glomerulus consists of a set of capillaries from which blood is filtered into Bowman's space. Large molecules, such as proteins, are usually too large to be filtered and instead are retained in the capillaries.<unk>  is primarily a disease of the renal glomerulus, the site of filtration of ions and solutes. Podocytes are specialized cells lining the Bowman's capsule that contribute to the filtration barrier, preventing molecules larger than 5 nm from being filtered.<unk>  involves damage to the renal podocytes such that larger molecules, most notably proteins, are filtered and lost through the kidney. Thus, many of the signs and symptoms of<unk>  are related to protein loss. On histology,<unk>  manifests as damage (sclerosis) to segments of glomeruli; moreover, only a portion of glomeruli are affected. The focal and<unk>  nature of disease seen on histology help to distinguish<unk>  from other types of glomerular sclerosis.<unk>  can be classified by the putative cause of damage to podocytes. Primary<unk>  involves cases in which no cause is readily identifiable. It is presumed that a set of unidentified circulating factors in the blood contribute to podocyte damage in these cases. Secondary<unk>  is caused by an identifiable stress or toxin that injures podocytes. Many causes of secondary<unk>  contribute to podocyte injury through hyperfiltration, which is a scenario of excess filtration by renal glomeruli. Hyperfiltration can be caused by obesity or loss of the contralateral kidney, among other causes. Secondary<unk>  can also be caused by toxins, including steroids and heroin. A number of genes have been implicated in<unk> . These include: NPHS1, which encodes the protein nephrin that contributes to the filtration barrier; NPHS2, which encodes the protein podocin found in podocytes; and INF2, which encodes the actin-binding protein formin. The pathogenesis of HIV-associated<unk>  is unclear, but may be primarily due to the presence of the G1/G2 risk alleles for APOL1. There is some data to suggest that HIV can infect tubular epithelial cells and podocytes, but much remains to be known.
Focal segmental glomerulosclerosis
Membranous glomerulonephritis
Minimal mesangial glomerulonephritis
Mesangial proliferative glomerulonephritis
Focal proliferative nephritis
IgA nephropathy
Mesoamerican nephropathy
Membranoproliferative glomerulonephritis