Utilización nutritiva de fósforo en el transcurso de la anemia ferropénica nutricional / Nutritive utilization of phosphorus during the course of nutritional ferropenic anaemia

Se ha estudiado el efecto de la evolución de la anemia ferropénica nutricional sobre la utilización digestiva y metabólica de fósforo en tres periodos 20, 30 y 40 días. Los animales de experimentación han sido 48 ratas macho de la raza Wistar albina que se dividieron en 6 grupos: tres grupos controles(C) y tres grupos ferrodeficientes (FD) que recibieron una dieta AIN 93G con contenido normal (45mg Fe/kg dieta) o con un bajo contenido de hierro (5 mg/Fe Kg dieta) respectivamente durante 20, 30 ó 40 días. Se ha encontrado un aumento significativo en la utilización digestiva y metabólica de fósforo en el transcurso de la anemia ferropénica nutricional, efecto que se va haciendo más patente a medida que evoluciona la ferrodeficiencia. Este incremento en la utilización nutritiva de fósforo es debido principalmente al mecanismo pasivo de absorción de fósforo que opera principalmente en el yeyuno-íleon y es predominante en situación de anemia ferropénica nutricional(AU)

The evolution of the nutritional iron deficiency anemia on the digestive and metabolic utilization of phosphorus has been studied during three periods: 20, 30 and 40 days. 48 male Wistar albino breedrats were divided in 6 groups: three control groups (C) and three Fe-deficient groups (FD) receiving AIN 93G with normal-Fe content (45 mg /kg diet) or with a low-Fe content (5 mg/Kg diet) respectively during 20, 30 ó 40 days. A significant increase in the digestive and metabolic utilization of phosphorus has been found in the course of the nutritional iron deficiency anemia, effect that become more pronounced as the ferrodeficiency is instaured. This increase in the nutritive utilization of phosphorus is due mainly to the passive mechanism of phosphorus absorption which operates principally in the jejunum-ileum and is predominant in situation of nutritional iron deficiency anemia(AU)

[Altered calcium-phosphorus metabolism and low-protein diet]. / Alterazione del metabolismo calcio-fosforo e dieta ipoproteica.

Many metabolic disorders associated with uremia can affect the long-term survival of patients with chronic kidney disease. Such disorders can be defined as: hypocalcemia, increased levels of phosphorus, reduced synthesis of 1,25-dihydroxyvitamin D and serum calcitriol, and reduced expression of vitamin D receptors on parathyroid cells with increased parathyroid hormone levels and secondary hyperparathyroidism. Phosphorus, which plays a crucial role in the progression of progressive renal disease, has been shown to be an independent risk factor for death in hemodialysis patients. Thus, reducing the phosphorus intake by decreasing dietary proteins may slow the progression of renal disease. Hypocalcemia is typically associated with chronic kidney disease. It is due to the reduced intestinal absorption of calcium and the spontaneously reduced protein intake that occur in patients with progressive renal disorders. Activated vitamin D and calcium supplements should be administered to patients who are following low-protein diets to prevent secondary hyperparathyroidism; the doses should be correlated with actual renal function and protein intake.

Practical approaches to management of hyperphosphatemia: can we improve the current situation?

Despite advanced technology and regular and efficient dialysis treatment, the prevalence of hyperphosphatemia still is unacceptably high. Nevertheless, a neutral phosphorus balance level can generally be achieved by optimization of dialysis prescription in combination with individualized dietary and medical strategies. Besides increasing the fraction of inorganic phosphate (iP) removed by convection through the application of hemodiafiltration, extension of daily or weekly treatment time is the most promising way to neutralize phosphorus balance. Dietary phosphate restriction, the second corner stone of phosphate management, bears the risk of development of protein malnutrition. Phosphate binders (PBs) effectively reduce intestinal iP absorption, but are mostly dosed inadequately in relation to meal phosphorus content. Phosphate management may be substantially improved by enabling patients to self-adjust the PB dose to individual meal phosphate content, similar to self-adjusting insulin dose to carbohydrate intake by diabetics. A recently developed Phosphate Education Program (PEP) provides simple training tools to instruct patients to eye-estimate meal phosphorus content based on newly defined phosphorus units instead of milligrams. PEP is the first approach applying the concept of patient empowerment in the management of hyperphosphatemia in dialysis patients.

Multidisciplinary approach for prescriptive management of mineral and bone metabolism in chronic kidney disease: development of a dietetic led protocol.

BACKGROUND: A number of mineral metabolism abnormalities occur as kidney function declines, these include hyperphosphatemia, hyperparathyroidism and altered vitamin D metabolism. These derangements are associated with increased morbidity and mortality amongst the chronic kidney disease patient group. Treatment requires a multidisciplinary team approach in which the dietitian plays a pivotal role. OBJECTIVES: The development of protocols to aid implementation of various international, national and local treatment strategies is described. Audit the protocol to evaluate their clinical effectiveness. RESULTS: A prescriptive Protocol for the management of mineral and bone metabolism abnormalities in chronic kidney disease was developed and implemented. Initial audit findings suggest the protocol has had a positive effect on the control of phosphate, corrected calcium and parathyroid (PTH) levels. CONCLUSION: The development and implementation of a dietetic-led prescriptive therapy protocol allows dietitians and clinicians to adopt an integrated approach for the diagnosis and timely management of these complicated conditions.

The use of telemedicine to assess and advise patients regarding dietary treatment of hyperphosphataemia.

