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| '''For patient information click [[{{PAGENAME}} (patient information)|here]]''' | | '''For patient information click [[{{PAGENAME}} (patient information)|here]]''' |
| {{Diabetic nephropathy}}
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| {{CMG}} | | {{CMG}} |
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| ==Case Studies== | | ==Case Studies== |
| [[Diabetic nephropathy case study one|Case #1]] | | [[Diabetic nephropathy case study one|Case #1]] |
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| ==Overview==
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| '''Diabetic nephropathy''' (''nephropatia diabetica''), also known as '''Kimmelstiel-Wilson syndrome''' and '''intercapillary glomerulonephritis''', is a progressive [[kidney disease]] caused by [[angiopathy]] of [[capillary|capillaries]] in the [[kidney]] [[glomerulus|glomeruli]]. It is characterized by [[nephrotic syndrome]] and nodular glomerulosclerosis. It is due to longstanding [[diabetes mellitus]], and is a prime cause for [[dialysis]] in many Western countries.
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| ==History==
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| The syndrome was discovered by British [[physician]] Clifford Wilson (1906-1997) and Germany-born American physician Paul Kimmelstiel (1900-1970) and was published for the first time in 1936.
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| ==Etiopathology==
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| The earliest detectable change in the course of diabetic nephropathy is a thickening in the glomerulus. At this stage, the kidney may start allowing more [[serum albumin]] (plasma protein) than normal in the [[urine]] ([[albuminuria]]), and this can be detected by sensitive [[medical test]]s for albumin. This stage is called "microalbuminuria". It can appear 5 to 10 years before other symptoms develop. As diabetic nephropathy progresses, increasing numbers of glomeruli are destroyed by nodular glomerulosclerosis. Now the amounts of albumin being excreted in the urine increases, and may be detected by ordinary [[urinalysis]] techniques. At this stage, a kidney [[biopsy]] clearly shows diabetic nephropathy.
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| ==Signs and symptoms==
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| Kidney failure provoked by glomerulosclerosis leads to fluid filtration deficits and other disorders of kidney function. There is an increase in [[blood pressure]] ([[hypertension]]) and of fluid retention in the body ([[oedema]]). Other [[complication (medicine)|complications]] may be [[arteriosclerosis]] of the [[renal artery]] and [[proteinuria]] (nephrotic syndrome).
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| Throughout its early course, diabetic nephropathy has no [[symptom]]s. They develop in late stages and may be a result of excretion of high amounts of protein in the urine or due to renal failure:
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| * [[edema]]: swelling, usually around the [[eye]]s in the mornings; later, general body swelling may result, such as swelling of the legs
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| * foamy appearance or excessive frothing of the urine
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| * unintentional weight gain (from fluid accumulation)
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| * [[anorexia (symptom)|anorexia]] (poor appetite)
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| * [[nausea]] and [[vomiting]]
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| * [[malaise]] (general ill feeling)
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| * [[fatigue (physical)|fatigue]]
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| * [[headache]]
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| * frequent [[hiccup]]s
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| * generalized [[itching]]
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| The first laboratory abnormality is a positive microalbuminuria test. Most often, the diagnosis is suspected when a routine urinalysis of a person with diabetes shows too much protein in the urine (proteinuria). The urinalysis may also show [[glucose]] in the urine, especially if blood glucose is poorly controlled. Serum [[creatinine]] and [[BUN]] may increase as kidney damage progresses.
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| A kidney [[biopsy]] confirms the diagnosis, although it is not always necessary if the case is straightforward, with a documented progression of proteinuria over time and presence of diabetic [[retinopathy]] on examination of the [[retina]] of the [[eye]]s.
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| ==Treatment==
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| The goals of treatment are to slow the progression of kidney damage and control related complications. The main treatment, once proteinuria is established, is [[ACE inhibitor]] drugs, which usually reduces proteinuria levels and slows the progression of diabetic nephropathy. Several effects of the ACEIs that may contribute to renal protection have been related to the association of rise in Kinins which is also responsible for some of the side effects associated with ACEIs therapy such as dry cough. The renal protection effect is related to the antihypertensive effects in normal and hypertensive patients, renal vasodilatation resulting in increased renal blood flow and dilatation of the efferent arterioles. [http://www.ksu.edu.sa/sites/Colleges/Medicine/Lists/Medical%20Subjects/Flat.aspx?RootFolder=http%3a%2f%2fwww%2eksu%2eedu%2esa%2fsites%2fColleges%2fMedicine%2fLists%2fMedical%20Subjects%2fDiabetes%20Mellitus%20and%20Angiotensin%20Converting%20Enzyme%20Inhibitors&FolderCTID=0x01200200CEDE56CEF8D11C46824F2F6116DF88AA] Many studies have shown that related drugs, [[angiotensin receptor blocker]]s (ARBs), have a similar benefit. In fact, a combination may be best.
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| Blood-glucose levels should be closely monitored and controlled. This may slow the progression of the disorder, especially in the very early ("microalbuminuria") stages. Medications to manage diabetes include oral hypoglycemic agents and [[insulin]] injections. As kidney failure progresses, less insulin is excreted, so smaller doses may be needed to control glucose levels.
