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14-September-2008 10:43:23 - Nephrotic syndrome Nephrotic syndrome Classification and external resources Histopathological image of diabetic glomerulosclerosis with nephrotic syndrome. HE stain. ICD-10 N04. ICD-9 581.9 DiseasesDB 8905 eMedicine med/1612 ped/1564 MeSH D009404 This article may require cleanup to meet 's quality standards. Please improve this article if you can. April 2008 Not to be confused with nephritic syndrome Nephrotic syndrome is a nonspecific disorder in which the kidneys are damaged, to leak large amounts of protein at least 3.5 grams per day per 1.73m2 body surface area from the blood into the urine. Contents 1 Presentation 2 Investigations 3 Pathogenesis 4 Classification and causes 4.1 Etiologic classification 4.2 Histologic classification 4.3 Primary causes 4.4 Secondary causes 4.4.1 Secondary causes by histologic pattern 5 Differential diagnosis of gross edema 6 Diagnosis 7 Treatment 7.1 General measures supportive 7.2 Specific treatment of underlying cause 7.3 Dietary recommendations 8 Complications 9 Prognosis 10 References 11 External links Presentation It is characterised by proteinuria 3.5g/day, hypoalbuminemia, hyperlipidemia and edema. A few other characteristics are: The most common sign is excess fluid in the body. This may take several forms: Puffiness around the eyes, characteristically in the morning. Edema over the legs which is pitting i.e. leaves a little pit when the fluid is pressed out, which resolves over a few seconds. Fluid in the pleural cavity causing pleural effusion. Fluid in the peritoneal cavity causing ascites. Hypertension rarely Some patients may notice foamy urine, due to a lowering of the surface tension by the severe proteinuria. Actual urinary complaints such as hematuria or oliguria are uncommon, and are seen commonly in nephritic syndrome. May have features of the underlying cause, such as the rash associated with Systemic Lupus Erythematosus, or the neuropathy associated with diabetes. Examination should also exclude other causes of gross edema-especially the cardiovascular and hepatic system. Investigations The following are baseline, essential investigations Urine sample shows proteinuria 3.5 per 1.73 m2 per 24 hour. It is also examined for urinary casts; which is more a feature of active nephritis. Comprehensive metabolic panel CMP shows Hypoalbuminemia: albumin level ≤2.5g/dL normal=3.5-5g/dL. High levels of cholesterol hypercholesterolemia, specifically elevated LDL, usually with concomitantly elevated VLDL Electrolytes, urea and creatinine EUCs: to evaluate renal function Further investigations are indicated if the cause is not clear Biopsy of kidney Auto-immune markers ANA, ASOT, C3, cryoglobulins, serum electrophoresis Pathogenesis The glomeruli of the kidneys are the parts that normally filter the blood. They consist of capillaries that are fenestrated leaky, due to little holes called fenestrae or windows and that allow fluid, salts, and other small solutes to flow through, but normally not proteins. In nephrotic syndrome, the glomeruli become damaged due to inflammation and hyalinisation so that small proteins, such as albumins immunoglobulins and anti-thrombin can pass through the kidneys into urine. Albumin is the major protein in the blood which maintains colloid osmotic pressure-this prevents leakage of blood from vessels into tissue. However, experiments show that the edema formation in nephrotic syndrome is more so due to microvascular damage and intense salt and water retention by the damaged kidneys due to increased angiotensin secretion. The mechanism is very complex and still not fully understood. In response to leakage of albumin, the liver begins to make more of all its proteins, and levels of large proteins such as alpha 2-macroglobulin and lipoproteins increase. The excess lipoproteins end up in the urine filtrate, which is then reabsorbed by the tubular cells, which end up shedding and forming oval fat bodies or fatty casts. Classification and causes Nephrotic syndrome has many causes and may either be the result of a disease limited to the kidney, called primary nephrotic syndrome, or a condition that affects the kidney and other parts of the body, called secondary nephrotic syndrome. Etiologic classification A broad classification of nephrotic syndrome based on etiology: Nephrotic syndrome Primary Secondary Histologic classification Nephrotic syndrome is often classified histologically: Nephrotic syndrome MCD FSGS MN MPGN Primary causes Primary causes of nephrotic syndrome are usually described by the histology, i.e. minimal change disease MCD, focal segmental glomerulosclerosis FSGS and membranous nephropathy MN. They are considered to be diagnoses of exclusion, i.e. they are diagnosed only after secondary causes have been excluded. Secondary causes Secondary causes of nephrotic syndrome have the same histologic patterns as the primary causes, though may exhibit some differences suggesting a secondary cause, such as inclusion bodies. They are usually described by the underlying cause. Secondary causes by histologic pattern Membranous nephropathy MN1 Hepatitis B Sjogren's syndrome Systemic lupus erythematosus SLE Diabetes mellitus Sarcoidosis Syphilis Drugs Malignancy cancer Focal segmental glomerulosclerosis FSGS1 Hypertensive Nephrosclerosis Human immunodeficiency virus HIV Diabetes mellitus Obesity Kidney loss Minimal change disease MCD1 Drugs Malignancy, especially Hodgkin's lymphoma Differential diagnosis of gross edema When someone presents with generalized edema, the following causes should be excluded: Heart failure: The patient is older, with a history of heart disease. Jugular venous pressure is elevated on examination, might hear heart murmurs. An echocardiogram is the gold standard investigation. Liver failure: History suggestive of hepatitis/ cirrhosis: alcoholic, IV drug user, some herary causes. Stigmata of liver disease are seen: jaundice yellow skin and eyes, dilated veins over umbilicus caput medusae, scratch marks due to widespread itching, known as pruritus, enlarged spleen, spider angiomata, encephalopathy, bruising, nodular