Acute Tubular Necrosis and Glomerulonephritis

Acute tubular necrosis (ATN) is a condition resulting from tubular cell apoptosis contributing to renal failure (1-3). It can result due to insult from extensive injury such as acute blood loss or septic shock, a specific renal disease such as glomerulonephritis, nephrotoxic drugs or bacterial products, or hypoxia (1-3).

ATN is identified via a rising serum urea creatinine and can be classified as pre-renal, renal or post-renal (1). If identified early, corrective action can stop damage and possible hyperkalemia (1).

Managing ATN includes caring for patient by replacing extra cellular fluid when necessary, controlling an underlying infection that may be cause, monitoring body fluid volume closely and via dialysis (1). Recovery involves three phases: initial oliguric phase (impairment), diuretic phase (high-urine output) and recovery phase (return of complete renal function) (1).

Glomerulonephritis is an inflammation of the glomeruli, which causes progressive renal damage that can lead to ATN and renal failure (4-6). The disease is mainly caused by infection such as streptococcal infection (7;8). In post-streptococcal glomerulonephritis, symptoms can include sudden hypertension, proteinuria, edema and hematuria (9). The inflammatory response causing the damage to the kidneys is thought to be related to hypersensitive immune response (9). Maintenance generally can include treatment of underlying disease, balancing electrolytes and fluids, and possible peritoneal dialysis (10).

Reference List

1. Gaw A, Murphy MJ, Cowan RA, O’Reilly DStJ, Stewart MJ, Shepherd J. Clinical Biochemistry: An Illustrated Colour Text. Edinburgh: Churchill Livingstone Elsevier, 2008.
2. Rosen S, Stillman IE. Acute tubular necrosis is a syndrome of physiologic and pathologic dissociation. J Am Soc Nephrol 2008;19:871-5.
3. Ortiz A, Justo P, Sanz A, Lorz C, Egido J. Targeting apoptosis in acute tubular injury. Biochem Pharmacol 2003;66:1589-94.
4. Vinen CS, Oliveira DB. Acute glomerulonephritis. Postgrad Med J 2003;79:206-13.
5. Feith GW, Assmann KJ, Wetzels JF. Acute renal failure in patients with glomerular diseases: a consequence of tubular cell damage caused by haematuria? Neth J Med 2003;61:146-50.
6. Ruiz P, Soares MF. Acute postinfectious glomerulonephritis: an immune response gone bad? Hum Pathol 2003;34:1-2.
7. Prakash J, Sen D, Kumar NS, Kumar H, Tripathi LK, Saxena RK. Acute renal failure due to intrinsic renal diseases: review of 1122 cases. Ren Fail 2003;25:225-33.
8. Faurie RE, Prado AC. [Streptococcal infection, acute kidney failure and interstitial nephritis]. Medicina (B Aires) 2000;60:953-5.
9. Yoshizawa N. Acute glomerulonephritis. Intern Med 2000;39:687-94.
10. Filler G. Acute renal failure in children: aetiology and management. Paediatr Drugs 2001;3:783-92.

Published by David Despain, MS, CFS

David is a science and health writer living on Long Island, New York. He's written for a variety of publications including Scientific American, Outside Online, the American Society for Nutrition's (ASN) Nutrition Notes Daily, and Institute of Food Technologists' (IFT) Food Technology magazine and Live! blog. He's also covered new findings reported at scientific meetings including Experimental Biology, AAAS, AOCS, CASW, Sigma Xi, IFT, and others on his personal blog "Evolving Health." David is also an active member of organizations including the National Association of Science Writers (NASW), the American Association for the Advancement of Science (AAAS), the American Society for Nutrition, the Institute of Food Technologists, and the National Audubon Society. David has a master's degree in human nutrition from the University of Bridgeport, and a bachelor's degree in English from University of Illinois at Springfield. He also earned his Certified Food Scientist credential from the Institute of Food Technologists.

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