Glomerulopatía C3: una nueva entidad basada en el complemento / C3 glomerulopathy: A new complement-based entity

La glomerulopatía C3 es una nueva entidad descrita recientemente que ha cambiado la visión, el tratamiento y la clasificación de algunas enfermedades glomerulares. Engloba 2patologías similares pero claramente diferenciadas: la enfermedad por depósitos densos y la glomerulonefritis C3 propiamente dicha. La vía alternativa del complemento juega un papel fundamental en su patogenia, y en concreto las mutaciones o defectos en sus factores reguladores (fundamentalmente factorH y factorI), así como la presencia de autoanticuerpos adquiridos (factor nefrítico C3) que generan una activación desenfrenada del sistema, y en último término un depósito de sus productos a nivel glomerular. Su mal pronóstico y la aparición en población joven hacen preciso el estudio de nuevas alternativas terapéuticas. Recientemente eculizumab, un anticuerpo anti C5, ha demostrado efectividad en el tratamiento de estos pacientes (AU)

C3 glomerulopathy is a new, recently described entity that has changed the perspective, treatment and classification of a number of glomerular diseases. It encompasses 2 similar but clearly differentiated pathologies —the dense-deposit disease and C3 glomerulonephritis itself. The alternative complement pathway plays a fundamental role in its pathogenesis and, specifically, the mutations and defects in its regulatory factors (mainly factor H and factorI), as well as the presence of acquired autoantibodies (C3 nephritic factor), which generates an unbridled activation of the system, and ultimately, a deposit of its products at the glomerular level. Its poor prognosis and onset in young populations makes the detailed study of new therapeutic alternatives for this disease essential. Recently eculizumab, an anti-C5 antibody, has demonstrated effectiveness in the treatment of these patients (AU)

C3 glomerulopathy: A new complement-based entity.

C3 glomerulopathy is a new, recently described entity that has changed the perspective, treatment and classification of a number of glomerular diseases. It encompasses 2 similar but clearly differentiated pathologies -the dense-deposit disease and C3 glomerulonephritis itself. The alternative complement pathway plays a fundamental role in its pathogenesis and, specifically, the mutations and defects in its regulatory factors (mainly factor H and factor I), as well as the presence of acquired autoantibodies (C3 nephritic factor), which generates an unbridled activation of the system, and ultimately, a deposit of its products at the glomerular level. Its poor prognosis and onset in young populations makes the detailed study of new therapeutic alternatives for this disease essential. Recently eculizumab, an anti-C5 antibody, has demonstrated effectiveness in the treatment of these patients.

The nephrologist's role in metformin-induced lactic acidosis.

Metformin is an antihyperglycemic agent commonly used in diabetic patients. It is very effective and is able to reduce the plasma glucose and HbA1C. However, in some patients, specially those with comorbidities, metformin can provoke severe lactic acidosis with high morbimortality. Treatment of the lactic acidosis induced by metformin is based on the use of supportive general measures; in severe cases, procedures of extrarrenal purification like hemodialysis or continuous hemodiafiltration have been successfully used.

Papel del nefrólogo en la acidosis láctica grave por metformina / The nephrologist's role in metformin-induced lactic acidosis

La metformina es un fármaco ampliamente utilizado en sujetos con diabetes mellitus y su eficacia para descender la glucemia y la hemoglobina A1C (HbA1C) es notable. Sin embargo, en algunos pacientes, sobre todo en los que presentan comorbilidades, puede provocar una acidosis láctica grave que origina una elevada morbimortalidad. El tratamiento de esta complicación se basa en la utilización de medidas de soporte y, en los casos más graves, en procedimientos de depuración extrarrenal, como la hemodiálisis o la hemodiafiltración continua (AU)

Metformin is an antihyperglycemic agent commonly used in diabetic patients. It is very effective and is able to reduce the plasma glucose and HbA1C. However, in some patients, specially those with comorbidities, metformin can provoke severe lactic acidosis with high morbimortality. Treatment of the lactic acidosis induced by metformin is based on the use of supportive general measures; in severe cases, procedures of extrarrenal purification like hemodialysis or continuous hemodiafiltration have been successfully used (AU)

Physicochemical and nutritional composition of dry-cured duck breast.

A total of 80 dry-cured duck breasts were used in this study. The gross composition, color and textural parameters, fatty acid and amino acid profiles, macro- and micromineral content, and sensory properties were analyzed. In comparison with other dry-cured meat products made from cuts of whole meat, dry-cured duck breast is characterized by low moisture and a higher protein content. Saturated, monounsaturated, and polyunsaturated fatty acid contents in intramuscular fat were approximately 35, 57, and 8% of the total fatty acid methyl esters, respectively. The main essential amino acids present in dry-cured duck breast were lysine and leucine, followed by valine, threonine, and isoleucine, with aspartic and glutamic acids being the most important in the nonessential fraction. Dry-cured duck breast proved to be a valuable source of iron, zinc, copper, and manganese (7.57, 4.66, 0.84, and 0.87 mg/100 g of edible portion, respectively), providing approximately 57, 45.2, 93, and 43.7% of the recommended daily allowances, respectively.

