title: Mechanisms of repair after kidney injury.
abstract: Kidney injury is repaired by inflammatory and non-inflammatory mechanisms, with the extent of recovery based on severity of the insult. Critical to the assessment of kidney repair is the ability to differentiate functional recovery from structural repair: compensatory increases in the function of intact residual nephrons often mask the inability of the kidney to heal or replace damaged structures. The mechanisms of repair reflect three levels of injury, which are handled differently by the kidney. First, DNA damage is countered by proof-reading DNA polymerases, backed by other controls for sequence misalignment/nucleotide replacement. If DNA cannot be repaired, cells harboring mutation(s) are lost through apoptosis, which is also critical to the disposal of kidney cells and infiltrating leukocytes in both acute and chronic ischemic, immunological, or chemical damage. This leaves room for a second mechanism of repair, i.e., cellular proliferation. At least 5 types of reparative proliferation are known to occur, some of which involve stem cell differentiation and perhaps immigration from distant reservoirs. The final type of repair is referred to as structural repair, actually quite limited by lack of postnatal nephrogenesis in the human kidney. Certain forms of recovery after acute tubular necrosis involve extensive remodeling of the proximal tubule, where integrity of the basement membrane is required for successful repair. Contrary to the long-held belief that only acute injury can be repaired, while ongoing chronic damage leads to progressive nephron loss, evidence is emerging that some degree of renal remodeling occurs even in the presence of persistent structural changes.
authors.affiliation: Department of Clinical Sciences, Division of Nephrology, University of Rome La Sapienza, 00161 Rome, Italy. Paolo.Mene@uniroma1.it
authors.forename: Paolo
authors.initials: P
authors.lastname: Menè
authors.forename: Rosaria
authors.initials: R
authors.lastname: Polci
authors.forename: Francescaromana
authors.initials: F
authors.lastname: Festuccia
mesh_terms: D058186:Acute Kidney Injury / Q000503:physiopathology*; D000222:Adaptation, Physiological; D017209:Apoptosis / Q000502:physiology*; D002454:Cell Differentiation; D002455:Cell Division / Q000502:physiology; D004249:DNA Damage / Q000502:physiology; D005260:Female; D006801:Humans; D007668:Kidney / Q000293:injuries* / Q000503:physiopathology; D007683:Kidney Tubular Necrosis, Acute / Q000503:physiopathology*; D008297:Male; D012038:Regeneration / Q000502:physiology*; D012680:Sensitivity and Specificity