Lupus nephritis overview: Difference between revisions
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===Laboratory Findings=== | ===Laboratory Findings=== | ||
Laboratory findings consistent with the diagnosis of systemic lupus erythematosus include [[autoantibody]] elevation of [[ANA]], [[anti-dsDNA antibody]], [[anti-SM antibody]], and [[antiphospholipid antibodies]], and a decrease in [[complement]] levels. Nonspecific laboratory findings include mild [[pancytopenia]], elevated levels of [[creatinine]] and [[proteinuria]] due to [[renal failure]] (secondary to [[nephritis]]), elevated levels of [[ESR]] and [[C-reactive protein|CRP]] as [[Acute phase reactant|acute phase reactants]], decreased level of [[Complement|complements]], and positive [[Coombs test|direct Coombs test]]. | |||
===Electrocardiogram=== | ===Electrocardiogram=== | ||
Revision as of 19:26, 27 July 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Omer Kamal, M.D.
Overview
Historical Perspective
Lupus Nephritis was first discovered by Osler and Jadassohn, two physicians, in 1948 by the discovery of the LE cell in 1948. The word "lupus" means wolf in Latin, as the destructive injuries SLE causes brought to mind wolf bites. The history of lupus erythematosus can be divided into three periods: classical, neoclassical, and modern. The classical period mostly refers to ancient history, when there was no exact definition of the disease. During the neoclassical lupus era, scientists investigated the manifestations of lupus and worked to define the disease's action. Modern history is mostly focused on a microscopical understanding of the disease and pathogenesis of SLE.
Classification
Lupus nephritis may be classified according to the Renal Pathology Society/International Society of Nephrology (RPS/ISN) classification which includes minimal mesangial lupus nephritis (class I), mesangial proliferative lupus nephritis (class II), focal lupus nephritis (class III), diffuse lupus nephritis (class IV), lupus membranous nephropathy (class V) and advanced sclerosing lupus nephritis (class VI)
Pathophysiology
Systemic lupus erythematosus (SLE, or lupus) is an autoimmune disease. This means there is a problem with the body's immune system. Normally, the immune system helps protect the body from harmful substances. But in patients with an autoimmune disease, the immune system cannot tell the difference between harmful substances and healthy ones. As a result, the immune system attacks otherwise healthy cells and tissue.
Causes
There are no established direct causes of systemic lupus erythematosus. Common contributory factors in the development of systemic lupus erythematosus include geneticpredisposition, auto-immune diseases, and use of drugs. Less common factors include environmental factors and exposure to ultraviolet (UV) light.
Differentiating Hereditary pancreatitis from Other Diseases
Lupus nephritis must be differentiated from other glomerular diseases that may cause hematuria, proteinuria, or renal failure. The various types of glomerular diseases should be differentiated from each other based on associations, presence of pitting edema, hemeturia, hypertension, hemoptysis, oliguria, peri-orbital edema, hyperlipidemia, type of antibodies, light and electron microscopic features. The following table differentiates between various types of glumerular diseases.
Epidemiology and Demographics
The incidence of lupus nephritis is 34 to 51 percent in Blacks, 31 to 43 percent in Hispanics, 33 to 55 percent in Asians, and 14 to 23 percent in Whites. In 2005, Incidence was fiund to be 5.1 (Overall), 1.9 (Adult men), 8.2 (Adult women).The incidence of Lupus nephritis increases with age upto 50 years; the median age at diagnosis is 25 years.Chronic disease name is usually first diagnosed among middle age patients. African Americans have a higher frequency of developing Lupus nephritis in the United States.
Risk Factors
Common risk factors in the development of Lupus nephritis may be occupational, environmental, genetic, and viral.
Screening
According to the United States Preventive Services Task Force, screening for systemic lupus erythematosus is not recommended.
Natural History, Complications, and Prognosis
Common complications of Lupus nephritis include microscopic hematuria, nephrotic syndrome, celluar casts, elevated creatinine and destruction of more than 50% of glomeruli.
Diagnosis
Diagnostic study of choice
In SLE, nephritis we suspect renal involvment by an abnormal urinalysis and/or increased serum creatinine. Histopathologic findings on renal biopsy confirm the diagnosis.
History and Symptoms
As a manifestation of SLE, Lupus nephritis shares most of the symptoms with SLE. A positive history of familial lupus, skin rashes (especially photosensitive skin rashes), arthritis, and fatigue may be suggestive of systemic lupus erythematosus. The most common symptoms of SLE include constitutional symptoms like fatigue, fever, myalgia, and weight changes. The organ-specific symptom mostly occur with disease progression. SLE may show a variety of symptoms in different organs depending on its complications. eg.g Foamy urine.
Physical Examination
In the earlier stages of the disease, patients appear well, while in the late stages of the disease, patients are clearly ill with multi-organ involvement. The patient may show a wide range of skin manifestations including urticaria, bullous lesions, malar rash, and scarring alopecia. The patient may develop nasal and oral ulcers. Arthritis may lead to a decreased range of motion, joint effusion, and arthralgia. Neurological manifestations including psychosis, cognitive impairment, and hallucinations, may also be present.
Laboratory Findings
Laboratory findings consistent with the diagnosis of systemic lupus erythematosus include autoantibody elevation of ANA, anti-dsDNA antibody, anti-SM antibody, and antiphospholipid antibodies, and a decrease in complement levels. Nonspecific laboratory findings include mild pancytopenia, elevated levels of creatinine and proteinuria due to renal failure (secondary to nephritis), elevated levels of ESR and CRP as acute phase reactants, decreased level of complements, and positive direct Coombs test.