Satellite units have the benefit of being local to patients and easily accessible. The main hospital where the dietitians are based is some distance away from the satellite unit. This has traditionally made it more difficult for the dietitians to assess satellite unit patients other than at set times when all the patients are assessed and advised in one visit. The aim of the telemedicine unit was to make dietary assessment of satellite unit patients easier by reducing travel time and to be more accessible to patients at times when visits by the dietitian were not scheduled. Telemedicine units were linked from the main hospital to the satellite unit. Fourteen patients were assessed and advised via this method and of these patients 8 patients were seen for help with their hyperphosphataemia. Phosphate levels on referral were 2.46 +/- 0.47mmols/l and by the following month after review by the dietitian had decreased to 2.06 +/- 0.43mmols/l (p=0.01) and 1.96 +/- 0.16mmols/l by month 6 (p=0.02). This small study shows that the telemedicine unit is an effective way to assess patients and communicate information. Travel time has been saved and patients have had the benefit of receiving dietary information soon after their raised phosphate result rather than having to wait for the next scheduled visit by the dietitian.

Treatment of secondary hyperparathyroidism by high calcium diet is associated with enhanced resistance artery relaxation in experimental renal failure.

BACKGROUND: Vasorelaxation is impaired in renal failure (RF) and hypertension. A high calcium diet enhances vasodilatation and reduces blood pressure in experimental hypertension. Oral calcium salts are used as phosphate binders in RF. However, the effect of increased calcium intake on arterial tone in RF is unknown. METHODS: We investigated the influence of an 8-week high calcium diet (0.3 vs 3.0%) on resistance artery tone in 5/6 nephrectomized (NTX) rats. Calcium was supplemented as carbonate salt, blood pressure measured by tail-cuff, urine collected in metabolic cages, and samples taken for blood chemistry and parathyroid hormone (PTH). Functional studies of isolated third-order branches of the mesenteric artery in vitro were performed using the Mulvany multimyograph. RESULTS: Plasma urea was elevated 1.6-fold and systolic blood pressure by 10 mmHg after NTX, while increased calcium intake was without effect on these variables. Plasma PTH and phosphate were raised following NTX, and suppressed by high calcium diet. Vasorelaxations induced by K(+) channel agonists 11,12-epoxyeicosatrienoic acid and levcromakalim were impaired after NTX. Vasorelaxation induced by acetylcholine was also reduced following NTX, and experiments with N(G)-nitro-L-arginine methyl ester, diclofenac and charybdotoxin + apamin suggested that the K(+) channel-mediated component of endothelium-dependent relaxation was deficient after NTX. Increased calcium intake corrected all impairments of vasodilatation in NTX rats. CONCLUSIONS: Deficient vasorelaxation via K(+) channels was normalized by high calcium diet in experimental RF. This effect was independent of the degree of renal impairment and blood pressure, but was associated with improved calcium metabolism: plasma levels of PTH and phosphate were decreased and ionized calcium was increased.

Tumoral calcinosis. Case report with treatment failure.

Periarticular calcifications are the hallmark of a rare entity: tumoral calcinosis. We have followed for 90 months a nine-year-old black girl with involvement of both shoulders. Seven initial local excisions of the mass on the right shoulder were attempted without complete removal and prompt recurrence after each attempt. The entire lesion on the right side, including a cutaneous ulceration, was managed by en masse surgical excision. Preoperative inpatient medical management in the form of low calcium and low phosphorus diet was unsuccessful. Postoperatively, she has remained free of ulceration; however, after two and a half years, the right mass has again increased in size with compression of the brachial plexus. This recurrence occurred despite strict dietary control starting immediately postoperatively. Although there are many advocates of surgical excision of these lesions and, more recently, several cases reported of successful medical management, we find that often a combination approach is necessary to effectively treat tumoral calcinosis and reduce the rate of recurrence.

[Phosphorus-calcium metabolism and dietetic correction of its disorders in chronic kidney diseases in children]. / Sostoianie fosforno-kal'tsievogo obmena i dieticheskaia korrektsiia ego narushenii pri khronicheskikh bolezniakh pochek u detei.

Ninety children with varying renal diseases were under observation. The investigations conducted have shown that disorders in phosphoric-calcium metabolism depend on the type, activity of chronic glomerulonephritis (CGN) and etiology of chronic renal insufficiency (CRI). Significant disorders in phosphoric-calcium metabolism were detected in patients with nephrotic and mixed types of CGN. Most manifest clinical and x-ray changes of the osseous system were observed in patients with CRI that developed as a result of the tubulointerstitial pathologic process. Low-phosphate diets with preset amounts of Ca and P were developed, composed of products with relatively low content of P, and of new dietetic products rich in Ca. The diets were used for correction of hyperphosphatemia in children with CGN and in those with CRI, simultaneously with drug therapy, to prevent or diminish disorders in phosphoric-calcium metabolism, and to reduce the risk of invalidism among children with chronic renal diseases.

[Bartter's disease associated with hypercorticism, phosphate and magnesium deficiencies and familial renal tubular disease]. / Un syndrome de bartter associant un hypercortisolisme, un diabete phosphore et magnesien et une tubulopathie d'origine familiale

A new case of Bartter's syndrome is described. There is a context of other cases of familial renal tubular disease with a sex-linked heredity. In this case, the Bartter's syndrome is associated with magnesium deficiency and hypomagnesemia, with a ricket and severe phosphate deficiency, and finally with an hypercorticism. The basal secretion rate of cortisol agree with a Cushing's syndrome. This hypercorticism is corrected by aminogluthetimide. The influence of the hyperreninism on the hypercorticism is discussed.