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Latest revision as of 14:32, 29 April 2019

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aarti Narayan, M.B.B.S [2], Aida Javanbakht, M.D., Mehrian Jafarizade, M.D [3]

Synonyms and keywords: light chain deposition disease, LCDD

Overview

Localized deposition of fibrils and proteins in glumerole is called glomerular deposition disease. Light chain deposition disease (LCDD) is one of the glomerular deposition disease. It's a rare blood cell disease which is characterized by deposition of fragments of infection-fighting immunoglobulins, called light chains, in the body. These light chain deposits damage organs and cause disease. The kidneys are almost always affected and this often leads to Chronic renal failure. About half of people with light chain deposition disease also have multiple myeloma. Unlike in AL Amyloidosis, in which light chains are laid down in characteristic amyloid deposits, in LCDD, light chains are deposited in non-amyloid granules. Light chains in LCDD are kappa light chains in granular shape.^[1]

Classification

Glomerular deposition disease may be classified according to pathology findings into into 5 groups: ^[2]^[3]

LCDD
Amyloidosis
Fabry's disease
Fibrillary immuno-tactoid glumerulopathy
Collagenofibrotic glomerulopathy

Pathophysiology

Pathogenesis:

Deposits of abnormal or extra production of proteins, lipids and fibrills in the glomeruls cause glomerular deposition diseases.

-In LCDD:

light chains are small polypeptides produced by B lymphocytes.They are sub units of antibodies. Kappa and Lambda are two types of light chains. Excess production of Kappa chain and accumulation in the renal glumerulus cause LCDD. The exact mechanism of increase production of light chains and reason that renal attracts them is unknown. These chains can deposit in all parts of renal glumeruls and tubuls.

Accumulation of monoclonal light chains and matrix proteins cause increase quantity and activity of transforming growth factor-beta (TGF-beta). TGF-beta inhibits mesangial cell proliferation and increase matrix protein production

Accumulation of matrix proteins compress the glomerular capillaryies and cause renal failure.^[4]

Besides glumerulus,light chains may accumulate in renal tubular and make tubular casts. These casts cause interstitial inflammation and renal failure.^[5]

- In Amyloidosis:

Amyloids (misfolding and aggregation of normally soluble proteins) deposit in the nephrones and cause renal failure.

- In Fabry's disease:

A deficiency of the enzyme alpha galactosidase A causes deposition of glycolipid in the nephrones and cause renal failure.

- In Fibrillary immuno-tactoid glomerulopathy:

Fibrills (larger than amyloids) deposit in subendothelial and mesangium of the nephrones and cause function impairment.

- In Collagenofibrotic glomerulopathy:

Type III collagen fibers deposit in the subendothelial and mesangium in the kidney.

Microscopic Pathology

On light microscopy:

-In LCDD:

No glomerular and vascular abnormality
Some tubular dilation with flattened epithelium suggest acute tubular injury
Negative Congo Red stain

- In Amyloidosis:

Typical green birefringence under polarized light after Congo red staining (appears in red under normal light)

- In Fabry's disease:

Hypertrophic podocytes of glomerul, foamy appearing vacuoles and mesangial widening. Vacuolated cells will be seen in PAS stain.^[6]

- In Fibrillary immuno-tactoid glumerulopathy:

Capillary wall thickening, matrix expansion,interstitial infiltration and necrosis in renal tubules and negative Congo red stain.^[7]

- In Collagenofibrotic glomerulopathy:

Diffuse increase in the mesangial matrix, capillary walls widening, and collagen fibers in the glomerular basement membrane.^[8]

On electron microscopy :

-In LCDD:

Ground-pepper–like deposits in the mesangial and the endothelial of the glomerular basement membrane. Also, in renal tubules if there is tubular involvement.

- In Amyloidosis:

Endothelium, glomerular basement membrane, and podocytes thickening.^[9]

- In Fabry's disease:

Deposition of glicolipids in lysosomes of podocytes and glomerular parietal epithelial cells.

- In Fibrillary immuno-tactoid glomerulopathy:

Predominant fibrils in the subepithelial of glomerular capillary.

- In Collagenofibrotic glomerulopathy:

Deposition of irregular collagenous fibers in the mesangium and subendothelial space of the renal glumerol.^[10]

Genetics

Fabry's disease is transmitted in X-linked recessive pattern.
Hereditory types of amyloidosis is transmitted in autosomal dominant pattern.
There exact genetic association for LCDD, Fibrillary immuno-tactoid glumerulopathy, and Collagenofibrotic glomerulopathy are unknown.

Causes

The specific etiology that cause extra or abnormal production of fibrills and chains in the glomerular depositional diseases is unknown.

Differentiating from Other Diseases

Glomerular deposition disease should be differentiate from other causes of glomerular disease. The various types of glomerular diseases may 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:

