It has been shown that in states where dietary fiber intake is low, as it holds true in CKD, the expansion of proteolytic bacteria may lead to a degradation of the goblet cell-derived mucin 2 (MUC-2) layer, which under normal circumstances facilitates the nutritional transit by lubricating the gut’s surface. A slower transit time affects uremic toxin generation by increasing the availability of amino acids to be fermented by proteolytic bacteria [118, 119]. Here, MUC2 is linked to chronic kidney disease.