Bloqueo del sistema renina-angiotensina-aldosterona en hipertensión arterial, diabetes y nefropatía / Blockade of the renin-angiotensin-aldosterone system in arterial hypertension, diabetes and nephropathy

El bloqueo del sistema renina-angiotensina con fármacos inhibidores de la enzima de conversión de la angiotensina o con antagonistas de los receptores de la angiotensina II ha demostrado su efectividad en hipertensos con y sin enfermedad cardiovascular previa. También en normotensos con alto riesgo vascular. Como además tienen efecto antiproteinúrico, se estima que estos agentes deben ocupar el primer escalón terapéutico en los pacientes con nefropatía diabética incipiente o establecida. Asimismo son agentes de primera línea en los casos de nefropatía no diabética con proteinuria > 0,5 g/24 h. Los estudios comparativos entre inhibidores de la enzima de conversión de angiotensina y los antagonistas de los receptores tipo 1 de la angiotensina II parecen mostrar una efectividad similar, con mejor tolerabilidad de estos últimos. En pacientes con nefropatía, la combinación de ambos agentes muestra una mayor capacidad antiproteinúrica que la monoterapia, aunque se desconoce si este efecto es independiente de una mayor reducción de la presión arterial (AU)

Blockade of the renin-angiotensin system with angiotensin-converting enzyme (ACE) inhibitors or angiotensin-II receptor antagonists has proved effective in hypertensive individuals with or without cardiovascular disease and also in normotensive individuals at a high cardiovascular risk. Moreover, due to their additional antiproteinuric effects, these drugs could also provide first-line therapy for patients with incipient or established diabetic nephropathy. Similarly, they could be the drugs of first choice in patients with non-diabetic nephropathy and a 24-hour urinary protein excretion >0.5 g. Comparative studies of ACE inhibitors and angiotensin-II type-1 receptor antagonists have shown that they appear to have a similar efficacy though the latter drugs are better tolerated. In patients with nephropathy, combinations of these two classes of drug have been found to have a greater antiproteinuric effect than monotherapy. However, it is not known whether this effect is independent of the greater reduction in blood pressure (AU)

Systemic and glomerular hypertension and progression of chronic renal disease: the dilemma of nephrosclerosis.

The link between the kidney and hypertension has been considered a villain-victim relationship. High blood pressure levels are a well-recognized feature in chronic renal disease, but the ability of mild-to-moderate hypertension to produce renal insufficiency has been questioned. Nephrosclerosis, benign nephrosclerosis, and hypertensive kidney disease are terms that clinicians use when renal damage is thought to be secondary to essential hypertension. Many cases of end-stage renal disease are ascribed to so-called benign nephrosclerosis. This entity could actually be a primary renal disease affecting the preglomerular microvasculature, perhaps genetically mediated and ethnically influenced, and showing a heterogeneous clinical expression. African Americans suffer from nephrosclerosis more frequently than Caucasians. Nephrosclerosis affecting Caucasians seems to show a less aggressive pattern and could represent early age-related renal sclerosis. The risk of end-stage renal disease is increased when atherosclerotic lesions in large renal arteries coexist. Age, systolic blood pressure, proteinuria, and concomitant cardiovascular disease are well-known promoters of renal failure. A multifactorial strategy, including antihypertensive and antiproteinuric drugs, and lipid-lowering and anti-platelet agents, could improve cardiovascular and renal outcomes in patients with nephrosclerosis.

Síndrome nefrótico y estado de anasarca, secundario al tratamiento con tiopronina en un caso de cistinuria / Nephrotic syndrome and massive edema following treatment with tiopronin

OBJETIVO: Presentar un caso de síndrome nefrótico y estado de anasarca en paciente con cistinuria que estaba recibiendo tratamiento con tiopronina. MÉTODO: Analizar la cistinuria como causa rara de litiasis renal, así como su clínica, diagnóstico, uso de la tiopronina como una de las opciones terapéuticas, y posibles eectos secundarios de la misma. RESULTADOS: Nosotros presentamos un caso de síndrome nefrótico, con ascitis y fallo cardiaco asociados, en paciente con cistinuria, que había recibido tiopronina, y que evolucionó favorablemente poco tiempo después de su suspensión. CONCLUSIONES: Recomendamos monitorizar estrechamente la proteinuria en pacientes tratados con tiopronina, y disminuir la dosis o suprimirla, si apareciese (AU)

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