الفهرس 
Pathophysiology of HTN in CKDOnly 14 pages are availabe for public view
 |  | from | 122 |  |  |
| | | from | 122 | | |
Abstract
Hypertension is highly prevalent in CKD and increases progressively as kidney function declines. The pathogenesis of hypertension in CKD is complex and multifactorial. Sodium and fluid retention and salt sen¬sitivity, sympathetic dysfunction and abnormalities in endothelial function are the prominent features which contribute to hypertension, and which potentiate the hypertensive effects of other factors.
Hypertensive crisis is usually defined as an acute and severe increase in SBP greater than or equal to 180 mm Hg or a DBP greater than or equal to 120 mm Hg Hypertensive crises have been further subdivided into hypertensive urgencies and emergencies.
Hypertensive emergency is the severe increase in BP which is associated with new or progressive end-organ damage and is a true emergency requiring immediate BP control usually over the course of minutes to hours. Hypertensive urgency is the severe increase in BP which is not associated with end-organ damage. It is not an emergency, and, contrary to its name, the BP does not require urgent reduction most of the time but instead can be reduced over the course of hours to days.
The overall acute increase in BP in hypertensive crisis is thought to result from an abrupt increase in SVR that occurs from an acute increase in humoral vasoconstrictors in conjunction with a failure of the normal autoregulatory function. This abrupt increase in SVR causes an increase in mechanical stress on the vascular wall resulting in endothelial injury and vascular permeability.
It is important to remember that, during the clinical assessment, regardless of the BP measurement, the emphasis remains on determining whether end-organ damage is present. The differentiation between hypertensive urgency and emergency using the encounter history, physical examination, and additional work-up options is vital because it determines the goals of treatment, including whether or not the patient should be transferred to the emergency department (ED).
Therapy can be initiated with fast and short-acting oral medications such as clonidine, captopril, labetalol, or nicardipine with a definitive plan to transition to longer acting antihypertensives that are more suitable for chronic therapy.
The goal after the exclusion of end-organ damage is to gradually reduce the BP over the next 24 to 48 hours to a more pathophysiologic safe level, generally defined as less than or equal to 160/95 mm Hg. There is rarely a compelling reason to treat hypertensive urgency with intravenous medications because safe and effective treatment can usually be accomplished using common oral medications.
Patients with evidence or high suspicion for end-organ damage (hypertensive emergency) should be referred from the outpatient setting to the ED because a rapid BP reduction over minutes to hours is often indicated to prevent additional end-organ damage. This need for immediate but controlled BP management usually indicates the requirement for monitoring in a critical care setting.
Several rapid-acting intravenous antihypertensive agents are available for the treatment of hypertensive emergencies and the choice of which agent to use is mainly related to the clinical manifestations of end-organ damage. Antihypertensive treatment should be individualized, taking into consideration factors such as comorbidities, and albuminuria.
In general, the BP should be reduced no more than 25% within the first hour and then to 160/100 to 110 mm Hg within 2 to 6 hours. An alternative and more conservative approach is to reduce the BP approximately 10% in the first few hours and then by no more than 25% during the first 24 hours.
Ongoing treatment of HTN in patients with CKD and type 1 diabetes with macroalbuminuria can be achieved using ACEI which reduce albuminuria and slow the decrease in GFR and onset of kidney failure. ARBs have the same efficacy as ACEI so, they can be used as an alternative in patients who do not tolerate ACEI.
In patients with CKD and type 2 diabetes with macroalbuminuria, ARBs are superior over other antihypertensive drugs in slowing progression of kidney disease.