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Query: UMLS:C0002871 (anemia)
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Osteopetrosis, a rare condition caused by a failure of osteoclasts to resorb bone, results in dense and deformed bones, growth failure, anemia, hypoplastic dentition, chronic infection, blindness, and massive splenomegaly. Children with infantile osteopetrosis have disease-related complications that affect nutritional status. Altered calcium and phosphorus intake has been reported in these patients, but previous studies did not include an assessment of dietary adequacy or nutrition-related complications. A prospective study of six children with severe infantile osteopetrosis was conducted to identify specific nutrition-related problems and effective nutrition intervention strategies. Patients were monitored by a registered dietitian while they participated in a clinical research protocol at St Jude Children's Research Hospital. Dietary records for each patient were obtained at set intervals during the 4-month study period. Because most patients lacked adequate dentition, they had difficulty obtaining adequate nutrition through normal oral intake. Three children required nutrition supplementation (enteral feedings for one and oral supplements for two). We conclude that oral and enteral nutrition support can provide nutrients needed for improved growth and response to treatment in patients with osteopetrosis.
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PMID:Managing osteopetrosis in children: a nutrition challenge. 855 44

We present a 72-year-old man who had episodes of severe, acute renal failure during severe attacks of diarrhea caused by Vibrio cholerae. Patterns of acute tubular necrosis and tubulointerstitial nephritis developed following hypotension and decrease in renal blood flow, causing secondary renal ischemia. There was severe dehydration with profound hypovolemia and infection. The clinical picture included fever, weakness, arthralgia, pedal edema, mild bilateral pleural effusions, anemia, leukocytosis, azotemia with a maximum of 330 mg/dl of urea, creatine to a maximum of 9.8 mg/dl, hypoproteinemia, severe metabolic acidosis, marked increase in lactate dehydrogenase (LDH) and creatine phosphokinase (CPK), microscopic hematuria, sterile leukocyturia, normoglycemic glucosuria and phosphaturia with diminished tubular reabsorption of phosphorus. A short oliguric phase was followed by a polyuric phase lasting about 10 days, and glomerular and tubular function became normal after about 3 weeks. Treatment was by intensive infusions of fluids, electrolytes, sodium bicarbonate, salt-free albumin and antibiotics. To the best of our knowledge, this renal complication of cholera has not yet been described in Israel.
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PMID:[Acute renal failure as a complication of cholera]. 868 55

We studied the effects of iron deficiency on the in vivo absorption (by using the intestinal perfusion technique in the duodenum) of different dietary sources of iron (haem, non-haem and equal parts of both forms) and investigated the interactions between iron and calcium, phosphorous, magnesium, copper and zinc in control and iron-deficient rats. Three perfusion solutions containing a different source of iron were used: solution 1, ferric citrate; solution 2, haemoglobin; solution 3, equal parts of ferric citrate and haemoglobin. We also tested the same perfusion solution with 2,4-dinitrophenol (2,4-DNP), an inhibitor or oxidative phosphorylation (solutions 1-I, 2-I and 3-I). In control rats we observed three mechanisms of iron absorption: passive for soluble iron salts, active receptor-mediated for non-haem iron complexes, and active receptor-mediated for haem iron. In anaemic rats iron absorption was greater than in controls, except after perfusion with solution 2 (containing haemoglobin). Absorption increased as a result of both the passive and active, receptor-mediated mechanism for non-haem iron complexes. The active component was influenced by the depletion of haem receptors under severe iron deficiency. The absorption of calcium, copper and zinc in iron-deficient animals was lower than in controls, whereas phosphorus and magnesium absorption were not significantly affected. After perfusion with solution 2 or 3, calcium, copper and zinc absorption were lower than after solution 1. We conclude that ferropoenic anaemia in the rat impairs the absorptive process of those minerals that are absorbed, at the duodenal level mainly via active transport (haem iron, calcium, copper and zinc), but does not affect the active component involved in non-haem iron absorption.
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PMID:Effect of source of iron on duodenal absorption of iron, calcium, phosphorous, magnesium, copper and zinc in rats with ferropoenic anaemia. 912 53

