Indian Journal of Anaesthesia

RESPONSE TO COMMENTS
Year
: 2018  |  Volume : 62  |  Issue : 4  |  Page : 325-

Reply to 'The link between pulmonary hypertension and adverse renal transplant outcome may be renal venous hypertension'


Sohan Lal Solanki1, Vipin Kumar Goyal2, Birbal Baj2,  
1 Department of Anaesthesiology, Critical Care and Pain, Tata Memorial Centre, Homi Bhabha National Institute, Mumbai, Maharashtra, India
2 Department of Anaesthesiology and Critical Care, Mahatma Gandhi Medical College and Hospital, Jaipur, Rajasthan, India

Correspondence Address:
Dr. Sohan Lal Solanki
Department of Anaesthesiology, Critical Care and Pain, 2nd Floor, Main Building, Tata Memorial Hospital, Parel, Mumbai-400012
India




How to cite this article:
Solanki SL, Goyal VK, Baj B. Reply to 'The link between pulmonary hypertension and adverse renal transplant outcome may be renal venous hypertension'.Indian J Anaesth 2018;62:325-325


How to cite this URL:
Solanki SL, Goyal VK, Baj B. Reply to 'The link between pulmonary hypertension and adverse renal transplant outcome may be renal venous hypertension'. Indian J Anaesth [serial online] 2018 [cited 2019 Sep 20 ];62:325-325
Available from: http://www.ijaweb.org/text.asp?2018/62/4/325/229796


Full Text



Sir,

We thank Dr. Grocott for the comment 'The link between pulmonary hypertension and adverse renal transplant outcome may be renal venous hypertension' on our recently published retrospective study.[1]

Mechanisms of development of delayed graft functioning (DGF) in patients with pulmonary hypertension (PH) by haemodynamic alterations and disturbances of vasoactive substances are well described in a study where thermodiffusion probes were inserted into the renal cortex of renal transplant recipients. Patients who developed DGF had evidence of lower renal microperfusion compared to patients with immediate graft function.[2],[3]

There is generally an inverse relationship between pulmonary artery systolic pressure and cardiac output. Furthermore, in most patients during the first 24–48 h after transplant, mean arterial pressure is maintained on higher side to assist with graft perfusion and this causes further stress on the pulmonary vasculature and perhaps, paradoxically, leads to low overall cardiac output and decreased renal perfusion.[3] Studies also showed that decrease in renal microperfusion may be, in part, the result of increased renovascular resistance from vasoconstriction.[4],[5]

So while we agree with the author's comment that DGF after renal transplant in patients having PH may be because of poor renal blood flow due to elevation in renal venous pressure that can result from PH-associated right ventricular dysfunction, it may not be the sole or principal cause of DGF in patients with PH.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

References

1Goyal VK, Solanki SL, Baj B. Pulmonary hypertension and post-operative outcome in renal transplant: A retrospective analysis of 170 patients. Indian J Anaesth 2018;62:131-5.
2Angelescu M, Kraus T, Wiesel M, Hergesell O, Haberkorn U, Klar E, et al. Assessment of renal graft function by perioperative monitoring of cortical microcirculation in kidney transplantation. Transplantation 2003;75:1190-6.
3Zlotnick DM, Axelrod DA, Chobanian MC, Friedman S, Brown J, Catherwood E, et al. Non-invasive detection of pulmonary hypertension prior to renal transplantation is a predictor of increased risk for early graft dysfunction. Nephrol Dial Transplant 2010;25:3090-6.
4Perico N, Cattaneo D, Sayegh MH, Remuzzi G. Delayed graft function in kidney transplantation. Lancet 2004;364:1814-27.
5Inman SR, Plott WK, Pomilee RA, Antonelli JA, Lewis RM. Endothelin-receptor blockade mitigates the adverse effect of preretrieval warm ischemia on posttransplantation renal function in rats. Transplantation 2003;75:1655-9.