The roles of sodium and volume overload on hypertension in chronic kidney disease

Abstract

Chronic kidney disease (CKD) is associated with increased risk of cardiovascular (CV) events, and the disease burden is rising rapidly. An important contributor to CV events and CKD progression is high blood pressure (BP). The main mechanisms of hypertension in early and advanced CKD are renin-angiotensin system activation and volume overload, respectively. Sodium retention is well known as a factor for high BP in CKD. However, a BP increase in response to total body sodium or volume overload can be limited by neurohormonal modulation. Recent clinical trial data favoring intensive BP lowering in CKD imply that the balance between volume and neurohormonal control could be revisited with respect to the safety and efficacy of strict volume control when using antihypertensive medications. In hemodialysis patients, the role of more liberal use of antihypertensive medications with the concept of functional dry weight for intensive BP control must be studied.

Association of serum creatinine to cystatin C to waist circumference ratios and hypertension: evidence from China health and retirement longitudinal study

“…An elevated level of CCR may suggest an increase in the GFR ( 35 – 37 ), which plays a pivotal role in maintaining fluid balance and regulating blood pressure ( 38 ). Enhanced GFR facilitates the effective excretion of sodium and waste, thereby aiding in the prevention of volume overload—a key contributor to the development of hypertension ( 39 ). Consequently, the heightened GFR, as indicated by an increased CCR, ostensibly lowers the risk of hypertension through effective fluid balance management and blood pressure regulation.…”

Recent updates in therapeutic approach using tolvaptan for autosomal dominant polycystic kidney disease

“…Based on the longterm open-label extension trial for patients who completed TEMPO 3:4, TEMPO 4:4, or REPRISE, representative symptoms such as thirst, polyuria, and nocturia were reduced following more prolonged exposure to the drug [34]. Osmolar excretion is the primary determinant of urine volume, and lowering dietary sodium intake helps reduce urine volume by reducing osmotic diuresis with active solutes [35][36][37][38]. Although the concomitant use of thiazides to reduce urine volume was considered based on a report on nephrogenic diabetes insipidus, there is insufficient evidence to support this hypothesis [39,40].…”

Therapeutic roles of thiazides and loop diuretics in blood pressure control and renal protection against chronic kidney disease

“…Therefore, early detection and proper management of hypertension are needed to reduce the risk of hypertension-related complications. Extracellular volume overload has been reported even in early stage of CKD [ 4 ]. However, a significant number of patients have subclinical volume overload without evident clinical signs [ 5 , 6 ].…”

“…However, a significant number of patients have subclinical volume overload without evident clinical signs [ 5 , 6 ]. Such existence of extracellular volume increase can be detected by noticing impressive blood pressure reduction when diuretics are added in a situation of uncontrolled hypertension during the use of antihypertensive agents other than diuretics [ 4 , 5 ]. Doubt on the effectiveness and safety related to use of diuretics in CKD patients has been present for many years.…”