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Membranoproliferative GN II   

Overview | Symptoms | Treatment | Prevention

Alternative names:

Membranoproliferative glomerulonephritis (type II); Glomerulonephritis - membranoproliferative (type II); Mesangiocapillary glomerulonephritis (type II); Dense deposit disease; MPGN II

Definition:

A kidney disorder causing decreased kidney function because of inflammation and changes in the tissues of the internal kidney structures.

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 II MPGN involves deposits within the glomerular basement membrane (the "bottom" layer of the membrane).

Membranoproliferative GN II is much less common than MPGN I. Both sexes are affected. The disorder affects mostly persons under age 30.

The effect of the disorder is very similar in both forms of MPGN. The glomerular membrane changes make the glomerulus permeable to protein and blood cells. The microscopic features of MPGN II are somewhat more variable and cellular compared to MPGN I. MPGN II also tends to have a more rapid progression to end stage renal disease than does MPGN I.

MPGN may present as acute nephritic syndrome, nephrotic syndrome, or abnormal urinalysis without symptoms. It accounts for less than 5% of all cases of idiopathic (unexplained) glomerulopathies (glomerular diseases). White blood cells may be excreted in the urine, causing it to have a cloudy appearance. Urine output decreases as glomerular filtration rate (the "speed" of blood purification) reduces.

Swelling of the body may occur as sodium and water are retained in the body. Protein in the bloodstream normally keeps fluid within the blood vessels. When protein is lost, fluid leaks from blood vessels into the tissues, which contributes to edema.

Hypertension occurs from the cumulative effects of water and sodium retention and increased production of renin (a hormone that regulates blood pressure) by the damaged kidney.

Nitrogen-containing waste products such as urea and creatinine may accumulate in the blood (azotemia) when kidney function is poor. These waste products are toxic to the tissues of the body. The disorder is often progressive and may result in chronic renal failure.

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