Uremia Clinical Presentation

  • Author: A Brent Alper Jr, MD, MPH; Chief Editor: Vecihi Batuman, MD, FACP, FASN   more...
 
Updated: Mar 17, 2010
 

History

  • Uremia can occur once the creatinine clearance is below 10-20 mL/min, and it is heralded by the clinical onset of nausea, vomiting, fatigue, anorexia, weight loss, muscle cramps, pruritus, mental status changes, visual disturbances, and increased thirst.
  • Uremic encephalopathy can progress to seizures, stupor, coma, and, eventually, death.
  • Patients may report of nonspecific symptoms, which become chronic and progressive over time because of the gradual onset of the disease.
  • Metabolic abnormalities such as anemia, acidemia, and electrolyte abnormalities are prominent.
  • Cardiovascular abnormalities such as hypertension, atherosclerosis, valvular stenosis and insufficiency, congestive heart failure, and angina accelerate as renal function declines. These abnormalities may contribute to clinical symptoms of uremia if not treated appropriately.
  • Diabetic patients may appear to be in better glycemic control but may tend to have more hypoglycemic episodes as renal function declines. This paradoxical improvement in glycemic control is a result of increased insulin secretion and insulin half-life, both of which occur as renal function declines.
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Physical

Typical physical findings found in persons with uremia are those associated with fluid retention, anemia, and acidemia. Severe malnutrition can contribute to muscle wasting, while electrolyte abnormalities may cause muscle cramping, cardiac arrhythmias, and mental status changes.

  • Skin: The classic skin finding in persons with uremia is uremic frost, which is a fine residue thought to consist of excreted urea left on the skin after evaporation of water. The skin may have a velvety appearance and feel, particularly in patients who are pigmented. Patients who are uremic also may have a sallow coloration of the skin due to urochrome, the pigment that gives urine its color. Patients may become hyperpigmented as uremia worsens (melanosis).
  • Head, ears, eyes, nose, and throat: Sclera may become slightly icteric. The oral pharynx may be dry. Stomatitis may be present. Calcium deposition in the sclera can cause "red eye."
  • Cardiovascular system: Uremic pericarditis can be associated with a pericardial rub or a pericardial effusion. Increased fluid retention may result in pulmonary edema, peripheral edema, and severe hypertension. Valvular calcification may cause aortic stenosis or accelerate underlying disease.
  • Lungs: Fluid retention may result in pulmonary edema and corresponding crackles in the lungs. Pleural rubs occur in the setting of uremic lungs.
  • Gastrointestinal system: Occult GI bleeding may occur. Nausea and vomiting are common in those with severe uremia. Uremic fetor (ammonia or urinelike odor to the breath) also may be present.
  • Extremities: Fluid retention, pruritus associated with calcium phosphate deposition, and nail atrophy are common in persons with uremia.
  • Neurologic system: Uremic encephalopathy symptoms include fatigue, muscle weakness, malaise, headache, restless legs, asterixis, polyneuritis, mental status changes, muscle cramps, seizures, stupor, and coma. Amyloid deposits may result in medial nerve neuropathy, carpal tunnel syndrome, or other nerve entrapment syndromes.
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Causes

The etiologies of CKD range from primary glomerular and tubular disorders (eg, membranoproliferative glomerulonephritis, focal segmental glomerulosclerosis, IgA nephropathy, polycystic kidney disease) to systemic disorders causing renal injury (eg, diabetes, lupus, amyloidosis, Goodpasture disease, multiple myeloma, thrombotic thrombocytopenic purpura, hemolytic uremic syndrome[9] ).

  • ARF may be caused by multiple etiologies but is associated with uremia when a rapid rise in urea or creatinine occurs.
  • Diabetes is the primary cause of ESRD in the United States and accounts for 40% of new dialysis patients, followed by hypertension (25.2%), glomerulonephritis (11.3%), interstitial disease (3.8%), cystitis (2.8%), and neoplasms (1.7%).
  • Diabetes is the primary cause of renal disease in most other countries; however, other glomerulonephropathies, particularly IgA nephropathy, may be the primary cause of ESRD, depending upon the country.
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Contributor Information and Disclosures
Author

A Brent Alper Jr, MD, MPH  Associate Professor of Medicine, Section of Nephrology and Hypertension, Department of Medicine, Tulane University School of Medicine

A Brent Alper Jr, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Society of Hypertension, American Society of Nephrology, National Kidney Foundation, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Coauthor(s)

Rajesh G Shenava, MD  Assistant Professor of Medicine, Section of Nephrology and Hypertension, Department of Internal Medicine, Louisiana State University Health Sciences Centre

Rajesh G Shenava, MD is a member of the following medical societies: American College of Physicians, American Society of Nephrology, National Kidney Foundation, and Renal Physicians Association

Disclosure: Nothing to disclose.

