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

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.[23]

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.[45]

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.

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