Renal and Electrolyte Disorders by Robert W. Schrier

Renal and Electrolyte Disorders by Robert W. Schrier

Author:Robert W. Schrier [Schrier, Robert W.]
Language: eng
Format: azw3
Publisher: Wolters Kluwer Health
Published: 2017-06-12T16:00:00+00:00


Conclusions

It is apparent that the kidney is both the villain and the victim in hypertension. The kidney has a central role in the pathogenesis of both essential hypertension and secondary hypertension caused by primary renal parenchymal disease, renal artery stenosis, and mineralocorticoid excess. Analysis of rare mendelian causes of hypertension has provided convincing evidence that abnormal renal sodium handling plays a central role in the pathogenesis of hypertension. Ongoing genetic linkage analysis studies may provide additional insights into the pathogenesis of essential hypertension and hopefully lead to the development of novel treatments to ameliorate the impairment in natriuretic capacity that characterizes both primary and secondary hypertension of all causes (16). At present, there is little hard evidence to support the widely held notion that benign essential hypertension is a common cause of ESRD although it is an important risk factor for cardiovascular disease and needs to be treated aggressively. Recent data indicate genetic disposition among black individuals for kidney disease associated with hypertension and suggest that hypertensive nephrosclerosis is a multifactorial disease. Although essential, hypertension by itself is not a likely cause of ESRD. Without question, hypertension does play a critical role in accelerating the progression of CKD. Rigorous control of BP with a regimen including an ACE inhibitor or ARB has been shown to slow the progression of both diabetic and nondiabetic renal disease. Large outcome trials have produced conflicting results regarding the utility of different classes of antihypertensive agents for reduction in cardiovascular mortality but confirm the importance of blood control as a general public health strategy (207, 209).



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