause hypoglycemia and most of them (linagliptin is an exception) require dose reduction in various stages of renal disease.
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PMID:Diabetes treatment in patients with renal disease: Is the landscape clear enough? 2531 42

In CKD, phosphate retention arising from diminished GFR is a key early step in a pathologic cascade leading to hyperthyroidism, metabolic bone disease, vascular calcification, and cardiovascular mortality. Tenapanor, a minimally systemically available inhibitor of the intestinal sodium-hydrogen exchanger 3, is being evaluated in clinical trials for its potential to (1) lower gastrointestinal sodium absorption, (2) improve fluid overload-related symptoms, such as hypertension and proteinuria, in patients with CKD, and (3) reduce interdialytic weight gain and intradialytic hypotension in ESRD. Here, we report the effects of tenapanor on dietary phosphorous absorption. Oral administration of tenapanor or other intestinal sodium-hydrogen exchanger 3 inhibitors increased fecal phosphorus, decreased urine phosphorus excretion, and reduced [(33)P]orthophosphate uptake in rats. In a rat model of CKD and vascular calcification, tenapanor reduced sodium and phosphorus absorption and significantly decreased ectopic calcification, serum creatinine and serum phosphorus levels, circulating phosphaturic hormone fibroblast growth factor-23 levels, and heart mass. These results indicate that tenapanor is an effective inhibitor of dietary phosphorus absorption and suggest a new approach to phosphate management in renal disease and associated mineral disorders.
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PMID:Gastrointestinal Inhibition of Sodium-Hydrogen Exchanger 3 Reduces Phosphorus Absorption and Protects against Vascular Calcification in CKD. 2540 58

The prevalence of chronic kidney disease (CKD) has now reached epidemic proportions and it is very likely that it will continue to rise with the increasing prevalence of juvenile diabetes mellitus, hypertension and aging population. CKD is a risk factor for cardiovascular disease (CVD) and cardiovascular disease can lead to CKD. It is also well known that patients with CKD have a higher risk of death from CVD than of progressing to end-stage renal disease that requires renal replacement therapy. In patients with CKD, there is a higher mortality from sudden cardiac death and congestive heart failure than coronary artery disease, which is not the case in the general population. The high prevalence of congestive heart failure in CKD is due to cardiac remodeling which progresses from concentric remodeling to concentric and eccentric hypertrophy, leading to left ventricular hypertrophy with both systolic and diastolic dysfunction. Recent studies have suggested that, in patients with chronic kidney disease, common traditional risk factors for cardiovascular disease such as hypertension, hyperlipidemia and obesity may not be the main determinants of cardiovascular disease. Among the various non-traditional cardiovascular risk factors present in patients with chronic kidney disease, abnormalities of CKD related mineral and bone disorder, which includes elevated fibroblast growth factor 23 (FGF23) have been one of the most extensively studied. However, after many years of research, the debate over the exact pathways by which FGF23 may lead to increased CVD still continues. FGF23 may have both direct and indirect effects on the cardiovascular system. Better understanding of the most relevant pathophysiologic pathways for FGF23 may lead to therapeutic interventions against cardiovascular disease in patients with CKD.
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PMID:[FGF23 and the heart]. 2550 70

This study analyze the characteristics and clinical medicine in 17 hospitals all over China, based on hospital information system diagnostic information database, including 4 497 cases of hospitalized patients with Parkinson's syndrome. Results indicate, the most common comorbidities are infarction, hypertension, coronary heart disease, diabetes and lung infections, including cerebral infarction, the combined incidence of hypertension in men reached 33.46% and 30.05%, respectively, it is slightly lower in the females. Men with coronary heart disease are more than women, women with diabetes and bone disease are more than men. Combined incidence of the disease increases with age, vascular factors occupy an important position. The most common combined diseases in patients with 90 years of age or older are coronary heart disease, lung infection, and often accompanied by metabolic disorders and nutritional emergency, critical care. Constipation, depression, anxiety, sleep disorders, cognitive impairment are common non-motor symptoms. The drug categories associated with Parkinson's core symptoms treatment are about 20% to 30% of clinical medicine, the others are associated with the treatment of combined disease, clinical medicine and disease spectrum consistent. Blood circulation topped Chinese agents applied frequency, reaching 44.52%; laxative drugs accounted for 11.66%; detoxification agent representing 9.46%. The first twenty Chinese medicine of the applying frequency reached 56.07% of the total utilization, including 12 kinds of traditional Chinese medicine injections, accounting for 60%. Therefore, in the diagnosis and treatment of Parkinsons syndrome, the treatment of comorbidities is very important, more attentions should be paid to vascular factors of the disease, Chinese medicine should be more concerned to improve the non-motor symptoms, give full play to the pharmaceutical multi-target, the overall regulation of advantages, integrative medicine, and improve the quality of life of patients.
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PMID:[Clinical and medicine characteristics of patients with Parkinson's syndrome]. 2553 83

