Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The incidence and prevalence of chronic renal failure (CKD), defined according to the NFK-KDOQI guidelines as a glomerular filtration rate less than 60 mL/min/1.73 m2 or the presence of microalbuminuria, is increasing worldwide, leading to an increased risk of cardiovascular disease. There is general agreement about the importance of early referral to the nephrologist and predialysis educational programs because this strategy prevents the progression (by the use of renin-angiotensin system blockers, low-protein diet) and complications (arterial hypertension, anemia, malnutrition, osteodystrophy, acidosis) of renal disease. Predialysis education helps patients choose the renal replacement therapy modality (hemodialysis, peritoneal dialysis, transplantation) and improve their quality of life. Furthermore, adequate predialysis care allows the nephrologist to prepare the vascular access well in advance. In contrast to the wished-for practice of early referral, patients are often referred to the nephrologist when renal failure is already advanced. This is mainly due to the fact that non-nephrologists pay little attention to identifying patients at risk for renal failure or defining the degree of renal failure according to the KDOQI classification. In addition, serum creatinine alone provides no adequate estimate of renal function, and both the MDRD equation and the Cockcroft-Gault formula permit a more accurate estimation of the glomerular filtration rate (GFR). Using the MDRD equation, the KDOQI guidelines recommend referral when GFR is less than 30 mL/min/1.73 m2. Late nephrology referral is an independent risk factor for early death while on dialysis, as well as being associated with a more frequent use of temporary catheters, particularly in the elderly but also in patients receiving regular nephrology care. This underlines the importance of a multidisciplinary predialysis approach which may bring additional benefits - beyond referral to a nephrologists - including a reduced hospitalization rate and improved survival. The KDOQI guidelines recommend evaluating the benefits and risks of starting renal replacement therapy when patients reach stage 5 (estimated GFR <15 mL/min/1.73 m2), although the ideal time for replacement therapy initiation remains a matter of debate and the results of prospective clinical trials are awaited to resolve this issue.
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PMID:[When to start dialysis. The predialysis patient]. 1847 14

(1) Pharmacological management of arterial hypertension is based on antihypertensive drugs with proven efficacy on morbidity and/or mortality endpoints. (2) Aliskiren is the first renin inhibitor to reach the market. (3) There are no published trials of aliskiren with clinical endpoints. Five double-blind short-term (8 weeks) placebo-controlled trials showed a moderate effect on blood pressure. This effect was not superior to that of other antihypertensive drugs with which aliskiren was compared: hydrochlorothiazide, amlodipine, irbesartan, losartan, valsartan, lisinopril and rampiril. (4) When added to another antihypertensive drug, aliskiren had little or no additional effect on blood pressure. In particular, there is no firm evidence that adding aliskiren to amlodipine 5 mg/day is any more effective than doubling the dose of amlodipine. (5) Aliskiren has not been tested in patients with renovascular hypertension or severe hypertension, but pharmacological data suggest that aliskiren might be less effective in these individuals. (6) Overall, the adverse effect profile of aliskiren does not seem to be any better than that of other antihypertensive drugs. Aliskiren contributes to the onset of angioedema, cough, diarrhea and abdominal pain, hyperuricaemia, gout attacks, kidney stones and skin rash. Pharmacovigilance should focus specifically on certain adverse effects that are known to occur with other drugs acting on renin-angiotensin axis, such as angioedema, muscle disorders and anaemia, even though few such cases were observed with aliskiren during clinical trials. (7) Aliskiren is contraindicated during pregnancy, as are other antihypertensive drugs acting on the renin-angiotensin axis. (8) In practice, it is better not to use aliskiren to treat hypertensive patients because better-assessed antihypertensive drugs with longer follow-up are available.
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PMID:Aliskiren: new drug. Arterial hypertension: no evidence of clinical efficacy. 1851 3

