Urinary podocyte excretion as a marker for preeclampsia

Garovic, Vesna D.; Wagner, Steven J.; Turner, Stephen T.; Rosenthal, David W.; Watson, William J.; Brost, Brian C.; Rose, Carl H.; Gavrilova, Larisa; Craigo, Paula; Bailey, Kent R.; Achenbach, Johannes; Schiffer, Mario; Grande, Joseph P.

doi:10.1016/j.ajog.2007.02.007

Cited by 182 publications

(115 citation statements)

References 17 publications

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“…Our group and others recently reported significantly higher numbers of podocytes in the urine (i.e., podocyturia) of women with preeclampsia compared with pregnant controls (5,6). This podocyturia remained in the patients with preeclampsia up to 1 month after delivery, although their proteinuria resolved (7).…”

Section: Introductionmentioning

confidence: 94%

Association of Preeclampsia with Podocyte Turnover

Penning¹,

Bloemenkamp

Zon³

et al. 2014

Clinical Journal of the American Society of Nephrology

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Background and objectives Preeclampsia is characterized by hypertension and proteinuria, and increased shedding of podocytes into the urine is a common finding. This finding raises the question of whether preeclamptic nephropathy involves podocyte damage. This study examined podocyte-related changes in a unique sample of renal tissues obtained from women who died of preeclampsia.Design, setting, participants, & measurements All patients with preeclampsia who died in The Netherlands since 1990 and had available autopsy tissue were identified using a nationwide database of the Dutch Pathology Registry (PALGA). This resulted in a cohort of 11 women who died from preeclampsia. Three control groups were also identified during the same time period, and consisted of normotensive women who died during pregnancy (n=25), and nonpregnant controls either with (n=14) or without (n=13) chronic hypertension. Glomerular lesions, including podocyte numbers, podocyte proliferation, and parietal cell activation, were measured.Results Patients with preeclampsia had prominent characteristic glomerular lesions. The results showed that the number of podocytes per glomerulus did not differ significantly between the patients with preeclampsia and the control groups. However, preeclampsia was associated with a significant increase in intraglomerular cell proliferation (7.3% [SD 9.4] Conclusions These findings suggest that the recently described mechanisms of podocyte replacement play a role in preeclampsia. These results provide key new insights into the pathogenesis of preeclamptic nephropathy, and they open new possibilities for developing therapeutic modalities.

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Section: Introductionmentioning

confidence: 94%

Association of Preeclampsia with Podocyte Turnover

Penning¹,

Bloemenkamp

Zon³

et al. 2014

Clinical Journal of the American Society of Nephrology

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“…The net consequence is the presence of podocytes in urine, a phenomenon called podocyturia. Low numbers of podocytes are usually excreted in the urine in the healthy state, whereas in some glomerular diseases podocyturia increases significantly (24), which renders this parameter a potentially valuable, noninvasive approach to monitor the progression of diseases such as focal segmental glomerulosclerosis, diabetic nephropathy, membranous and IgA nephropathy, and preeclampsia (25)(26)(27).…”

Section: What Do We Know?mentioning

confidence: 99%

Biomarkers of Fabry Disease Nephropathy

Schiffmann¹,

Waldek²,

Benigni³

et al. 2010

Clinical Journal of the American Society of Nephrology

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It is suggested that biomarkers of renal complications of Fabry disease are likely to be useful for diagnosis and to follow the natural disease progression or the effect of specific therapeutic interventions. Traditionally, globotriaosylceramide (Gb 3 ) in urine has been used to evaluate the effect of specific therapy, such as enzyme replacement therapy (ERT). Although urinary Gb 3 decreases significantly with ERT, it has not yet been shown to be a valid surrogate marker in treatment trials. We propose a detailed study of the nature and origin of Gb 3 combined with a prospective collaborative trial that combines Gb 3 changes with the effect of ERT on clinical nephrological outcome measures. Existing biomarkers such as general proteinuria/ albuminuria or specific proteins such as N-acetyl-␤-D-glucosaminidase should be evaluated along with novel proteomic or metabolomic studies for biomarker discovery using mass spectrometry or nuclear magnetic resonance. Standard scoring of all pathologic aspects of kidney biopsies may also be a promising way to assess the effect of therapy.

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“…Proteinuria, for example, is due to characteristic changes in the renal glomeruli (glomerular endotheliosis). Indeed, a strict diagnosis of preeclampsia, differentiating it from other forms of pregnancy hypertension, requires a renal biopsy (Chesley 1980) or demonstration of podocytes in the urine (Garovic et al 2007).…”

Section: Introductionmentioning

confidence: 99%

Comparative studies of placentation and immunology in non-human primates suggest a scenario for the evolution of deep trophoblast invasion and an explanation for human pregnancy disorders

Carter

2011

Reproduction

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Deep trophoblast invasion in the placental bed has been considered the hallmark of human pregnancy. It occurs by two routes, interstitial and endovascular, and results in transformation of the walls of the spiral arteries as they traverse the decidua and the inner third of the myometrium. Disturbances in this process are associated with reproductive disorders such preeclampsia. In contrast, trophoblast invasion in Old World monkeys occurs only by the endovascular route and seldom reaches the myometrium. Recently, it was shown that this pattern is maintained in gibbons, but that the human arrangement also occurs in chimpanzee and gorilla. There is an interesting parallel with results from placental immunology regarding the evolution of the major histocompatability complex class I antigen HLA-C and its cognate receptors. HLA-C is not present in Old World monkeys or gibbons. It emerged in the orangutan and became polymorphic in the lineage leading to gorilla, bonobo, chimpanzee, and human. Interaction between HLA-C1 and HLA-C2 on the surface of trophoblast and killer immunoglobulin-like receptors (KIRs) expressed by uterine natural killer cells are important regulators of trophoblast invasion. Evolution of this system in great apes may have been one prerequisite for deep trophoblast invasion but seems to have come at a price. The evidence now suggests that certain combinations of maternal genotype for KIRs and fetal genotype for HLA-C imply an increased risk of preeclampsia, fetal growth restriction, and recurrent abortion. The fetal genotype is in part derived from the father providing an explanation for the paternal contribution to reproductive disorders.

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Urinary podocyte excretion as a marker for preeclampsia

Cited by 182 publications

References 17 publications

Association of Preeclampsia with Podocyte Turnover

Association of Preeclampsia with Podocyte Turnover

Biomarkers of Fabry Disease Nephropathy

Comparative studies of placentation and immunology in non-human primates suggest a scenario for the evolution of deep trophoblast invasion and an explanation for human pregnancy disorders

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