Chronic kidney disease: Difference between revisions
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Revision as of 12:09, 14 October 2009
In medicine, chronic kidney disease is defined as "kidney damage or glomerular filtration rate (GFR) <60 mL/min/1.73 m(2) for 3 months or more, irrespective of cause. Kidney damage in many kidney diseases can be ascertained by the presence of albuminuria, defined as albumin-to-creatinine ratio >30 mg/g in two of three spot urine specimens."[1]
Classification
There are five stages:[1]
- Stage 1 - glomerular filtration rate is 90 ml/min/1.73 m2 or more
- Stage 2 - glomerular filtration rate is 60-89 ml/min/1.73 m2
- Stage 3 - glomerular filtration rate is 30-59 ml/min/1.73 m2
- Stage 4 - glomerular filtration rate is 15-29 ml/min/1.73 m2
- Stage 5 - glomerular filtration rate is less than 15 ml/min/1.73 m2 or on renal dialysis
Etiology/cause
Bilateral renal artery stenosis (RAS) may cause 5% to 15% of cases of chronic kidney disease.[2]
Signs and symptoms
Uremia, "the illness accompanying kidney failure", may have subtle manifestations when the glomerular filtration rate falls below 60 ml/min/1.73 m2.[3]
Treatment
The National Kidney Disease Education Program provides guidance on dosing drugs in patients with reduced glomerular filtration rate.[4]
Various drugs have been studied for slowing the progression of chronic kidney disease.[5][6][7]
| Treatment | Setting | Results |
|---|---|---|
| Protein restriction[5] | Diabetic renal disease | relative risk of end stage renal disease or death: |
| Protein restriction[6] | Non-diabetic renal disease | relative risk of renal death: |
| Angiotensin converting enzyme inhibitors[7] | Diabetic renal disease |
Medications
Angiotensin inhibition
Angiotensin can be inhibited with either angiotensin-converting enzyme inhibitors[8] or angiotensin II receptor antagonists. These medications can help patients with an elevated creatinine,[9] including those with a creatinine of 1.5 to 5.0 mg per deciliter.[10]
Combining angiotensin-converting enzyme inhibitors and angiotensin II receptor antagonists increases effect, but at uncertain increase in drug toxicity such as hyperkalemia according to a meta-analysis.[11] Adding an aldosterone receptor antagonist such as spironolactone may add further benefit, but presumably more hyperkalemia.[12]
Secondary hyperparathyroidism
Clinical practice guidelines from the "Kidney Disease: Improving Global Outcomes (KDIGO)" address management of renal osteodystrophy.[13]
- Phosphate binders (calcium carbonate 650 mg tabs three times - Calcichew™, Titrala™) or calcium acetate (Phosex™, PhosLo™) per day by mouth.
- Vitamin D preparations such as calcitriol (0.25-0.5 µg orally once per day) or intravenous paricalcitol (Zemplar™)are given once a patient has Stage 3 disease in order to prevent secondary hyperparathyroidism.
- Calcimimetic such as cinacalcet (Sensipar™) may help.
Allopurinol
A single randomized controlled trial found that giving allopurinol to hyperuricemic patients with chronic kidney disease had a relative risk ratio of 0.35 in the prevention of "significant deterioration in renal function and dialysis dependence."[14]
Renal replacement therapy
Prognosis
The estimated glomerular filtration rate and the urinary albumin/creatinine ratio can help predict who will progress to CKD5.[15]
References
- ↑ 1.0 1.1 Levey AS, Eckardt KU, Tsukamoto Y, et al (2005). "Definition and classification of chronic kidney disease: a position statement from Kidney Disease: Improving Global Outcomes (KDIGO)". Kidney Int. 67 (6): 2089–100. DOI:10.1111/j.1523-1755.2005.00365.x. PMID 15882252. Research Blogging.
- ↑ Rimmer JM, Gennari FJ (May 1993). "Atherosclerotic renovascular disease and progressive renal failure". Ann. Intern. Med. 118 (9): 712–9. PMID 8460859. [e]
- ↑ Meyer TW, Hostetter TH (2007). "Uremia.". N Engl J Med 357 (13): 1316-25. DOI:10.1056/NEJMra071313. PMID 17898101. Research Blogging.