Glomerular diseases	Disease		History and Symtoms									Laboratory Findings		Pathology
Glomerular diseases	Disease		History	Systemic symptoms	Hemeturia	Proteinuria	Hypertension	Pitting edema	Oliguria	Nephrotic features	Nephritic features	Hyperlipidemia and hypercholesterolemia	Auto-antibodies, Complements	Light microscope	Electron microscope	Immunoflourescence pattern
Acute Nephritic Syndromes	Poststreptococcal Glomerulonephritis^[11]^[12]^[13]		Streptococcal skin infections Streptococcal pharyngitis 2-3 weeks after infection	Fever Fatigue Skin rash	+/-	+	+/-	+/-	+/-	+/-	+/-	+/-	Anti-dsDNA antibodies Anti-C1q antibodies Antineutrophil cytoplasmic antibodies (ANCA)	Hypercellular and inflamed glomeruli	Sub-epithelial immune complex deposits Obliteration of epithelial cell foot processes	Immune complex GN Granular deposit
	Renal disease due to Subacute Bacterial Endocarditis, or cardiac shunt (Atrioventricular)^[14]^[15]		History of infective endocarditis mostly due to S. aureus Cardiac shunt	Fever Fatigue Weight loss	+/-	+	+/-	+/-	+/-	+/-	+/-	+/-	ANCA (myeloperoxidase) positive in 1/3 Activation of the alternative complement pathway (Decreased C3, C4) Positive RF Positive anti-GBM autoantibodies	Crescentic GN is the most common pathological features Diffuse membranoproliferative glomerulonephritis features Focal proliferative GN Mesangial proliferative GN	Mesangial deposits, Subendothelial deposits Subepithelial "humps," in minority of cases	Pauci-immune GN
	Lupus Nephritis^[16]		History of SLE features	Lupus criteria: Malar rash Arthritis Arthralgia Anemia Easy bruising	+/-	+	+/-	+/-	+/-	+/-	+/-	+/-	Anti-C1q antibodies Anti-dsDNA	Differs based on the disease classification	Differs based on the disease classification	Differs based on the disease classification, mostly immune complex GN Granular deposit
	Antiglomerular Basement Membrane Disease (Goodpasture's syndrome)^[17]^[18]		Young adults	Dry cough Hemoptysis Malaise Fever and chills Arthralgia Fatigue Lethargy Pallor Anorexia Easy bruising	+	+	+	+	+	+	-	-	ANCA (myeloperoxidase) Positive anti-GBM autoantibodies	Hypercellular and inflamed glomeruli (Crescent formation)	Diffuse thickening of the glomerular basement membrane with absence of sub-epithelial and sub-endothelial deposits	Immune complex GN Linear deposit
	IgA Nephropathy^[19]^[20]		Young children History of mucosal infections (e.g. gastroenteritis) and upper respiratory tract infection 2-3 days after infection (synpharyngitic)	Low grade fever Flank pain	+	+/-	+	+/-	+	-	+	-	Immune complex deposition	Crescent formation	Mesangial proliferation	Immune complex GN, granular deposite
	Disease		History	Systemic symptoms	Hemeturia	Proteinuria	Hypertension	Pitting edema	Oliguria	Nephrotic features	Nephritic features	Hyperlipidemia and hypercholesterolemia	Auto-antibodies, Complements	Light microscope	Electron microscope	Immunoflourescence pattern
	ANCA Small-Vessel Vasculitis^[21]^[22]	Granulomatosis with Polyangiitis (Wegener's)^[23]^[24]^[25]	Middle age male	Constitutional symptoms Dyspnea Purpura Arthralgias Neurologic dysfunction Sinusitis Otitis media Epistaxis.	+	+	+	+/-	+	-	+	-	ANCA	Necrotizing and crescentic glomerulonephritis	Subendothelial edema Microthrombosis Degranulation of neutrophils	Pauci-immune GN
		Microscopic Polyangiitis^[26]	+/-	Constitutional symptoms Dyspnea Purpura Arthralgias Neurologic dysfunction	+	+	+	+	+	+		-	P-ANCA	Hypercellular and inflamed glomeruli (Crescent formation)	Hypercellular and inflamed glomeruli (Crescent formation)	Pauci-immune GN
		Churg-Strauss Syndrome^[27]	+/-	Asthma Sinusitis Myalgia Arthralgia Purpura Arrythmias Peripheral neuropathy	+	+	+	+	+	+		-	C-ANCA	Hypercellular and inflamed glomeruli (Crescent formation)	Hypercellular and inflamed glomeruli (Crescent formation)	Pauci-immune GN
	Membranoproliferative Glomerulonephritis^[28]^[29]		Idiopathic Hepatitis B and C (Type 1) C3 nepritic factor (Type2)	Hematuria Oliguria Periorbital edema Hypertension	+	+	+	+/-	+	+	-	-	-	Thick glomerular basement membrane (Tram-track appearance)	Mesangial proliferation Leukocyte infiltration	Immune complex GN Granular deposite
	Henoch-Schönlein purpura ^[30]		Most common in young male, following upper respiratory infections	Skin manifestations- Palpable purpura on buttocks Gastrointestinal manifestations- Abdominal pain Melena Bloody diarrhea Hematemesis Joints manifestations- Arthralgia	+	+	+	+/-	+	+	-	-	-	Diffuse mesangial IgA deposits often associated with mesangial hypercellularity	Diffuse mesangial IgA deposits often associated with mesangial hypercellularity	Immune complex GN, granular deposite
	Disease		History	Systemic symptoms	Hemeturia	Proteinuria	Hypertension	Pitting edema	Oliguria	Nephrotic features	Nephritic features	Hyperlipidemia and hypercholesterolemia	Auto-antibodies, Complements	Light microscope	Electron microscope	Immunoflourescence pattern
	Cryoglobulinemia^[31]		Patients having cryoglobulinemia may have positive history of: Hepatitis C infection Hepatitis B infection Leg ulcers Recurrent thrombosis	Pulmonary symptoms: Difficulty breathing Cough Cutaneous symptoms: Purpura Skin ulcer Gastrointestinal symptoms: Abdominal pain General symptoms: Fever Arthralgia, Myalgia Fatigue Blurring/loss of vision Diplopia Confusion	+/-	+	+/-	+	+/-	+/-	+/-	+/-	+/-	Membranoproliferative glomerulonephritis	Mesangial and subendothelial deposits	Prominent IgM and C3
Nephrotic Syndrome	Minimal Change Disease^[32]^[33]		Young children Recent infection and immunization Atopy Hodgkin lymphoma Thrombosis (due to urinary loss of antithrombin-III)		-	+	-	+	+/-	+	-	+		Normal	Fusion of podocytes	-
	Focal Segmental Glomerulosclerosis^[34]^[35]^[36]		Idiopathic HIV Heroine use Sickle cell disease Interferon Severe obesity Mixed cryoglobulinemia (Hepatitis C)		-	+	-	+	+/-	+	-	+		Focal (some glomeruli) and segmental (only part of glomerulus)	Effacement of podocytes	-
	Membranous Glomerulonephritis^[37]^[38]		Idiopathic Hepatitis B and C Solid tumors Systemic lupus erythematosus Drugs (NSAIDS, pencilamine, gold, captopril)		-	+	-	+	+/-	+	-	+	Immune complex deposition	Thick glomerular basement membrane	Sub-epithelial immune complex depositis with 'spike and dome' appearance	Immune complex GN, granular deposite
	Diabetic Nephropathy^[39]^[40]^[41]^[42]^[43]^[44]^[45]^[46]^[47]^[48]		For more information on diabetes click here.		-	+	-	+	+/-	+	-	+		Diffuse mesangial matrix expansion (nodular glomerulosclerosis) Increased mesangial hypercellularity Prominent glomerular basement membranes Thick basement membrane without any deposit	Nodular glomerulosclerosis	-
	Disease		History	Systemic symptoms	Hemeturia	Proteinuria	Hypertension	Pitting edema	Oliguria	Nephrotic features	Nephritic features	Hyperlipidemia and hypercholesterolemia	Auto-antibodies, Complements	Light microscope	Electron microscope	Immunoflourescence pattern
	Glomerular Deposition Diseases	Light Chain Deposition Disease^[49]	Occurs in the setting of high tumor burden	-	-	+	-	+	+/-	+	-	+	-	Light-chain deposits	Granular deposits on electron microscopy	Detection of light chain deposits using anti–light chain antibody
		Renal Amyloidosis^[50]^[51]^[52]^[53]	For the secondary causes of amloidosis: Tuberculosis Familial Mediterranean fever Rheumatoid arthritis Multiple myeloma	Dyspnea Lethargy Weight loss Bleeding tendency	-	+	-	+	+/-	+	-	+	-	Diffuse glomerular deposition of amorphous hyaline material (nodular pattern), in mesangium (weakly staining with periodic acid-Schiff (PAS)	Nodular deposit	AA amyloidosis type: negative for immunoglobulins and complement AL amyloidosis type: Positive for lambda or kappa light chains
		Fibrillary-Immunotactoid Glomerulopathy^[54]	Malignancy Monoclonal gammopathy Autoimmune disease	-	+/-	+	+/-	+/-	+/-	+	+/-	+/-	-	Diffuse sclerosing glomerulonephritis Diffuse proliferative glomerulonephritis Membranoproliferative glomerulonephritis Mesangioproliferative/sclerosing disease Membranous glomerulonephritis	Large fibrillar deposits in the mesangium randomly Glomerular capillary walls different from amloidosis No staining with Congo red or thioflavine-T or with antibodies to a specific type	Positive for immunoglobulin G (IgG), C3 Kappa and lambda (ie, polyclonal) light chains
		Fabry's Disease^[6]^[55]^[56]	Family history suggestive of the disorder	Anhidrosis or decreased sweating Fatigue Angiokeratomas Burning pain of the extremities Corneal opacities. Dysphagia Abdominal pain Steatorrhea Delayed puberty Raynaud's phenomenon Hearing loss Telangiectasis Ataxia	-	+	-	+	+/-	+	-	+	-	Vacuolization of visceral glomerular epithelial cells (podocytes) and distal tubular epithelial cells Glycolipid accumulation	Myeloid or zebra bodies: Gb3 deposition within enlarged secondary lysosomes as lamellated membrane structures Inclusions, composed of concentric layers (onion skin appearance)	-
Basement Membrane Syndrome	Alport's Syndrome^[57]^[58]^[59]^[60]^[61]^[62]		Positive family history	Auditary: Early Tinnitus Vertigo High-frequency progressive bilateral hearing loss Occular problems: Refractory Error Arcus Glaucoma Band Keratopathy Lenticonus Spherophakia Cataracts	-	+	-	+	+/-	+	-	+	-	Early stage: unremarkable Late stages: glomerulosclerosis, interstitial fibrosis, and interstitial foam cells (due to prolonged proteinuria).	Within glomerular basement membrane (GBM): longitudinal splitting of the lamina densa	Absence of staining of the alpha-3, alpha-4, and alpha-5 (IV) chains in the glomerular basement membrane Minimal binding to a glomerulus in indirect immunofluorescence microscopy with anti-glomerular basement membrane antibodies
	Disease		History	Systemic symptoms	Hemeturia	Proteinuria	Hypertension	Pitting edema	Oliguria	Nephrotic features	Nephritic features	Hyperlipidemia and hypercholesterolemia	Auto-antibodies, Complements	Light microscope	Electron microscope	Immunoflourescence pattern
	Thin Basement Membrane Disease^[63]^[64]		Positive family history Gross hematuria following upper respiratory tract infection	-	-	+	-/+	-	-/+	-	-/+	-	-	-	Diffuse thinning of the glomerular basement membranes (GBM)	-
	Nail-Patella Syndrome^[65]^[66]		Positive family history	Poorly developed fingernails, toe nails, and patellae (kneecaps). Elbow deformities Abnormally shaped pelvis bone (hip bone) Knee may be small, deformed or absent	+	+	-	-	-	-	-	-	-	Mostly unremarkable changes Secondary FSGS Late stages: Global glomerulosclerosis, Tubulointerstitial fibrosis	Glomerular basement membranes (GBMs): Focal or diffuse irregular thickening with electron-lucent areas (moth-eaten appearance) containing type III collagen bundles. Similar collagen fibrils can be seen in mesangial matrix. Podocytes: Segmental effacement of foot processes.	Immunofluorescence studies are typically negative. Nonspecific IgM and C3 deposition may be seen in sclerotic glomeruli.
Glomerular-Vascular Syndromes	Hypertensive Nephrosclerosis^[67]		Chronic hypertension	Hypertensive retinal changes. High jugular venous pressure Rales from pulmonary edema on auscultation .Signs of left ventricular hypertrophy Left ventricular heave Shifting of apex towards the left S3 and gallop rhythm Loud S2 Ascites Paralysis from stroke secondary to hypertension Inferior limb edema	+/-	+/-	+	+/-	+/-	+/-	-	+/-	-	Interstitial fibrosis and atrophy Medial thickening and intimal fibrosis of medium-sized and larger vessels Arteriolar thickening, and hyalinosis Chronic stages: Global sclerosis Focal segmental sclerosis
	Cholesterol Emboli^[68]		Atherosclerotic cardiovascular disease Anticoagulation therapy Cardiopulmonary resuscitation Hypertension Aortic aneurysm Hypercholesterolemia Smoking history Male sex Age over 55 years Vascular procedures Invasive angiography Aortic aneurysm rupture or surgery Vascular surgery	Depends on the organ involved	+/-	+/-	+	+/-	+/-	+/-	-	+/-	-	Atheroemboli are seen in interlobular and arcuate arteries, as lance-shaped clefts, due to dissolution of cholesterol crystals Acute lesions: Atheroemboli are surrounded by red blood cells, fibrin, and leukocytes, with multinucleated giant cell reactions Chronic lesions: Cholesterol clefts are surrounded by intimal fibrosis Vessel recanalization of chronic lesions can occur. Global and segmental sclerosis of glomeruli may be present.	Extensive foot process effacement can be seen	Not specific changes
	Disease		History	Systemic symptoms	Hemeturia	Proteinuria	Hypertension	Pitting edema	Oliguria	Nephrotic features	Nephritic features	Hyperlipidemia and hypercholesterolemia	Auto-antibodies, Complements	Light microscope	Electron microscope	Immunoflourescence pattern
	Sickle Cell Disease^[69]		Positive family history	Pain and/or bone pain Dactylitis Blurry vision Persistent and painful erection Numbness Tingling Motor skill loss Speech deficits Gait disturbance Leg ulceration Jaundice	+/-	+/-	+/-	-	-	-	-	-	-	Glomerular hypertrophy Hemosiderin deposits Focal areas of hemorrhage or necrosis Chronic stage: interstitial inflammation, edema, fibrosis, tubular atrophy, and papillary infarcts Glomerular enlargement and focal segmental glomerulosclerosis (FSGS)
	Thrombotic Microangiopathies^[70]		Click for more information on Thrombotic Microangiopathies.		+	+/-	+	+/-	+/-	+/-	-	-	-	Acute stage: Inravasculr fibrin thrombi Chronic stage: Endocapillary hypercellularity. Intimal proliferation of arterioles	Swollen glomerular endothelial cells with loss of fenestrations Chronic stage: interposed cells with new GBM matrix material deposition.	Thrombi stain positive for fibrinogen
	Antiphospholipid Antibody Syndrome ^[71]^[72]^[73]		Thrombosis Miscarriage History of nephropathy History of hematologic abnormalities Nonthrombotic neurologic symptoms, such as migraine headaches Pulmonary hypertension	Fatigue Fever Weight loss Venous thrombosis Arterial thrombosis Thrombocytopenia Recurrent fetal loss	+	+/-	+	+/-	+/-	+/-	-	-	-	Acute stage: Inravasculr fibrin thrombi Chronic stage: Endocapillary hypercellularity. Intimal proliferation of arterioles	Swollen glomerular endothelial cells with loss of fenestrations Chronic stage: interposed cells with new GBM matrix material deposition.	Thrombi stain positive for fibrinogen

