Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypertension and osteoporosis are characteristic clinical features in patients with Cushing's syndrome or in those on glucocorticoid (GC) treatment. These two distinct complications of GC excess share one common denominator: an abnormal handling of cations, sodium (Na(+)) and calcium (Ca(2+)), either primarily or in part by the kidney tubule. The principal mechanism of GC-induced hypertension is overstimulation of the non-selective mineralocorticoid receptor (MR), resulting in renal Na(+) retention, volume expansion and finally to an increase in blood pressure. In mineralocorticoid target organs, such as the kidney, the MR is protected from GC occupation by the enzyme 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2), a gate-keeping enzyme, which converts cortisol to receptor-inactive cortisone. This enzyme allows aldosterone to be the physiological agonist of the MR despite significantly higher circulating levels of cortisol. Kinetic properties of 11betaHSD2 suggest that saturability of this enzyme can already be achieved at high-normal physiological plasma cortisol levels, thereby leading to ovestimualtion of the MR by cortisol in states of GC excess. The mechanisms of GC action on bone turnover are more complex. GCs increase bone resorption, inhibit bone formation and have an indirect action on bone by decreasing intestinal Ca(2+) absorption, but also inducing a sustained renal Ca(2+) excretion. The latter appears to be mediated through stimulation of the MR by GC. The prevention and treatment of GC-induced hypertension and osteoporosis include the use of the minimal effective dose of GC, some general measures, and the use of some specific drugs. Modulation of renal Na(+) and Ca(2+) excretion with some, but not all, diuretics represents an important specific (for hypertension) or supportive (for bone disease) therapeutic intervention.
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PMID:Cortisol and the renal handling of electrolytes: role in glucocorticoid-induced hypertension and bone disease. 1468 90

Post-transplant diabetes mellitus (PTDM) is a frequent and serious complication after kidney transplantation. Its ethiopathogenesis is multifactorial and includes the immunosuppressive regimen, the ethnicity, older age and the body mass index. Among these, calcineurine inhibitor and steroid use seems to have outstanding relevance. Both patient and graft survival is significantly reduced in recipients affected by PTDM. The main clinical aspects of transplant recipients with PTDM are patient and graft survival rate, infections, cardiovascular complications and late complications of diabetes that include nephropathy, neuropathy, retinopathy, micro-macroangiopathy and bone disease. The main stages of PTDM prophylaxis and treatment are: to identify patients at risk pre-transplantation; to control modifiable risk factors post-transplantation; to control hypertension and lipid profiles and a strict metabolic control. Insulin treatment is indicated mainly in thin patients and oral hypoglycemic agents should be reserved for overweight patients. Transplant centers are currently accepting higher risk candidates for post-transplant complications; therefore, attention needs to shift to the prevention and the control of complications, such as PTDM, because they can lead to a poor quality of life and an increased mortality in patients with functioning grafts.
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PMID:Post-transplant diabetes mellitus. 1473 7

The Pituitary Society in conjunction with the European Neuroendocrine Association held a consensus workshop to develop guidelines for diagnosis and treatment of the co-morbid complications of acromegaly. Fifty nine pituitary specialists (endocrinologists, neurosurgeons and cardiologists) assessed the current published literature on acromegaly complications in light of recent advances in maintaining tight therapeutic control of GH hypersecretion. The impact of elevated GH levels on cardiovascular disease, hypertension, diabetes, sleep apnea, colon polyps, bone disease, reproductive disorders, and neuropsychologic complications were considered. Guidelines are proposed for effective management of these complications in the context of overall acromegaly control. When appropriate, requirements for prospective evidence-based studies and surveillance database development are enunciated. Effective management of co-morbid acromegaly complications will lead to improved morbidity and mortality in acromegaly.
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PMID:Diagnosis and treatment of acromegaly complications. 1505 79