liver Acute fluid overload in someone with kidney failure: These people are known to have kidney failure, and have either drunk too much or missed their dialysis. Metastatic cancer: When cancer seeds the lungs or abdomen it causes effusions and fluid accumulation due to obstruction of lymphatics and veins as well as serous exudation. Diagnosis Diagnosis is based on blood and urine tests and sometimes imaging of the kidneys, a biopsy of the kidneys, or both. Treatment This section does not cite any references or sources. Please help improve this section by adding citations to reliable sources. August 2008 Treatment includes: General measures supportive Monitoring and maintaining euvolemia the correct amount of fluid in the body: monitoring urine output, BP regularly fluid restrict to 1L diuretics IV furosemide Monitoring kidney function: do EUCs daily and calculating GFR Prevent and treat any complications see below Albumin infusions are generally not used because their effect lasts only transiently. Specific treatment of underlying cause Immunosupression for the glomerulonephritides Corticosteroids2, cyclosporin. Standard ISKDC Regime for first episode:Prednisolone -60mg/m2 /day in 3 divided doses for 4weeks followed by 40mg/m2/day in a single dose on every alternate day for 4 weeks. Relapses by prednisolone 2mg/kg/day till urine becomes negative for protein.Then,1.5mg/kg/day for 4 weeks. Frequent Relapses treated by:cyclophosphamide or nitrogen mustard or cyclosporin or levamisole. Achieving stricter blood glucose control if diabetic. Blood pressure control. ACE inhibitors are the drug of choice. Independent of their blood pressure lowering effect, they have been shown to decrease protein loss. Dietary recommendations This section does not cite any references or sources. Please help improve this section by adding citations to reliable sources. August 2008 Reduce sodium intake to 1000-2000 milligrams daily. Foods high in sodium include salt used in cooking and at the table, seasoning blends garlic salt, Adobo, season salt, etc. canned soups, canned vegetables containing salt, luncheon meats including turkey, ham, bologna, and salami, prepared foods, fast foods, soy sauce, ketchup, and salad dressings. On food labels, compare milligrams of sodium to calories per serving. Sodium should be less than or equal to calories per serving. Eat a moderate amount of high protein animal food: 3-5 oz per meal preferably lean cuts of meat, fish, and poultry Avoid saturated fats such as butter, cheese, fried foods, fatty cuts of red meat, egg yolks, and poultry skin. Increase unsaturated fat intake, including olive oil, canola oil, peanut butter, avocadoes, fish and nuts. Eat low-fat desserts. Increase intake of fruits and vegetables. There is no potassium or phosphorus restriction necessary. Monitor fluid intake, which includes all fluids and foods that are liquid at room temperature. Fluid management in nephrotic syndrome is tenuous, especially during an acute flare. Complications Venous thrombosis: due to leak of anti-thrombin 3, which helps prevent thrombosis. This often occurs in the renal veins. Treatment is with oral anticoagulants not heparin as heparin acts via anti-thrombin 3 which is lost in the proteinuria so it will be ineffective. Infection: due to leakage of immunoglobulins, encapsulated bacteria such as Haemophilus influenzae and Streptococcus pneumonia can cause infection. Acute renal failure is due to hypovolemia. Despite the excess of fluid in the tissues, there is less fluid in the vasculature. Decreased blood flow to the kidneys causes them to shutdown. Thus it is a tricky task to get rid of excess fluid in the body while maintaining circulatory euvolemia. Pulmonary edema: again due to fluid leak, sometimes it leaks into lungs causing hypoxia and dyspnoea. Growth retardation: does not occur in MCNS.It occurs in cases of relapses or resistance to therapy. Causes of growth retardation are protein deficiency from the loss of protein in urine, anorexia reduced protein intake, and steroid therapy catabolism. Vitamin D deficiency can occur. Thyroxine is reduced due to decreased thyroid binding globulin. Microcytic hypochromic anaemia is typical. It is iron-therapy resistant. Prognosis The prognosis depends on the cause of nephrotic syndrome. It is usually good in children, because minimal change disease responds very well to steroids and does not cause chronic renal failure. However other causes such as focal segmental glomerulosclerosis frequently lead to end stage renal disease. Factors associated with a poorer prognosis in these cases include level of proteinuria, blood pressure control and kidney function GFR. References ^ a b c Fogo AB, Bruijn JA. Cohen AH, Colvin RB, Jennette JC. Fundamentals of Renal Pathology. Springer. ISBN 978-0387-31126-5. ^ Hodson E, Willis N, Craig J 2007. Corticosteroid therapy for nephrotic syndrome in children. Cochrane database of systematic reviews Online 4: CD001533. doi:10.1002/14651858.CD001533.pub4. PMID 17943754. Brenner, Barry M. or 2004. Brenner Rector's The Kidney, seventh ion. W.B. Saunders Company. ISBN 0-7216-0164-2. External links Nutrition Care Manual from the American Dietetic Association Information from the NephCure Foundation Childhood Nephrotic Syndrome - National Institute of Diabetes and Digestive and Kidney Diseases NIDDK, NIH Adult Nephrotic Syndrome - National Institute of Diabetes and Digestive and Kidney Diseases NIDDK, NIH http://www.nephroticsyndrome.com Nephrotic Syndrome expalined and Homeopathic treatment view described. From the Homoeopathy India Foundation, India 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 Retrieved from http://en..org/wiki/Nephrotic_syndrome Categories: Kidney diseases | Pediatrics | SyndromesHidden categories: Cleanup from April 2008 | All pages needing cleanup | Articles needing additional references from August 2008 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 Deutsch Eesti Español Français Hrvatski Italiano Nederlands 日本語 Polski Português Svenska 中文 This page was last modified on 3 September 2008, at 05:21
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