Glomerulonephritis

GLOMERULAR DISEASESYjnah D. Lim BMLS III-A

Riverside College Inc.

GLOMERULAR DISEASES

➤ Membranous Glomerulonephritis (MGN)

➤ Membranoproliferative Glomerulonephritis (MPGN)

➤ Chronic Glomerulonephritis

➤ Berger Disease

GLOMERULUS

FILTRATION MEMBRANE

MEMBRANOUS GLOMERULONEPHRITIS

(MGN)

MEMBRANOUS GLOMERULONEPHRITIS

➤ Pronounced thickening of the glomerular basement membrane resulting from the deposition of immunoglobulin G immune complexes in the sub-epithelial space.

MEMBRANOUS GLOMERULUNEPHRITIS


➤ The immune complex serves as an activator that triggers a response from the C5b - C9 complements, which form a membrane attack complex (MAC) on the glomerular epithelial cells.

LABORATORY FINDINGS➤Proteinuria and microscopic hematuria. ➤ In some cases the protein loss can be large

enough to be associated with water retention, and swelling of the face, hands or feet.

COMPLICATIONS

➤ High blood pressure may develop. This damages the kidneys and puts a strain on the heart and the rest of the circulation.

➤ Kidney failure may sometimes occur.

DISEASES ASSOCIATED WITH MGN DEVELOPMENT

SYSTEMIC LUPUS ERYTHEMATOSUS


➤ Usually arises within 5 years of diagnosis.

➤ Production of autoantibodies directed against nuclear elements.

➤ These autoantibodies form pathogenic immune complexes intravascularly, which are deposited in glomeruli.

➤ Alternatively, autoantibodies may bind to antigens already located in the glomerular basement membrane, forming immune complexes in situ.

➤ Immune complexes promote an inflammatory response by activating complement and attracting inflammatory cells, including lymphocytes, macrophages, and neutrophils.

SJÖGREN'S SYNDROME➤ Autoimmune disease of salivary and tear glands.

➤ Most patients with Sjögren's syndrome are female.

➤ Primary: Inflammation of the lacrimal glands and parotid glands leading to dry eyes, dry mouth and lips.

➤ Secondary: Associated with a connective tissue disease, such as rheumatoid arthritis, systemic lupus erythematosus, or scleroderma.

http://www.medicinenet.com/dry_eyes/article.htm

http://www.medicinenet.com/rheumatoid_arthritis/article.htm

http://www.medicinenet.com/systemic_lupus_erythematosus_quiz/quiz.htm

http://www.medicinenet.com/scleroderma/article.htm

SJÖGREN'S SYNDROME

SECONDARY SYPHILIS

➤ Systemic invasion of Treponama pallidum

➤ Usually marked by a non-itchy rash. The rash might be confined to one part of your body, or it could spread over several parts.

OTHERS

➤ Hepatitis B: Hepadnaviridae. Liver disease. Immune complexes on glomerular membrane.

➤ Gold and mercury treatments: Kidney is the main mercury accumulation and excretion organ.

➤ Malignancy: Cancerous cells that have the ability to metastasize or to invade and destroy locla tissues.

➤ Thrombosis: Decreased antithrombin III.

MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS


➤ Marked by two different alterations in the cellularity of the glomerulus and peripheral capillaries.

➤ Histopathologic findings:

➤ Proliferation of mesangial and endothelial cells and expansion of the mesangial matrix.

➤ Thickening of the peripheral capillary walls by subendothelial immune deposits and/or intramembranous dense deposits.


➤ Type 1 – Increased cellularity in the subendothelial cells of the mesangium causing thickening of the capillary walls.

➤ Type 2 – Dense deposits in the glomerular basement membrane

➤ Type 3 – Subepithelial and subendothelial deposits

LABORATORY FINDINGS

➤ Hematuria

➤ Proteinuria

➤ Decreased serum complement levels

CHRONIC GLOMERULONEPHRITIS


➤ Caused by slow, cumulative damage and scarring of the glomeruli.

➤ Scarring of the glomeruli impedes the filtering process, trapping waste products in the blood while allowing red blood cells or proteins to escape into the urine.

MANIFESTATIONS

➤ Hematuria, proteinuria, glucosuria as a result of tubular dysfunction, and many varieties of casts, including broad casts.

➤ A markedly decreased glomerular filtration rate is present in conjunction with increased BUN and creatinine levels and electrolyte imbalance.

MANIFESTATIONS

BERGER DISEASEImmunoglobulin A Nephropathy

BERGER DISEASE

➤ IgA immune complexes are deposited on mesangial region causing glomerulonephritis and gradually affecting its filtering ability.

➤ Immunoglobulin A (IgA) is an antibody synthesized in plasma cells found in mucosal-associated lymphoid tissue.

➤ Most common form of primary glomerulonephritis worldwide.

BERGER DISEASE

LABORATORY FINDINGS

➤ A patient with the disorder may remain essentially asymptomatic for 20 years or more.

➤ Cola- or tea-colored urine following an infection or strenuous exercise.

➤ Asymptomatic microhematuria and elevated serum levels of IgA remain.

BERGER DISEASE

MANIFESTATIONS

➤ High blood pressure. Damage to kidneys from IgA deposits can raise blood pressure, and high blood pressure can cause further damage to kidneys.

➤ High cholesterol. High levels of cholesterol may increase risk of a heart attack.

➤ Acute kidney failure. If kidneys lose their filtering ability due to IgA deposits, waste products build up quickly in the blood.

➤ Chronic kidney disease. IgA nephropathy can cause kidneys to gradually stop functioning. In such cases, permanent dialysis or a kidney transplant is needed to sustain life.

➤ Nephrotic syndrome. This is a group of problems that can be caused by damage to the glomeruli, including high urine protein levels, low blood protein levels, high cholesterol and lipids, and swelling of your eyelids, feet and abdomen.

Glomerulonephritis

Health & Medicine

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