Lesäo renal na hipertensäo essencial / Renal damage in essential hypertension

Na última década, a incidência de insuficiência renal crônica terminal atribuída à hipertensão tem aumentado significativamente. Esse aumento parece paradoxal, uma vez que o melhor controle da pressão arterial, nesse período, tem levado à diminuição na incidência de hipertensão maligna e a outras complicações da hipertensão, como acidentes vasculares cerebrais e infarto do miocárdio. Evidências atuais apontam a hipertensão arterial como fator de risco independente para o desenvolvimento de insuficiência renal crônica terminal. O mecanismo pelo qual a hipertensão pode lesar o rim ainda não foi completamente definido. Dois mecanismos são propostos para explicar o desenvolvimento de insuficiência renal na presença de hipertensão: 1) isquemia glomerular devido ao progressivo estreitamento vascular; e 2) esclerose glomerular devido à perda da auto-regulação renal e transmissão da hipertensão sistêmica para o capilar glomerular. Na prática, o diagnóstico de nefroesclerose hipertensiva é difícil e, em geral, é feito excluindo clinicamente outras causas de insuficiência renal. Como nefroesclerose, doença primária renal, aterosclerose de artérias renais e microembolização do colesterol podem apresentar quadro clínico similar, a prevalência de nefroesclerose pode ser superestimada. Entretanto, uma fração importante dos pacientes hipertensos pode desenvolver nefroesclerose efetivamente e esse número tende a aumentar com a melhora da sobrevida dos hipertensos.

Inappropriately high plasma renin activity accompanies chronic loss of renal function.

Stimulation of both the systemic and local renin-angiotensin systems participates in the pathogenesis of tissue injury observed in experimental renal disease. However, substantial information demonstrating excessive activation of the renin-angiotensin system in patients with chronic renal disease is not available in spite of the well-established role of this system in the progression of renal damage. This investigation examined the plasma renin activity (PRA) and the ratio of this parameter to the simultaneously measured glomerular filtration rate (PRA/GFR) in normal volunteers (mean values 3.2 ng/ml/h and 3.0 ng/ml/h/100 ml GFR, respectively) and in patients with chronic renal disease (1.6 ng/ml/h and 28.5 ng/ml/h/100 ml GFR, respectively). A mean tenfold increase in the PRA/GFR ratio was observed in patients with chronic renal disease as compared to normal volunteers. The observed augmentation in PRA was not caused by physiologic mechanisms aimed at conserving urinary sodium since a positive correlation was found between PRA/GFR and the fractional excretion of sodium (y = 2.75 + 2.23x; r = 0.781, p < 0.01), as opposed to that of normal controls (y = 5.3 - 1.46x; r = -0.640, p < 0.01). Consequently, our results support the existence of inappropriate activation of the renin-angiotensin system in humans with chronic renal disease. Such stimulation might play a critical role in the pathophysiology of advanced renal injury.

Rarity of hypertensive stigmata in aging renocortical arteries of Bolivians.

Numerous reports have accumulated from around the world throughout the twentieth century of small, remote, self-sufficient populations that do not show a rise of blood pressure with age. Knowing that renocortical arteriosclerosis, a defining feature of hypertensive nephrosclerosis, is a close commensurate of blood pressure, it can be predicted that the elderly members of such populations should fail to show arteriosclerosis of hypertensive degree in the renal cortex. Emigrants from such populations sometimes come to medical attention in places like La Paz, Bolivia. Reported here are findings in autopsy samples of kidney tissue examined in La Paz. These samples have revealed remarkably little renovasculopathy at all ages up to 80 years, a phenomenon that has not previously been observed. Because of these findings, it can now be seen as biologically possible for a whole population of elderly persons to avoid renovasculopathy of hypertensive degree, and by implication, perhaps never experience hypertensive cardiovascular disease.