We examined renal abnormalities in Greek patients with sickle-cell beta thalassemia (S-beta thal). A total of 17 patients aged 16-59 years suffering from S-beta thal and 17 age- and sex-matched healthy controls were studied. In all individuals we carried out a detailed study of renal function including electrolytes in serum and urine, concentrating or diluting ability, urine acidification ability, glomerular filtration rate (GFR), and hormones [such as plasma renin activity (PRA), serum aldosterone, and erythropoietin (EPO)]. Though the GFR did not differ significantly in patients and controls, half the patients had either supranormal or subnormal values. Serum potassium and uric acid were significantly higher in patients than controls. Serum phosphorus was similar in both groups, though patients with S-beta thal had significantly lower phosphate excretion indices. All patients were unable to maximally concentrate the urine, and seven also had limited ability to maximally dilute it. Five patients had incomplete distal renal tubular acidosis. Four had mild proteinuria, and six had microalbuminuria. Serum EPO and aldosterone were higher in S-beta thal patients than controls, but there was no difference in PRA between the two groups. There was a strong correlation between hemoglobin concentration and EPO levels, which was strongest in patients with GFR < 50 ml/min. We conclude that patients with S-beta thal, like sickle-cell anemia patients, present multiple abnormalities of renal function.
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PMID:Renal abnormalities in patients with sickle cell-beta thalassemia. 923 25

The nephrology nurses in collaboration with the nephrologist worked closely to avoid severe symptomatology related to calcium phosphorus imbalance. The surgical team support was discontinued 48 hours after the removal of the autotransplant. The patient exhibited classic signs of secondary hyperparathyroidism, as indicated by laboratory tests, anemia, and pruritus. Despite the level of anemia, the patient did not complain of fatigue or dyspnea. A hypocalcemic crisis was avoided by the ongoing assessment and intervention the patient received from the nursing staff. Four of the five stated goals were met. The patient is free of disability as evidenced by steady gait, normal range of motion, and adequate muscle strength. The calcium and phosphorus levels and the calcium phosphorus product are within acceptable ranges (see Figure 1). J.I. has always had information about diet and medication management but has demonstrated variable adherence to the regimen. However, the nephrology nurses plan to continue with counseling and education as needed.
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PMID:Patient, nurses, and physicians collaborating in the management of a patient following autotransplant parathyroidectomy. 932 98

In this report, the outcome, diagnosis, management, and complications of pregnancy in dialysis patients are discussed. The advantages and disadvantages to the use of peritoneal dialysis and hemodialysis and the changes in dialysis regimen used in pregnant women are addressed. Maternal complications, particularly hypertension and anemia, are reviewed. This report looks at the approach to the management of anemia and calcium/phosphorus metabolism in the setting of limited information. The report also discusses pregnancy outcome for the mother and fetus, including the problem of prematurity and fetal loss. Special considerations in women with lupus and diabetes are noted. Pregnancy in dialysis patients remains a high-risk undertaking for both the patient and the infant. There are large gaps in our knowledge base regarding the effect of the abnormalities associated with renal failure on pregnancy. The survival of the infant and the safety of the mother depend on close cooperation among all the specialities involved, including nurses, doctors, nutritionists, and social workers from nephrology, perinatology, and neonatology.
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PMID:Management of the pregnant dialysis patient. 947 12

