acute tubular necrosis; tubulorrhexis (ATN)
Jump to navigation
Jump to search
Etiology
- ischemia
- hypovolemia
- low cardiac output
- renal vasoconstriction
- systemic vasodilatation
- obstetric complications
- recent hemorrhage
- hypotension
- surgery (30%)[7]
- sepsis[4]
- pharmaceutical agents (nephrotoxic agents)
- toxins: ethylene glycol
- endogenous toxins
- risk factors[5]
Epidemiology
- most common form of acute renal failure
Pathology
- oliguric phase
- intratubular obstruction secondary to oncosis of renal tubular epithelial cells
- backleak of glomerular filtrate through a disrupted proximal tubular barrier
- decreased glomerular permeability & GFR
- diuretic phase
- improved GFR
- inability of regenerating tubules to reabsorb Na+ & water normally
- alterations in fluid & electrolyte balance may occur
Clinical manifestations
- 60% of patients are not oliguric
- oliguric phase
- duration 1-2 weeks
- seldom > 4 weeks
- consider biopsy to seek other causes of renal failure if oliguric phase lasts > 4 weeks
- diuretic phase
- increases in urine flow not necessarily associated with improvement in serum creatinine early
- serum creatinine improves as glomerular filtration rate (GFR) increases
- severe hypercalcemia may occur in rhabdomyolysis-induced renal failure during this phase
- recovery phase
- glomerular filtration rate improves over 3-12 months
- generally, GFR stabilizes at a reduced rate, especially in patients who have been oliguric for > 16 days
- hypotension
Laboratory
- urinalysis
- muddy brown granular or tubular epithelial cell casts
- urinary sodium > 20 meq/L
- specific gravity < 1.015
- fractional excretion of sodium (FENA) > 2%[4]
- urine sodium > 30 meq/L[9]
- urine osmolality similar to serum osmolality
- urine creatinine is generally low (oliguric phase)
- urine protein may be elevated (2+)
- hematuria & pyuria may be observed, 10-25 RBC/HPF, 10-25 WBC/HPF (GRS11)[7]
- serum chemistries
- serum potassium (hyperkalemia or hypokalemia[9])
- serum phosphorous (hyperphosphatemia)
- serum calcium (hypocalcemia)
- serum magnesium (hypomagnesemia)[9]
- serum uric acid (hyperuricemia)
- serum myoglobin (increased)
- serum creatine kinase (increased)
- serum sodium (hyponatremia)
- serum bicarbonate (metabolic acidosis)
- serum urea nitrogen (uremia)
- serum creatinine (increased)
- serum complement C3, serum complement C4 normal
- serum protein electrophoresis (SPE)/immunofixation electrophoresis (IFE) if indicated
- osmolal gap (if ethylene glycol is suspected)
- complete blood count (CBC): leukocytosis associated with infection
Complications
- infection is the most common morbidity
- GI bleeding (platelet dysfunction secondary to uremia)
- hypervolemia with congestive heart failure (CHF)
- hyponatremia
Differential diagnosis
- glomerulonephritis (normal serum complement, RBC casts in urine)
- acute interstitial nephritis
- leukocyte casts in urine, eosinophiluria, proteinuria
Management
- restore systemic hemodynamics & renal perfusion
- eliminate nephrotoxins
- ref[10] (NEJM) includes ACE inhibitors & ARBS among the nephrotoxins due to interference with glomerular autoregulation & risk of hyperkalemia
- consider specific methods
- forced alkaline diuresis to remove uric acid, myoglobin (rhabdomyolysis), methotrexate
- loop diuretic not likely to be useful for ATN with oliguria[4]
- not likely to remove K+
- chelation therapy
- hemodialysis[5] QD is better than QOD
- removes K+ if hyperkalemia
- continuous hemodialysis (CRRT) recommended in[4]
- fenoldopam may benefit a subgroup of patients[6]
- forced alkaline diuresis to remove uric acid, myoglobin (rhabdomyolysis), methotrexate
- once injured, renal tubular epithelial cells take 3-4 weeks to regenerate
- dialysis
- fluid & electrolyte management
- once tubular regeneration occurs, the patient enters a diuretic phase
- trial of low dose (renal) dopamine plus furosemide (Lasix)
- prognosis: non oliguric patients have better prognosis than oliguric patients
- see acute renal failure
More general terms
Additional terms
References
- ↑ Harrison's Principles of Internal Medicine, 13th ed. Companion Handbook, Isselbacher et al (eds), McGraw-Hill Inc. NY, 1995, pg 829-39
- ↑ Harrison's Principles of Internal Medicine, 14th ed. Fauci et al (eds), McGraw-Hill Inc. NY, 1998, pg 1504-1513
- ↑ Applied Laboratory Medicine, Teitz NW, Conn RB & Pruden EL editors, WB Saunders, Philadelphia, 1992
- ↑ 4.0 4.1 4.2 4.3 4.4 Medical Knowledge Self Assessment Program (MKSAP) 11, 15, 16, 17, 19. American College of Physicians, Philadelphia 1998, 2009, 2012, 2015, 2021
- ↑ 5.0 5.1 5.2 Journal Watch 22(5):38, 2002 Schiffl H et al Daily hemodialysis and the outcome of acute renal failure. N Engl J Med 346:305, 2002 PMID: https://www.ncbi.nlm.nih.gov/pubmed/11821506 Bonventre JV et al, Daily hemodialysis-will treatment each day improve the outcome in patients with acute renal failure? N Engl J Med 346:362, 2002 PMID: https://www.ncbi.nlm.nih.gov/pubmed/11821514
- ↑ 6.0 6.1 Journal Watch 25(17):135, 2005 Tumlin JA, Finkel KW, Murray PT, Samuels J, Cotsonis G, Shaw AD. Fenoldopam mesylate in early acute tubular necrosis: a randomized, double-blind, placebo-controlled clinical trial. Am J Kidney Dis. 2005 Jul;46(1):26-34. PMID: https://www.ncbi.nlm.nih.gov/pubmed/15983954
- ↑ 7.0 7.1 7.2 Geriatric Review Syllabus, 7th edition Parada JT et al (eds) American Geriatrics Society, 2010
Geriatric Review Syllabus, 11th edition (GRS11) Harper GM, Lyons WL, Potter JF (eds) American Geriatrics Society, 2022 - ↑ 8.0 8.1 Shah-Khan F, Scheetz MH, Ghossein C. Biopsy-Proven Acute Tubular Necrosis due to Vancomycin Toxicity. Int J Nephrol. 2011;2011:436856 PMID: https://www.ncbi.nlm.nih.gov/pubmed/21716699
Belen C, Budhiraja P, Bracamonte E, Popovtzer M. Biopsy-proven acute tubular necrosis associated with vancomycin in an adult patient. Ren Fail. 2012;34(4):502-5 PMID: https://www.ncbi.nlm.nih.gov/pubmed/22329801 - ↑ 9.0 9.1 9.2 9.3 NEJM Knowledge+ Nephrology/Urology
- ↑ 10.0 10.1 NEJM Knowledge+ Complex Medical Care