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)

According to a k/DOQI work group, chronic kidney disease (CKD) can be present also in subjects with glomerular filtration rate (GFR) >90 mL/min or a serum creatinine (sCr) below 1.3 mg/dL. The aim of this study was to document the prevalence of clinical or biologic abnormalities among 190 cadaveric renal transplant patients with excellent and stable renal function at 6 months after transplantation as well as 5 years later. The recipients were 82 women and 108 men of mean age at transplantation of 44.56 +/- 11.73 years. All patients were on Neoral-based immunosuppression with at least 5-year follow-up. Mean sCr was 1.18 +/- 0.2 mg/dL. Mean GFR was 78.57 +/- 27.06 mL/min. Systolic blood pressure was >130 mm Hg in 56.6%, although 78.3% of patients were on antihypertensive therapy; 34.3% were anemic; 75.4% had serum cholesterol >200 mg/dL; 62.2% had serum triglyceride levels >170 mg/dL. Serum intact parathyroid hormone >100 pg/mL was observed in 38% of patients and 43% were on vitamin D supplementation, and 11.4% had developed posttransplant diabetes mellitus. With respect to controls, von Willebrand factor was higher in 81.2% (P < .0001; RR = 11); serum homocysteine levels in 75% (P < 0.001; RR = 7.61); PAI-1 in 37.5% (P = .0009; RR = 4). At 5 years posttransplantation we observed an overall improvement in these abnormalities. The vast majority of renal transplant patients with excellent graft function belong to stage 1 of CKD being affected by hypertension, dyslipidemia, anemia, and residual hyperparathyroidism. Markers of endothelial dysfunction were largely abnormal, a condition that could predispose to cardiovascular events.
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PMID:Chronic kidney disease is still present after renal transplantation with excellent function. 1675 52

During recent years, it was shown, that treatment with recombinant human erythropoietin (rHuEPO) stimulates erythropoiesis in patients both with renal and nonrenal anaemia. Additionally in patients with chronic renal failure treated with rHuEPO a significant, however only transient, influence on function of endocrine glands was also found. The present study aimed to asses for the first time the influence of rHuEPO on function of endocrine organs in anaemic patients with rheumatoid arthritis and normal renal function. Twenty two woman with rheumatoid arthritis and concomitant anaemia (Ht < or = 30%) were enrolled into the study. In 13 of them rHuEPO was used during 4 months (5000 IU 2 times per week s.c.). The rest 9 woman with similar degree of anaemia did not receive rHuEPO therapy. In woman of both groups intensive clinical and biochemical monitoring during 4 months period was performed. Blood samples were withdrawn before and after 4 months of rHuEPO therapy or clinical observation only. In these blood samples plasma concentrations of somatotropin (HGH), insulin (IRI), aldosterone (ALD), atrial natriuretic peptide (ANP), 25-hydroxycholecalciferol (25OHD3), intact parathyroid hormone (iPTH) and plasma renin activity (PRA) were estimated. After 4 months of rHuEPO therapy significant increase of plasma IRI, ANP concentrations and significant decrease of PRA and plasma ALD, HGH concentrations were found. Therapy with rHuEPO does not influence significantly plasma iPTH and 25OHD3 concentration. During 4 months of clinical observation in patients not treated with rHuEPO, plasma concentrations of HGH, IRI, ALD, ANP, 25OHD3, iPTH and plasma renin activity (PRA) did not change significantly. Results obtained in this study suggest, that rHuEPO therapy does influence the function of endocrine organs also in patients with rheumatoid arthritis with normal renal function.
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PMID:[Influence of recombinant human erythropoietin (rHuEPO) on plasma levels of selected hormones in females with rheumatoid arthritis]. 1680 10

A 6-mo longitudinal study of 48 hemodialysis patients (HPs) with chronic renal failure was performed. Three blood samplings were done. Samples of whole blood from each patient were collected during hemodialysis sessions after passing through the artificial kidney. Zinc and copper levels were measured by atomic absorption spectrometry. Additionally, 36 biochemical indexes were evaluated during the study. Fifty-two healthy matched controls were also considered. Mean serum zinc and copper concentrations in HPs were significantly decreased (Zn) and increased (Cu), when compared with healthy controls (p < 0.01). Zinc concentrations found in the first and second blood samplings from patients were significantly lower than those measured for the third sampling (p < 0.01). The etiology of chronic renal failure influenced the statistically serum Zn levels of patients (p < 0.05). Serum copper levels of HPs were significantly diminished by the existence of secondary associated diseases (p < 0.01). Uric acid and parathyroid hormone, and total-cholesterol and glutamic-pyruvic-transaminase levels were significantly (p < 0.05) and linearly related with serum zinc and copper concentrations, respectively. From all of indexes, creatinine, direct bilirubin, magnesium, calcium, parathyroid hormone, transferrin, and albumin were statistically modified along the longitudinal study (p < 0.05). Transferrin serum levels were significantly diminished in the third blood sampling, indicating the tendency toward anemia in the patients. This result is reinforced by low levels of biochemical and hematological indexes related with iron body staus.
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PMID:Longitudinal study of serum zinc and copper levels in hemodialysis patients and their relation to biochemical markers. 1719 22

