FLUID OVERLOAD IN CHRONIC KIDNEY DISEASE (CKD)

In end-stage renal disease (ESRD), the reduced ability of the kidneys to excrete urine results in water being retained by the patient, leading to fluid overload.

The accumulation of excess fluid in the body (referred to variously as ’chronic volume’ or ‘fluid overload’, ‘overhydration’ or ‘hypervolemia’) leads to an increase of interstitial fluid (that bathes and surrounds the cells).

Hypertension as comorbid condition
In the absence of adequate kidney function, but with sufficient cardiac function, the fluid that accumulates in the blood vessels may lead to ‘secondary hypertension’ (high blood pressure), a comorbid condition that affects the vast majority of patients with CKD. Persistent volume-dependent hypertension can also lead to ‘left ventricular hypertrophy’ (LVH) and congestive heart failure. Cardiovascular disease-related complications affect almost every other patient with CKD.

Complications
Patients with chronic kidney disease (CKD 5) require renal replacement therapy (dialysis or transplantation) to sustain life and to remove not only accumulated uremic toxins but also excess fluid which is removed by the process of ‘ultrafiltration’.

The removal of excess fluid during dialysis by ultrafiltration, may itself lead to complications: ‘intradialytic hypotension’ – occurring in up to 20 % of all hemodialysis sessions – is a major cause of morbidity and vascular complications.

Intradialytic Hypotension
Hypotension – abnormally low blood pressure – during dialysis is usually the result of too fast or non adequate removal of excess fluid via ultrafiltration.


Summary

Chronic fluid overload in dialysis patients is a two-edged sword – with hypertension and cardiac hypertrophy being one edge and intradialytic hypotension, primarily due to high ultrafiltration rates, being the other.

“Chronic overhydration contributes to the development of left ventricular hypertrophy and a high cardiovascular mortality in end-stage renal disease.”

Source:
Kuhlmann MK, Zhu F, Seibert E, Levin NW
Curr Opin Nephrol Hypertens. 2005 14(6) 543- 549