Acute kidney injury pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Farima Kahe M.D. [2]

Overview

Acute kidney injury is defined as spontaneous deficit in kidney functions leading to urea retention and electrolyte imbalance. Etiologies of AKI can be divided based on pathophysiologic mechanisms into 3 broad categories: prerenal, intrinsic renal, and postrenal causes. Pre-renal AKI is most common and typically results from hypovolemia. Intrinsic renal is due to damage to renal paranchyma. Post-renal AKI is usually result of an obstruction, may be due to stones or strictures.

Pathophysiology

Physiology

Etiologies of AKI can be divided based on pathophysiologic mechanisms into 3 broad categories: prerenal, intrinsic renal, and postrenal causes.


Prerenal AKI

  • Prerenal AKI, known as prerenal azotemia, is by far the most common cause of AKI representing 30-50% of all cases.
  • It is provoked by inadequate renal blood flow commonly due to decreased effective circulating blood flow.
  • This causes a decrease in the intraglomerular hydrostatic pressure required to achieve proper glomerular filtration.
  • As such, the pathophysiology of prerenal azotemia entails a drop in renal plasma flow beyond the capacity of autoregulation, a blunted or inadequate renal compensation for an otherwise tolerable change in perfusion, or a combination of both.
  • This eventually leads to ischemic renal injury particularly to the medulla which is maintained in hypoxic conditions at baseline.
  • Causes of prerenal injury are summarized in the figure below. To note, as prerenal AKI progresses with further ischemia, it transforms into acute tubular necrosis (ATN) crossing into the realm of intrinsic AKI.

Intrinsic Renal AKI

Intrinsic renal AKI generally occurs due to renal parenchymal injury and may be classified according to the site of injury into: glomerular, tubular, interstitial, and vascular.

Tubular AKI

Sepsis
Nephrotoxins
Contrast-induced Nephropathy
  • Contrast induced nephropathy (CIN) recently called contrast induced AKI (CIAKI) is also major cause of intrinsic injury caused by iodinated contrast media used in cardiovascular imaging.
  • This entity is virtually non-existent in healthy young individuals.
  • Risk factors that increase susceptibility to CIN include advanced age, pre-existing CKD, diabetic nephropathy, severe heart failure, and concomitant exposure to other nephrotoxins.
    • The pathophysiology of CIN is not clearly understood; however, several attempts have been made to explain the underlying mechanism.
    • It is generally agreed that CIN is due to a combination of several influences brought on by contrast-media infusion rather than a single process.
    • The most important mechanism thought to be involved in CIN is a reduction in renal perfusion at the level of the microvasculature leading to tubular damage.
    • This is attributed to several alterations in the renal microenvironment including activation of the tubuloglomerular feeback, local vasoactive metabolites including adenosine, prostaglandin, NO, and endothelin as well as increased interstitial pressure.
    • Studies have also proposed injury to renal tubular cells may occur via a direct cytotoxic effect of the contrast media and via reactive oxygen species production.[13]

Glomerular AKI

Vascular AKI

Interstitial AKI

Postrenal AKI

Genetics

There is no genetics associated with AKI.

Associated Conditions

Gross Pathology

  • On gross pathology, characteristic findings for AKI are not present.

Microscopic Pathology

  • On microscopic histopathological analysis, characteristic findings of AKI depends on the etiology of disease.

References

  1. Loutzenhiser R, Griffin K, Williamson G, Bidani A (2006). "Renal autoregulation: new perspectives regarding the protective and regulatory roles of the underlying mechanisms". Am J Physiol Regul Integr Comp Physiol. 290 (5): R1153–67. doi:10.1152/ajpregu.00402.2005. PMC 1578723. PMID 16603656.
  2. Badr KF, Ichikawa I (1988). "Prerenal failure: a deleterious shift from renal compensation to decompensation". N Engl J Med. 319 (10): 623–9. doi:10.1056/NEJM198809083191007. PMID 3045546.
  3. Cupples WA, Braam B (2007). "Assessment of renal autoregulation". Am J Physiol Renal Physiol. 292 (4): F1105–23. doi:10.1152/ajprenal.00194.2006. PMID 17229679.
  4. Herbaczynska-Cedro K, Vane JR (1973). "Contribution of intrarenal generation of prostaglandin to autoregulation of renal blood flow in the dog". Circ Res. 33 (4): 428–36. PMID 4355037.
  5. Winkelmayer WC, Waikar SS, Mogun H, Solomon DH (2008). "Nonselective and cyclooxygenase-2-selective NSAIDs and acute kidney injury". Am J Med. 121 (12): 1092–8. doi:10.1016/j.amjmed.2008.06.035. PMID 19028206.
  6. Arendshorst WJ, Brännström K, Ruan X (1999). "Actions of angiotensin II on the renal microvasculature". J Am Soc Nephrol. 10 Suppl 11: S149–61. PMID 9892156.
  7. Abuelo JG (2007). "Normotensive ischemic acute renal failure". N Engl J Med. 357 (8): 797–805. doi:10.1056/NEJMra064398. PMID 17715412.
  8. Bonventre JV, Weinberg JM (2003). "Recent advances in the pathophysiology of ischemic acute renal failure". J Am Soc Nephrol. 14 (8): 2199–210. PMID 12874476.
  9. Conger JD, Weil JV (1995). "Abnormal vascular function following ischemia-reperfusion injury". J Investig Med. 43 (5): 431–42. PMID 8528754.
  10. Devarajan P (2006). "Update on mechanisms of ischemic acute kidney injury". J Am Soc Nephrol. 17 (6): 1503–20. doi:10.1681/ASN.2006010017. PMID 16707563.
  11. Bonventre JV (2010). "Pathophysiology of AKI: injury and normal and abnormal repair". Contrib Nephrol. 165: 9–17. doi:10.1159/000313738. PMID 20427950.
  12. Choudhury D, Ahmed Z (2006). "Drug-associated renal dysfunction and injury". Nat Clin Pract Nephrol. 2 (2): 80–91. doi:10.1038/ncpneph0076. PMID 16932399.
  13. Wong PC, Li Z, Guo J, Zhang A (2012). "Pathophysiology of contrast-induced nephropathy". Int J Cardiol. 158 (2): 186–92. doi:10.1016/j.ijcard.2011.06.115. PMID 21784541.
  14. Erwig LP, Rees AJ (1999). "Rapidly progressive glomerulonephritis". J Nephrol. 12 Suppl 2: S111–9. PMID 10688410.
  15. Chen YX, Chen N (2013). "Pathogenesis of rapidly progressive glomerulonephritis: what do we learn?". Contrib Nephrol. 181: 207–15. doi:10.1159/000348633. PMID 23689582.
  16. Naesens M, Kuypers DR, Sarwal M (2009). "Calcineurin inhibitor nephrotoxicity". Clin J Am Soc Nephrol. 4 (2): 481–508. doi:10.2215/CJN.04800908. PMID 19218475.
  17. 17.0 17.1 Ruggenenti P, Noris M, Remuzzi G (2001). "Thrombotic microangiopathy, hemolytic uremic syndrome, and thrombotic thrombocytopenic purpura". Kidney Int. 60 (3): 831–46. doi:10.1046/j.1523-1755.2001.060003831.x. PMID 11532079.
  18. Michel D and Kelly C. Acute Interstitial Nephritis. JASN 1998; 9(3): 506-515.
  19. Patel TV, Kumar S, Singh AK (2007). "Post-renal acute renal failure". Kidney Int. 72 (7): 890–4. doi:10.1038/sj.ki.5002301. PMID 17495862.

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