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Chronic kidney disease
Classification and external resources
ICD-10 N18.
ICD-9 585 403
DiseasesDB 11288
MedlinePlus 000471
eMedicine med/374
MeSH D007676

Chronic kidney disease (CKD), also known as chronic renal disease, is a progressive loss of renal function over a period of months or years. The symptoms of worsening kidney function are unspecific, and might include feeling generally unwell and experiencing a reduced appetite. Often, chronic kidney disease is diagnosed as a result of screening of people known to be at risk of kidney problems, such as those with high blood pressure or diabetes and those with a blood relative with chronic kidney disease. Chronic kidney disease may also be identified when it leads to one of its recognized complications, such as cardiovascular disease, anemia or pericarditis.[1]

Chronic kidney disease is identified by a blood test for creatinine. Higher levels of creatinine indicate a falling glomerular filtration rate and as a result a decreased capability of the kidneys to excrete waste products. Creatinine levels may be normal in the early stages of CKD, and the condition is discovered if urinalysis (testing of a urine sample) shows that the kidney is allowing the loss of protein or red blood cells into the urine. To fully investigate the underlying cause of kidney damage, various forms of medical imaging, blood tests and often renal biopsy (removing a small sample of kidney tissue) are employed to find out if there is a reversible cause for the kidney malfunction.[1] Recent professional guidelines classify the severity of chronic kidney disease in five stages, with stage 1 being the mildest and usually causing few symptoms and stage 5 being a severe illness with poor life expectancy if untreated. Stage 5 CKD is also called established chronic kidney disease and is synonymous with the now outdated terms end-stage renal disease (ESRD), chronic kidney failure (CKF) or chronic renal failure (CRF).[1]

There is no specific treatment unequivocally shown to slow the worsening of chronic kidney disease. If there is an underlying cause to CKD, such as vasculitis, this may be treated directly with treatments aimed to slow the damage. In more advanced stages, treatments may be required for anemia and bone disease. Severe CKD requires one of the forms of renal replacement therapy; this may be a form of dialysis, but ideally constitutes a kidney transplant.[1]

Contents

Signs and symptoms

CKD is initially without specific symptoms and can only be detected as an increase in serum creatinine or protein in the urine. As the kidney function decreases:

People with chronic kidney disease suffer from accelerated atherosclerosis and are more likely to develop cardiovascular disease than the general population. Patients afflicted with chronic kidney disease and cardiovascular disease tend to have significantly worse prognoses than those suffering only from the latter.

Diagnosis

In many CKD patients, previous renal disease or other underlying diseases are already known. A small number presents with CKD of unknown cause. In these patients, a cause is occasionally identified retrospectively.[citation needed]

It is important to differentiate CKD from acute renal failure (ARF) because ARF can be reversible. Abdominal ultrasound is commonly performed, in which the size of the kidneys are measured. Kidneys with CKD are usually smaller (< 9 cm) than normal kidneys with notable exceptions such as in diabetic nephropathy and polycystic kidney disease. Another diagnostic clue that helps differentiate CKD and ARF is a gradual rise in serum creatinine (over several months or years) as opposed to a sudden increase in the serum creatinine (several days to weeks). If these levels are unavailable (because the patient has been well and has had no blood tests) it is occasionally necessary to treat a patient briefly as having ARF until it has been established that the renal impairment is irreversible.[citation needed]

Additional tests may include nuclear medicine MAG3 scan to confirm blood flows and establish the differential function between the two kidneys. DMSA scans are also used in renal imaging; with both MAG3 and DMSA being used chelated with the radioactive element Technetium-99.[citation needed]

In chronic renal failure treated with standard dialysis, numerous uremic toxins accumulate. These toxins show various cytotoxic activities in the serum, have different molecular weights and some of them are bound to other proteins, primarily to albumin. Such toxic protein bound substances are receiving the attention of scientists who are interested in improving the standard chronic dialysis procedures used today.[citation needed]

Stages

All individuals with a Glomerular filtration rate (GFR) <60 mL/min/1.73 m2 for 3 months are classified as having chronic kidney disease, irrespective of the presence or absence of kidney damage. The rationale for including these individuals is that reduction in kidney function to this level or lower represents loss of half or more of the adult level of normal kidney function, which may be associated with a number of complications.[1]

All individuals with kidney damage are classified as having chronic kidney disease, irrespective of the level of GFR. The rationale for including individuals with GFR 60 mL/min/1.73 m2 is that GFR may be sustained at normal or increased levels despite substantial kidney damage and that patients with kidney damage are at increased risk of the two major outcomes of chronic kidney disease: loss of kidney function and development of cardiovascular disease.[1]

The loss of protein in the urine is regarded as an independent marker for worsening of renal function and cardiovascular disease. Hence, British guidelines append the letter "P" to the stage of chronic kidney disease if there is significant protein loss.[3]