Metabolic acidosis is a frequent but asymptomatic complication in chronic kidney disease (CKD). In early stages of CKD acidosis is limited to the renal tissue and progresses to reduced serum bicarbonate levels. Reduced renal tissue pH and increased ammoniagenesis are the key mechanisms of the kidney to enhance acid excretion to the urine. The expressed protein patterns in the proximal tubular epithelial cells change remarkably, the proximal convoluted tubule develops hypertrophy, and an intra-renal enhanced renin-angiotensin-system leads to interstitial fibrosis. Since nephrons are numerically reduced in CKD each remaining functional unit has to progressively increase these mechanisms to keep up the equilibrium. The adverse effects of chronic metabolic acidosis include aside from acceleration of progression of kidney disease, the development or exacerbation of bone disease, increased degradation of muscle with muscle wasting, enhanced protein degradation and inflammation. Genome wide association studies demonstrated that tubular acid-base transporters are involved in the development of arterial hypertension. Several retrospective analyses have indicated that low serum bicarbonate predicts death in cohorts with CKD and cardiovascular disease. All studies confirmed a U-shaped association of mortality and serum bicarbonate, indicating that both, acidosis and alkalosis are associated with increased mortality. Randomized controlled trials showed that base substitution, either by modification of the diet or by simply adding alkalizing agents, might halt the decline of kidney function in subjects with CKD. In 2012 a meta-analysis concluded that alkali therapy might provide a long-term favorable effect on renal function in patients with CKD.
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PMID:Effect of oral alkali supplementation on progression of chronic kidney disease. 2554 43

Most patients receiving dialysis have other common chronic conditions in addition to end-stage renal disease, including hypertension, diabetes, cardiovascular disease, and mineral and bone disorder, all of which require long-term medication management. Dialysis patients take an average of 10-12 prescribed and over-the-counter medications from an average of 4.7 prescribers, and an average of 19 pills per day. Thus, reducing polypharmacy is not adequate as a medication therapy goal for these patients. Instead, the dialysis community should focus on ensuring that all patients receive medications that are appropriate, effective, safe and convenient. Barriers to this include a fragmented health care system with inadequate communication between multiple prescribers and pharmacies, and frequent care transitions between ambulatory care sites (dialysis centre, ambulatory primary care practice, ambulatory specialty practice) and the hospital, skilled nursing facility or long-term care facility. Three distinct processes are necessary to prevent and solve the resultant medication-related problems (and reduce polypharmacy). These are medication reconciliation (creating an accurate medication list that reflects all medications the patients is taking and how they are being taken), medication review (evaluating the list for appropriateness, effectiveness, safety and convenience in conjunction with the patient's health status), and ongoing patient-centred medication therapy management (e.g., developing treatment plans centred on each patient's medication-related goals). A team approach including pharmacists as part of the dialysis team with the dialysis facility as the primary medication home is needed.
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PMID:Management of Polypharmacy in Dialysis Patients. 2586 28

Noncommunicable diseases, such as cardiovascular disease, hypertension, renal and bone disease, and malignancies are an ongoing concern during the course of treated HIV disease. Research in this area continues to focus on the epidemiology and risk factors associated with these conditions, identifying the contributions of HIV-related immunopathology to specific and collective end-organ diseases, and evaluating interventions to prevent or reduce the morbidity associated with these conditions. Infectious complications of HIV, such as tuberculosis and cryptococcal disease, also continue to cause substantial morbidity and mortality; diagnosis, prevention, and treatment of these is an area of focus. The 2015 Conference on Retroviruses and Opportunistic Infections provided new insights into all of these areas.
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PMID:CROI 2015: Complications of HIV Infection and Antiretroviral Therapy. 2596 12

Hypovitaminosis D is a worldwide disorder, with a high prevalence in the general population of both Western and developing countries. In HIV patients, several studies have linked vitamin D status with bone disease, neurocognitive impairment, depression, cardiovascular disease, high blood pressure, metabolic syndrome, type 2 diabetes mellitus, infections, autoimmune diseases like type 1 diabetes mellitus, and cancer. In this review, we focus on the most recent epidemiological and experimental data dealing with the relationship between vitamin D deficiency and HIV infection. We analysed the extent of the problem, pathogenic mechanisms, clinical implications, and potential benefits of vitamin D supplementation in HIV-infected subjects.
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PMID:Vitamin D Deficiency in HIV Infection: Not Only a Bone Disorder. 2600 Mar 2


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