Some infectious diseases such as HIV, HBV, HCV, syphilis, leprosy, malaria, and schistosomiasis may cause glomerular diseases.

Epidemiology and Demographics

The incidence of glomerular deposition disease depends on the type of the disease. Collagenofibrotic glomerulopathy and Fibrillary immuno-tactoid glumerulopathy are rare. LCDD is unknown. Most of the patients are men with the mean age of 58 years ^[1]. The incidence of amyloidosis is 1.2 per 100,000 individuals per year ^[74]. The incidence of Fabry's disease is 1 in 50,000 males ^[75].

Renal involvement is the most common cause of mortality and morbidity in these patients. Survival varies between months to 10 years in patients with LCDD ^[76].

Risk Factors

There are no established risk factors for glomerular deposition disease.

Screening

There is insufficient evidence to recommend routine screening for glomerular deposition disease.

Natural History, Complications, and Prognosis

If left untreated, most of the patients will suffer from ESRD in the future. Common complication of glomerular deposition diseases is renal failure. Prognostic factors of glomerular deposition diseases include:^[1]

Age
underlying hematologic disease
Light chain deposition in other organs
Renal function
other medical diseases like diabetic nephropathy

Prognosis is generally not good. The median time to progression to chronic renal failure in LCDD is 2.7 years. After 5 years, about 37% of patients with LCDD are alive and do not have end stage renal disease.

Diagnosis

Diagnostic Study of Choice

Biopsy is the gold standard test for the diagnosis of glomerular deposition disease.^[77]

History and Symptoms

Usually patients are asymptomatic in early stages. Symptoms are nonspecific like fatigue and weight loss. In case of edema patients may come with edema. Patients may come with abdominal pain because of deposition of light chains in the liver may lead to hepatomegaly, portal hypertension and liver failure. Patients may come with palpitation because the heart is affected in up to 80% of patients with LCDD, and may cause arrhythmias restrictive cardiomyopathy, cardiomegaly, and congestive heart failure.^[78]

Physical Examination

Physical exam is normal most of the time.
Sometimes there is an organomegaly which depends on involvement of the organ like hepatomegaly

Laboratory Findings

Laboratory findings consistent with the diagnosis of glomerular deposition disease include:^[79]^[80]^[81]

Proteinuria (30-50% of cases have nephrotic syndrome)
Hematuria (usually microscopic)
Abnormal liver enzyme ( in case of liver involvement)
Presence of a monoclonal protein in serum or urine

Electrocardiogram

Arrhythmia like atrial fibrillation ( in case of heart involvement).

X-ray

There are no x-ray findings associated with glomerular deposition disease.

Echocardiography or Ultrasound

Echocardiography:

Echocardiography may be helpful in the diagnosis of glomerular deposition disease. Findings on echocardiography suggestive of glomerular deposition disease in case of heart involvement include:^[82]

Low EF
Diffuse hypokinesia
Left ventricular concentric hypertrophy
Low diastolic compliance

Ultrasound:

There are no ultrasound findings associated with glomerular deposition disease.

CT scan

There are no CT scan findings associated with glomerular deposition disease.
In severe cases the size of the organ will increase.

MRI

There are no MRI findings associated with glomerular deposition disease.
In severe cases the size of the organ will increase.

Other Imaging Findings

There are no other imaging findings associated with Glomerular deposition diseases.

Other Diagnostic Studies

There are no other diagnostic studies associated with Glomerular deposition diseases.

Treatment

Medical therapy:

70% of cases untreated patients will become to ESRD. There is no standard treatment for Glomerular deposition diseases. Medical therapy options for LCDD include:^[83]^[84]^[85]

Symptomatic treatment for renal dysfunction like ACE inhibitors like Lisinopril 2.5 to 5 mg orally once a day ( dose depends on the level of the kidney damage).

If patient has LCDD and Multiple Myeloma (MM), should receive treatment per MM guideline like Bortezomib1.3 mg/m^2 IV on days 1,4,8,11,22,25,29,32 of 42 day cycle for cycles 1-4.
High-dose melphalan in conjunction with autologous stem cell transplantation

Surgery

Surgery is not the first-line treatment option for patients with glomerular deposition disease. Surgery is usually reserved for patients with either:^[86]^[87]

LCDD patients who have detectable light chains in urine or serum
ESRD

Primary Prevention

There are no established measures for the primary prevention of Glomerular deposition diseases.

Secondary Prevention

There are no established measures for the secondary prevention of Glomerular deposition diseases.