Despite the enormous cardiovascular disease epidemic and poor survival among individuals with chronic kidney disease (CKD), traditional risk factors such as hypercholesterolemia, hypertension, and obesity appear not as relevant as was previously thought, nor would their management improve survival in patients with CKD who are undergoing dialysis. On the contrary, kidney disease wasting (KDW) (also known as the malnutrition-inflammation complex), renal anemia, and kidney bone disease (KBD) appear to be the 3 most important nontraditional risk factors associated with cardiovascular disease in CKD. KBD-associated hyperparathyroidism may contribute to worsening refractory anemia and KDW/inflammation. The main cause of secondary hyperparathyroidism is active vitamin D deficiency. Hence, treatment of patients with KBD with vitamin D analogs, especially those with lesser effects on calcium and phosphorus such as paricalcitol, may be the most promising option for improving CKD outcomes. By conducting survival analyses in a 2-year (7/2001 to 6/2003) cohort of 58,058 patients on hemodialysis, we recently found that associations between high serum parathyroid hormone and increased death risk were masked by the demographic and clinical characteristics of patients, and that alkaline phosphatase had an incremental association with mortality. Administration of paricalcitol was associated with improved survival in time-varying models. We now present additional subgroup analyses that show that administration of any dose of paricalcitol, when compared with no paricalcitol, is associated with better likelihood of survival in virtually all subgroups of patients on hemodialysis. Because these associations may be secondary to bias by indication, randomized clinical trials are necessary to verify the findings of this and similar observational studies.
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PMID:Impact of kidney bone disease and its management on survival of patients on dialysis. 1719 30

Sixty-three-year-old woman requested medical attention for osteoporosis. Bone densitometry revealed: T(spine (L1-L4))= -3.5 SD [Bone mineral density (BMD): 0.766 g/cm(2)]. T(femoral neck) = -2.4 SD (BMD: 0.716 g/cm(2)). She has been in calcium and vitamin D supplementation for 2 years. She informed a 5-year-history of hypothyroidism in levothyroxine replacement. Alendronate sodium 70 mg/week was initiated with significant increase in BMD in the first year (6.1% equally in spine and femoral neck). After a 5-year follow-up, the patient presented with weight loss, anemia and decrease in BMD (12.6% in spine and 20.9% in femoral neck). Clinical history revealed intermittent diarrhea episodes for 2 years and the hypothesis of celiac disease was suspected. Anti-gliadin and anti-endomysium antibodies were positive: 25.3 U/mL (< 20) e 1/5 U/mL (RV: negative), respectively. Bone biochemical parameters revealed normal levels of calcium and phosphate, increased parathyroid hormone: 283 pg/mL (10-65) and increased levels of bone reabsortion markers, consistent with secondary hyperparathyroidism in response to malabsorptive syndrome. One year after gluten-free diet, patient improved of malabsorptive symptoms and gained BMD (47.3% in spine and 31.6% in femoral neck), confirming the hypothesis of celiac disease as aggravating factor of osteoporosis in this patient.
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PMID:[Case report: recently diagnosed celiac disease as aggravating factor of osteoporosis in an old woman]. 1722 Nov 22

Although the clinical symptoms of patients with benign parathyroid adenoma are usually nonspecific and benign, a malignant presentation of the benign disease may sometimes occur. Here, we report a case of a 58-year-old woman who presented with aggravated sacrum pain, general malaise, and polydipsia. Initial laboratory findings revealed hypercalcemia, normocytic anemia, and impaired renal function. Acute hypercalcemic crisis manifested and primary hyperparathyroidism was diagnosed together with myelofibrosis on account of the result of bone marrow biopsy. Excision of a parathyroid adenoma was performed, and the anemia and bone marker regressed later. These findings suggested that benign parathyroid adenoma may mimic the clinical presentation of parathyroid carcinoma, releasing excess parathyroid hormone and resulting in hyperparathyroid crisis. In addition, primary hyperparathyroidism can be associated with anemia and myelofibrosis.
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PMID:Benign parathyroid adenoma presenting with unusual parathyroid crisis, anemia and myelofibrosis. 1749 90

