Reducing the incidents of infectious disease is one of the most critical challenges of post-transplant kidney care. Such incidents can be directly linked to the change in gut microbiome diversity. Gene sequencing of the gut microbiome has shed light on some previously unexplainable dynamics of immunosuppressive medication effectiveness. All investigations point out to the fact that gut microbiota has a critical role in the development of post-transplant complications (Xiao et. al; 2018).

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Studies conclude that dysbiosis in the gut microbiome leads to an increased risk of post-transplant infection (ibid).  Imbalance in the gut microbiota is associated with increased risk of graft failure in renal transplants by influencing the dosing of immunosuppressants (Zaza et al., 2017).  For example, Fecal Faecalibacterium Prausnitzii abundance in the first week of transplantation is positively associated with higher Tacrolimus dosing at 1 month (Lee et al., 2014).  Other studies have also observed the role of gut microbiome in the prognosis of kidney transplant outcomes (Ardalan et al., 2017;  Ahmad et al., 2016; Fricke et al., 2014).  Ardalan et al. reported that gut dysbiosis causes accumulation of uremic toxins, systemic inflammation, and infection that influence the pathogenesis of acute kidney injury, chronic kidney disease, emergence of infection, changes in drug metabolism and graft rejection (Ardalan et al., 2017).  Dysbiosis can be caused by immunosuppression and antimicrobial therapies, ischemia-reperfusion (I/R) injury, and dietary restrictions (ibid). ​