Aging impairs vascular function, but the mechanisms involved are unknown. The aim of this study was to analyze whether aging-related hyperphosphatemia is implied in this effect by elucidating the role of oxidative stress. C57BL6 mice that were aged 5 months (young) and 24 months (old), receiving a standard (0.6%) or low-phosphate (0.2%) diet, were used. Isolated mesenteric arteries from old mice showed diminished endothelium-dependent vascular relaxation by the down-regulation of NOS3 expression, increased inflammation and increased fibrosis in isolated aortas, compared to those isolated from young mice. In parallel, increased Nox4 expression and reduced Nrf2, Sod2-Mn and Gpx1 were found in the aortas from old mice, resulting in oxidant/antioxidant imbalance. The low-phosphate diet improved vascular function and oxidant/antioxidant balance in old mice. Mechanisms were analyzed in endothelial (EC) and vascular smooth muscle cells (SMCs) treated with the phosphate donor ß-glycerophosphate (BGP). In EC, BGP increased Nox4 expression and ROS production, which reduced NOS3 expression via NFκB. BGP also increased inflammation in EC. In SMC, BGP increased Collagen I and fibronectin expression by priming ROS production and NFκB activity. In conclusion, hyperphosphatemia reduced endothelium-dependent vascular relaxation and increased inflammation and vascular fibrosis through an impairment of oxidant/antioxidant balance in old mice. A low-phosphate diet achieved improvements in the vascular function in old mice.

Leprosy is a chronic infectious disease caused by Mycobacterium leprae. The main clinical manifestations involve the skin and the peripheral nervous system. Several types of nephropathy have been described in leprosy. One frequent form of renal involvement is amyloidosis, especially in patients with lepromatous leprosy. In these patients, end-stage renal disease is an important contributor to morbidity and mortality. Here, we present the case of a patient with nephrotic syndrome caused by secondary amyloidosis, chronic peripheral neuropathy and a history of leprosy. The patient was correctly treated in her youth, which is the best way to avoid renal pathology, but she developed a nephrotic syndrome years later.

Acute endocapillary glomerulonephritis, as its name suggests, is a one-time process, which usually resolves within weeks. However, in a small percentage of patients, the disease becomes chronic. In these cases, a deregulation in the alternative complement pathway, which can be caused by mutations or autoantibodies, has been proposed as a pathophysiological mechanism. As a result, the alternative complement pathway remains active after resolution of infection. We report a patient with two episodes of acute renal failure, both times diagnosed by renal biopsy of acute endocapillary glomerulonephritis, with slow recovery after two episodes of low-serum complement C3, haematuria and proteinuria.

La amiloidoisis renal hereditaria es un trastorno autosómico dominante cuya clínica se solapa con la de otros tipos de amiloidoisis. Hacer un adecuado diagnóstico diferencial puede ser difícil, pero tiene una gran relevancia respecto al pronóstico y tratamiento, que difiere según sea el origen de la enfermedad. Presentamos el caso clínico de un paciente con síndrome nefrótico e insuficiencia renal progresiva, con antecedente familiar de madre con amiloidosis renal. En la biopsia renal se observó depósito de amiloide a nivel glomerular, con negatividad para cadenas ligeras y proteína AA. La sospecha clínica inicial fue la de amiloidosis por depósito de cadena A alfa de fibrinógeno, que es la causa más frecuente de amiloidosis hereditaria en Europa, con afectación preferentemente glomerular. Sin embargo, el estudio genético determinó una nueva mutación previamente no descrita de la Apolipoproteina AI (APO AI). En la biopsia de la madre se detectó depósito glomerular, pero también depósito masivo en médula, lo que caracteriza a la amiloidosis por depósito de APO AI. El diagnóstico se confirmó mediante inmunohistoquímica. La amiloidosis por depósito de Apo AI progresa a enfermedad renal crónica terminal en el plazo de de 3 a 15 años. Se diferencia clínicamente de la amiloidosis AL por su menor afectación extrarrenal y su mejor pronóstico. El trasplante renal ofrece una supervivencia del injerto aceptable y el trasplante hepato-renal se podría tener en cuenta en pacientes con disfunción significativa de ambos órganos