References

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↑ Aoki T, Hayashi K, Morinaga T, Tomida H, Hishida M, Yamamoto S, Kajiwara N, Tamai H (May 2015). "Two brothers with collagenofibrotic glomerulopathy". CEN Case Rep. 4 (1): 85–89. doi:10.1007/s13730-014-0145-y. PMC 5413714. PMID 28509277.
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↑ Suzuki H, Kiryluk K, Novak J, Moldoveanu Z, Herr AB, Renfrow MB, Wyatt RJ, Scolari F, Mestecky J, Gharavi AG, Julian BA (October 2011). "The pathophysiology of IgA nephropathy". J. Am. Soc. Nephrol. 22 (10): 1795–803. doi:10.1681/ASN.2011050464. PMC 3892742. PMID 21949093.
↑ Wyatt RJ, Julian BA (June 2013). "IgA nephropathy". N. Engl. J. Med. 368 (25): 2402–14. doi:10.1056/NEJMra1206793. PMID 23782179.
↑ Higgins RM, Goldsmith DJ, Connolly J, Scoble JE, Hendry BM, Ackrill P, Venning MC (January 1996). "Vasculitis and rapidly progressive glomerulonephritis in the elderly". Postgrad Med J. 72 (843): 41–4. PMC 2398323. PMID 8746284.
↑ Jennette JC (March 2003). "Rapidly progressive crescentic glomerulonephritis". Kidney Int. 63 (3): 1164–77. doi:10.1046/j.1523-1755.2003.00843.x. PMID 12631105.
↑ Renaudineau Y, Le Meur Y (October 2008). "Renal involvement in Wegener's granulomatosis". Clin Rev Allergy Immunol. 35 (1–2): 22–9. doi:10.1007/s12016-007-8066-6. PMID 18172777.
↑ Weiss MA, Crissman JD (October 1984). "Renal biopsy findings in Wegener's granulomatosis: segmental necrotizing glomerulonephritis with glomerular thrombosis". Hum. Pathol. 15 (10): 943–56. PMID 6384024.
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↑ Sinico RA, Di Toma L, Maggiore U, Tosoni C, Bottero P, Sabadini E, Giammarresi G, Tumiati B, Gregorini G, Pesci A, Monti S, Balestrieri G, Garini G, Vecchio F, Buzio C (May 2006). "Renal involvement in Churg-Strauss syndrome". Am. J. Kidney Dis. 47 (5): 770–9. doi:10.1053/j.ajkd.2006.01.026. PMID 16632015.
↑ Alchi B, Jayne D (August 2010). "Membranoproliferative glomerulonephritis". Pediatr. Nephrol. 25 (8): 1409–18. doi:10.1007/s00467-009-1322-7. PMC 2887509. PMID 19908070.
↑ Davis AE, Schneeberger EE, Grupe WE, McCluskey RT (May 1978). "Membranoproliferative glomerulonephritis (MPGN type I) and dense deposit disease (DDD) in children". Clin. Nephrol. 9 (5): 184–93. PMID 657595.
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↑ Fogo AB, Lusco MA, Najafian B, Alpers CE (February 2016). "AJKD Atlas of Renal Pathology: Cryoglobulinemic Glomerulonephritis". Am. J. Kidney Dis. 67 (2): e5–7. doi:10.1053/j.ajkd.2015.12.007. PMID 26802335.
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↑ Jefferson JA, Shankland SJ (September 2014). "The pathogenesis of focal segmental glomerulosclerosis". Adv Chronic Kidney Dis. 21 (5): 408–16. doi:10.1053/j.ackd.2014.05.009. PMC 4149756. PMID 25168829.
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@@ Line 3: / Line 3: @@
 {{SI}}
-{{CMG}}; {{AE}} {{AN}},{{AIDA}} {{MJ}}
+{{CMG}}; {{AE}}{{AN}}, {{AIDA}}, {{MJ}}
 {{SK}} light chain deposition disease, LCDD
 ==Overview==
-Localized deposition of fibrils and proteins in glumerole is called glomerular deposition disease.
+Localized deposition of fibrils and proteins in glumerole is called [[glomerular deposition disease]].
+Light chain deposition disease (LCDD) is one of the glomerular deposition disease. It's a rare blood cell disease which is characterized by deposition of fragments of infection-fighting [[immunoglobulins]], called [[light chain]]s, in the body. These light chain deposits damage organs and cause disease. The kidneys are almost always affected and this often leads to [[Chronic renal failure]]. About half of people with [[light chain]] deposition disease also have [[multiple myeloma]]. Unlike in AL [[Amyloidosis]], in which [[light chain]]s are laid down in characteristic [[amyloid]] deposits, in LCDD, [[light chain]]s are deposited in non-amyloid granules. Light chains in LCDD are [[Light chain|kappa]] light chains in [[Granular cell|granular]] shape.<ref name="pmid14655186">{{cite journal |vauthors=Pozzi C, D'Amico M, Fogazzi GB, Curioni S, Ferrario F, Pasquali S, Quattrocchio G, Rollino C, Segagni S, Locatelli F |title=Light chain deposition disease with renal involvement: clinical characteristics and prognostic factors |journal=Am. J. Kidney Dis. |volume=42 |issue=6 |pages=1154–63 |date=December 2003 |pmid=14655186 |doi= |url=}}</ref>
-Light chain deposition disease (LCDD) is one of the glomerular deposition disease. It's a rare blood cell disease which is characterized by deposition of fragments of infection-fighting [[immunoglobulins]], called [[light chain]]s, in the body. These light chain deposits damage organs and cause disease. The kidneys are almost always affected and this often leads to [[Chronic renal failure]]. About half of people with [[light chain]] deposition disease also have [[multiple myeloma]]. Unlike in AL [[Amyloidosis]], in which [[light chain]]s are laid down in characteristic [[amyloid]] deposits, in LCDD, [[light chain]]s are deposited in non-amyloid granules. Light chains in LCDD are [[Light chain|kappa]] light chains in granular shape<ref name="pmid14655186">{{cite journal |vauthors=Pozzi C, D'Amico M, Fogazzi GB, Curioni S, Ferrario F, Pasquali S, Quattrocchio G, Rollino C, Segagni S, Locatelli F |title=Light chain deposition disease with renal involvement: clinical characteristics and prognostic factors |journal=Am. J. Kidney Dis. |volume=42 |issue=6 |pages=1154–63 |date=December 2003 |pmid=14655186 |doi= |url=}}</ref>.
 ==Classification==
-[[Glomerular deposition disease]]<nowiki/>s are classified in 5 types of diseases:
+Glomerular deposition disease may be classified according to pathology findings into into 5 groups: <ref name="pmid18045849">{{cite journal |vauthors=Alpers CE, Kowalewska J |title=Fibrillary glomerulonephritis and immunotactoid glomerulopathy |journal=J. Am. Soc. Nephrol. |volume=19 |issue=1 |pages=34–7 |date=January 2008 |pmid=18045849 |doi=10.1681/ASN.2007070757 |url=}}</ref><ref name="pmid28182050">{{cite journal |vauthors=Nimmagadda S, Mukku K, Devaraju SR, Uppin MS |title=Unusual cause of glomerular deposition disease: Collagenofibrotic glomerulopathy |journal=Indian J Nephrol |volume=27 |issue=1 |pages=62–65 |date=2017 |pmid=28182050 |pmc=5255993 |doi=10.4103/0971-4065.179300 |url=}}</ref>
-# LCDD
+*LCDD
-# [[Amyloidosis]]
+*Amyloidosis
-# [[Fabry's disease]]
+*[[Fabry's disease]]
-# Fibrillary immuno-tactoid glumerulopathy: The diagnosis is based on [[pathology]] finding. [[Infiltration (medical)|Infiltration]] of fibrills make glomerular structures in the kidney. Fibrills are larger than [[amyloid]] fibrils. Patients usually asymtomatic but, sometimes have [[proteinuria]] and [[hematuria]]. Prognosis is poor and [[ESRD]] will happen in half of the patients  <ref name="pmid18045849">{{cite journal |vauthors=Alpers CE, Kowalewska J |title=Fibrillary glomerulonephritis and immunotactoid glomerulopathy |journal=J. Am. Soc. Nephrol. |volume=19 |issue=1 |pages=34–7 |date=January 2008 |pmid=18045849 |doi=10.1681/ASN.2007070757 |url=}}</ref>.
+*Fibrillary immuno-tactoid glumerulopathy
-# Collagenofibrotic glomerulopathy: A rare disease and the diagnosis is based on [[pathology]] finding. Type III [[Collagen, type III, alpha 1|collagen]] fibers deposit in the subendothelial  and [[mesangium]] in the kidney. Negetive with [[Congo red]] and [[thioflavin]] stains. There is no specific threatment for it<ref name="pmid28182050">{{cite journal |vauthors=Nimmagadda S, Mukku K, Devaraju SR, Uppin MS |title=Unusual cause of glomerular deposition disease: Collagenofibrotic glomerulopathy |journal=Indian J Nephrol |volume=27 |issue=1 |pages=62–65 |date=2017 |pmid=28182050 |pmc=5255993 |doi=10.4103/0971-4065.179300 |url=}}</ref> .
+*Collagenofibrotic glomerulopathy
 ==Pathophysiology==
 === Pathogenesis: ===
-Deposits of abnormal or extra production of proteins, lipids and fibrills in the glomeruls cause glomerular deposition diseases.
+Deposits of abnormal or extra production of proteins, [[lipids]] and fibrills in the glomeruls cause glomerular [[Deposition (chemistry)|deposition]] diseases.
 -In LCDD:
 [[light chain]]<nowiki/>s are small [[polypeptides]] produced by [[B lymphocyte]]<nowiki/>s.They are sub units of [[antibodies]]. [[Kappa-chain immunoglobulin|Kappa]] and Lambda are two types of [[light chain]]<nowiki/>s. Excess production of [[Kappa-chain immunoglobulin|Kappa]] chain and accumulation in the [[Renal|renal glumerulus]] cause LCDD. The exact [[Mechanism (biology)|mechanism]] of increase production of light chains and reason that [[renal]] attracts them is unknown. These chains can deposit in all parts of [[Renal|renal glumeruls]] and [[Renal tubular|tubuls]].
 Accumulation of monoclonal [[light chains]] and [[matrix protein]]<nowiki/>s cause increase quantity and activity of transforming growth factor-beta ([[TGF-beta]]). TGF-beta inhibits [[mesangial cell]] proliferation and increase [[matrix protein]] production
-* Accumulation of [[matrix protein]]<nowiki/>s  compress the [[Glomerular capillaries|glomerular]] capillaryies and cause [[renal failure]] <ref name="pmid7639331">{{cite journal |vauthors=Zhu L, Herrera GA, Murphy-Ullrich JE, Huang ZQ, Sanders PW |title=Pathogenesis of glomerulosclerosis in light chain deposition disease. Role for transforming growth factor-beta |journal=Am. J. Pathol. |volume=147 |issue=2 |pages=375–85 |date=August 1995 |pmid=7639331 |pmc=1869812 |doi= |url=}}</ref>.
+* Accumulation of [[matrix protein]]<nowiki/>s  compress the [[Glomerular capillaries|glomerular]] capillaryies and cause [[renal failure]].<ref name="pmid7639331">{{cite journal |vauthors=Zhu L, Herrera GA, Murphy-Ullrich JE, Huang ZQ, Sanders PW |title=Pathogenesis of glomerulosclerosis in light chain deposition disease. Role for transforming growth factor-beta |journal=Am. J. Pathol. |volume=147 |issue=2 |pages=375–85 |date=August 1995 |pmid=7639331 |pmc=1869812 |doi= |url=}}</ref>
-Besides glumerulus,[[light chain]]<nowiki/>s may accumulate in [[renal tubular]]<nowiki/> and make [[tubular]] casts. These casts cause interstitial [[inflammation]] and [[renal failure]] <ref name="pmid10919389">{{cite journal |vauthors=Herrera GA |title=Renal manifestations of plasma cell dyscrasias: an appraisal from the patients' bedside to the research laboratory |journal=Ann Diagn Pathol |volume=4 |issue=3 |pages=174–200 |date=June 2000 |pmid=10919389 |doi= |url=}}</ref>.
