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)

We retrospectively evaluated the factors that are prognostic in long-term continuous ambulatory peritoneal dialysis (CAPD). From 1986 to 1997, 91 CAPD patients (59 male, 32 female, mean age 48 years) entered the study. Their primary renal diseases were chronic glomerulonephritis (CGN, n = 80), diabetic nephropathy (DN, n = 10), and polycystic kidney disease (PKD, n = 1). The roles of primary renal disease, hypertension, left ventricular hypertrophy (LVH), left ventricular ejection fraction (LVEF), cardiac sympathetic activity, anemia, hypoalbuminemia, and plasma concentration of parathyroid hormone (PTH) on patient prognosis were analyzed. Among the 91 CAPD patients, 26 died during the observation period. Of these deaths, 17 resulted from cardiovascular diseases including cerebrovascular events (n = 7), myocardial infarction (n = 2), sudden death (n = 7), and aortic aneurysmal rupture (n = 1). Nine patients died of non cardiovascular events. Sclerosing encapsulating peritonitis and others, mainly cachexia, accounted for 2 and 7 of these deaths, respectively. The 5-year survival rate was 74%; the 10-year rate was 49%. The cumulative 5- and 10-year success rates of CAPD were 69% and 39%, respectively. DN, hypertension, severe LVH (more than 200 g/m2), and hypoalbuminemia were contributors to poor prognosis. Among these, DN and severe LVH were the two main predictors by Cox proportional hazards model. We conclude that CAPD patients with DN or severe LVH, or both, have a greater chance of drop-out from cardiovascular events.
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PMID:Predictors of survival in continuous ambulatory peritoneal dialysis patients: the importance of left ventricular hypertrophy and diabetic nephropathy. 1068 78

Patients with severe secondary hyperparathyroidism, usually associated with osteitis fibrosa on bone histology, show considerable resistance to Epoetin, partly because of replacement of the cellular components of the bone marrow by fibrous tissue. In case of unexplained resistance to Epoetin, investigation of secondary hyperparathyroidism is strongly recommended, with measurement of serum parathyroid hormone, calcium, phosphate, and alkaline phosphatase levels and, where needed, skeletal radiology and bone biopsy. Treatment of severe secondary hyperparathyroidism consists of active vitamin D metabolites or parathyroidectomy, although the marrow fibrosis, if present, may be irreversible. The finding of a progressive inability of the bone marrow to respond to Epoetin treatment with higher levels of parathyroid hormone suggests the importance to prevent metabolic bone disease and in particular secondary hyperparathyroidism. Moreover, there are several reports of a beneficial action on hemoglobin levels of an effective treatment of hyperparathyroidism. Larger, controlled studies are necessary to confirm these preliminary and exciting findings, and to elucidate the mechanisms underlying the improvement in anemia after medical or surgical treatment of hyperparathyroidism.
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PMID:Hyperparathyroidism and anemia in renal failure. 1077 7

Parathyroid hormone and calcitonin, both endocrine modulators of calcium homeostasis, may influence blood rheology. Parathyroid hormone is known to reduce erythrocyte survival, leading to anemia. Calcitonin has been found to have some vascular effects. We have analyzed the Influence of parathyroid hormone (10(-7) to 10(-10) mol/L), calcitonin (10(-6) to 10(-12) mol/L), 1,25(OH)2 cholecalciferol (10(-7) to 10(-10) mol/L), additional calcium in plasma (+1 and 2 mmol/L), and the calcium lonophore A23187 (50 micromol/L) on erythrocyte morphology and blood viscosity at high shear rate (94 s(-1)) and low shear rate (0.1 s(-1)) in vitro. The loading of erythrocytes with calcium by the ionophore A23187 produced a marked echinocytic shape transformation, an increased blood viscosity at high shear rate caused by decreased deformability of these cells, and a decreased viscosity at low shear rate caused by decreased aggregation of echinocytes. In contrast, increasing plasma calcium concentrations, parathyroid hormone, calcitonin, and 1,25(OH)2 vitamin D3 had no effect on erythrocyte morphology and blood viscosity. We conclude that an increase in intraerythrocytic calcium leads to severe echinocytosis and altered blood viscosity. The endocrine modulators of calcium homeostasis--namely, parathyroid hormone, calcitonin, and 1,25(OH)2 vitamin D3--apparently do not influence intraerythrocytic calcium to a significant degree and have, therefore, no influence on cell morphology and blood viscosity.
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PMID:Influence of parathyroid hormone, calcitonin, 1,25(OH)2 cholecalciferol, calcium, and the calcium ionophore A23187 on erythrocyte morphology and blood viscosity. 1077 51

It is suggested that parathyroid hormone (PTH), when in excessive amounts, interferes with normal erythropoiesis by downregulating the erythropoietin receptors on erythroid progenitor cells in the bone marrow. Therefore, physiologic concentrations of EPO can no longer sustain normal red cell counts, so normocytic and normochromic anaemia ensues. In primary hyperparathyroidism (HPT), this effect is observed with very high concentrations of PTH. In secondary HPT during chronic renal failure, this effect is more pronounced because erythropoietin synthesis is impaired.
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PMID:Pathogenesis of anaemia in hyperparathyroidism. 1079 Jul 58

