Recent Progress in HIV-Associated Nephropathy

Ross, Michael J.; Klotman, Paul E.

doi:10.1097/01.asn.0000040750.40907.99

Cited by 133 publications

(90 citation statements)

References 70 publications

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“…Direct cytopathic effect, expression of intracellular antigens and deposition of in situ immune complexes, abnormal activation of the immune system with formation of circulating immune complexes, and subsequent renal deposition are all possible explanations. 12 In this present case, renal pathology showed an acute glomerulonephritis, with signs of splitting of the basement membrane and the appearance of double contours. This histological pattern associated with the presence of tubuloreticular inclusions suggests the diagnosis of HIVassociated immune complex glomerulonephritis.…”

Section: Discussionsupporting

confidence: 49%

Hiv Infection and Acute Glomerulonephritis

Titan¹,

Testagrossa²,

Saldanha³

et al. 2007

Clinics

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Section: Discussionsupporting

confidence: 49%

Hiv Infection and Acute Glomerulonephritis

Titan¹,

Testagrossa²,

Saldanha³

et al. 2007

Clinics

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“…As discussed above, podocytes are the target of many forms of injury, including antibodies to podocyte membrane antigens (membranous nephropathy, minimal change disease) (98), hemodynamic injury (reduced nephron number, diabetes, metabolic diabetes) (99 -101) [104]), and unknown causes (idiopathic FSGS) (105). Moreover, in secondary forms of FSGS, such as after loss of nephron number, hypertension, and tubulointerstitial disease, podocytes are also injured (106).…”

Section: Podocyte Number Contributes To Glomerulosclerosismentioning

confidence: 99%

“…Although the vast majority of human podocyte diseases are not associated with proliferation, podocyte proliferation does occur in idiopathic collapsing glomerulopathy and HIV-associated nephropathy (see review by Ross and Klotman in this issue [104]). In these diseases, there is increased expression of cyclin A and Ki-67 and a reduction in p27 and p57 in cells that are proliferating (139,140).…”

Section: Lack Of Proliferationmentioning

confidence: 99%

Podocyte Biology and Response to Injury

Mündel¹,

Shankland²

2002

Journal of the American Society of Nephrology

595

541

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The visceral glomerular epithelial cell, also called podocyte, is a terminally differentiated cell that lines the outer aspect of the glomerular basement membrane (GBM). It therefore forms the final barrier to protein loss, which explains why podocyte injury is typically associated with marked proteinuria. Indeed, all forms of nephrotic syndrome are characterized by abnormalities in the podocyte. In this review, we will provide an update of the known functions of recent podocyte-specific proteins and focus on the slit diaphragm (SD) and the mechanisms underlying foot process (FP) flattening and how the podocyte responds to injury. Molecular Anatomy of the Podocyte FP CytoskeletonPodocyte FP are not static, but rather contain a contractile system similar to that seen in pericytes. This contractile apparatus is composed of actin, myosin-II, ␣-actinin-4, talin, and vinculin (1). The actin filament bundles form arches between adjacent FP of the same podocyte (2). Figure 1 is a schema of our current understanding of the molecular composition of the cytoskeleton in podocyte FP. Importantly, the actin filaments are connected to the underlying GBM at focal contacts via an ␣3␤1 integrin complex (3,4). The bends of the actin filament arches appear to be connected directly to the microtubules of the major processes (own unpublished results). FP are anchored to the GBM via ␣3␤1 integrin (5) and dystroglycans (6,7). Neighboring FP are connected by a cell-cell junction, the glomerular SD, which represents the main size selective filter barrier in the kidney (8 -10). The SD is thought to be a modified adherens junction (11) that is composed of a growing number of proteins, including nephrin (12-14), P-cadherin, CD2AP (15-18), , FAT (20), podocin (16,21), and possibly Neph1 (see reference 22 and below). In addition to the contractile proteins described above, we have reported the association of synaptopodin with the actin filaments in FP (23). Synaptopodin is the first member of a novel class of prolinerich proteins (24) and, like ␣-actinin-4, interacts with the tight junction protein MAGI-1 (25) that is also expressed in podocytes (26). Four Major Causes of FP EffacementThe basolateral portion of the foot processes represents the center of podocyte function and is defined by three membrane domains: the apical membrane domain, the SD protein complex, and the basal membrane domain or sole plate (27). The submembranous regions of all compartments are connected to the FP actin cytoskeleton, e.g., on the apical membrane domain, podocalyxin associates with the actin cytoskeleton through interactions with ezrin and the actin cytoskeleton via Na ϩ /H ϩ -exchanger regulatory factor 2 (NHERF2), a scaffold protein containing two PDZ (PSD-95/Dlg/ZO-1) domains and an ERM-binding region (28,29). The FP actin cytoskeleton is highly dynamic and ultimately determines the structural maintenance of the filtration slits as demonstrated in the acute PS/heparin model by several groups (30 -32). Interference with one of the three domains eventually ...

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“…It has been suggested, for example, that parvovirus infection is associated with the development of FSGS (99,100). HIV infection is associated with a distinct podocytopathy (see review by Ross and Klotman in this issue [101]). We will ultimately need to explain why some people with HIV infection (and perhaps parvovirus) develop disease and others do not.…”

Section: Sporadic Fsgsmentioning

confidence: 99%

Inherited Podocytopathies

Pollak¹

2002

Journal of the American Society of Nephrology

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Recent Progress in HIV-Associated Nephropathy

Cited by 133 publications

References 70 publications

Hiv Infection and Acute Glomerulonephritis

Hiv Infection and Acute Glomerulonephritis

Podocyte Biology and Response to Injury

Inherited Podocytopathies

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