+Besides glumerulus,[[light chain]]<nowiki/>s may accumulate in [[renal tubular]]<nowiki/> and make [[tubular]] casts. These [[casts]] cause interstitial [[inflammation]] and [[renal failure]].<ref name="pmid10919389">{{cite journal |vauthors=Herrera GA |title=Renal manifestations of plasma cell dyscrasias: an appraisal from the patients' bedside to the research laboratory |journal=Ann Diagn Pathol |volume=4 |issue=3 |pages=174–200 |date=June 2000 |pmid=10919389 |doi= |url=}}</ref>
 - In [[Amyloidosis]]:
@@ Line 41: / Line 40: @@
 A deficiency of the [[enzyme]] [[Alpha galactosidase|alpha galactosidase A]] causes deposition of [[glycolipid]]  in the [[Nephron|nephrone]]<nowiki/>s and cause [[renal failure]].
-- In Fibrillary immuno-tactoid glumerulopathy:
+- In Fibrillary immuno-tactoid [[glomerulopathy]]:
 Fibrills (larger than [[amyloid]]<nowiki/>s) deposit in subendothelial  and [[mesangium]] of the [[nephron]]<nowiki/>es and cause function impairment.
--  In Collagenofibrotic glomerulopathy:
+-  In Collagenofibrotic [[glomerulopathy]]:
-Type III [[Collagen, type III, alpha 1|collagen]] fibers deposit in the subendothelial  and [[mesangium]] in the kidney.
+Type III [[Collagen, type III, alpha 1|collagen]] fibers deposit in the subendothelial  and [[mesangium]] in the [[kidney]].
 == Microscopic Pathology ==
 On [[Light microscope|light microscop]]<nowiki/>y:
 -In LCDD:
@@ Line 59: / Line 58: @@
 * Typical green [[birefringence]] under [[Polarization|polarized]] light after [[Congo red]] staining (appears in red under normal light)
 - In [[Fabry's disease]]:
-* [[Hypertrophic]] [[podocytes]] of glomerul, foamy appearing [[Vacuoles|vacuole]]<nowiki/>s and [[Mesangial cells|mesangial]] widening. Vacuolated cells will be seen in [[Periodic acid-Schiff stain|PAS]] stain <ref name="pmid12068025">{{cite journal |vauthors=Alroy J, Sabnis S, Kopp JB |title=Renal pathology in Fabry disease |journal=J. Am. Soc. Nephrol. |volume=13 Suppl 2 |issue= |pages=S134–8 |date=June 2002 |pmid=12068025 |doi= |url=}}</ref>.
+* [[Hypertrophic]] [[podocytes]] of glomerul, foamy appearing [[Vacuoles|vacuole]]<nowiki/>s and [[Mesangial cells|mesangial]] widening. Vacuolated cells will be seen in [[Periodic acid-Schiff stain|PAS]] stain.<ref name="pmid12068025">{{cite journal |vauthors=Alroy J, Sabnis S, Kopp JB |title=Renal pathology in Fabry disease |journal=J. Am. Soc. Nephrol. |volume=13 Suppl 2 |issue= |pages=S134–8 |date=June 2002 |pmid=12068025 |doi= |url=}}</ref>
 - In Fibrillary immuno-tactoid glumerulopathy:
-* [[Capillary]] wall thickening, [[matrix]] expansion,[[interstitial]] [[Infiltration (medical)|infiltration]] and [[necrosis]] in [[renal]] [[tubules]] and negative [[Congo red]] stain <ref name="pmid12631361">{{cite journal |vauthors=Rosenstock JL, Markowitz GS, Valeri AM, Sacchi G, Appel GB, D'Agati VD |title=Fibrillary and immunotactoid glomerulonephritis: Distinct entities with different clinical and pathologic features |journal=Kidney Int. |volume=63 |issue=4 |pages=1450–61 |date=April 2003 |pmid=12631361 |doi=10.1046/j.1523-1755.2003.00853.x |url=}}</ref>.
+* [[Capillary]] wall thickening, [[matrix]] expansion,[[interstitial]] [[Infiltration (medical)|infiltration]] and [[necrosis]] in [[renal]] [[tubules]] and negative [[Congo red]] stain.<ref name="pmid12631361">{{cite journal |vauthors=Rosenstock JL, Markowitz GS, Valeri AM, Sacchi G, Appel GB, D'Agati VD |title=Fibrillary and immunotactoid glomerulonephritis: Distinct entities with different clinical and pathologic features |journal=Kidney Int. |volume=63 |issue=4 |pages=1450–61 |date=April 2003 |pmid=12631361 |doi=10.1046/j.1523-1755.2003.00853.x |url=}}</ref>
 -  In Collagenofibrotic glomerulopathy:
-* Diffuse increase in the [[Mesangial cells|mesangial]] matrix, [[capillary]] walls widening, and [[collagen]] fibers in the [[glomerular basement membrane]]<ref name="pmid8398640">{{cite journal |vauthors=Gubler MC, Dommergues JP, Foulard M, Bensman A, Leroy JP, Broyer M, Habib R |title=Collagen type III glomerulopathy: a new type of hereditary nephropathy |journal=Pediatr. Nephrol. |volume=7 |issue=4 |pages=354–60 |date=August 1993 |pmid=8398640 |doi= |url=}}</ref>.
+* Diffuse increase in the [[Mesangial cells|mesangial]] [[matrix]], [[capillary]] walls widening, and [[collagen]] fibers in the [[glomerular basement membrane]].<ref name="pmid8398640">{{cite journal |vauthors=Gubler MC, Dommergues JP, Foulard M, Bensman A, Leroy JP, Broyer M, Habib R |title=Collagen type III glomerulopathy: a new type of hereditary nephropathy |journal=Pediatr. Nephrol. |volume=7 |issue=4 |pages=354–60 |date=August 1993 |pmid=8398640 |doi= |url=}}</ref>
 On [[Electron-micrograph|electron]] microscopy :
@@ Line 69: / Line 68: @@
 * Ground-pepper–like deposits in the [[Mesangial cells|mesangia]]<nowiki/>l  and  the [[endothelial]] of the [[glomerular basement membrane]]. Also, in [[renal tubule]]<nowiki/>s if there is [[Tubular|tubular involvement]].
 - In [[Amyloidosis]]:
-* Endothelium, [[glomerular basement membrane]], and [[podocytes]] thickening <ref name="pmid13617410">{{cite journal |vauthors=SPIRO D |title=The structural basis of proteinuria in man; electron microscopic studies of renal biopsy specimens from patients with lipid nephrosis, amyloidosis, and subacute and chronic glomerulonephritis |journal=Am. J. Pathol. |volume=35 |issue=1 |pages=47–73 |date=1959 |pmid=13617410 |pmc=1934814 |doi= |url=}}</ref>.
+* Endothelium, [[glomerular basement membrane]], and [[podocytes]] thickening.<ref name="pmid13617410">{{cite journal |vauthors=SPIRO D |title=The structural basis of proteinuria in man; electron microscopic studies of renal biopsy specimens from patients with lipid nephrosis, amyloidosis, and subacute and chronic glomerulonephritis |journal=Am. J. Pathol. |volume=35 |issue=1 |pages=47–73 |date=1959 |pmid=13617410 |pmc=1934814 |doi= |url=}}</ref>
 - In [[Fabry's disease]]:
 * Deposition of glicolipids in [[Lysosomes|lysosome]]<nowiki/>s of [[Podocytes|podocyte]]<nowiki/>s and [[glomerular]] parietal [[Epithelial cell|epithelial]] cells.
-- In Fibrillary immuno-tactoid glumerulopathy:
+- In Fibrillary immuno-tactoid [[glomerulopathy]]:
 * Predominant [[Fibril|fibri]]<nowiki/>ls in the [[Subepithelial connective tissue graft|subepithelial]] of glomerular capillary.
--  In Collagenofibrotic glomerulopathy:
+-  In Collagenofibrotic [[glomerulopathy]]:
-* Deposition of irregular collagenous fibers in the mesangium and subendothelial space of the renal glumerol <ref name="pmid28509277">{{cite journal |vauthors=Aoki T, Hayashi K, Morinaga T, Tomida H, Hishida M, Yamamoto S, Kajiwara N, Tamai H |title=Two brothers with collagenofibrotic glomerulopathy |journal=CEN Case Rep |volume=4 |issue=1 |pages=85–89 |date=May 2015 |pmid=28509277 |pmc=5413714 |doi=10.1007/s13730-014-0145-y |url=}}</ref>.
+* Deposition of irregular collagenous fibers in the [[mesangium]] and subendothelial space of the renal glumerol.<ref name="pmid28509277">{{cite journal |vauthors=Aoki T, Hayashi K, Morinaga T, Tomida H, Hishida M, Yamamoto S, Kajiwara N, Tamai H |title=Two brothers with collagenofibrotic glomerulopathy |journal=CEN Case Rep |volume=4 |issue=1 |pages=85–89 |date=May 2015 |pmid=28509277 |pmc=5413714 |doi=10.1007/s13730-014-0145-y |url=}}</ref>
 == Genetics ==
-* Fabry's disease is  [[X-linked recessive]].
+* Fabry's disease is transmitted in [[X-linked recessive]] pattern.
-* Hereditory types of [[amyloidosis]] is [[autosomal dominant]].
+* Hereditory types of [[amyloidosis]] is transmitted in [[autosomal dominant]] pattern.
 * There exact genetic association for LCDD, Fibrillary immuno-tactoid glumerulopathy, and Collagenofibrotic glomerulopathy are unknown.
@@ Line 90: / Line 89: @@
 <small>
 {| class="wikitable"
-! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Glomerular diseases
+! rowspan="2" style="background:#4479BA; color: #FFFFFF;" align="center" + |Glomerular diseases
-! colspan="2" rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Disease
+! colspan="2" rowspan="2" style="background:#4479BA; color: #FFFFFF;" align="center" + |Disease
-! colspan="9" align="center" style="background:#4479BA; color: #FFFFFF;" + |History and Symtoms
+! colspan="9" style="background:#4479BA; color: #FFFFFF;" align="center" + |History and Symtoms
-! colspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Laboratory Findings
+! colspan="2" style="background:#4479BA; color: #FFFFFF;" align="center" + |Laboratory Findings
-! colspan="3" align="center" style="background:#4479BA; color: #FFFFFF;" + |Pathology
+! colspan="3" style="background:#4479BA; color: #FFFFFF;" align="center" + |Pathology
 |-
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |History
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |History
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Systemic symptoms
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Systemic symptoms
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hemeturia
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hemeturia
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Proteinuria
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Proteinuria
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hypertension
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hypertension
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Pitting edema
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Pitting edema
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Oliguria
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Oliguria
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Nephrotic features
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Nephrotic features
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Nephritic features
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Nephritic features
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hyperlipidemia and hypercholesterolemia
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hyperlipidemia and hypercholesterolemia
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Auto-antibodies,
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Auto-antibodies,
 Complements
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Light microscope
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Light microscope
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Electron microscope
