Diabetic nephropathy
You don't need to be Editor-In-Chief to add or edit content to WikiDoc. You can begin to add to or edit text on this WikiDoc page by clicking on the edit button at the top of this page. Next enter or edit the information that you would like to appear here. Once you are done editing, scroll down and click the Save page button at the bottom of the page.
| Diabetic nephropathy Classification and external resources | |
 | |
|---|---|
| Photomicrography of nodular glomerulosclerosis in Kimmelstein-Wilson syndrome. Source: CDC | |
| ICD-10 | E10.2, E11.2, E12.2, E13.2, E14.2 |
| ICD-9 | 250.4 |
| MeSH | D003928 |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Phone:617-632-7753
Please Take Over This Page and Apply to be Editor-In-Chief for this topic: There can be one or more than one Editor-In-Chief. You may also apply to be an Associate Editor-In-Chief of one of the subtopics below. Please mail us [2] to indicate your interest in serving either as an Editor-In-Chief of the entire topic or as an Associate Editor-In-Chief for a subtopic. Please be sure to attach your CV and or biographical sketch.
Diabetic nephropathy (nephropatia diabetica), also known as Kimmelstiel-Wilson syndrome and intercapillary glomerulonephritis, is a progressive kidney disease caused by angiopathy of capillaries in the kidney 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.
History
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.
Epidemiology
The syndrome can be seen in patients with chronic diabetes (15 years or more after onset), so patients are usually of older age (between 50 and 70 years old). The disease is progressive and may cause death two or three years after the initial lesions, and is more frequent in men. Diabetic nephropathy is the most common cause of chronic kidney failure and end-stage kidney disease in the United States. People with both type 1 and type 2 diabetes are at risk. The risk is higher if blood-glucose levels are poorly controlled. Further, once nephropathy develops, the greatest rate of progression is seen in patients with poor control of their blood pressure. Also people with high cholesterol level in their blood have much more risk than others.
Etiopathology
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 tests 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.
Signs and symptoms
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 complications may be arteriosclerosis of the renal artery and proteinuria (nephrotic syndrome).
Throughout its early course, diabetic nephropathy has no symptoms. 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:
- oedema: swelling, usually around the eyes in the mornings; later, general body swelling may result, such as swelling of the legs
- foamy appearance or excessive frothing of the urine
- unintentional weight gain (from fluid accumulation)
- anorexia (poor appetite)
- nausea and vomiting
- malaise (general ill feeling)
- fatigue
- headache
- frequent hiccups
- generalized itching
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.
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 eyes.
Treatment
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. [3] Many studies have shown that related drugs, angiotensin receptor blockers (ARBs), have a similar benefit. In fact, a combination may be best.
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.
The diet may be modified to help control blood-sugar levels. Modification of protein intake can effect hemodynamic and nonhemodynamic injury. 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.
Patients with diabetic nephropathy should avoid taking the following drugs:
- Contrast agents containing iodine
- Commonly used non-steroidal anti-inflammatory drugs (NSAIDs) like ibuprofen and naproxen, or COX-2 inhibitors like Celebrex, because they may injure the weakened kidney.
Urinary tract and other infections are common and can be treated with appropriate antibiotics.
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.
C-peptide, a by-product of insulin production, may provide new hope for patients sufering from diabetic nephropathy [1] [2].
Prognosis
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.
Complications
Possible complications include:
- hypoglycemia (from decreased excretion of insulin)
- rapidly progressing chronic kidney failure
- end-stage kidney disease
- hyperkalemia
- severe hypertension
- complications of hemodialysis
- complications of kidney transplant
- coexistence of other diabetes complications
- peritonitis (if peritoneal dialysis used)
- increased infections
Additional images
 Histopathological image of diabetic glomerulosclerosis with nephrotic syndrome. H&E stain. |
 Histopathological image of diabetic glomerulosclerosis with nephrotic syndrome. Another glomerulus. H&E stain. |
 Histopathological image of diabetic glomerulosclerosis with nephrotic syndrome. Another glomerulus. H&E stain. |
 Histopathological image of diabetic glomerulosclerosis with nephrotic syndrome. PAS stain. |
 Histopathological image of diabetic glomerulosclerosis with nephrotic syndrome. PAS stain. |
 Histopathological image of diabetic glomerulosclerosis with nephrotic syndrome. PAM stain. |
 Histopathological image of diabetic glomerulosclerosis with nephrotic syndrome. PAM stain. |
References
- ↑ C-peptide is a bioactive peptide. [Diabetologia. 2007] - PubMed Result
- ↑ Wahren J, Ekberg K, Jörnvall H (2007). "C-peptide is a bioactive peptide". Diabetologia 50 (3): 503–9. doi:10.1007/s00125-006-0559-y. PMID 17235526.
Additional Resource
- Kimmelstiel P, Wilson C. Benign and malignant hypertension and nephrosclerosis. A clinical and pathological study. Am J Pathol 1936;12:45-48.
External links
- Diabetic nephropathy. HealthCentral.
- Diabetic nephropathy. MedlinePlus Medical Encyclopedia. Text from this public domain article was partially used here.