Informe de diálisis y trasplante de la Sociedad Española de Nefrología y Registros Autonómicos, año 2000 / Rapport of the dialysis and transplant registry in Spain. The Spanish Society of Nephrology and Regional Registries

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Uso de asistentes personales digitales (PDAs) en medicina / The use of personal digital assistant (PDAs) in medicine

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Abnormal calcaemic response to PTH in the uraemic rat without secondary hyperparathyroidism.

BACKGROUND: Skeletal resistance to the calcaemic action of parathyroid hormone (PTH) is an important pathogenic factor in the development of secondary hyperparathyroidism. Since parathyroidectomy normalizes the calcaemic response to PTH in uraemic animals, the increase in PTH levels has been advanced as a cause of skeletal resistance to the calcaemic action of PTH. This study was designed to evaluate in uraemic rats the effect of normal PTH levels on the calcaemic response to PTH. METHODS: To maintain normal PTH levels, rats were parathyroidectomized (PTX) and rat 1-34 PTH was infused at a rate of 0.022 microg/100 g per hour via a subcutaneously implanted miniosmotic pump; this rate of infusion was considered to be the normal PTH replacement dose since it normalized serum calcium and phosphorus in PTX rats with normal renal function. Two separate studies were performed. In the first study, rats were maintained on a moderate-phosphorus (0.6%) diet and rats were divided into four groups: (I) normal; (II) uraemic; (III) PTX with normal PTH replacement; and (IV) uraemic with PTX and normal PTH replacement. In a second study, the groups were the same except that a high-phosphorus (1.2%) diet was given to increase the magnitude of hyperparathyroidism in rats with intact parathyroid glands; an additional group (V) identical to group IV except that rats received daily calcitriol was included. After 14 days, rats received a 48-h infusion of high-dose rat 1-34 PTH (0.11 microg/100 g per hour) to evaluate the calcaemic response to PTH. Results. The calcaemic response to PTH was similar in normal rats and PTX rats replacement on both a moderate and high-phosphorus diet. In uraemic rats, the calcaemic response to PTH was decreased and the maintenance of normal PTH levels by PTH replacement did not correct the decreased calcaemic response to PTH; moreover, calcitriol supplementation did not improve the calcaemic response to PTH. Finally, hypocalcaemia was observed in uraemic rats with PTH replacement and was more profound than in rats on a high-phosphorus diet. CONCLUSIONS: This study demonstrates that the maintenance of a normal PTH level in uraemic rats did not correct the impaired calcaemic response to PTH, suggesting that factors intrinsic to uraemia, independent of phosphorus, calcitriol, and PTH participate in the decreased calcaemic response to PTH in uraemia.

Relative effects of PTH and dietary phosphorus on calcitriol production in normal and azotemic rats.

In moderate renal failure, the serum calcitriol level is influenced by the stimulatory effect of high PTH and the inhibitory action of phosphorus retention. Our goal was to evaluate the relative effect that high PTH levels and increased dietary phosphorus had on calcitriol production in normal rats (N) and rats with moderate renal failure (Nx). Normal and Nx (3/4 nephrectomy) rats were divided into two groups: (1) rats with intact parathyroid glands (IPTG) and (2) parathyroidectomized rats in which PTH was replaced (PTHR) by the continuous infusion of rat 1-34 PTH, 0.022 microgram/hr/100 g body wt, using a miniosmotic Alzet pump. To test the effect of dietary phosphorus, rats received either a moderate (MPD, 0.6% P) or a high phosphorus (HPD, 1.2%) diet for 14 days. The experimental design included pair-fed N and Nx rats with either IPTG or PTHR. Serum calcitriol and PTH levels in N rats fed a MPD were 69 +/- 3 and 40 +/- 5 pg/ml, respectively. In Nx rats on a MPD, serum calcitriol levels decreased only if hyperparathyroidism was not allowed to occur (76 +/- 4 vs. 62 +/- 4 pg/ml in Nx-IPTG-MPD and Nx-PTHR-MPD groups respectively, P < 0.05). Even in N rats on a HPD, high PTH levels (67 +/- 8 pg/ml in the N-IPTG-HPD group) were required to maintain normal serum calcitriol levels (69 +/- 4 vs. 56 +/- 6 pg/ml in Nx-IPTG-HPD and Nx-PTHR-HPD groups, respectively; P < 0.05). In Nx rats on a HPD, the development of secondary hyperparathyroidism (286 +/- 19 pg/ml in the Nx-IPTG-HPD group) prevented a decrease in serum calcitriol levels (68 +/- 7 pg/ml). In contrast, serum calcitriol levels were low in the Nx-PTHR-HPD group (52 +/- 4 pg/ml, P < 0.05), which were deprived of the adaptative increase in endogenous PTH production. In conclusion, our results in rats indicate that in moderate renal failure, an elevated PTH level maintains calcitriol production and overcomes the inhibitory action of phosphorus retention.