Membranoproliferative glomerulonephritis

Membranoproliferative glomerulonephritis, or MPGN, is a kidney disease triggered by immune deposits which end up in the walls of the glomerulus, which are the tufts of capillaries where blood is filtered.

These deposits lead to inflammation and result in structural changes to the glomerulus, that cause a decrease in kidney function, which commonly presents as a nephrotic syndrome.

But what exactly is nephrotic syndrome? Well usually the glomerulus only lets small molecules, like sodium and water, move from the blood into the kidney nephron, where it eventually makes its way into the urine. But with nephrotic syndromes, the glomeruli are damaged and they become more permeable, so they start letting plasma proteins come across from the blood to the nephron and then into the urine, which causes proteinuria, typically greater than 3.5 grams per day.

An important protein in the blood is albumin, and so when it starts leaving the blood, people get hypoalbuminemia—low albumin in the blood.

With less protein in the blood the oncotic pressure falls, which lowers the overall osmotic pressure, which drives water out of the blood vessels and into the tissues, called edema.

Finally, it’s thought that as a result of either losing albumin or losing some protein or proteins that inhibit the synthesis of lipids, or fat, you get increased levels of lipids in the blood, called hyperlipidemia.

Just like the proteins, these lipids can also get into the urine, causing lipiduria.

And those are the hallmarks of nephrotic syndrome—proteinuria, hypoalbuminemia, edema, hyperlipidemia, and lipiduria.

Okay so membranoproliferative glomerulonephritis is a type of nephrotic syndrome, got it. But how exactly do these glomeruli start letting plasma proteins like albumin through? Well, with MPGN, there are actually three types, so let’s go through one by one.

Type I MPGN is the most common form, and it usually starts one of two ways. The first way involves circulating immune complexes, made up of antigens and antibodies, that might form, for example, because of antigen release from a chronic infection like hepatitis B or hepatitis C which gets bound by antibody in the blood.