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14-September-2008 18:02:39 - Diabetic nephropathy 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 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. Contents 1 History 2 Epidemiology 3 Etiopathology 4 Signs and symptoms 5 Treatment 6 Prognosis 7 Complications 8 References 9 References 10 Additional images 11 External links History Diabetes mellitus Types of Diabetes Diabetes mellitus type 1 Diabetes mellitus type 2 Gestational diabetes Pre-diabetes: Impaired fasting glycaemia Impaired glucose tolerance Disease Management Diabetes management: Diabetic diet Anti-diabetic drugs Conventional insulinotherapy Intensive insulinotherapy Other Concerns Cardiovascular disease Diabetic comas: Diabetic hypoglycemia Diabetic ketoacidosis Nonketotic hyperosmolar Diabetic myonecrosis Diabetic nephropathy Diabetic neuropathy Diabetic retinopathy Diabetes and pregnancy Blood tests Blood sugar Fructosamine Glucose tolerance test Glycosylated hemoglobin 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. 1 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. 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 References Kimmelstiel P, Wilson C. Benign and malignant hypertension and nephrosclerosis. A clinical and pathological study. Am J Pathol 1936;12:45-48. References ^ 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 images Histopathological image of diabetic glomerulosclerosis with nephrotic syndrome. HE stain. Histopathological image of diabetic glomerulosclerosis with nephrotic syndrome. Another glomerulus. HE stain. Histopathological image of diabetic glomerulosclerosis with nephrotic syndrome. Another glomerulus. HE 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. External links Diabetic nephropathy. HealthCentral. Diabetic nephropathy. MedlinePlus Medical Encyclopedia. Text from this public domain article was partially used here. Texas University Classification v d e Urinary system - Pathology - Urologic disease N00-N39, 580-599 Abdominal Kidney/ nephropathy Glomerulus Nephritis/ glomerulonephritis by structure: Membranoproliferative glomerulonephritis - Membranous glomerulonephritis/Membranous nephritis - IgA nephropathy/glomerulonephritis by disease: Post-streptococcal glomerulonephritis - Lupus nephritis other: Rapidly progressive glomerulonephritis - Nephritic syndrome Nephrosis/ noninflammatory Glomerulosclerosis Focal segmental glomerulosclerosis, Diabetic nephropathy/glomerulosclerosis - Nephrotic syndrome Minimal change disease - Familial renal amyloidosis Tubulointerstitial/ Renal tubule Interstitial nephritis Pyelonephritis, Danubian endemic familial nephropathy Uropathy Obstructive uropathy, Hydronephrosis, Pyonephrosis Inborn errors of renal tubular transport Renal tubular acidosis, Gitelman syndrome Reflux nephropathy - Nephrogenic diabetes insipidus - Renal papillary necrosis Renal failure Acute renal failure Acute tubular necrosis - Chronic renal failure Other Renal osteodystrophy - Nephroptosis - Abderhalden-Kaufmann-Lignac syndrome vascular Renal artery stenosis, Hypertensive nephropathy, Renovascular hypertension Ureter Ureteritis - Ureterocele - Megaureter Pelvic Bladder Cystitis Interstitial cystitis, Trigonitis - Neurogenic bladder - Vesicointestinal fistula - Vesicoureteral reflux Urethra Urethritis Non-gonococcal urethritis - Urethral syndrome - Urethral stricture Other/general Urinary tract infection - Retroperitoneal fibrosis - Urolithiasis Kidney stone, Renal colic See also congenital, neoplasia, symptoms/signs v d e Endocrine pathology: endocrine diseases E00-35, 240-259 Pancreas/ glucose metabolism Diabetes mellitus types: type 1, type 2, MODY, complications: coma, angiopathy, ketoacidosis, nephropathy, neuropathy, retinopathy Hypoglycemia - Hyperinsulinism - Zollinger-Ellison syndrome - insulin receptor Rabson-Mendenhall syndrome - Insulin resistance Hypothalamic/ pituitary axes Pituitary Hyperpituitarism Acromegaly, Hyperprolactinaemia, SIADH Hypopituitarism Sheehan's syndrome, Kallmann syndrome, Growth hormone deficiency, Diabetes insipidus Adiposogenital dystrophy - Empty sella syndrome - Pituitary apoplexy - ACTH deficiency 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 - Thyroid hormone resistance - Thyroid nodule Parathyroid Hypoparathyroidism Pseudohypoparathyroidism - Hyperparathyroidism Primary, Secondary, Tertiary Adrenal Adrenocortical hyperfunction: Cushing's syndrome Nelson's syndrome, Pseudo-Cushing's syndrome - Hyperaldosteronism Conn syndrome, Bartter syndrome CAH Lipoid, 3β, 11β, 17α, 21α Adrenal insufficiency Addison's disease, Waterhouse-Friderichsen syndrome - Hypoaldosteronism Gonads ovarian Polycystic ovary syndrome, Premature ovarian failure testicular 5-alpha-reductase deficiency, 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 - thymus Abscess of thymus, Thymus hyperplasia see also congenital, neoplasia Retrieved from http://en..org/wiki/Diabetic_nephropathy Categories: Kidney diseases | Angiology | Diabetes Views Article Discussion this page History Personal tools Log in / create account Navigation Main page Contents Featured content Current events Random article Search Go Search Interaction Community portal Recent changes Contact Donate to Help Toolbox What links here Related changes Upload file Special pages Printable version Permanent link Cite this page Languages العربية Deutsch Español עברית СрпÑ?ки / Srpski Suomi Svenska This page was last modified on 2 September 2008, at 03:28
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