Optic nerve sheath decompression (ONSD) maintains a role in the management of visual loss complicating papilloedema in selected patients primarily with idiopathic intracranial hypertension. The evidence base for this intervention is reviewed and audit data on visual outcomes for patients with acute, chronic, and atrophic forms of papilloedema are contrasted. Optic canal decompression has a role in the management of compressive optic neuropathies complicating mass lesions arising from paranasal sinuses and intracranially and can be achieved by transethmoidal, transbasal, and open craniotomy routes. The evidence base supporting this intervention in traumatic optic neuropathy and in primary bone disease causing canal stenosis (in particular fibrous dysplasia) is reviewed where the indications are more controversial.
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PMID:Optic nerve disorders: role of canal and nerve sheath decompression surgery. 1553 2

Vitamin D3 is modified by vitamin D3-25-hydroxylase in the liver, and 25-hydroxyvitamin D3-1alpha-hydroxylase in the kidney, to form the active metabolite, 1,25-dihydroxyvitamin D3. Chronic kidney disease (CKD) is characterized by reduced synthesis of 1,25-dibydroxyvitamin D3, inadequate renal phosphate clearance and calcium imbalance, secondary hyperparathyroidism (SHPT) and bone disease. CKD patients encounter a much higher risk of cardiovascular disease (CVD) than the general public. The cardiovascular risk factors for CKD patients include conventional factors such as age, gender, hypertension, diabetes, dyslipidemia and smoking, and non-conventional factors, such as anemia, uremia, reduced vascular compliance, inflammation and various hormonal factors. Several vitamin D analogs are currently available for the treatment of SHPT, and recent clinical data show that these analogs provide survival benefit for CKD patients in the order of paricalcitol > calcitriol > no vitamin D analog, independent of parathyroid hormone and calcium. Moreover, the survival benefit seems to be associated with cardiovascular causes. The observations made from these clinical studies raised intriguing questions about the involvement of the vitamin D receptor locus (VDR) in the cardiovascular system. This review discusses recent data regarding the role of vitamin D and its analogs in the CVD associated with CKD.
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PMID:Cardiovascular disease in chronic kidney failure: is there a role for vitamin D analogs? 1581

Long-term survival of children with end-stage renal disease (ESRD) has increased in the last 20 years, but the mortality rate remains high. Cardiovascular disease accounts for 40 to 50% of all deaths, infectious disease for about 20%. A prolonged period of dialysis versus having a renal graft and persistent hypertension are mortality risk factors. The prevalence of the various morbidities is high among those who have reached adulthood. Nearly 50% of all these patients suffer from left ventricular hypertrophy and life-threatening vascular changes; nearly one third has clinical signs of metabolic bone disease. This accounts for both dialysis and transplant recipients. The chance of getting cancer is increased ten times compared to the general population; skin cancer and non-Hodgkin lymphomas are most commonly reported. A long period of dialysis at childhood is associated with impairment of both cognitive and educational attainment. However, despite all these negative outcomes, the health perception of young adults with childhood onset ESRD is positive. Research and therapy in children with ESRD should focus not only on prevention of graft failure, but also on prevention of co-morbidity, especially cardiovascular disease, life-threatening infections and malignancies. Early transplantation, more extended forms of frequent hemodialysis in those who can not be transplanted, a more rigorous treatment of hypertension, avoidance or at least dosage reduction of calcium-containing phosphate binders, reduction of the chronic inflammatory state, and tailor made anti-rejection therapy after transplantation may all be targets to improve the outcome in future patients.
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PMID:Long-term outcomes of children with end-stage renal disease. 1583 18

The aim of the project was to establish the somatic and psycho-social consequences in adulthood of paediatric end-stage renal disease (ESRD). A long term follow up study of all Dutch patients who started renal replacement therapy at age 0-15 years between 1972 and 1992 and who were born before 1979 was undertaken. The study was performed between 1998 and 2000. About 25% of patients had died at time of investigation. Cardiovascular abnormalities were prominent in both transplanted and dialysis patients and cardiovascular disease was also found to be the most prominent cause of death. Skeletal disorders as a result of metabolic bone disease accounted for most frequent occurring disabilities. The risk for malignancies was 10-fold that of the normal population. Mean IQ and educational attainment were low as compared to the normal population. The overall quality of life was good, despite the co-morbidity and disabilities. Adverse outcomes were in nearly all cases related to a prolonged period of dialysis in the past and to (current) hypertension, not to the state of dialysis at time of investigation.
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PMID:Late somatic and psycho-social consequences of renal insufficiency in children. 1583 15