The pathophysiological condition, in which combined cardiac and renal dysfunction amplifies a progression in the failure of the individual organ, has been denoted as severe cardiorenal syndrome (SCRS). An interactive network of cardiorenal connectors, i.e., the renin-angiotensin system (RAS), nitric oxide (NO) and reactive oxygen species (ROS) balance, the sympathetic nervous system (SNS), and inflammation, has been proposed as the cornerstones of the pathophysiology of SCRS. Because erythropoietin (Epo) production declinesin chronic renal failure (CRF) and Epo sensitivity might decrease by the cardiorenalconnectors in patients with the SCRS, it is not surprising thatanaemia is a commonly occurring state coinciding with CRF and chronic heart failure (CHF). Epo treatment in patients with SCRS acts via haematopoietic effects, but also may intervenes in the vicious circle of cardiorenal connectors with subsequent deteriorating effects on cardiac, renal, and vascular function. It appears that regular Epo treatment in anaemic patients with diminished renal function improves cardiac performance, delays the progression of kidney disease, and may be of clinical benefit even to patients suffering from CHF with relatively mild anaemia. Despite growing evidence about Epo having positive effects on both renal and cardiac function, little is known about the underlying mechanisms of action.
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PMID:[The cardiorenal syndrome and erythropoietin]. 1857 29

Cardiovascular risk profiling and therapy have traditionally been based on established risk factors, such as age, smoking, sex, hypertension, dyslipidemia, body weight, and diabetes mellitus. Despite optimum therapy, cardiovascular mortality and morbidity remain high. Attention is being devoted, therefore, to identifying new risk factors that can also be used as therapeutic targets. Renal dysfunction manifesting as low glomerular filtration rate, albuminuria, or anemia is a strong risk factor for cardiovascular disease and is prevalent in the general population and among patients with cardiovascular disease. Epidemiological data suggest that 10-11% of the general population have low glomerular filtration rates, 5-7% have increased urinary albumin excretion, and 5-10% have anemia. Each of these features represents an independent but additive cardiovascular risk. Treatments for all these indications can reduce cardiovascular mortality and morbidity as well as renal risk. Such findings suggest that treatment should be directed towards improving renal function in order to achieve optimum cardiovascular benefit. Such a strategy would offer the possibility of multiorgan therapy in diseases characterized by multiorgan impairment, such as type 2 diabetes. I present the evidence that renal dysfunction is a common and powerful cardiovascular risk factor and that treatment strategies intervening in the renin-angiotensin-aldosterone system can be used to target albuminuria and reduce cardiovascular and renal risk.
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PMID:Renal disease: a common and a silent killer. 1858 Aug 63

Intraglomerular hypertension, and glomerular hypertrophy, leading to glomerular scarring are suggested to have an effect on the progression in chronic kidney disease, unrelated to the initial cause of kidney injury. Tubulointerstitial disease is another factor, which may affect the prognosis. Strategies to prevent or minimize the progression of kidney disease consist of treating these disease-worsening mechanisms, including smoking cessation, treatment of hyperlipidemia, sodium and protein restriction, antihypertensive therapy, inhibition of renin-angiotensin-aldosterone system, and treatment of anemia. Studies in experimental animals and humans suggest that these therapies are effective to prevent the progression in chronic kidney disease and there are some evidences that these therapies have benefits in the patients with chronic kidney disease.
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PMID:[Management of chronic kidney disease--preventing the progression of renal disease]. 1878 3

In this pandemic of diabetes and obesity, Asia will have the highest number of affected people with the greatest increase in the young-to-middle aged group. Asian patients have increased risk for diabetic kidney disease which may be compounded by low grade infection, obesity and genetic factors. In these subjects, the onset of albuminuria and diabetic kidney disease causes further perturbation of metabolic milieu with increased oxidative stress, anaemia and vascular calcification which interact to markedly increase the risk of cardiovascular disease. Despite receiving optimal care to control blood pressure and metabolic risk factors as well as inhibition of the renin-angiotensin system in a clinical trial setting, there is a considerable residual risk for cardio-renal complications in patients with diabetic kidney disease. Control of obesity and low grade inflammation as well as correction of anaemia may represent areas where novel strategies can be developed and tested to curb this rising global burden of cardio-renal complications.
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PMID:Diabetic nephropathy--what are the unmet needs? 1895 13

