Previous attempts to maintain cultures of the
so - called
nephron progenitor cells often failed, as the cells died or gradually lost their developmental potential rather than staying in a more medically useful precursor state.
-RCB- elevated sodium level within kidneys, either as a result of pathological bottleneck such as reduced number of
nephrons, or simply due to heightened intake - or both - may activate pro-inflammatory cytokines and chemokines in proximal tubular cells, may cause oxidative stress by activating ROS - producing NADH oxidase enzymes, or blood vessel constriction by inhibiting kidney arginine transport and nitric oxide synthesis; elevated renal inflammation, oxidative stress and restricted blood flow all can impair the efficacy of sodium excretion, more
so combined (if extensive, it can also result in post-natal reduction of
nephron units)