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Definition of Nephritis: Inflammation of the kidney. Nephritis can be acute or chronic.
Acute nephritis is most commonly caused by hypersensitivity (allergy) to drug therapy. Recognition of a drug-related cause is important because severe renal damage is often preventable or reversible. The most frequent drugs involved include analgesics (e.g., acetaminophen and aspirin), cyclosporine and tacrolimus (immunosuppressants used in transplantation and treatment of some autoimmune disorders), anti-cancer drugs (e.g., cisplatin; nitrosoureas; rarely, carboplatin), and lithium (for depressive disease). Sarcoidosis, Legionella, leptospirosis, Streptococcus, and viral infections, and certain Chinese herbs may also be responsible for acute nephritis.
Chronic nephritis can similarly be due to a very large number of causes, including drug hypersensitivity, autoimmunity, infections, radiation of the kidney, obstruction of the urinary tract, hypertension (high blood pressure is a very well known cause of chronic nephritis), sickle cell disease, and polycystic disease of the kidney.
Nephritis also results from metabolic and toxic disorders, including the deposition of urates (uric acid) in the kidney, hypercalcemia (high blood calcium) with deposition of calcium in the kidney, chronic lead intoxication, and cadmium toxicity.
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Urticaria, nephritis, and pseudotumor cerebri.Department of Rheumatic and Immunologic Disease, Cleveland Clinic Foundation, Ohio 44195.
ReplyDeleteThe spectrum of chronic urticarial disease ranges from chronic urticarial skin lesions alone to well-characterized systemic lupus erythematosus with urticarial vasculitis as the major skin manifestation. Within this spectrum is the syndrome of urticarial vasculitis associated with systemic disease manifestations. There have been six previously recorded cases of urticarial vasculitis associated with pseudotumor cerebri. At least two of these have included membranoproliferative glomerulonephritis. The authors report a case of chronic urticarial disease associated with pseudotumor cerebri and membranoproliferative glomerulonephritis, but without demonstrable vasculitis. It is possible that this represents a distinct entity within the spectrum of chronic urticarial disease and cca be easily screened for in clinical practice.
Muckle-Wells Syndrome and Urticaria
ReplyDeleteMuckle-Wells Syndrome (MWS) is another CAPS disorder that has been found to be caused by genetic mutations on the CIAS1 gene that encodes the cryopyrin protein. MWS gene mutations have been found to be transmitted as an autosomal DOMINANT disorder (meaning if one parent has the mutation, it can be given to the children, and DOES NOT require two parents to have the mutation to pass the syndrome genetically to their offspring, like other syndromes that are caused by recessive mutations). There can be a variable level of expression of symptoms and number of cases of MWS within families, and even from one family to another. Most people with MWS do not have the same degree of inflammatory damage to their bodies NOMID, and do not have mental or cognitive affects like NOMID, so many more people with MWS have been able to get married and have children over generations. This has led to the syndrome being present in some families. However, the mutation can occur randomly and spontaneously during early cell divisions at conception as well.
Muckle-Wells Syndrome and Urticaria
ReplyDeleteMuckle-Wells Syndrome (MWS) is another CAPS disorder that has been found to be caused by genetic mutations on the CIAS1 gene that encodes the cryopyrin protein. MWS gene mutations have been found to be transmitted as an autosomal DOMINANT disorder (meaning if one parent has the mutation, it can be given to the children, and DOES NOT require two parents to have the mutation to pass the syndrome genetically to their offspring, like other syndromes that are caused by recessive mutations). There can be a variable level of expression of symptoms and number of cases of MWS within families, and even from one family to another. Most people with MWS do not have the same degree of inflammatory damage to their bodies NOMID, and do not have mental or cognitive affects like NOMID, so many more people with MWS have been able to get married and have children over generations. This has led to the syndrome being present in some families. However, the mutation can occur randomly and spontaneously during early cell divisions at conception as well.
Testing for Muckle-Wells Syndrome
ReplyDeleteDiagnosing and Testing for Muckle-Wells Syndrome
Chronic Urticaria and Nephritis
ReplyDeleteA 34-year-old white female first presented with fatigue, oedema and a Raynaud's phenomenon. She was found to be hypertensive and had a nephrotic syndrome with elevated serum creatinine. The medical history was unremarkable except for chronic urticaria and hypothyroidism of unknown origin. She denied any arthralgias, myalgias, dysphagia, dyspnoea or abortions. Immunoserology showed an elevated ANA, positive SS-A antibodies and a profound hypocomplementemia. Kidney biopsy was performed, which showed some intracapillary glomerular precipitations, an irregular contour of glomerular capillaries and a moderate mesangial cell proliferation as well as a mild, focal interstitial nephritis. Immunofluorescence staining showed mesangial deposits of IgM with some IgG as well as C3 and C1q in the glomerular capillary loops. EM revealed immunoprecipitations in the mesangial cells including scarce deposits in the subepithelial space.
Glomerulonephritis, Membranoproliferative (Nephritis)
ReplyDeleteMembranoproliferative glomerulonephritis (MPGN) is an uncommon cause of chronic nephritis that occurs primarily in children and young adults. This entity refers to a pattern of glomerular injury based on characteristic histopathologic findings, including (1) proliferation of mesangial and endothelial cells and expansion of the mesangial matrix; (2) thickening of the peripheral capillary walls by subendothelial immune deposits and/or intramembranous dense deposits; and (3) mesangial interposition into the capillary wall, giving rise to a double-contour or tram-track appearance on light microscopy.
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ReplyDeleteKey Words
ReplyDeleteHypocomplementemic urticarial vasculitis
Membranoproliferative glomerulonephritis
Membranous nephropathy
Steroid therapy
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Abstract
A 49-year-old-man developed proteinuria in 1978. He was diagnosed as having membranous nephropathy by renal biopsy and was treated with prednisolone. The proteinuria disappeared completely and the treatment was stopped. In 1995, after complete remission, he developed nephrotic syndrome with chronic urticaria and hypocomplementemia. Renal biopsy revealed membranoproliferative glomerulonephritis (type I) and skin biopsy showed leukocytoclastic vasculitis, which was compatible with hypocomplementemic vasculitis syndrome. Steroid therapy was very effective.
Copyright © 2001 S. Karger AG, Basel
Membranoproliferative Glomerulonephritis Associated with Hypocomplementemic Urticarial Vasculitis after Complete Remission of Membranous Nephropathy