Objective To study the clinical significance of detecting urine glycyl -proline dipeptidyl arninopeptidase (GPDA) at convalescence of acute glomerulonephritis.
Information about their glomerular target antigens is inconsistent, and whether aailability of target antigens, antibody specificity or aidity are nephritogenic parameters, is not determined.
So focal segmental glomerulosclerosis is a type of nephrotic syndrome, that's helpful, but why does the glomerulus develop segmental sclerosis in the first place?
So when there is glomerular injury, red blood cells sneak into the urine —causing hematuria, which contributes to this being a type of nephritic syndrome.
Chronic vesicoureteral reflux can cause pyelonephritis, or inflammation of the kidney, and renal scarring, or fibrosis which damages the kidney tissue.
So for ascending infections that cause acute pyelonephritis, the most common organisms are E. coli, Proteus species, and Enterobacter species, all of which are commonly found in the bowel flora.
Other potential causes of renal papillary necrosis are chronic use of analgesics, like aspirin, as well as diabetes mellitus, sickle cell disease, and pyelonephritis.
If Leptospira gets to the kidneys, it may infect the interstitium, causing interstitial nephritis, or it may cause an inflammatory reaction that damages the renal tubules, resulting in acute tubular necrosis.
Alright, quick recap—membranous glomerulonephritis is where immune complexes deposit in the GBM, causing a thickening of that GBM and a " spike and dome" appearance that leads to nephrotic syndrome.