Chronic kidney disease (CKD) guidelines recommend evaluating patients with GFR <60 ml/min per 1.73 m(2) for complications, but little evidence supports the use of a single GFR threshold for all metabolic disorders. We used data from the NephroTest cohort, including 1038 adult patients who had stages 2 through 5 CKD and were not on dialysis, to study the occurrence of metabolic complications. GFR was measured using renal clearance of (51)Cr-EDTA (mGFR) and estimated using two equations derived from the Modification of Diet in Renal Disease study. As mGFR decreased from 60 to 90 to <20 ml/min per 1.73 m(2), the prevalence of hyperparathyroidism increased from 17 to 85%, anemia from 8 to 41%, hyperphosphatemia from 1 to 30%, metabolic acidosis from 2 to 39%, and hyperkalemia from 2 to 42%. Factors most strongly associated with metabolic complications, independent of mGFR, were younger age for acidosis and hyperphosphatemia, presence of diabetes for acidosis, diabetic kidney disease for anemia, and both male gender and the use of inhibitors of the renin-angiotensin system for hyperkalemia. mGFR thresholds for detecting complications with 90% sensitivity were 50, 44, 40, 39, and 37 ml/min per 1.73 m(2) for hyperparathyroidism, anemia, acidosis, hyperkalemia, and hyperphosphatemia, respectively. Analysis using estimated GFR produced similar results. In summary, this study describes the onset of CKD-related complications at different levels of GFR; anemia and hyperparathyroidism occur earlier than acidosis, hyperkalemia, and hyperphosphatemia.
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PMID:Timing of onset of CKD-related metabolic complications. 1900 10

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

Twin-twin transfusion syndrome (TTTS) is a fascinating condition in which fetuses of identical genotype adopt discordant cardiovascular phenotypes, secondary to unbalanced placental inter-twin transfusion. Flow along the primary units of inter-twin transfusion, unidirectional arteriovenous anastomoses, can be as high as litres/day each, and TTTS develops when the placenta has insufficient compensatory counter-transfusional anastomoses. The initial phenotype reflects dysvolaemia, with added contributions from uteroplacental insufficiency in the donor, and raised afterload with diastolic dysfunction secondary to discordant endothelin and placentally derived renin-angiotensin system effectors in the recipient. Endoscopic laser ablation of placental anastomoses has become the primary treatment modality, supported by a randomised trial showing improved survival and short but not long-term neurological morbidity. Its uptake has facilitated comparative pre- and post-laser studies, which provide considerable insight into the pathophysiology. Despite the therapeutic advance, placental laser remains associated with a 25% incidence of fetal death within a week, and a 10% risk each of recurrence and twin anaemia/polycythaemia sequence due to residual anastomoses. In Stage I, high rates of non-progression with more conservative management have resulted in therapeutic equipoise as to whether laser is indicated primarily or only for progressive disease. The challenge ahead lies in improving double intact survival rates, which in addition to randomised trials will require technical advances, better understanding of the circulatory pathophysiology and more sophisticated surveillance tools.
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PMID:The basic and clinical science of twin-twin transfusion syndrome. 1929 17

Twin anemia-polycythemia sequence (TAPS) is a rare variant of twin-twin transfusion syndrome (TTTS) without the characteristic twin oligohydramnios-polyhydramnios sequence and cardiovascular milieu attributed to renin-angiotensin system mediators. It can occur spontaneously or iatrogenically after fetoscopic laser surgery. We report the case of a woman, gravida 2 para 1, with a monochorionic diamniotic pregnancy who developed Quintero Stage III TTTS. She underwent laser photocoagulation of identifiable anastomotic vessels and subsequently developed suspected TAPS 2 weeks later. The pregnancy was successfully treated with serial intrauterine intraperitoneal transfusions (IUT-PTs) of red blood cells. Although TAPS is a rare condition, serial middle cerebral artery peak systolic velocity measurements are warranted as follow-up in patients who have undergone fetoscopic laser surgery for TTTS. IUT-PTs may be superior to intravascular intrauterine transfusions in the treatment of this condition.
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PMID:Fetal intraperitoneal transfusion for iatrogenic twin anemia-polycythemia sequence after laser therapy. 1940 3


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