Role of the podocyte in proteinuria

Menzel, Sylvia; Moeller, Marcus J.

doi:10.1007/s00467-010-1725-5

Cited by 46 publications

(24 citation statements)

References 33 publications

(32 reference statements)

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“…One possible explanation for this unexpected finding is that an improvement in glomerular filtration and a reduction in albuminuria and other filtered tubulotoxins directly leads to decreased proximal tubulointerstitial damage . We have found that the absence of CB 1 R from podocytes mitigated the hyperglycaemia‐induced lipocalin 2 overexpression in tubular cells, which may be related also to the decrease in albuminuria in diabetic pCB1Rko mice, as it was previously shown that an increase in albumin promotes tubular cell death by inducing Ca 2+ ‐dependent endoplasmic reticulum stress, leading to lipocalin 2 overexpression .…”

Section: Discussionsupporting

confidence: 59%

Cannabinoid‐1 receptor deletion in podocytes mitigates both glomerular and tubular dysfunction in a mouse model of diabetic nephropathy

Jourdan

Park

Varga

et al. 2017

Diabetes Obesity Metabolism

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Section: Discussionsupporting

confidence: 59%

Cannabinoid‐1 receptor deletion in podocytes mitigates both glomerular and tubular dysfunction in a mouse model of diabetic nephropathy

Jourdan

Park

Varga

et al. 2017

Diabetes Obesity Metabolism

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“…Significant podocyte loss may result in permanent injury to the glomerular filtration barrier and slit diaphragm with subsequent proteinuria [28,29,30,31,32,33,34,35,36]. The ability of these shed cells to attach to tissue culture plates in vitro suggests that they are still viable, as has been previously demonstrated in animal models by our group and by others [17,22,28].…”

Section: Discussionsupporting

confidence: 55%

Urinary Podocyte Excretion and Proteinuria in Patients Treated with Antivascular Endothelial Growth Factor Therapy for Solid Tumor Malignancies

Hayman¹,

Calle

Jatoi³

et al. 2014

Oncology

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Background: Urinary podocyte excretion (podocyturia) may function as a more specific marker of ongoing glomerular damage. This study sought to analyze the relationship between proteinuria and podocyturia in cancer patients treated with antivascular endothelial growth factor (anti-VEGF) agents. Methods: Thirty-seven patients treated with anti-VEGF medications were analyzed in a single-institution, cross-sectional study. Podocyte cultures were performed on random urine collections (50-100 ml), and podocytes were identified by positive podocin staining. The corresponding urine samples were analyzed for protein and creatinine (Cr) measurements. Results: Proteinuria ≥0.5 g/g Cr was found in 30% of the patients (median, 0.12; interquartile range, 0.04-0.86), and 62% had podocyturia. There was a significant difference in the amount of podocyturia between patients with proteinuria ≥0.5 g/g Cr and those with a value <0.5 g/g Cr (median podocyturia, 1.08 cells/mg Cr, range, 0-14.55 vs. 0.03 cells/mg Cr, range, 0-1.64, respectively; p < 0.001). A statistically significant correlation was observed between the cumulative dose of bevacizumab and both proteinuria (r = 0.48, p = 0.004) and podocyturia (r = 0.34, p = 0.045) as well as between proteinuria and podocyturia (r = 0.63, p < 0.001), suggesting that these are mechanistically related. Discussion: Ongoing podocyte loss may be mechanistically related to the onset and severity of proteinuria in patients treated with anti-VEGF agents.

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“…Podocytes are critically important in overall glomerular function and structure. Injury to podocytes commonly leads to proteinuria and glomerulosclerosis . Podocytes have VDR, which is markedly upregulatable, and the podocyte nucleus has a VDRE (vitamin D response element) in its DNA near the promoter start site for the nephrin gene .…”

Section: Renoprotective Roles Of Vdra In Ckd Patientsmentioning

confidence: 99%

Calcitriol, calcidiol, parathyroid hormone, and fibroblast growth factor‐23 interactions in chronic kidney disease

Galvao¹,

Nagode

Schenck

et al. 2013

J Vet Emergen Crit Care

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ObjectiveTo review the inter-relationships between calcium, phosphorus, parathyroid hormone (PTH), parent and activated vitamin D metabolites (vitamin D, 25(OH)-vitamin D, 1,25(OH)2-vitamin D, 24,25(OH)2-vitamin D), and fibroblast growth factor-23 (FGF-23) during chronic kidney disease (CKD) in dogs and cats.Data SourcesHuman and veterinary literature.Human Data SynthesisBeneficial effects of calcitriol treatment during CKD have traditionally been attributed to regulation of PTH but new perspectives emphasize direct renoprotective actions independent of PTH and calcium. It is now apparent that calcitriol exerts an important effect on renal tubular reclamation of filtered 25(OH)-vitamin D, which may be important in maintaining adequate circulating 25(OH)-vitamin D. This in turn may be vital for important pleiotropic actions in peripheral tissues through autocrine/paracrine mechanisms that impact the health of those local tissues.Veterinary Data SynthesisLimited information is available reporting the benefit of calcitriol treatment in dogs and cats with CKD.ConclusionsA survival benefit has been shown for dogs with CKD treated with calcitriol compared to placebo. The concentrations of circulating 25(OH)-vitamin D have recently been shown to be low in people and dogs with CKD and are related to survival in people with CKD. Combination therapy for people with CKD using both parental and activated vitamin D compounds is common in human nephrology and there is a developing emphasis using combination treatment with activated vitamin D and renin-angiotensin-aldosterone-system (RAAS) inhibitors.

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Role of the podocyte in proteinuria

Cited by 46 publications

References 33 publications

Cannabinoid‐1 receptor deletion in podocytes mitigates both glomerular and tubular dysfunction in a mouse model of diabetic nephropathy

Cannabinoid‐1 receptor deletion in podocytes mitigates both glomerular and tubular dysfunction in a mouse model of diabetic nephropathy

Urinary Podocyte Excretion and Proteinuria in Patients Treated with Antivascular Endothelial Growth Factor Therapy for Solid Tumor Malignancies

Calcitriol, calcidiol, parathyroid hormone, and fibroblast growth factor‐23 interactions in chronic kidney disease

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