To establish a useful animal model of Itai-Itai disease (IID) of humans, we conducted the following experiments. Experiment 1: Toxic effects of Cd were compared between ovariectomized (OX) and non-OX rats after daily, intravenous injection of cadmium (Cd) chloride for 14 days. In this experiment, we demonstrated that OX rats were more susceptible to Cd-induced nephrotoxicity and hepatotoxicity than non-OX rats. Experiment 2: OX rats were injected with Cd at doses of 1.0 and 2.0 mg/kg, 5 days a week, for 13 weeks. The bone Cd content was gradually increased for 13 weeks in a dose-dependent manner. Calcium and phosphorus contents in the bone and serum levels of parathyroid hormone and osteocalcin were not significantly different between Cd-treated and control rats. Mild osteomalacic lesions in the cortical bones of the midshaft haversian canals as well as chronic nephropathy appeared in the rats of the 2.0 mg/kg group. Experiment 3: OX rats were treated with Cd at doses of 0.5 and 0.05 mg/kg for 70 weeks. The rats of the 0.05 mg/kg group showed slight anemia and mild degeneration of tubular epithelium after 50 weeks of treatment. In the 0.5 mg/kg group, the rats showed definite osteomalacia of bones and nephrosclerosis. The Cd concentration in the bones increased for the first 25 weeks, but was replaced gradually with iron at from 50 to 70 weeks of the administration period. Iron deficiency anemia appeared in the 0.5 mg/kg group at from 12 to 25 weeks, and changed to renal anemia after 50 weeks of administration. The anemia at 50 and 70 weeks was normocytic and normochromic, and serum erythropoietin levels were not elevated in response to the decrease of hemoglobin concentrations of red blood cells. Experiment 4: Ten, OX cynomolgus monkeys were given intravenous injections of 0, 1.0 or 2.5 mg/kg/day Cd, 2 or 3 days per week, for 13 to 15 months. Normocytic and normochromic anemia, renal lesions characterized by tubular atrophy and interstitial fibrosis (Cd nephropathy), and bone lesions characterized by an increase of osteoid and osteopenia (Cd osteopathy) were induced in the monkeys treated with Cd. These results demonstrated that chronic cadmium toxicosis similar to IID of humans was reproducible in rats and monkeys by repeated intravenous injection of Cd and that a disease entity closely resembling IID of humans could be induced in experimental animals by chronic Cd toxicosis without participation of malnutrition, vitamin D deficiency, impaired absorption at the intestinal mucosa or multiparous birth.
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PMID:Experimental reproduction of itai-itai disease, a chronic cadmium poisoning of humans, in rats and monkeys. 1092 82

Blood-dialyzer interaction in hemodialysis has the potential to activate mononuclear cells leading to the production of inflammatory cytokines. The extent of activation is dependent on the dialyzer material used and is considered an index of biocompatibility. Cytokines, such as interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), and IL-6, may induce an inflammatory state and are believed to play a significant role in dialysis-related morbidity. The interleukin hypothesis suggests that the release of proinflammatory cytokines acts as an underlying pathophysiologic event in hemodialysis-related acute manifestations, such as fever and hypotension. Nevertheless, a cytokine overproduction may alter sleep pattern in chronic hemodialyzed patients, thus explaining the presence of sleep disorders in these patients. A potential role of cytokines in chronic-related morbidity has also been suggested. High levels of some inflammatory cytokines are often associated with anemia caused by hyporesponsiveness to erythropoietin. Cytokine production may also play a relevant role in bone remodeling by regulating osteoblast/osteoclast cell functions and parathyroid hormone (PTH). Finally, cytokine release may have a long-term deleterious effect on mortality of uremic patients by altering immune response and increasing susceptibility to infections. Bioincompatibility of dialytic membranes may also contribute to malnutrition in dialysis patients by increasing the monocyte release of catabolic cytokines such as TNF-alpha and IL-6. Bioincompatible dialytic treatment may induce an inappropriate monocyte activation and cytokine production, which, in turn, may mediate some of the immune and metabolic dysfunction associated with hemodialysis. The use of biocompatible dialytic membranes appears to reduce the monocyte activation and to improve the survival of hemodialysis patients.
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PMID:Clinical relevance of cytokine production in hemodialysis. 1093 6