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Electron microscope
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Immunoflourescence pattern
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Immunoflourescence pattern
 |-
-! rowspan="13" align="center" style="background:#4479BA; color: #FFFFFF;" + |Acute Nephritic Syndromes
+! rowspan="13" style="background:#4479BA; color: #FFFFFF;" align="center" + |Acute Nephritic Syndromes
 ! colspan="2" |[[Poststreptococcal glomerulonephritis|Poststreptococcal Glomerulonephritis]]<ref name="pmid13022878">{{cite journal| author=GERMUTH FG| title=A comparative histologic and immunologic study in rabbits of induced hypersensitivity of the serum sickness type. | journal=J Exp Med | year= 1953 | volume= 97 | issue= 2 | pages= 257-82 | pmid=13022878 | doi= | pmc=PMC2136196 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=13022878 }}</ref><ref name="pmid5031005">{{cite journal| author=Germuth FG, Senterfit LB, Dreesman GR| title=Immune complex disease. V. The nature of the circulating complexes associated with glomerular alterations in the chronic BSA-rabbit system. | journal=Johns Hopkins Med J | year= 1972 | volume= 130 | issue= 6 | pages= 344-57 | pmid=5031005 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=5031005 }}</ref><ref name="pmid22895519">{{cite journal| author=Radhakrishnan J, Cattran DC| title=The KDIGO practice guideline on glomerulonephritis: reading between the (guide)lines--application to the individual patient. | journal=Kidney Int | year= 2012 | volume= 82 | issue= 8 | pages= 840-56 | pmid=22895519 | doi=10.1038/ki.2012.280 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22895519 }}</ref>
 |
@@ Line 263: / Line 262: @@
 * Immune complex GN, granular deposite
 |-
-! colspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Disease
+! colspan="2" style="background:#4479BA; color: #FFFFFF;" align="center" + |Disease
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |History
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |History
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Systemic symptoms
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Systemic symptoms
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hemeturia
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hemeturia
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Proteinuria
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Proteinuria
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hypertension
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hypertension
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Pitting edema
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Pitting edema
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Oliguria
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Oliguria
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Nephrotic features
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Nephrotic features
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Nephritic features
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Nephritic features
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hyperlipidemia and hypercholesterolemia
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hyperlipidemia and hypercholesterolemia
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Auto-antibodies,
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Auto-antibodies,
 Complements
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Light microscope
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Light microscope
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Electron microscope
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Electron microscope
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Immunoflourescence pattern
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Immunoflourescence pattern
 |-
 ! rowspan="3" |[[Vasculitis|ANCA Small-Vessel Vasculitis]]<ref name="pmid8746284">{{cite journal |vauthors=Higgins RM, Goldsmith DJ, Connolly J, Scoble JE, Hendry BM, Ackrill P, Venning MC |title=Vasculitis and rapidly progressive glomerulonephritis in the elderly |journal=Postgrad Med J |volume=72 |issue=843 |pages=41–4 |date=January 1996 |pmid=8746284 |pmc=2398323 |doi= |url=}}</ref><ref name="pmid12631105">{{cite journal |vauthors=Jennette JC |title=Rapidly progressive crescentic glomerulonephritis |journal=Kidney Int. |volume=63 |issue=3 |pages=1164–77 |date=March 2003 |pmid=12631105 |doi=10.1046/j.1523-1755.2003.00843.x |url=}}</ref>
@@ Line 421: / Line 420: @@
 * Immune complex GN, granular deposite
 |-
-! colspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Disease
+! colspan="2" style="background:#4479BA; color: #FFFFFF;" align="center" + |Disease
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |History
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |History
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Systemic symptoms
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Systemic symptoms
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hemeturia
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hemeturia
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Proteinuria
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Proteinuria
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hypertension
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hypertension
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Pitting edema
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Pitting edema
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Oliguria
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Oliguria
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Nephrotic features
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Nephrotic features
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Nephritic features
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Nephritic features
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hyperlipidemia and hypercholesterolemia
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hyperlipidemia and hypercholesterolemia
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Auto-antibodies,
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Auto-antibodies,
 Complements
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Light microscope
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Light microscope
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Electron microscope
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Electron microscope
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Immunoflourescence pattern
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Immunoflourescence pattern
 |-
 ! colspan="2" |[[Cryoglobulinemia]]<ref name="pmid26802335">{{cite journal |vauthors=Fogo AB, Lusco MA, Najafian B, Alpers CE |title=AJKD Atlas of Renal Pathology: Cryoglobulinemic Glomerulonephritis |journal=Am. J. Kidney Dis. |volume=67 |issue=2 |pages=e5–7 |date=February 2016 |pmid=26802335 |doi=10.1053/j.ajkd.2015.12.007 |url=}}</ref>
@@ Line 478: / Line 477: @@
 * Prominent [[IgM]] and C3
 |-
-! rowspan="9" align="center" style="background:#4479BA; color: #FFFFFF;" + |Nephrotic Syndrome
+! rowspan="9" style="background:#4479BA; color: #FFFFFF;" align="center" + |Nephrotic Syndrome
 ! colspan="2" |[[Minimal change disease|Minimal Change Disease]]<ref name="pmid17195422">{{cite journal |vauthors=Saha TC, Singh H |title=Minimal change disease: a review |journal=South. Med. J. |volume=99 |issue=11 |pages=1264–70 |date=November 2006 |pmid=17195422 |doi=10.1097/01.smj.0000243183.87381.c2 |url=}}</ref><ref name="pmid27092244">{{cite journal |vauthors=Saleem MA, Kobayashi Y |title=Cell biology and genetics of minimal change disease |journal=F1000Res |volume=5 |issue= |pages= |date=2016 |pmid=27092244 |pmc=4821284 |doi=10.12688/f1000research.7300.1 |url=}}</ref>
 | colspan="2" |
@@ Line 567: / Line 566: @@
 | -
 |-
-! colspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Disease
+! colspan="2" style="background:#4479BA; color: #FFFFFF;" align="center" + |Disease
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |History
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |History
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Systemic symptoms
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Systemic symptoms
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hemeturia
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hemeturia
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Proteinuria
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Proteinuria
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hypertension
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hypertension
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Pitting edema
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Pitting edema
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Oliguria
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Oliguria
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Nephrotic features
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Nephrotic features
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Nephritic features
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Nephritic features
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hyperlipidemia and hypercholesterolemia
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hyperlipidemia and hypercholesterolemia
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Auto-antibodies,
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Auto-antibodies,
 Complements
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Light microscope
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Light microscope
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Electron microscope
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Electron microscope
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Immunoflourescence pattern
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Immunoflourescence pattern
 |-
 ! rowspan="4" | [[Glomerular deposition disease|Glomerular Deposition Diseases]]
@@ Line 702: / Line 701: @@
 |<nowiki>-</nowiki>
 |-
-! rowspan="4" align="center" style="background:#4479BA; color: #FFFFFF;" + |Basement Membrane Syndrome
