COVID-19 Sequalae and Formation of Kidney Stone by Decrease in Mitochondrial Sulfur Metabolism Transsulfuration and Hyperuricemia during CKD

Post severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2, Covid-19) sequalae’s, immune and RNA based treatments are associated with the development of micro-stones and chronic kidney disease (CKD). In addition, circulating cytokines cocktail and viral envelope spike protein (SP) instigates CKD. During epigenetic regulation, Covid-19 methyltransferase (MT) methylates the DNA/RNA/Proteins/Histones and generates homocysteine (Hcy). Although cysteine promotes the growth and aggregation of calcium oxalate crystals in normal undiluted human urine. However, during elevated levels of Hcy (i.e., hyperhomocysteinemia, HHcy) due in part to the impaired transsulfuration (i.e., mitochondrial sulfur metabolism) pathways, homocysteine is the only sulfur-denoting non-protein amino acid may promote crystals. HHcy is associated with severity of Covid-19 infection and pneumonia post Covid-19. It is unclear however whether the HHcy facilitates homocysteine crystals. Although an E. coli strain degrades tricarboxylic acid (TCA, citric acid), and disrupts mitochondrial TCA cycle, to dicarboxylic acid (DCA, oxalic acid), DCA also promotes calcium oxalate crystals and may contributes to kidney stones, it is unclear whether gut-dysbiosis by Covid-19 infection contributes to kidney stones. There is robust succinylation of enzymes in TCA cycle which causes dysfunctional mitochondrial bioenergetics during Covid-19 infection. In this regards interaction between SIRT5 and mitochondrial transsulfuration during Covid-19 infection attenuates TCA cycle. Interestingly, the mitochondrial bioenergetics though sulfur metabolism participate in TCA cycle and epigenetic acetylation/succinylation, therefore, Covid-19 infection transition acute kidney injury (AKI) to CKD by defective mitochondria sulfur metabolism (transsulfuration) pathways, forming uricemia micro stones.