Stage 1 CKD

Slightly diminished function; Kidney damage with normal or relatively high GFR (>90 mL/min/1.73 m2). Kidney damage is defined as pathologic abnormalities or markers of damage, including abnormalities in blood or urine test or imaging studies.[1]

Stage 2 CKD

Mild reduction in GFR (60-89 mL/min/1.73 m2) with kidney damage. Kidney damage is defined as pathologic abnormalities or markers of damage, including abnormalities in blood or urine test or imaging studies.[1]

Stage 3 CKD

Moderate reduction in GFR (30-59 mL/min/1.73 m2).[1] British guidelines distinguish between stage 3A (GFR 45-59) and stage 3B (GFR 30-44) for purposes of screening and referral.[3]

Stage 4 CKD

Severe reduction in GFR (15-29 mL/min/1.73 m2)[1] Preparation for renal replacement therapy

Stage 5 CKD

Established kidney failure (GFR <15 mL/min/1.73 m2, or permanent renal replacement therapy (RRT)[1]

Causes

The most common causes of CKD are diabetic nephropathy, hypertension, and glomerulonephritis. Together, these cause approximately 75% of all adult cases. Certain geographic areas have a high incidence of HIV nephropathy.[citation needed]

Historically, kidney disease has been classified according to the part of the renal anatomy that is involved, as:[citation needed]

Treatment

The goal of therapy is to slow down or halt the otherwise relentless progression of CKD to stage 5. Control of blood pressure and treatment of the original disease, whenever feasible, are the broad principles of management. Generally, angiotensin converting enzyme inhibitors (ACEIs) or angiotensin II receptor antagonists (ARBs) are used, as they have been found to slow the progression of CKD to stage 5.[4][5] Although the use of ACE inhibitors and ARBs represents the current standard of care for patients with CKD, patients progressively lose kidney function while on these medications, as seen in the IDNT[6] and RENAAL[7] studies, which reported a decrease over time in estimated glomerular filtration rate (an accurate measure of CKD progression, as detailed in the K/DOQI guidelines[1]) in patients treated by these conventional methods.

Currently, several compounds are in development for CKD. These include, but are not limited to, bardoxolone methyl[8], olmesartan medoxomil, sulodexide, and avosentan[9].

Replacement of erythropoietin and vitamin D3, two hormones processed by the kidney, is usually necessary in patients with CKD, as is calcium. Phosphate binders are used to control the serum phosphate levels, which are usually elevated in chronic kidney disease.

When one reaches stage 5 CKD, renal replacement therapy is required, in the form of either dialysis or a transplant.

In some cases, dietary modifications have been proven to slow and even reverse further progression. Generally this includes limiting a persons intake of protein.[citation needed]

The normalization of hemoglobin has not been found to be of any benefit.[10]

Prognosis

The prognosis of patients with chronic kidney disease is guarded as epidemiological data has shown that all cause mortality (the overall death rate) increases as kidney function decreases.[11] The leading cause of death in patients with chronic kidney disease is cardiovascular disease, regardless of whether there is progression to stage 5.[11][12][13]

While renal replacement therapies can maintain patients indefinitely and prolong life, the quality of life is severely affected.[14][15] Renal transplantation increases the survival of patients with stage 5 CKD significantly when compared to other therapeutic options;[16][17] however, it is associated with an increased short-term mortality (due to complications of the surgery). Transplantation aside, high intensity home hemodialysis appears to be associated with improved survival and a greater quality of life, when compared to the conventional three times a week hemodialysis and peritoneal dialysis.[18]

Epidemiology

In Canada 1.9 to 2.3 million people have chronic kidney disease.[19]

UK estimates suggest that 8.8% of the population of Great Britain and Northern Ireland have symptomatic CKD. [20]

Organizations

In the USA, the National Kidney Foundation is a national organization representing patients and professionals who treat kidney diseases. The American Kidney Fund (AKF) is a national non-profit organization providing treatment-related financial assistance to 1 out of every 5 dialysis patients each year. The Renal Support Network (RSN) is a nonprofit, patient-focused, patient-run organization that provides non-medical services to those affected by CKD. The American Association of Kidney Patients (AAKP) is a non-profit, patient-centric group focused on improving the health and well-being of CKD and dialysis patients. The Renal Physicians Association (RPA) is an association representing nephrology professionals.

In the United Kingdom, the UK National Kidney Federation represents patients, and the Renal Association represents renal physicians and works closely with the National Service Framework for kidney disease.

The International Society of Nephrology is an international body representing specialists in kidney diseases.