Bessie A Young, MD, MPH  Associate Professor, Division of Nephrology, Department of Medicine, University of Washington; Director of Home Hemodialysis, Northwest Kidney Center, Seattle

Bessie A Young, MD, MPH is a member of the following medical societies: American College of Physicians, American Diabetes Association, American Society of Nephrology, International Society of Nephrology, and National Kidney Foundation

Disclosure: NxStage Grant/research funds Principal Investigator; Amgen Grant/research funds Principal Investigator

Specialty Editor Board

Donald A Feinfeld, MD, FACP, FASN  Consulting Staff, Division of Nephrology & Hypertension, Beth Israel Medical Center

Donald A Feinfeld, MD, FACP, FASN is a member of the following medical societies: American Academy of Clinical Toxicology, American Society of Hypertension, American Society of Nephrology, and National Kidney Foundation

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Eleanor Lederer, MD  Consulting Staff, Louisville VA Hospital; Professor of Medicine; Interim Chief of Nephrology; Director of Nephrology Training Program; Director, Metabolic Stone Clinic; Director of Outpatient Clinics, Kidney Disease Program, University of Louisville School of Medicine

Eleanor Lederer, MD is a member of the following medical societies: American Association for the Advancement of Science, American Federation for Medical Research, American Society for Biochemistry and Molecular Biology, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, International Society of Nephrology, Kentucky Medical Association, National Kidney Foundation, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Rebecca J Schmidt, DO, FACP, FASN  Professor of Medicine, Section Chief, Department of Medicine, Section of Nephrology, West Virginia University School of Medicine

Rebecca J Schmidt, DO, FACP, FASN is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Nephrology, International Society of Nephrology, National Kidney Foundation, Renal Physicians Association, and West Virginia State Medical Association

Disclosure: Abbott Grant/research funds Speaking and teaching; Genzyme Honoraria Consulting; Amgen Honoraria Speaking and teaching; Ortho Biotech Honoraria Speaking and teaching

Chief Editor

Vecihi Batuman, MD, FACP, FASN  Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Medicine Service, Southeast Louisiana Veterans Health Care System

Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, and International Society of Nephrology

Disclosure: Nothing to disclose.

References
  1. Piorry PA, l'Heritier D. Traite des Alterations du Sang. Paris, France: Bury & JB Bailliere; 1840.

  2. Carrero JJ, Witasp A, Stenvinkel P, et al. Visfatin is increased in chronic kidney disease patients with poor appetite and correlates negatively with fasting serum amino acids and triglyceride levels. Nephrol Dial Transplant. Mar 2010;25(3):901-6. [Medline].

  3. Almoznino-Sarafian D, Shteinshnaider M, Tzur I, et al. Anemia in diabetic patients at an internal medicine ward: Clinical correlates and prognostic significance. Eur J Intern Med. Apr 2010;21(2):91-96. [Medline].

  4. Teng M, Wolf M, Lowrie E, Ofsthun N, Lazarus JM, Thadhani R. Survival of patients undergoing hemodialysis with paricalcitol or calcitriol therapy. N Engl J Med. Jul 31 2003;349(5):446-56. [Medline].

  5. Sprague SM, Llach F, Amdahl M, Taccetta C, Batlle D. Paricalcitol versus calcitriol in the treatment of secondary hyperparathyroidism. Kidney Int. Apr 2003;63(4):1483-90. [Medline].

  6. Schlieper G, Aretz A, Verberckmoes SC, et al. Ultrastructural Analysis of Vascular Calcifications in Uremia. J Am Soc Nephrol. Mar 4 2010;[Medline].

  7. El-Agroudy AE, El-Baz A. Soluble Fas: a useful marker of inflammation and cardiovascular diseases in uremic patients. Clin Exp Nephrol. Jan 26 2010;[Medline].

  8. Muscaritoli M, Molfino A, Bollea MR, et al. Malnutrition and wasting in renal disease. Curr Opin Clin Nutr Metab Care. Jul 2009;12(4):378-83. [Medline].

  9. Fakhouri F, Roumenina L, Provot F, et al. Pregnancy-Associated Hemolytic Uremic Syndrome Revisited in the Era of Complement Gene Mutations. J Am Soc Nephrol. Mar 4 2010;[Medline].

  10. Chuang YW, Shu KH, Yu TM, et al. Hypokalaemia: an independent risk factor of Enterobacteriaceae peritonitis in CAPD patients. Nephrol Dial Transplant. May 2009;24(5):1603-8. [Medline].

