Classically the course of ischemic ATN has been divided into 3 phases initiation, maintenance, and recovery. During the initiation phase, immediately following the insult, sublethal cellular injury occurs, with loss of cell polarity and brush border. The maintenance phase is reached after the irreversible renal parenchymal injury has been established. During the last 2 phases, both<unk>  cell death and cell regeneration occur simultaneously. Apoptosis has been reported in the initial phase of<unk><unk>  necrosis and during the recovery phase. With initial ischemic or cytotoxic injury, a number of<unk>  cells may undergo apoptosis. The ET-1 gene has also been shown to be upregulated during ischemic injuries. When exposed to ischemic stress,<unk>  cells are prone to loss polarity and even detachment of viable cells due to the disruption of key structural anchors. Several important proteins are required for<unk>  cells to maintain their structure and polarity including the actin cytoskeleton, microvilli, and junctional complexes such as tight junctions and adherents junctions.
Acute tubular necrosis pathophysiology
Renal papillary necrosis pathophysiology
Acute kidney injury pathophysiology
Contrast induced nephropathy pathophysiology
Interstitial nephritis pathophysiology
Analgesic nephropathy pathophysiology
Contrast induced nephropathy risk factors
Renal papillary necrosis causes