LVAD & Kidney Dysfunction: The Chicken & the Egg

This is part 2 of a blog on LVAD for the nephrologist. Part 1 may be found here.

Predicting reversibility of renal dysfunction is a difficult task in the setting of heart disease and has a significant effect on patient prognosis. Patients with low GFR may have their kidney function improved after LVAD implantation due to an increase in kidney perfusion. Or it may continue to be poor due to pre-existing intrinsic kidney disease. 

• Some studies show that patients with low GFR prior to LVAD had initial improvement in creatinine but a gradual decline in GFR over the next several months. Despite this, GFR at one year was still more than the pre-LVAD level. Interestingly patients with normal pre-LVAD GFR had a small but steady decline in kidney function after the implantation. Probable reasons for the late decline in kidney function could due to a measurement bias (less muscle mass at the time of LVAD surgery, so low creatinine levels post LVAD, muscle mass improves with rise in creatinine), hemolysis or RV dysfunction (seen in up to 10 % patients post–LVAD). 
• Another unique possibility is an effect of continuous flow physiology on renal vessel walls (animal studies show arterial smooth muscle hyperplasia, periarteritis and interstitial inflammation & fibrosis; no human data). Bresco et al, demonstrated an unexpected survival analysis based on GFR change in first month of LVAD implantation. They showed that patients who had greater than 88 % rise in GFR within one month had a poor survival rate, followed by patients with any degree of worsening of kidney function after LVAD implantation. The best survival was in patients with modest GFR improvement (22-47%). One possible explanation for this could be that patients who are severely ill prior to LVAD are likely to be those with worse kidney function. Could they then have a larger improvement in kidney perfusion and therefore kidney function, in the early post LVAD period?

Dialysis Post LVAD:

The incidence of AKI varies between studies, ranging from 7 to 56%, possibly due to different definitions of AKI, severity of underlying of cardiac & kidney disease, and has an adverse impact on patient survival post-LVAD. Patient with AKI also have poor bridge to transplantation rates (52.4 %vs 83.5 %).

LVAD implantation in the ESRD population has an even worse prognosis, with one recent study describing a mortality rate of 81.9 % compared to 36.4 % in a non-ESRD group after a median follow up of over 2 years. Does this preclude patients with advanced renal failure from LVAD implantation? Combined heart-kidney transplantation may be a viable option for some, and for those who do not have recovery of kidney function after LVAD-associated AKI.

Dialysis options in patients with LVAD include HD & PD. There are no head to head trials comparing the two. PD appears more attractive in my view as it offers more gentle ultrafiltration, less risk of systemic infections and it`s a home modality which keeps the infection prone LVAD patients away from hospital. Very few case reports of PD in LVAD have been published which described successful dialysis in these patients. A couple of practical aspects about PD in this setting:

• imaging of the abdomen should be done prior to PD catheter insertion to confirm that no element of LVAD is intra peritoneal
• PD catheter exit site should be far away from the drive line exit site.

HD is the most frequently used dialysis modality in this population.  There are case reports of all forms of HD done in these patients-regular HD, CRRT and even home HD. Access is an important issue to be discussed. 

• For catheter insertion, we need to remember not to reverse the anticoagulation in these patients. The person doing the cannulation should be trained to do the intervention in a fully anticoagulated individual. It's always prudent to use fluoroscopy for these procedures as it reduces the risk of complications, like a guide wire inadvertently damaging the VAD pump. It's important to perform the procedure under aseptic conditions and avoid bedside procedures. Tunneled catheters are preferred in this regard as they are associated with less risk of infections. If we are forced to do the cannulation without fluoroscopy guidance, it`s preferable to use a short guide wire (10-12 cm).
• Long term access should be a fistula or graft if possible. There are no direct studies comparing these 2 accesses. While the initial preference was for graft due to concerns of poor fistula maturation with the continuous flow, there are published cases of patients who had successful fistula creation while on LVAD. Of the 6 cases described, 2 of them required balloon assisted maturation and the other 4 had unassisted maturation which were successfully cannulated. The more difficult aspect of long term access is a thrill or bruit cannot be appreciated in these patients. The only way of assessing patency of the access is with the help of Doppler or direct cannulation.
• Very few case series of patients on HD have been described. One of them included 10 patients who underwent 281 sessions of HD after post-LVAD AKI. 15 of these sessions were interrupted with symptomatic hypotension being the reason in 6 instances (3 catheter related blood stream infections; 3 volume related).
• Dialysis centres accepting patients on LVAD for HD should have their nurses and doctors trained to interpret the basic LVAD parameters and make necessary changes to hemodialysis prescription accordingly. Specifics about BP measurement were described in part 1 of this post.

The increasing number of patients with LVADs definitely poses a challenge to the Nephrologist. Learning about the device parameters and monitoring is fast becoming essential for us to manage these patients. More research is warranted to understand the implications of this extraordinary treatment for renal function and provision of renal replacement therapy.

Post by Sriram Sriperumbuduri