+! rowspan="4" style="background:#4479BA; color: #FFFFFF;" align="center" + |Basement Membrane Syndrome
 ! colspan="2" |[[Alport syndrome|Alport's Syndrome]]<ref name="pmid111374282">{{cite journal| author=McCarthy PA, Maino DM| title=Alport syndrome: a review. | journal=Clin Eye Vis Care | year= 2000 | volume= 12 | issue= 3-4 | pages= 139-150 | pmid=11137428 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11137428 }}</ref><ref name="pmid84141532">{{cite journal| author=Chugh KS, Sakhuja V, Agarwal A, Jha V, Joshi K, Datta BN et al.| title=Hereditary nephritis (Alport's syndrome)--clinical profile and inheritance in 28 kindreds. | journal=Nephrol Dial Transplant | year= 1993 | volume= 8 | issue= 8 | pages= 690-5 | pmid=8414153 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8414153 }}</ref><ref name="pmid8414153">{{cite journal| author=Chugh KS, Sakhuja V, Agarwal A, Jha V, Joshi K, Datta BN et al.| title=Hereditary nephritis (Alport's syndrome)--clinical profile and inheritance in 28 kindreds. | journal=Nephrol Dial Transplant | year= 1993 | volume= 8 | issue= 8 | pages= 690-5 | pmid=8414153 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8414153 }}</ref><ref name="pmid11137428">{{cite journal| author=McCarthy PA, Maino DM| title=Alport syndrome: a review. | journal=Clin Eye Vis Care | year= 2000 | volume= 12 | issue= 3-4 | pages= 139-150 | pmid=11137428 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11137428 }}</ref><ref name="pmid7819734">{{cite journal| author=Amari F, Segawa K, Ando F| title=Lens coloboma and Alport-like glomerulonephritis. | journal=Eur J Ophthalmol | year= 1994 | volume= 4 | issue= 3 | pages= 181-3 | pmid=7819734 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7819734 }}</ref><ref name="pmid6871140">{{cite journal| author=Govan JA| title=Ocular manifestations of Alport's syndrome: a hereditary disorder of basement membranes? | journal=Br J Ophthalmol | year= 1983 | volume= 67 | issue= 8 | pages= 493-503 | pmid=6871140 | doi= | pmc=PMC1040106 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6871140 }}</ref>
 |
@@ Line 739: / Line 738: @@
 * Minimal binding to a glomerulus in indirect [[immunofluorescence]] microscopy with [[Anti-glomerular basement membrane antibody|anti-glomerular basement membrane]] antibodies
 |-
-! colspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Disease
+! colspan="2" style="background:#4479BA; color: #FFFFFF;" align="center" + |Disease
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |History
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |History
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Systemic symptoms
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Systemic symptoms
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hemeturia
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hemeturia
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Proteinuria
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Proteinuria
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hypertension
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hypertension
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Pitting edema
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Pitting edema
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Oliguria
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Oliguria
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Nephrotic features
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Nephrotic features
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Nephritic features
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Nephritic features
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hyperlipidemia and hypercholesterolemia
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hyperlipidemia and hypercholesterolemia
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Auto-antibodies,
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Auto-antibodies,
 Complements
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Light microscope
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Light microscope
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Electron microscope
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Electron microscope
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Immunoflourescence pattern
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Immunoflourescence pattern
 |-
 ! colspan="2" |[[Thin basement membrane disease|Thin Basement Membrane Disease]]<ref name="pmid12969134">{{cite journal |author=Savige J, Rana K, Tonna S, Buzza M, Dagher H, Wang YY |title=Thin basement membrane nephropathy |journal=Kidney Int. |volume=64 |issue=4 |pages=1169–78 |year=2003 |month=October |pmid=12969134 |doi=10.1046/j.1523-1755.2003.00234.x}}</ref><ref name="pmid17726307">{{cite journal |author=Hou P, Chen Y, Ding J, Li G, Zhang H |title=A novel mutation of COL4A3 presents a different contribution to Alport syndrome and thin basement membrane nephropathy |journal=Am. J. Nephrol. |volume=27 |issue=5 |pages=538–44 |year=2007 |pmid=17726307 |doi=10.1159/000107666 |url=http://content.karger.com/produktedb/produkte.asp?typ=fulltext&file=000107666}}</ref>
@@ Line 809: / Line 808: @@
 * Nonspecific [[IgM]] and C3 deposition may be seen in sclerotic glomeruli.
 |-
-! rowspan="6" align="center" style="background:#4479BA; color: #FFFFFF;" + | Glomerular-Vascular Syndromes
+! rowspan="6" style="background:#4479BA; color: #FFFFFF;" align="center" + | Glomerular-Vascular Syndromes
 ! colspan="2" |[[Hypertensive nephropathy|Hypertensive Nephrosclerosis]]<ref name="pmid24327566">{{cite journal |vauthors=Hughson MD, Puelles VG, Hoy WE, Douglas-Denton RN, Mott SA, Bertram JF |title=Hypertension, glomerular hypertrophy and nephrosclerosis: the effect of race |journal=Nephrol. Dial. Transplant. |volume=29 |issue=7 |pages=1399–409 |date=July 2014 |pmid=24327566 |pmc=4071048 |doi=10.1093/ndt/gft480 |url=}}</ref>
 |Chronic [[hypertension]]
@@ Line 887: / Line 886: @@
 * Not specific changes
 |-
-! colspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Disease
+! colspan="2" style="background:#4479BA; color: #FFFFFF;" align="center" + |Disease
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |History
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |History
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Systemic symptoms
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Systemic symptoms
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hemeturia
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hemeturia
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Proteinuria
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Proteinuria
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hypertension
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hypertension
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Pitting edema
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Pitting edema
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Oliguria
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Oliguria
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Nephrotic features
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Nephrotic features
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Nephritic features
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Nephritic features
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hyperlipidemia and hypercholesterolemia
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hyperlipidemia and hypercholesterolemia
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Auto-antibodies,
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Auto-antibodies,
 Complements
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Light microscope
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Light microscope
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Electron microscope
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Electron microscope
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Immunoflourescence pattern
+! style="background:#4479BA; color: #FFFFFF;" align="center" + |Immunoflourescence pattern
 |-
 ! colspan="2" |[[Sickle-cell disease|Sickle Cell Disease]]<ref name="pmid12028473">{{cite journal |vauthors=Wesson DE |title=The initiation and progression of sickle cell nephropathy |journal=Kidney Int. |volume=61 |issue=6 |pages=2277–86 |date=June 2002 |pmid=12028473 |doi=10.1046/j.1523-1755.2002.00363.x |url=}}</ref>
@@ Line 1,014: / Line 1,013: @@
 ==Natural History, Complications, and Prognosis==
-Prognostic factors of glomerular deposition diseases at presentation <ref name="pmid14655186" />:
+If left untreated, most of the patients will suffer from ESRD in the future.
+Common complication of glomerular deposition diseases is renal failure.
+Prognostic factors of glomerular deposition diseases include:<ref name="pmid14655186" />
 * Age
 * underlying [[Hematologic diseases|hematologic]] disease
@@ Line 1,020: / Line 1,021: @@
 * [[Renal function]]
 * other medical diseases like [[diabetic nephropathy]]
-The median time to progression to [[chronic renal failure]] in LCDD is 2.7 years. After 5 years, about 37% of patients with LCDD are alive and do not have [[Chronic renal failure|end stage renal disease]].
+Prognosis is generally not good. The median time to progression to [[chronic renal failure]] in LCDD is 2.7 years. After 5 years, about 37% of patients with LCDD are alive and do not have [[Chronic renal failure|end stage renal disease]].
 ==Diagnosis==
 ===Diagnostic Study of Choice===
-* Complete [[Blood tests|blood test]]
+*Biopsy is the gold standard test for the diagnosis of glomerular deposition disease.<ref name="pmid17685926">{{cite journal |vauthors=Joh K |title=Pathology of glomerular deposition diseases |journal=Pathol. Int. |volume=57 |issue=9 |pages=551–65 |date=September 2007 |pmid=17685926 |doi=10.1111/j.1440-1827.2007.02139.x |url=}}</ref>
-* Urine and serum [[electrophoresis]]
-* Serum and urine immunoglobulin free [[light chain]] assays <ref name="pmid25296094">{{cite journal |vauthors=Yadav P, Leung N, Sanders PW, Cockwell P |title=The use of immunoglobulin light chain assays in the diagnosis of paraprotein-related kidney disease |journal=Kidney Int. |volume=87 |issue=4 |pages=692–7 |date=April 2015 |pmid=25296094 |pmc=4863638 |doi=10.1038/ki.2014.333 |url=}}</ref>
