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Treatment with cinacalcet of secondary hyperparathyroidism after renal transplantation.

BACKGROUND: The treatment of posttransplant secondary hyperparathyroidism (SHP) with vitamin D analogues is determined by their effectiveness to reverse hypercalcemia. Calcimimetics inhibit parathyroid hormone (PTH) secretion by modulating the calcium-sensing receptor in the parathyroid gland. Cinacalcet, a calcimimetic drug, has proven its effectiveness for the treatment of SHP among patients in phase V of chronic renal disease. PATIENTS AND METHODS: This retrospective analysis included 48 patients with SHP who were treated with cinacalcet. The initial dose of 30 mg/d could be increased to 180 mg, administering calcitriol also, depending on the serum calcium and PTH levels. The objectives were a PTH level between 75 and 125 pg/mL or a decrease >40%, and a serum calcium level below 10.5 mg/dL. RESULTS: The average PTH at baseline was 244 pg/mL, decreasing to 131 pg/mL at 1 year (P < .01). The average calcium at baseline was 10.1 mg/dL descending to 9.2 mg/dL at 1 year (P < .01). Among patients with hypercalcemia, the calcium decreased from 11 to 9.6 mg/dL at 1 year (P < .01). Seventy percent of patients without hypercalcemia reached the desired value of PTH, and 100% of those with hypercalcemia. Among patients with hypercalcemia, the desired calcium level was reached in 91% of cases. Ten patients developed hypocalcemia. In 3 cases we stopped the treatment with cinacalcet due to digestive intolerance. CONCLUSIONS: Treatment with cinacalcet controlled hyperparathyroidism and hypercalcemia among patients with posttransplant SHP. It was a safe drug, with a low incidence of side effects.

[Acute renal failure due to sulfadiazine crystalluria]. / Insuficiencia renal aguda por depósito de cristales de Sulfadiacina.

Focal necrotizing encephalitis due to Toxoplasma gondii infection represents one of the most common opportunistic infection in patients with the acquired inmunodeficiency syndrome (AIDS), and the treatment is commonly with a combination sulphadiazine, and pyrimethamine. A major side effect of sulfadiazine therapy is the occurrence of crystallization in the urinary collecting system. We report a patient with AIDS and Toxoplasmic encephalitis treated with sulfadiazine who developed acute renal failure. Renal ultrasound demonstrated echogenic areas within the renal parenchyma, presumed to be sulfa crystals. Renal failure and ultrasound findings resolved rapidly with hydratation and administration of alkali. Patients infected with AIDS frequently have characteristic that increase intratubular crystal precipitation and they require treatment with one or more of the drugs that are associated with crystal-induced renal failure. Controlled alkalinization of the urine and high fluid intake are recommended for prophylaxis of crystalluria. The literature concerning crystalluria and renal failure due to sulfadiazine is reviewed.

Insuficiencia renal aguda por depósito de cristales de Sulfadiacina / Acute renal failure due to sulfadiazine crystalluria

La encefalitis necrotizante focal por Toxoplasma Gondii es una de las infecciones oportunistas más frecuente en pacientes con síndrome de inmunodeficiencia adquirida. (SIDA). El tratamiento de elección consiste en la combinación de Pirimetamida y Sulfadiacina. Uno de los principales efectos adversos de la Sulfadiazina es su precipitación en el sistema urinario. Presentamos a una paciente con SIDA y encefalitis por Toxoplasma Gondii que desarrolla insuficiencia renal aguda reversible por depósito de cristales de sulfadiacina a nivel renal. La ecografía mostró múltiples calcificaciones en el seno renal, que desaparecieron tras hidratación y administración de bicarbonato sódico endovenoso. Estos pacientes y otros inmunodeprimidos, presentan factores favorecedores de la precipitación de éste y otros fármacos, siendo necesario una adecuada monitorización de la función renal y del sedimento urinario, junto con medidas profilácticas como el aumento de la ingesta de líquidos y la alcalinización urinaria

Focal necrotizing encephalitis due to Toxoplasma gondii infection represents one of the most common oportunistic infection in patients with the acquired inmunodeficiency syndrome (AIDS), and the treatment is commonly with a combination sulphadiazine, and pyrimethamine. A major side effect of sulfadiazine therapy is the occurrence of cristallization in the urinary collecting system. We report a patient with AIDS and Toxoplasmic encephalitis treated with sulfadiazine who developed acute renal failure. Renal ultrasound demonstrated echogenic areas within the renal parenchyma, presumed to be sulfa crystals. Renal failure and ultrasound findings resolved rapidly with hidratation and administration of alkali. Patients infected with AIDS frequently have characteristic that increase intratubular crystal precipitation and they require treatment with one or more of the drugs that are associated with crystal-induced renal failure. Controlled alkalinization of the urine and high fluid intake are recommended for prophylaxis of crystalluria. The literature concerning crystalluria and renal failure due to sulfadiazine is reviewed