Metabolic acidosis is noted in the majority of patients with chronic kidney disease (CKD) when glomerular filtration rate (GFR) decreases to less than 20% to 25% of normal, although as many as 20% of individuals can have acid-base parameters close to or within the normal range. Acidosis generally is mild to moderate in degree, with plasma bicarbonate concentrations ranging from 12 to 22 mEq/L (mmol/L), and it is rare to see values less than 12 mEq/L (mmol/L) in the absence of an increased acid load. Degree of acidosis approximately correlates with severity of renal failure and usually is more severe at a lower GFR. The metabolic acidosis can be of the high-anion-gap variety, although anion gap can be normal or only moderately increased even with stage 4 to 5 CKD. Several adverse consequences have been associated with metabolic acidosis, including muscle wasting, bone disease, impaired growth, abnormalities in growth hormone and thyroid hormone secretion, impaired insulin sensitivity, progression of renal failure, and exacerbation of beta 2 -microglobulin accumulation. Administration of base aimed at normalization of plasma bicarbonate concentration might be associated with certain complications, such as volume overload, exacerbation of hypertension, and facilitation of vascular calcifications. Whether normalization of plasma bicarbonate concentrations in all patients is desirable therefore requires additional study. In the present review, we describe clinical and laboratory characteristics of metabolic acidosis, discuss potential adverse effects, and address benefits and complications of therapy.
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PMID:Metabolic acidosis of CKD: diagnosis, clinical characteristics, and treatment. 1595 26

Vitamin D is taken for granted and is not appreciated for its importance in overall health and well-being. Vitamin D, known as the sunshine vitamin, is appreciated as being important for the prevention of rickets in children. It is now recognized that vitamin D is important for not only the growing skeleton, but for the maintenance of a healthy musculoskeletal system throughout life. Vitamin D deficiency in adults precipitates and exacerbates osteoporosis and causes the painful bone disease osteomalacia. The revelation that vitamin D is biologically inactive and requires sequential hydroxylations in the liver and kidney to form 1,25-dihydroxyvitamin D helps explain why patients with renal failure are often resistant to vitamin D and suffer from secondary hyperparathyroidism and renal osteodystrophy. In addition to its role in maintaining calcium and phosphorus homeostasis, vitamin D is now being recognized as important for maintaining maximum muscle strength and for the prevention of many chronic diseases, including type I diabetes, multiple sclerosis, rheumatoid arthritis, hypertension, cardiovascular heart disease, and many common cancers. Vitamin D status is best determined by the measurement of circulating levels of 25-hydroxyvitamin D. Vigilance for maintaining a 25-hydroxyvitamin D level of at least 20 ng/ml and preferably 30-50 ng/ml has important benefits for both healthy children and adults, as well as children and adults suffering from chronic kidney disease.
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PMID:Vitamin D for health and in chronic kidney disease. 1607 48

Chronic kidney disease (CKD) is a permanent, progressive loss of kidney function characterized by a decline in glomerular filtration rate (GFR). Early identification of CKD risk factors provides an opportunity to prevent or delay the progression of kidney disease and decrease morbidity and mortality. There is increasing evidence to suggest that the adverse outcomes of CKD can be delayed or prevented by early detection and treatment. Current literature suggests that a low-protein, low-phosphorus diet may retard the progression of kidney disease. Other modifiable risk factors affecting CKD include proteinuria, hypertension, hyperglycemia, dyslipidemia, bone disease, anemia, and obesity. This discussion will review the current clinical nutrition guidelines for managing adult patients with CKD.
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PMID:Integrating clinical nutrition practice guidelines in chronic kidney disease. 1620 58


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