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| The [[diet (nutrition)|diet]] may be modified to help control blood-sugar levels. Modification of protein intake can effect hemodynamic and nonhemodynamic injury.
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| High blood pressure should be aggressively treated with antihypertensive medications, in order to reduce the risks of kidney, eye, and blood vessel damage in the body. It is also very important to control lipid levels, maintain a healthy weight, and engage in regular physical activity.
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| Patients with diabetic nephropathy should avoid taking the following drugs:
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| * Contrast agents containing [[iodine]]
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| * Commonly used non-steroidal anti-inflammatory drugs ([[NSAID]]s) like [[ibuprofen]] and [[naproxen]], or [[COX-2]] inhibitors like [[Celebrex]], because they may injure the weakened kidney.
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| [[Urinary tract]] and other [[infections]] are common and can be treated with appropriate [[antibiotics]].
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| [[Dialysis]] may be necessary once end-stage renal disease develops. At this stage, a [[kidney transplantation]] must be considered. Another option for type 1 diabetes patients is a combined kidney-pancreas transplant.
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| [[C-peptide]], a by-product of insulin production, may provide new hope for patients sufering from diabetic nephropathy <ref>[http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&list_uids=17235526&cmd=Retrieve&indexed=google C-peptide is a bioactive peptide. [Diabetologia. 2007] - PubMed Result<!-- Bot generated title -->]</ref> <ref>{{cite journal |author=Wahren J, Ekberg K, Jörnvall H |title=C-peptide is a bioactive peptide |journal=Diabetologia |volume=50 |issue=3 |pages=503–9 |year=2007 |pmid=17235526 |doi=10.1007/s00125-006-0559-y |url=}}</ref>.
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| ==Prognosis==
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| Diabetic nephropathy continues to get gradually worse. Complications of chronic kidney failure are more likely to occur earlier, and progress more rapidly, when it is caused by diabetes than other causes. Even after initiation of dialysis or after transplantation, people with diabetes tend to do worse than those without diabetes.
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| ==Complications==
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| Possible complications include:
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| * [[hypoglycemia]] (from decreased excretion of insulin)
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| * rapidly progressing chronic [[kidney failure]]
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| * [[end-stage kidney disease]]
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| * [[hyperkalemia]]
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| * severe [[hypertension]]
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| * complications of [[hemodialysis]]
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| * complications of [[kidney transplant]]
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| * coexistence of other [[diabetes]] complications
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| * [[peritonitis]] (if peritoneal dialysis used)
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| * increased [[infections]]
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| ==Additional images==
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| <gallery>Image:Diabetic glomerulosclerosis (1) HE.jpg|Histopathological image of diabetic glomerulosclerosis with nephrotic syndrome. H&E stain.
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| Image:Diabetic glomerulosclerosis (2) HE.jpg|Histopathological image of diabetic glomerulosclerosis with nephrotic syndrome. Another glomerulus. H&E stain.
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| Image:Diabetic glomerulosclerosis (3) HE.jpg|Histopathological image of diabetic glomerulosclerosis with nephrotic syndrome. Another glomerulus. H&E stain.
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| Image:Diabetic glomerulosclerosis (4) PAS.jpg|Histopathological image of diabetic glomerulosclerosis with nephrotic syndrome. PAS stain.
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| Image:Diabetic glomerulosclerosis (5) PAS.jpg|Histopathological image of diabetic glomerulosclerosis with nephrotic syndrome. PAS stain.
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| Image:Diabetic glomerulosclerosis (7) PAM.jpg|Histopathological image of diabetic glomerulosclerosis with nephrotic syndrome. PAM stain.
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| Image:Diabetic glomerulosclerosis (8) PAM.jpg|Histopathological image of diabetic glomerulosclerosis with nephrotic syndrome. PAM stain.
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| </gallery>
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| ==References==
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| {{Reflist}}
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| ==Additional Resource==
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| * Kimmelstiel P, Wilson C. ''Benign and malignant hypertension and nephrosclerosis. A clinical and pathological study.'' Am J Pathol 1936;12:45-48.
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| ==External links== | | ==External links== |
| * [http://www.healthcentral.com/mhc/top/000494.cfm Diabetic nephropathy]. HealthCentral.
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| * [http://www.nlm.nih.gov/medlineplus/ency/article/000494.htm Diabetic nephropathy]. MedlinePlus Medical Encyclopedia. Text from this public domain article was partially used here. | | * [http://www.nlm.nih.gov/medlineplus/ency/article/000494.htm Diabetic nephropathy]. MedlinePlus Medical Encyclopedia. Text from this public domain article was partially used here. |
| * [http://www.podomedic.it/modules/news/article.php?storyid=108 Texas University Classification]
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| {{Nephrology}} | | {{Nephrology}} |
| {{Endocrine pathology}} | | {{Endocrine pathology}} |
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| {{Diabetes}} | | {{Diabetes}} |
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| [[Category:Kidney diseases]] | | [[Category:Kidney diseases]] |
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| [[sv:Diabetesnefropati]] | | [[sv:Diabetesnefropati]] |
| [[Category:Mature chapter]] | | [[Category:Mature chapter]] |
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| {{WH}} | | {{WH}} |
| {{WS}} | | {{WS}} |