-* [[Biopsy]] is the [[Gold standard (test)|gold standard]] test
 ===History and Symptoms===
-All organs can be effected by Glomerular deposition diseases especially in LCDD. Most of the time [[kidney]] is involved <ref name="pmid11423587">{{cite journal |vauthors=Ronco PM, Alyanakian MA, Mougenot B, Aucouturier P |title=Light chain deposition disease: a model of glomerulosclerosis defined at the molecular level |journal=J. Am. Soc. Nephrol. |volume=12 |issue=7 |pages=1558–65 |date=July 2001 |pmid=11423587 |doi= |url=}}</ref>. Usually patients are asymptomatic in early stages. Symptoms are nonspecific like fatigue and weight loss. Rapidly progressive [[glomerulonephritis]] or acute [[tubulointerstitial nephritis]] cause [[renal failure]] in these patients. Other than the [[kidneys]], [[liver]] and [[heart]] are the most commonly involved organs. Deposition of [[light chain]]s in the [[liver]] may lead to [[hepatomegaly]], [[portal hypertension]] and [[liver failure]]. The [[heart]] is affected in up to 80% of patients with LCDD, and may cause [[arrhythmia]]s [[restrictive cardiomyopathy]], [[cardiomegaly]], and [[congestive heart failure]] <ref name="pmid20128164">{{cite journal |vauthors=Koopman P, Van Dorpe J, Maes B, Dujardin K |title=Light chain deposition disease as a rare cause of restrictive cardiomyopathy |journal=Acta Cardiol |volume=64 |issue=6 |pages=821–4 |date=December 2009 |pmid=20128164 |doi=10.2143/AC.64.6.2044752 |url=}}</ref>.
+Usually patients are asymptomatic in early stages. Symptoms are nonspecific like fatigue and weight loss. In case of edema patients may come with edema. Patients may come with abdominal pain because of deposition of [[light chain]]s in the [[liver]] may lead to [[hepatomegaly]], [[portal hypertension]] and [[liver failure]]. Patients may come with palpitation because the [[heart]] is affected in up to 80% of patients with LCDD, and may cause [[arrhythmia]]s [[restrictive cardiomyopathy]], [[cardiomegaly]], and [[congestive heart failure]].<ref name="pmid20128164">{{cite journal |vauthors=Koopman P, Van Dorpe J, Maes B, Dujardin K |title=Light chain deposition disease as a rare cause of restrictive cardiomyopathy |journal=Acta Cardiol |volume=64 |issue=6 |pages=821–4 |date=December 2009 |pmid=20128164 |doi=10.2143/AC.64.6.2044752 |url=}}</ref>
 ===Physical Examination===
-* Depends on involvement of the organ you may find [[organomegaly]] like [[hepatomegaly]]
+* Physical exam is normal most of the time.
-* [[Polyneuropathy]]
+* Sometimes there is an organomegaly which depends on involvement of the organ like [[hepatomegaly]]
 ===Laboratory Findings===
-* [[Proteinuria]] (30-50% of cases have [[nephrotic syndrome]])<ref name="pmid2106817">{{cite journal |vauthors=Buxbaum JN, Chuba JV, Hellman GC, Solomon A, Gallo GR |title=Monoclonal immunoglobulin deposition disease: light chain and light and heavy chain deposition diseases and their relation to light chain amyloidosis. Clinical features, immunopathology, and molecular analysis |journal=Ann. Intern. Med. |volume=112 |issue=6 |pages=455–64 |date=March 1990 |pmid=2106817 |doi= |url=}}</ref>
+Laboratory findings consistent with the diagnosis of glomerular deposition disease include:<ref name="pmid2106817">{{cite journal |vauthors=Buxbaum JN, Chuba JV, Hellman GC, Solomon A, Gallo GR |title=Monoclonal immunoglobulin deposition disease: light chain and light and heavy chain deposition diseases and their relation to light chain amyloidosis. Clinical features, immunopathology, and molecular analysis |journal=Ann. Intern. Med. |volume=112 |issue=6 |pages=455–64 |date=March 1990 |pmid=2106817 |doi= |url=}}</ref><ref name="pmid12194920">{{cite journal |vauthors=Katzmann JA, Clark RJ, Abraham RS, Bryant S, Lymp JF, Bradwell AR, Kyle RA |title=Serum reference intervals and diagnostic ranges for free kappa and free lambda immunoglobulin light chains: relative sensitivity for detection of monoclonal light chains |journal=Clin. Chem. |volume=48 |issue=9 |pages=1437–44 |date=September 2002 |pmid=12194920 |doi= |url=}}</ref><ref name="pmid21162651">{{cite journal |vauthors=Ozsan GH, Dispenzieri A |title=Serum free light chain analysis in multiple myeloma and plasma cell dyscrasias |journal=Expert Rev Clin Immunol |volume=7 |issue=1 |pages=65–73 |date=January 2011 |pmid=21162651 |doi=10.1586/eci.10.80 |url=}}</ref>
+* [[Proteinuria]] (30-50% of cases have [[nephrotic syndrome]])
 * [[Hematuria]] (usually microscopic)
 * Abnormal [[liver enzyme]] ( in case of liver involvement)
+*Presence of a monoclonal protein in serum or urine
 ===Electrocardiogram===
 [[Arrhythmia]] like [[atrial fibrillation]] ( in case of heart involvement).
 ===X-ray===
-There are no [[pathognomonic]] and specific x-ray findings associated with LCDD.
+There are no x-ray findings associated with glomerular deposition disease.
 ===Echocardiography or Ultrasound===
-* Echocardiography:
+*Echocardiography:
-In case of heart involvement: Low [[Ejection fraction|EF]], diffuse [[hypokinesia]], left ventricular [[Left ventricular hypertrophy|concentric hypertrophy]], Low [[diastolic]] compliance <ref name="pmid26988342">{{cite journal |vauthors=Mohan M, Gokden M, Gokden N, Schinke C |title=A Case of Cardiac Light Chain Deposition Disease in a Patient with Solitary Plasmacytoma |journal=Am J Case Rep |volume=17 |issue= |pages=173–6 |date=March 2016 |pmid=26988342 |pmc=4801155 |doi= |url=}}</ref>
+Echocardiography may be helpful in the diagnosis of glomerular deposition disease. Findings on echocardiography suggestive of glomerular deposition disease in case of heart involvement include:<ref name="pmid26988342">{{cite journal |vauthors=Mohan M, Gokden M, Gokden N, Schinke C |title=A Case of Cardiac Light Chain Deposition Disease in a Patient with Solitary Plasmacytoma |journal=Am J Case Rep |volume=17 |issue= |pages=173–6 |date=March 2016 |pmid=26988342 |pmc=4801155 |doi= |url=}}</ref>
+:*Low [[Ejection fraction|EF]]
+:*Diffuse [[hypokinesia]]
+:*Left ventricular [[Left ventricular hypertrophy|concentric hypertrophy]]
+:*Low [[diastolic]] compliance
 * Ultrasound:
-No findings associated with renal Glomerular deposition diseases.
+There are no ultrasound findings associated with glomerular deposition disease.
 ===CT scan===
-* In severe cases the size of the organ will increase.
+*There are no CT scan findings associated with glomerular deposition disease.
-* No  [[pathognomonic]] and specific finding associated with Glomerular deposition diseases.
+* In severe cases the size of the organ will increase.
 ===MRI===
-* In severe cases the size of the organ will increase.
+*There are no MRI findings associated with glomerular deposition disease.
-* No  [[pathognomonic]] and specific finding associated with Glomerular deposition diseases.
+*In severe cases the size of the organ will increase.
 ===Other Imaging Findings===
@@ Line 1,069: / Line 1,074: @@
 '''Medical therapy:'''
-% of cases without therapy will have [[ESRD]]. There is no standard treatment for Glomerular deposition diseases. Medical therapy options for LCDD are:
+% of cases untreated patients will become to [[ESRD]]. There is no standard treatment for Glomerular deposition diseases. Medical therapy options for LCDD include:<ref name="pmid21913808">{{cite journal |vauthors=Gertz MA |title=Managing light chain deposition disease |journal=Leuk. Lymphoma |volume=53 |issue=2 |pages=183–4 |date=February 2012 |pmid=21913808 |doi=10.3109/10428194.2011.622423 |url=}}</ref><ref name="pmid21181954">{{cite journal |vauthors=Rajkumar SV |title=Multiple myeloma: 2011 update on diagnosis, risk-stratification, and management |journal=Am. J. Hematol. |volume=86 |issue=1 |pages=57–65 |date=January 2011 |pmid=21181954 |doi=10.1002/ajh.21913 |url=}}</ref><ref name="pmid21479696">{{cite journal |vauthors=Gharwan H, Truica CI |title=Bortezomib-based chemotherapy for light chain deposition disease presenting as acute renal failure |journal=Med. Oncol. |volume=29 |issue=2 |pages=1197–201 |date=June 2012 |pmid=21479696 |doi=10.1007/s12032-011-9938-4 |url=}}</ref>
-* Symptomatic treatment for [[Renal dysfunction|renal dysfunctio]]<nowiki/>n like [[Angiotensin Converting Enzyme Inhibitor|ACE inhibitors]]
+* Symptomatic treatment for [[Renal dysfunction|renal dysfunctio]]<nowiki/>n like [[Angiotensin Converting Enzyme Inhibitor|ACE inhibitors]] like Lisinopril 2.5 to 5 mg orally once a day ( dose depends on the level of the kidney damage).
-* [[Chemotherapy]] with [[Bortezomib]]
+* If patient has LCDD and [[Multiple Myeloma]] (MM), should receive treatment per [[Multiple myeloma|MM]] guideline like [[Bortezomib]]1.3 mg/m^2 IV on days 1,4,8,11,22,25,29,32 of 42 day cycle for cycles 1-4.
 * High-dose [[melphalan]] in conjunction with [[autologous]] [[stem cell transplantation]]
-* If patient has LCDD and [[Multiple Myeloma]] (MM), should receive treatment per [[Multiple myeloma|MM]] guideline
 ===Surgery===
-In case of [[ESRD]]→ [[Kidney transplant]]
+Surgery is not the first-line treatment option for patients with glomerular deposition disease. Surgery is usually reserved for patients with either:<ref name="pmid14712438">{{cite journal |vauthors=Leung N, Lager DJ, Gertz MA, Wilson K, Kanakiriya S, Fervenza FC |title=Long-term outcome of renal transplantation in light-chain deposition disease |journal=Am. J. Kidney Dis. |volume=43 |issue=1 |pages=147–53 |date=January 2004 |pmid=14712438 |doi= |url=}}</ref><ref name="pmid11423695">{{cite journal |vauthors=Short AK, O'Donoghue DJ, Riad HN, Short CD, Roberts IS |title=Recurrence of light chain nephropathy in a renal allograft. A case report and review of the literature |journal=Am. J. Nephrol. |volume=21 |issue=3 |pages=237–40 |date=2001 |pmid=11423695 |doi=10.1159/000046254 |url=}}</ref>
+*LCDD patients who have detectable light chains in urine or serum
+*ESRD
 ===Primary Prevention===

Glomerular deposition disease: Difference between revisions

Latest revision as of 14:32, 29 April 2019

Overview

Classification

Pathophysiology

Pathogenesis:

Microscopic Pathology

Genetics

Causes

Differentiating from Other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications, and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X-ray

Echocardiography or Ultrasound

CT scan

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Surgery

Primary Prevention

Secondary Prevention

References

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