- ↑ The National Kidney Disease Education Program. (2009) Chronic Kidney Disease and Drug Dosing: Information for Providers National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), National Institutes of Health (NIH), U.S. Department of Health & Human Services (DHHS).
- ↑ 5.0 5.1 Robertson L, Waugh N, Robertson A (2007). "Protein restriction for diabetic renal disease". Cochrane Database Syst Rev (4): CD002181. DOI:10.1002/14651858.CD002181.pub2. PMID 17943769. Research Blogging.
- ↑ 6.0 6.1 Fouque D, Laville M, Boissel JP (2006). "Low protein diets for chronic kidney disease in non diabetic adults". Cochrane Database Syst Rev (2): CD001892. DOI:10.1002/14651858.CD001892.pub2. PMID 16625550. Research Blogging.
- ↑ 7.0 7.1 Strippoli GF, Bonifati C, Craig M, Navaneethan SD, Craig JC (2006). "Angiotensin converting enzyme inhibitors and angiotensin II receptor antagonists for preventing the progression of diabetic kidney disease". Cochrane Database Syst Rev (4): CD006257. DOI:10.1002/14651858.CD006257. PMID 17054288. Research Blogging.
- ↑ Jafar TH, Stark PC, Schmid CH, et al (2003). "Progression of chronic kidney disease: the role of blood pressure control, proteinuria, and angiotensin-converting enzyme inhibition: a patient-level meta-analysis". Ann. Intern. Med. 139 (4): 244–52. PMID 12965979. [e]
- ↑ Ruggenenti P, Perna A, Remuzzi G (2001). "ACE inhibitors to prevent end-stage renal disease: when to start and why possibly never to stop: a post hoc analysis of the REIN trial results. Ramipril Efficacy in Nephropathy". J. Am. Soc. Nephrol. 12 (12): 2832–7. PMID 11729254. [e]
- ↑ Hou FF, Zhang X, Zhang GH, et al (2006). "Efficacy and safety of benazepril for advanced chronic renal insufficiency". N. Engl. J. Med. 354 (2): 131–40. DOI:10.1056/NEJMoa053107. PMID 16407508. Research Blogging.
- ↑ Kunz R, Friedrich C, Wolbers M, Mann JF (January 2008). "Meta-analysis: effect of monotherapy and combination therapy with inhibitors of the renin angiotensin system on proteinuria in renal disease". Ann. Intern. Med. 148 (1): 30–48. PMID 17984482. [e]
- ↑ Tylicki L, Rutkowski P, Renke M, et al (September 2008). "Triple pharmacological blockade of the renin-angiotensin-aldosterone system in nondiabetic CKD: an open-label crossover randomized controlled trial". Am. J. Kidney Dis. 52 (3): 486–93. DOI:10.1053/j.ajkd.2008.02.297. PMID 18423812. Research Blogging.
- ↑ Moe S, Drüeke T, Cunningham J, Goodman W, Martin K, Olgaard K et al. (2006). "Definition, evaluation, and classification of renal osteodystrophy: a position statement from Kidney Disease: Improving Global Outcomes (KDIGO).". Kidney Int 69 (11): 1945-53. DOI:10.1038/sj.ki.5000414. PMID 16641930. Research Blogging. Free full text
- ↑ Siu YP, Leung KT, Tong MK, Kwan TH (January 2006). "Use of allopurinol in slowing the progression of renal disease through its ability to lower serum uric acid level". Am. J. Kidney Dis. 47 (1): 51–9. DOI:10.1053/j.ajkd.2005.10.006. PMID 16377385. Research Blogging.
- ↑ Hallan SI, Ritz E, Lydersen S, Romundstad S, Kvenild K, Orth SR (April 2009). "Combining GFR and Albuminuria to Classify CKD Improves Prediction of ESRD". J. Am. Soc. Nephrol.. DOI:10.1681/ASN.2008070730. PMID 19357254. Research Blogging.