See also

References

  1. ^ a b c d e f g h i j k l National Kidney Foundation (2002). "K/DOQI clinical practice guidelines for chronic kidney disease". http://www.kidney.org/professionals/KDOQI/guidelines_ckd. Retrieved 2008-06-29. 
  2. ^ Adrogué HJ, Madias NE (September 1981). "Changes in plasma potassium concentration during acute acid-base disturbances". Am. J. Med. 71 (3): 456–67. doi:10.1016/0002-9343(81)90182-0. PMID 7025622. 
  3. ^ a b National Institute for Health and Clinical Excellence. Clinical guideline 73: Chronic kidney disease. London, 2008.
  4. ^ Ruggenenti P, Perna A, Gherardi G, Gaspari F, Benini R, Remuzzi G (October 1998). "Renal function and requirement for dialysis in chronic nephropathy patients on long-term ramipril: REIN follow-up trial. Gruppo Italiano di Studi Epidemiologici in Nefrologia (GISEN). Ramipril Efficacy in Nephropathy". Lancet 352 (9136): 1252–6. doi:10.1016/S0140-6736(98)04433-X. PMID 9788454. 
  5. ^ Ruggenenti P, Perna A, Gherardi G, et al. (July 1999). "Renoprotective properties of ACE-inhibition in non-diabetic nephropathies with non-nephrotic proteinuria". Lancet 354 (9176): 359–64. doi:10.1016/S0140-6736(98)10363-X. PMID 10437863. 
  6. ^ Lewis EJ, Hunsicker LG, Clarke WR, et al. (2001). "Renoprotective effect of the angiotensin-receptor antagonist irbesartan in patients with nephropathy due to type 2 diabetes". N Engl J Med 345: 851–60. 
  7. ^ Brenner BM, Cooper ME, de ZD, et al. (2001). "Effects of losartan on renal and cardiovascular outcomes in patients with type 2 diabetes and nephropathy". N Engl J Med 345: 861–9. 
  8. ^ http://www.medscape.com/viewarticle/590644
  9. ^ http://www.medicalnewstoday.com/articles/139028.php
  10. ^ Levin A, Hemmelgarn B, Culleton B, et al. (November 2008). "Guidelines for the management of chronic kidney disease". CMAJ 179 (11): 1154–62. doi:10.1503/cmaj.080351. PMID 19015566. 
  11. ^ a b Perazella MA, Khan S (March 2006). "Increased mortality in chronic kidney disease: a call to action". Am. J. Med. Sci. 331 (3): 150–3. doi:10.1097/00000441-200603000-00007. PMID 16538076. 
  12. ^ Sarnak MJ, Levey AS, Schoolwerth AC, et al. (October 2003). "Kidney disease as a risk factor for development of cardiovascular disease: a statement from the American Heart Association Councils on Kidney in Cardiovascular Disease, High Blood Pressure Research, Clinical Cardiology, and Epidemiology and Prevention". Circulation 108 (17): 2154–69. doi:10.1161/01.CIR.0000095676.90936.80. PMID 14581387. http://circ.ahajournals.org/cgi/content/full/108/17/2154. 
  13. ^ Tonelli M, Wiebe N, Culleton B, et al. (July 2006). "Chronic kidney disease and mortality risk: a systematic review". J. Am. Soc. Nephrol. 17 (7): 2034–47. doi:10.1681/ASN.2005101085. PMID 16738019. http://jasn.asnjournals.org/cgi/content/full/17/7/2034. 
  14. ^ Heidenheim AP, Kooistra MP, Lindsay RM (2004). "Quality of life". Contrib Nephrol 145: 99–105. doi:10.1159/000081673. PMID 15496796. 
  15. ^ de Francisco AL, Piñera C (January 2006). "Challenges and future of renal replacement therapy". Hemodial Int 10 Suppl 1: S19–23. doi:10.1111/j.1542-4758.2006.01185.x. PMID 16441862. 
  16. ^ Groothoff JW (July 2005). "Long-term outcomes of children with end-stage renal disease". Pediatr. Nephrol. 20 (7): 849–53. doi:10.1007/s00467-005-1878-9. PMID 15834618. 
  17. ^ Giri M (2004). "Choice of renal replacement therapy in patients with diabetic end stage renal disease". Edtna Erca J 30 (3): 138–42. PMID 15715116. 
  18. ^ Pierratos A, McFarlane P, Chan CT (March 2005). "Quotidian dialysis--update 2005". Curr. Opin. Nephrol. Hypertens. 14 (2): 119–24. PMID 15687837. 
  19. ^ Levin A, Hemmelgarn B, Culleton B, et al. (November 2008). "Guidelines for the management of chronic kidney disease". CMAJ 179 (11): 1154–62. doi:10.1503/cmaj.080351. PMID 19015566. 
  20. ^ The Association of Public Health Observatories – Chronic Kidney Disease Prevalence Estimates. 2007 [cited 1/3/2010]; Available from: http://www.apho.org.uk/resource/item.aspx?RID=63798.

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