Síndrome pneumo-renal en paciente con vasculitis de Schönlein-Henoch / Schölein-Henoch nephriis complicated with pulmonary renal syndrome

El síndrome de Schönlein-Henoch es una vasculítis sistémica que afecta a arteriolas y capilares. Aunque es un enfermedad típica de la infancia puede aparecer en edades más tardías. La enfermedad parece ser más severa en los adultos que la desarrollan. Las manifestaciones clínicas incluyen la clásica tétrada de rash cutáneo, artralgias, dolor abdominal y enfermedad renal, pero pueden verse afectados otros órganos como el miocardio, el pulmón, el uréter o el sistema nervioso central. La hemorragia pulmonar es una complicación rara del síndrome de Shönlein-Henoch, que aparece generalmente en adolescentes y adultos, y está asociada con una mortalidad significativa. Presentamos a un paciente de 76 años de edad con afectación renal severa, diagnosticado por biopsia renal de síndrome de Schönlein-Henoch, que desarrolla hemorragia pulmonar tras un tratamiento inicial con bolus de esteroides por glomerulonefrítis, desapareciendo la afectación pulmonar tras un segundo ciclo de bolus de esteroides

Schönlein-Henoch purpura is a systemic vasculitic disorder involving both arterioles and capillaries. Although it is mainly a disease of early chilhood, it can occur at any age. The disease may be more severe in the few adults who develop this disorder. The clinical manifestations include a classic tetrad: rash, arthralgias, abdominal pain and renal disease. However it may affect almost every other bodily organ such us myocardium, lungs, ureter and nervous system. Pulmonary hemorrhage, a rare complication of Schönlein-Henoch purpura, has been found mainly in adolescents and adults, and it is associated with significant mortality. We present a case of 76-year-old men with Schönlein-Henoch purpura, pulmonary haemorrhage and severe renal involvement. Therapy with intravenous prednisolone resulted in resolution of the pulmonary lesions and renal failure

[Shönlein-Henoch nephritis complicated with pulmonary renal syndrome]. / Síndrome pneumo-renal en paciente con vasculitis de Schönlein-Henoch.

Schönlein-Henoch purpura is a systemic vasculitic disorder involving both arterioles and capillaries. Although it is mainly a disease of early chilhood, it can occur at any age. The disease may be more severe in the few adults who develop this disorder. The clinical manifestations include a classic tetrad: rash, arthralgias, abdominal pain and renal disease. However it may affect almost every other bodily organ such us myocardium, lungs, ureter and nervous system. Pulmonary hemorrhage, a rare complication of Schönlein-Henoch purpura, has been found mainly in adolescents and adults, and it is associated with significant mortality. We present a case of 76-year-old men with Schönlein-Henoch purpura, pulmonary haemorrhage and severe renal involvement. Therapy with intravenous prednisolone resulted in resolution of the pulmonary lesions and renal failure.

[Atheroembolic disease and pulmonary haemorrhage]. / Enfermedad ateroembólica y hemorragia pulmonar.

The cholesterol embolism syndrome is a multisystemic disease resulting from cholesterol crystal emboli deriving from ulcerous atherosclerotic plaques of the aorta or large arteries. Cholesterol crystal embolization can affect multiple organ, including the skin, kidney, brain, eyes, gastrointestinal tract and extremities, and mimic other systemic diseases like vasculitis. Cholesterol crystal embolization of lungs has been described and should be included in the differential diagnostic of pulmonary-renal syndromes. The diagnosis of cholesterol embolism should be considered in elderly patients with pre-existing atherosclerotic disease who develop renal failure and clinical features of peripheral cholesterol crystal embolization in association with precipitating event, without the need for histological demonstration of cholesterol clefts. This syndrome is associated with high morbidity and mortality but recent reports suggest that an aggressive therapeutic management with patient-tailored supportive measures, avoids precipitating factors, and the use of corticosteroids may be associated with a favorable clinical outcome.

Enfermedad ateroembólica y hemorragia pulmonar / Atheroembolic disease and pulmonary haemorrhage

El síndrome de embolismo de colesterol se produce por la liberación de cristales de colesterol de placas ateroscleróticas ulceradas de grandes arterias. Puede afectar múltiples órganos simulando enfermedades sistémicas como las vasculítis, y debe ser incluido en el diagnóstico diferencial de los síndromes neumo-renales. El diagnóstico de embolismo de colesterol debería contemplarse en pacientes de edad, con enfermedad aterosclerótica previa, que desarrollan fallo renal o deterioro de una insuficiencia renal previa, y en los que aparecen hallazgos clínicos sugestivos de embolismos de colesterol periféricos, asociado a factores precipitantes, sin necesidad de demostración histológica. Este síndrome se ha asociado tradicionalmente a una alta morbi-mortalidad, aunque en recientes series se sugiere que un manejo agresivo con medidas de soporte, evitando factores precipitantes y el uso de corticoides a bajas dosis pueden proporcionar una mejoría en su pronóstico (AU)