ABSTRACT
Renal tubular acidosis (RTA) is a hyperchloremic metabolic acidosis characterized by a normal anion gap due to reduced urinary acidification.Multiple mechanisms act in the renal tubule to maintain balance in hydrogen ion secretions and bicarbonate absorption.In recent years,more and more proteins have been found to be associated with RTA,so hereditary RTA has attracted people's attention.Mutations in the gene SLC4A1,encoding C1-/HCO3-exchanger (kAE1);in the gene ATP6V1B1,encoding B1 subunit of H+-ATP ase;in the gene ATP6V0A4,encoding a4 subunit of H +-ATP ase;in the gene SLC4A4,encoding Na+/HCO3-cotransporter(kNBCe1);in the gene CA2,encoding carbonic anhydrase Ⅱ are identified in the pathogenesis of hereditary RTA.The search for pathogenetic genes for clinically suspected hereditary RTA patients can help us to make accurate genetic diagnosis and provide targeted treatment interventions.
ABSTRACT
Objective To elucidate the role of renal progenitor-like tubular cells in the repair process after acute tubular necrosis(ATN)induced by ischemia. Methods Rat ATN was developed by clamping left kidney artery for 60 minutes,and bromodeoxyuridine(BrdU),a cell division and proliferation marker,was administrated one hour before rats were sacrificed.Kidneys were isolated at 1,3,5,7,14,21,28 days after injury.The proliferative and apoptotic cells were determined by immunostaining using anti-BrdU,Pax2(an embryonic renal marker),vimentin(an immature mesenchymal cell marker),and activated caspase-3(a cell apoptosis marker). Results Cell death was found in tubules at day 1 after ischemia and reperfusion injury.BrdU-positive cells were dramatically increased and reached peak at day 3 after injury.In addition,the number of BrdU positive cells in the contralateral kidney was significantly increased compared to sham operated group.Double immunostaining showed that BrdU-positive cells co-expressed Pax2 or vimentin,but not activated caspase-3. Conclusions Renal progenitor-like tubular cells may play a predominant role in repair process following ATN in rats.They may dedifferentiate,proliferate,and then redifferentiate into mature tubular cells.Growth factors may regulate the repair process.