  11. Seyffart G, Schulz T, Stiller S. Use of two calcium concentrations in hemodialysis--report of a 20-year clinical experience. Clin Nephrol. Mar 2009;71(3):296-305. [Medline].

  12. [Best Evidence] Singh AK, Szczech L, Tang KL, Barnhart H, Sapp S, Wolfson M, et al. Correction of anemia with epoetin alfa in chronic kidney disease. N Engl J Med. Nov 16 2006;355(20):2085-98. [Medline].

  13. Drüeke TB, Locatelli F, Clyne N, Eckardt KU, Macdougall IC, Tsakiris D, et al. Normalization of hemoglobin level in patients with chronic kidney disease and anemia. N Engl J Med. Nov 16 2006;355(20):2071-84. [Medline].

  14. Fouque D, Laville M. Low protein diets for chronic kidney disease in non diabetic adults. Cochrane Database Syst Rev. Jul 8 2009;CD001892. [Medline].

  15. Baigent C, Burbury K, Wheeler D. Premature cardiovascular disease in chronic renal failure. Lancet. Jul 8 2000;356(9224):147-52. [Medline].

  16. Bolton WK, Kliger AS. Chronic renal insufficiency: current understandings and their implications. Am J Kidney Dis. Dec 2000;36(6 Suppl 3):S4-12. [Medline].

  17. Fort J. Chronic renal failure: a cardiovascular risk factor. Kidney International. 2005;99:S25-29.

  18. IV. NKF-K/DOQI Clinical Practice Guidelines for Anemia of Chronic Kidney Disease: update 2000. Am J Kidney Dis. Jan 2001;37(1 Suppl 1):S182-238. [Medline].

  19. K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification. Am J Kidney Dis. Feb 2002;39(2 Suppl 1):S1-266. [Medline].

  20. Kausz AT, Obrador GT, Arora P, Ruthazer R, Levey AS, Pereira BJ. Late initiation of dialysis among women and ethnic minorities in the United States. J Am Soc Nephrol. Dec 2000;11(12):2351-7. [Medline].

  21. Levey AS, Adler S, Caggiula AW, England BK, Greene T, Hunsicker LG, et al. Effects of dietary protein restriction on the progression of advanced renal disease in the Modification of Diet in Renal Disease Study. Am J Kidney Dis. May 1996;27(5):652-63. [Medline].

  22. Lim VS, Kopple JD. Protein metabolism in patients with chronic renal failure: role of uremia and dialysis. Kidney Int. Jul 2000;58(1):1-10. [Medline].

  23. May RC, Mitch WE. Pathophysiology of uremia. In: Brenner BM, ed. Brenner & Rector's The Kidney. Vol 2. 5th ed. Philadelphia, Pa: WB Saunders; 1996:2148-69.

  24. Noris M, Remuzzi G. Uremic bleeding: closing the circle after 30 years of controversies?. Blood. Oct 15 1999;94(8):2569-74. [Medline].

  25. Palmer BF. Sexual dysfunction in uremia. J Am Soc Nephrol. Jun 1999;10(6):1381-8. [Medline].

  26. Roubicek C, Brunet P, Huiart L, et al. Timing of nephrology referral: influence on mortality and morbidity. Am J Kidney Dis. Jul 2000;36(1):35-41. [Medline].

  27. US Renal Data System. Excerpts from the USRDS 2000 Annual Data Report: Atlas of End-Stage Renal Disease in the United States. Am J Kidney Dis. 2000;36 (Suppl 2):S1-S239.

  28. US Renal Data System. USRDS 1999 Annual Data Report. Bethesda, Md: National Institutes of Health; 1999:[Full Text].

  29. Vanholder R. The Uremic Syndrome. In: Greenberg A, ed. Primer on Kidney Disease. 2nd ed. San Diego, Calif: Academic Press; 1998:403-7.

  30. Vanholder R, De Smet R. Pathophysiologic effects of uremic retention solutes. J Am Soc Nephrol. Aug 1999;10(8):1815-23. [Medline].

  31. Vanholder R, De Smet R, Lameire N. Protein-bound uremic solutes: the forgotten toxins. Kidney Int Suppl. Feb 2001;78:S266-70. [Medline].

  32. Walker R. General management of end stage renal disease. BMJ. Nov 29 1997;315(7120):1429-32. [Medline].

  33. Xu X, Fang W, Ling H, et al. Diffusion-weighted MR imaging of kidneys in patients with chronic kidney disease: initial study. Eur Radiol. Sep 30 2009;[Medline].

  34. Yavuz A, Tetta C, Ersoy FF, D'intini V, Ratanarat R, De Cal M, et al. Uremic toxins: a new focus on an old subject. Semin Dial. May-Jun 2005;18(3):203-11. [Medline].

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