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Membranoproliferative GN I   

Overview | Symptoms | Treatment | Prevention

Alternative names:

Mesangiocapillary glomerulonephritis (type I); Membranoproliferative glomerulonephritis (type I); Lobular GN; Glomerulonephritis - membranoproliferative (type I); MPGN type I

Definition:

A kidney disorder that results in disrupted kidney function, caused by inflammation and changes in the microscopic structure of kidney cells.

Causes and Risks

The glomeruli are the inner structures of the kidney. They include small capillaries surrounded by membranes through which the blood is filtered to form urine. Glomerulonephritis involves inflammation of the glomeruli. Membranoproliferative glomerulonephritis (MPGN) is a form of glomerulonephritis caused by an abnormal immune response, with deposits of antibodies in the kidneys. Certain cells in the capillary wall (mesangial cells) increase in number and the parts of the glomerular membranes change in structure. Type I MPGN involves deposits of antibodies in the subendothelial layer of the glomerular membrane.

Most cases of membranoproliferative glomerulonephritis are type I. (A few are type II or III MPGN). Both sexes are affected. The disorder affects mostly people under age 30.

Membranoproliferative GN I may present in several forms. The glomerular membrane disruption causes a change in urine filtration, making the glomerulus permeable to protein and blood cells. This is manifested as acute nephritic syndrome, nephrotic syndrome, or abnormal urinalysis without symptoms. MPGN accounts for about 5% of all cases of idiopathic glomerulopathies (diseases of the glomerulus).

White blood cells may be excreted in the urine, causing it to have a cloudy appearance. Urine output decreases because of reduced glomerular filtration rate. Swelling may occur as sodium and water are retained in the body.

Protein in the bloodstream keeps fluid within the blood vessels. Edema is increased when protein is lost because fluid leaks out of blood vessels into the tissues. Hypertension occurs due to the cumulative effects of water and sodium retention, and increased production of renin (a hormone that regulates blood pressure) by the damaged kidney.

Nitrogenous waste products such as urea (see BUN) and creatinine may accumulate in the blood (azotemia) because of poor kidney functioning. The disorder is often progressive and eventually results in chronic renal failure.

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