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Renal tubular acidosis
Minimal change disease
Focal segmental glomerulosclerosis (NORD)
Rapidly progressive glomerulonephritis
IgA nephropathy (NORD)
Acute tubular necrosis
Renal papillary necrosis
Renal cortical necrosis
Chronic kidney disease
Polycystic kidney disease
Multicystic dysplastic kidney
Medullary cystic kidney disease
Medullary sponge kidney
Renal artery stenosis
Renal cell carcinoma
Nephroblastoma (Wilms tumor)
Posterior urethral valves
Hypospadias and epispadias
Lower urinary tract infection
Transitional cell carcinoma
Non-urothelial bladder cancers
Congenital renal disorders: Pathology review
Renal tubular defects: Pathology review
Renal tubular acidosis: Pathology review
Acid-base disturbances: Pathology review
Electrolyte disturbances: Pathology review
Renal failure: Pathology review
Nephrotic syndromes: Pathology review
Nephritic syndromes: Pathology review
Urinary incontinence: Pathology review
Urinary tract infections: Pathology review
Kidney stones: Pathology review
Renal and urinary tract masses: Pathology review
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autoantibody p. 113
Tanner Marshall, MS
Membranous glomerulonephritis, also known as membranous nephropathy, is where the glomerular basement membrane, or GBM, which lines the glomeruli in the kidney, becomes inflamed and damaged, which results in increased permeability and proteins being able to filter through into the urine, causing 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 lipid in the blood, called hyperlipidemia.
Just like the proteins, these lipids can also get into the urine, causing hyperlipiduria.
And those are the hallmarks of nephrotic syndrome—proteinuria, hypoalbuminemia, edema, hyperlipidemia, and lipiduria.
Alright, so with membranous glomerulonephritis, the basement membrane becomes damaged which causes nephrotic syndrome. How does this happen, though? Well, ultimately this damage is caused by immune complexes—complexes composed of an antigen with an antibody bound to it.
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