- Texas University Classification
Endocrine pathology: endocrine diseases (E00-35, 240-259) | |
|---|---|
| Thyroid | Hypothyroidism (Iodine deficiency, Cretinism, Congenital hypothyroidism, Goitre, Myxedema) - Hyperthyroidism (Graves disease, Toxic multinodular goitre, Teratoma with thyroid tissue or Struma ovarii) - Thyroiditis (De Quervain's thyroiditis, Hashimoto's thyroiditis, Riedel's thyroiditis) - Euthyroid sick syndrome |
| Pancreas | Diabetes mellitus (type 1, type 2, coma, angiopathy, ketoacidosis, nephropathy, neuropathy, retinopathy) - Hypoglycemia - Hyperinsulinism - Zollinger-Ellison syndrome - insulin receptor (Rabson-Mendenhall syndrome) |
| Parathyroid | Hypoparathyroidism (Pseudohypoparathyroidism) - Hyperparathyroidism (Primary, Secondary, Tertiary) |
| Pituitary | Hyperpituitarism (Acromegaly, Hyperprolactinaemia, SIADH) - Hypopituitarism (Simmonds' disease/Sheehan's syndrome, Kallmann syndrome, Growth hormone deficiency, Diabetes insipidus) - Adiposogenital dystrophy - Empty sella syndrome |
| Adrenal | Cushing's syndrome (Nelson's syndrome, Pseudo-Cushing's syndrome) - CAH (Lipoid, 3β, 11β, 17α, 21α) - Hyperaldosteronism (Conn syndrome, Bartter syndrome) - Adrenal insufficiency (Addison's disease) - Hypoaldosteronism |
| Gonads | ovarian dysfunction (Polycystic ovary syndrome, Premature ovarian failure) - testicular dysfunction (5-alpha-reductase deficiency) - testosterone biosynthesis (17-beta-hydroxysteroid dehydrogenase deficiency) - general (Hypogonadism, Delayed puberty, Precocious puberty) |
| Other | Androgen insensitivity syndrome - Autoimmune polyendocrine syndrome - Carcinoid syndrome - Gigantism - Short stature (Laron syndrome, Psychogenic dwarfism) - Multiple endocrine neoplasia (1, 2) - Progeria - Woodhouse-Sakati syndrome |
WikiDoc Research Resources for Diabetic nephropathy | |
|---|---|
| Articles on Diabetic nephropathy | Most recent articles on Diabetic nephropathy • Most cited articles on Diabetic nephropathy • Review articles on Diabetic nephropathy • Articles on Diabetic nephropathy in N Eng J Med, Lancet, BMJ |
| Media (Slides, Video, Images, MP3) on Diabetic nephropathy | Powerpoint slides on Diabetic nephropathy • Images of Diabetic nephropathy • Photos of Diabetic nephropathy • Podcasts & MP3s on Diabetic nephropathy • Videos on Diabetic nephropathy |
| Evidence Based Medicine Regarding Diabetic nephropathy | Cochrane Collaboration on Diabetic nephropathy • Bandolier on Diabetic nephropathy • TRIP on Diabetic nephropathy |
| Cost Effectiveness of Diabetic nephropathy | Cost Effectiveness of Diabetic nephropathy |
| Clinical Trials Involving Diabetic nephropathy | Ongoing Trials on Diabetic nephropathy at Clinical Trials.gov • Trial results on Diabetic nephropathy • Clinical Trials on Diabetic nephropathy at Google |
| Guidelines / Policies / Government Resources (FDA/CDC) Regarding Diabetic nephropathy | US National Guidelines Clearinghouse on Diabetic nephropathy • NICE Guidance on Diabetic nephropathy • NHS PRODIGY Guidance • FDA on Diabetic nephropathy • CDC on Diabetic nephropathy |
| Textbook Information on Diabetic nephropathy | Books and Textbook Information on Diabetic nephropathy |
| Pharmacology Resources on Diabetic nephropathy | Dosing of Diabetic nephropathy • Drug interactions with Diabetic nephropathy • Side effects of Diabetic nephropathy • Allergic reactions to Diabetic nephropathy • Overdose information on Diabetic nephropathy • Carcinogenicity information on Diabetic nephropathy • Diabetic nephropathy in pregnancy • Pharmacokinetics of Diabetic nephropathy • |
| Genetics, Pharmacogenomics, and Proteinomics of Diabetic nephropathy | Genetics of Diabetic nephropathy • Pharmacogenomics of Diabetic nephropathy • Proteomics of Diabetic nephropathy |
| Newstories on Diabetic nephropathy | Diabetic nephropathy in the news • Be alerted to news on Diabetic nephropathy • News trends on Diabetic nephropathy |
| Commentary on Diabetic nephropathy | Blogs on Diabetic nephropathy |
| Patient Resources on Diabetic nephropathy | Patient resources on Diabetic nephropathy • Discussion groups on Diabetic nephropathy • Patient Handouts on Diabetic nephropathy • Directions to Hospitals Treating Diabetic nephropathy • Risk calculators and risk factors for Diabetic nephropathy |
| Healthcare Provider Resources on Diabetic nephropathy | Symptoms of Diabetic nephropathy • Causes & Risk Factors for Diabetic nephropathy • Diagnostic studies for Diabetic nephropathy • Treatment of Diabetic nephropathy |
| Continuing Medical Education (CME) Programs on Diabetic nephropathy | CME Programs on Diabetic nephropathy |
| International Resources on Diabetic nephropathy | Diabetic nephropathy en Espanol • Diabetic nephropathy en Francais |
| Business Resources on Diabetic nephropathy | Diabetic nephropathy in the Marketplace • Patents on Diabetic nephropathy |
| Informatics Resources on Diabetic nephropathy | List of terms related to Diabetic nephropathy |
sr:Дијабетесна нефропатија fi:Diabeettinen nefropatia sv:Diabetesnefropati
| ||||
Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .
