A systematic review showed a significant reduction in the incidence of stone formation RR 0.26, 95% CI 0.10 to 0.68.It is also used as an alkalizing agent in the treatment of mild urinary tract infections, such as cystitis.It is also used in many soft drinks as a buffering agent.Frequently used in an aqueous solution with other potassium salts, it is a wet chemical fire suppressant that is particularly useful against kitchen fires. Its alkaline pH encourages saponification to insulate the fuel from oxidizing air, and the endothermic dehydration reaction absorbs heat energy to reduce temperatures. Administration
Potassium citrate is usually administered by mouth in dilute aqueous solution, because of its somewhat caustic effect on the stomach lining, and the potential for other mild health hazards. References
External links
Tanner, G.A. "Potassium citrate improves renal function in rats with polycystic kidney disease". Journal of the American Society of Nephrology. Retrieved December 17, 2016.
White blood cells may also bind to the endothelium of small capillaries, obstructing them and leading to more ischemia.Reperfusion injury plays a major part in the biochemistry of hypoxic brain injury in stroke. Similar failure processes are involved in brain failure following reversal of cardiac arrest; control of these processes is the subject of ongoing research. Repeated bouts of ischemia and reperfusion injury also are thought to be a factor leading to the formation and failure to heal of chronic wounds such as pressure sores and diabetic foot ulcer. Continuous pressure limits blood supply and causes ischemia, and the inflammation occurs during reperfusion. As this process is repeated, it eventually damages tissue enough to cause a wound.The main reason for the acute phase of ischemia-reperfusion injury  is oxygen deprivation and, therefore, arrest of generation of ATP (cellular energy currency) by mitochondria oxidative phosphorylation. Tissue damage due to the general energy deficit during ischemia is followed by reperfusion (increase of oxygen level) when the injury is enhanced. Mitochondrial complex I is thought to be the most vulnerable enzyme to tissue ischemia/reperfusion but the mechanism of damage is different in different tissues. For example brain ischemia/reperfusion injury is mediated via complex I redox-dependent inactivation. It was found that lack of oxygen leads to conditions in which mitochondrial complex I loses its natural cofactor, flavin mononucleotide (FMN) and become inactive. When oxygen is present the enzyme catalyzes a physiological reaction of NADH oxidation by ubiquinone, supplying electrons downstream of the respiratory chain (complexes III and IV).