This is a report about two cases of hereditary spherocytosis complicated by severe hypophosphatemia, while recovering from aplastic crisis. Case #1: A 31-year-old male, who had jaundice and splenomegaly since the age of 15 and who has a son diagnosed with hemolytic anemia, was admitted because of fever lymphadenopathy, and jaundice. A diagnosis of hereditary spherocytosis was made based on microspherocytes observed in his peripheral blood smear. After admission, the anemia became more serious for a few days and he was considered suffering from bone marrow aplastic crisis. His serum phosphorus level fell to 0.5 mg/dl on the second day, but it rapidly returned to normal as reticulocyte counts rose. Case #2: A 29-year-old male with known transient jaundice and splenomegaly suffered from fever, anemia and jaundice, but recovered two weeks later. Laboratory examination revealed positive human Parvovirus B19 (HPV-B19) DNA, anti-HPV-19 IgM and IgG-antibody. His serum phosphorus level fell to 1.2 mg/dl on the eighth day, but it rose in the same manner as seen in case #1. The fall in serum phosphorus is probably due to its shift to the erythroblasts during erythroid hyperplasia.
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PMID:[Hereditary spherocytosis associated with severe hypophosphatemia in patients recovering from aplastic crisis]. 963 90

Metabolic bone disease was diagnosed in an 11-month-old female common marmoset (Callithrix jacchus). It was depressed, reluctant to move, and was cachectic and small for its age. Laboratory findings included anaemia, azotaemia and an inverse calcium to phosphorus ratio. The radiological findings showed simultaneous signs of osteomalacia and soft-tissue calcification. There was decreased bone density with lytic areas in the pelvis and femur, and severe bilateral nephrocalcinosis. Postmortem examination revealed marked focal dystrophic calcification of the epi- and myocardium. Calcium and vitamin D3 deficiency (nutritional secondary hyperparathyroidism) was the most likely cause of the osteomalacia.
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PMID:Unusual case of metabolic bone disease in a common marmoset (Callithrix jacchus). 971 24

Chronic renal insufficiency ultimately culminating in end-stage renal disease requiring dialysis or transplantation is a major health problem in the United States. The first task confronting the physician caring for a patient with renal disease is to decide whether the renal insufficiency is acute or chronic. The initial differential diagnostic approach to chronic renal insufficiency consists of determining whether the patient has glomerular disease or interstitial or vascular disease on the basis of a careful history taking, urinalysis, and measurement of 24-hour protein excretion. Further refinement of diagnostic considerations often requires serologic studies, renal biopsy, or imaging the urinary tract with ultrasonography or computed tomography. Management considerations begin with the identification and correction of any acute reversible causes of renal insufficiency in patients with chronic renal disease. Recent studies have shown that effective antihypertensive therapy, especially with angiotensin-converting enzyme inhibitors, restriction of dietary protein, and excellent glycemic control in patients with diabetes, can retard the progression of chronic renal disease. Once these therapeutic strategies are in place, it is important to anticipate and treat the multiple manifestations of chronic progressive renal insufficiency: fluid overload, hyperkalemia, metabolic acidosis, abnormalities of calcium, phosphorus, and vitamin D metabolism, and anemia.
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PMID:Chronic renal insufficiency: a diagnostic and therapeutic approach. 1021 59

We studied the development of nutritional iron deficiency 0, 10, 20, 30 and 40 days after the intake of a semisynthetic diet lacking iron (diet 0) and the possible interactions with calcium, phosphorus and magnesium in both control rats and rats after 40 days of iron deficiency. During this period, iron deficiency was found to produce stress in the rats, as evidenced by high levels of cortisol in the serum. High levels of parathyroid hormone (PTH) were also found. There was a considerable increase in the absorption of calcium, phosphorus and magnesium, but the phosphorus and magnesium balance decreased and that of calcium remained practically unchanged, although there was an increase in calcium urinary elimination. Despite the noticeable degree of bone demineralization, which was evident in the femur, serum levels of calcium, phosphorus and magnesium remained constant. The present study shows that severe nutritional ferropenic anaemia provokes significant alterations in the metabolism of calcium, phosphorus and magnesium. We conclude that these alterations should be taken into account in the treatment of this pathology, given its prevalence and the fact that it may exacerbate other pathologies, particularly those related to the metabolism of calcium and phosphorus.
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PMID:Interactions among iron, calcium, phosphorus and magnesium in the nutritionally iron-deficient rat. 978 87


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