Renal Pathophysiology

CHAPTER 11 Acute Kidney Injury


Recovery requires the regeneration of tubular cells, mediated in part by the activation of growth response genes and the release of growth factors. The recovery process can be accelerated in experimental animals; for exam ple, the administration of insulin-like growth factor I or epidermal growth factor can enhance tubular regeneration and the rate of improvement in re nal function. However, as with other experimental treatment options for AKI, growth factor trials in human AKI have been disappointing and not currently utilized. Assuming that the underlying insult has been removed or corrected, the GFR rises and, as a result of the increased filtered creatinine load, the plasma creatinine concentration begins to fall within 3 to 21 days. The in terval is shorter with a mild, self-limited injury and longer with a severe and persistent injury. For example, patients with continued infection may have recurrent episodes of renal ischemia and prolonged renal injury, whereas pa tients with uncomplicated contrast nephropathy typically show peak creati nine concentrations at 3 to 5 days and then begin to improve. Recovery of renal function is usually preceded by a progressive in crease in urine output, which is an indicator of the enhanced number of functioning nephrons. Most patients return to their previous baseline plasma creatinine concentration, although careful measurements of GFR will often reveal some degree of permanent injury. Episodes of AKI can lead to the development of CKD, and CKD is a risk factor for developing AKI. What remains to be determined is whether an episode of AKI in a patient with CKD accelerates the decline in GFR after the AKI resolves. Furthermore, it remains unknown how the different etiologies of AKI affect the subsequent renal course. In patients with prolonged ATN ( > 6 weeks), only partial recovery may be seen and some will remain dialysis dependent. AKI is common in hospitalized patients and is associated with adverse outcomes. Patients with AKI are usually identified by decreased urine output and/or in creased serum creatinine (although exact definitions vary). The differential diag nosis of AKI includes disorders of the collecting system and bladder (postrenal); conditions that result in renal hypoperfusion (prerenal); and intrinsic diseases that affect glomeruli, tubules, or blood vessels. The approach to the patient with AKI is to identify the timing of the likely injury, and in combination with clinical scenario, urinalysis findings, and other laboratories, the etiology can usually be identified. Unfortunately, only supportive measures are currently available to manage AKI, but high-risk situations can often be anticipated (patients with ex isting CKD, hemodynamic instability, exposure to contrast agents, surgery, and specific nephrotoxic medications). SUMMARY

CHAPTER 11 Acute Kidney Injury

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