A prospective study was planned to follow the clinical and laboratory data of hemodialysis (HD) patients after change of treatment to continuous ambulatory peritoneal dialysis (CAPD). Patients who had been on the HD program for more than 6 months were selected and followed for at least 6 months under CAPD treatment. Measured parameters included hemoglobin, ferritin, C-reactive protein (CRP), calcium, phosphorus, and intact parathyroid hormone (iPTH) levels; lipid profile; total protein and albumin; body mass index and triceps skin fold thickness; echocardiographic findings; and medications administered. We followed 34 patients (12 males, 22 females; mean age: 43.5 +/- 14.5 years; mean HD duration: 36.6 +/- 24.76 months) for a mean period of 19.8 +/- 11.9 months after change of treatment to CAPD. We saw a significant increase in mean hemoglobin, cholesterol, triglyceride, high-density lipoprotein (HDL), lipoprotein (a) [Lp(a)], phosphorus, and iPTH levels. We observed a decrease in erythropoietin dose, mean ferritin levels, systolic blood pressure (139.4 +/- 22.8 mmHg vs 114.4 +/- 21.0 mmHg, p = 0.001), diastolic blood pressure (85.7 +/- 12.6 mmHg vs 73.5 +/- 17.6 mmHg, p = 0.002), percentage of left ventricular hypertrophy, systolic and diastolic dysfunction, and the number of hypertensive drugs received. A significant improvement in the nutritional status of the patients (total protein, body mass index and triceps skin fold thickness) was also seen. In conclusion, CAPD treatment has a short-term outcome superior to that of HD in terms of better nutritional status and better control of hypertension and anemia.
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PMID:What happens after conversion of treatment to continuous ambulatory peritoneal dialysis from hemodialysis? 1104 88

The index patient is a 23-year-old female with end-stage renal disease (ESRD) secondary to chemotherapeutic agents. Continuous cycling peritoneal dialysis (CCPD) has been the renal replacement therapy for the past 5 years since a failed cadaveric renal transplant. Past medical history was significant for diabetes mellitus, hypertension, anemia, bilateral subclavian vein thrombosis with superior vena cava syndrome, secondary hyperparathyroidism, leukemia (at age 8), and hyperlipidemia. On presentation, soft tissue nodules were noted in the anterolateral surfaces of the legs. After 3 months of continued low-calcium-dialysate CCPD, calcitriol, and oral phosphate binders, a 2 x 3 cm nodule was noted on the posterior aspect of the thorax at the scapula. The only complaint at this time was shoulder pain at the acromioclavicular joint. Radiological examination revealed a 3 x 4 cm soft tissue opacity in the superior segment of the left lower lobe laterally. Despite a prior subtotal parathyroidectomy, phosphate binders, and calcitriol, the parathyroid hormone levels continued to increase, with development of tumoral calcinosis, worsening renal osteodystrophy, and calciphylaxis. Computed tomography examination revealed extensive soft tissue calcification consistent with tumoral calcinosis. An ulcerative lesion (1 cm) developed on the lateral aspect of the upper thigh owing to warfarin necrosis versus calciphylaxis. At this time, the phosphate binder was changed from calcium acetate to sevelamer hydrochloride. Aggressive wound treatment and aggressive calcium and phosphate control added to the treatment regimen has resulted in healing of the single ulcer and a decrease in the size of the tumoral lesions. In conclusion, early recognition and aggressive treatment of calciphylaxis can result in reduced morbidity and mortality from calciphylaxis in ESRD patients.
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PMID:Spectrum of complications related to secondary hyperparathyroidism in a peritoneal dialysis patient. 1104 12

Adynamic bone disease (ABD) has an increasing prevalence in the dialysis population, more so in peritoneal dialysis patients. Anemia in patients with high turnover bone disease and high intact parathyroid hormone (iPTH) tends to be resistant to recombinant human erythropoietin (rHuEPO). The same problem may occur in patients with ABD; however, data are scarce. This study evaluates the effectiveness of rHuEPO in 32 chronic peritoneal dialysis patients, 9 with iPTH levels below 100 pg/mL for more than 6 months (group A, with ABD) and 23 with iPTH levels above 100 pg/mL (group B, without ABD). In group A and group B respectively, the dosage of rHuEPO was 141.8 +/- 59 U/kg/week and 144.8 +/- 77 U/kg/week, and hematocrit was 33.2% +/- 4.3% and 31.7% +/- 4.5% (p > 0.05). Iron indices, nutritional parameters, and bone indices were similar, except that group A had lower alkaline phosphatase and serum ferritin levels. The data suggest that patients with ABD may not be resistant to rHuEPO, but may even have a slightly better hematocrit at a similar rHuEPO dosage. Further studies in a larger number of patients are needed to confirm these findings.
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PMID:Influence of adynamic bone disease on responsiveness to recombinant human erythropoietin in peritoneal dialysis patients. 1104 14

The anemia associated with renal failure is largely due to inappropriate erythropoietin production. There is also good evidence, however, that substances present in uremic serum can inhibit erythropoiesis, although the exact identity of these substances and the mechanism(s) by which they exert this effect remain obscure. Candidates that have been suggested to play a role in uremic inhibition of erythropoiesis include the polyamines (such as spermine, spermidine, putrescine, and cadaverine), parathyroid hormone, and some of the inflammatory cytokines. The potential role of each of these inhibitory substances is discussed in this article.
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PMID:Role of uremic toxins in exacerbating anemia in renal failure. 1116 86


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