The mortality rate in patients with end-stage renal disease (ESRD) is extremely high, mainly because of the high prevalence of cardiovascular disease. In addition to traditional cardiovascular risk factors, other factors peculiar to chronic kidney disease play a role. Anemia and calcium-phosphate disorders are of particular interest, not only because they have been related to an increased risk of death but, more importantly, because they can be reversed by treatment, thereby providing the opportunity to prevent or delay the onset of cardiovascular disease. Despite a clear association between higher hemoglobin levels and better survival, data from interventional trials do not seem to show a significant positive effect of hemoglobin normalization with erythropoiesis-stimulating agents on survival and left ventricular mass in ESRD patients. Nevertheless, partial correction of anemia is still an important goal to be reached, as is also suggested by international guidelines. Disorders of calcium-phosphate metabolism have also been clearly related to increased mortality. Unlike anemia, which can be easily corrected by treatment in most cases, mineral metabolism is much less effectively treated. New agents, such as phosphate binders not containing calcium and aluminum, vitamin D analogs with lower calcemic activity, and calcimimetics, are becoming increasingly available in everyday clinical practice and are likely to allow a higher percentage of patients to achieve the recommended targets for calcium-phosphate and parathyroid hormone. Given that these molecules have only been introduced recently, clear data from interventional studies showing improved survival after adequate correction of mineral metabolism parameters are still lacking.
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PMID:[Recent advances in the prevention of cardiovascular morbidity and mortality in end-stage renal disease: role of anemia, hyperparathyroidism and calcifications]. 1792 44

A significant number of children with chronic kidney disease (CKD) have eccentric left ventricular hypertrophy (LVH), suggesting the role of preload overload. Therefore, we hypothesized that increased cardiac output (CO) might be a contributing factor for increased left ventricular mass index (LVMI) in these children. Patients aged 6-20 years with CKD stages 2-4 were enrolled. Echocardiograms were performed to assess LV function and geometry at rest and during exercise. Heart rate, stroke volume, and CO were also assessed at rest and during exercise. Twenty-four-hour ambulatory blood pressure (AMBP) monitoring was performed. Of the patients enrolled in this study, 17% had LVH. Increased stroke volume and CO were observed in patients with LVH compared to patients without LVH. Univariate analysis revealed significant positive associations between LVMI and CO, stroke volume, body mass index, pulse pressure from mean 24-h AMBP, and mean 24-h systolic BP load. No association with heart rate, age, parathyroid hormone, glomerular filtration rate, or anemia was observed. Only CO (beta = 1.98, p = 0.0005) was independently associated with increased LVMI in multivariate modeling (model R (2) = 0.25). The results of this study suggest that increased CO might predispose to increased LVMI in pediatric patients with CKD. Adaptations may be required to meet increased metabolic demand in these patients.
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PMID:Cardiac output and associated left ventricular hypertrophy in pediatric chronic kidney disease. 1904 1

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

Primary hyperparathyroidism and malignancy are responsible for greater than 90% of all cases of hypercalcemia. Compared with the hypercalcemia of malignancy, hyperparathyroidism tends to be associated with lower serum calcium levels (< 12 mg/dL) and a longer duration of hypercalcemia (more than 6 months). The hypercalcemic symptoms are usually fewer and subtle. Hyperparathyroidism tends to cause kidney calculi, hyperchloremic metabolic acidosis, and the characteristics of metabolic bone disease osteitis fibrosa cystica, but no anemia. In contrast, hypercalcemia of malignancy is typically rapid in onset, with higher serum calcium levels, and more severe symptoms. Patients so affected show marked anemia, but they never have kidney calculi or metabolic acidosis. Parathyroid hormone assay is the most useful test for differentiating hyperparathyroidism from malignancy and other causes of hypercalcemia. In hyperparathyroidism, serum parathyroid hormone levels will be elevated. In other cases, the high serum calcium concentration usually results in suppression of parathyroid hormone. Treatment of hypercalcemia should be started with hydration. Loop diuretics may be required in individuals with renal insufficiency or heart failure to prevent fluid overload. Calcitonin is administered for the immediate short-term management of severe symptomatic hypercalcemia. For long-term control of severe or symptomatic hypercalcemia, the addition of biphosphonate is typically required. Among intravenous bisphosphonates, zoledronic acid or pamidronate are the agents of choice. Glucocorticoids are effective in hypercalcemia due to lymphoma or granulomatous diseases. Dialysis is generally reserved for those with severe hypercalcemia complicated with kidney failure.
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PMID:Hypercalcemia: an evidence-based approach to clinical cases. 1939 81


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