Urinary and glomerular podocytes in patients with chronic kidney diseases

Hanamura, Kikuno; Tojo, Akihiro; Fujita, Toshiro

doi:10.1007/s10157-013-0814-8

Cited by 19 publications

(25 citation statements)

References 39 publications

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“…Podocalyxin[40] (PCX) is a highly negatively charged molecule which is abundantly expressed on the surface of podocytes and hence is a sensitive marker of these cells commonly used in podocyturia studies[13, 41, 42]; however, since some of the parietal cells covering Bowman's capsule also express podocalyxin[42], we used claudin-1 (CL-1) which, in glomeruli, is specifically expressed in parietal epithelial cells, as an exclusion marker. The cytospin slides were stained with antibodies against PCX (Invitrogen, Camarillo, CA.…”

Section: Methodsmentioning

confidence: 99%

Urinary Podocyte Loss Is Increased in Patients with Fabry Disease and Correlates with Clinical Severity of Fabry Nephropathy

et al. 2016

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Chronic kidney disease is a major complication of Fabry disease. Podocytes accumulate globotriaosylceramide inclusions more than other kidney cell types in Fabry patients. Podocyte injury occurs early in age, and is progressive. Since injured podocytes detach into the urine (podocyturia), we hypothesized that podocyturia would increase in Fabry patients and correlate with clinical severity of Fabry nephropathy. Urine specimens from 39 Fabry patients and 24 healthy subjects were evaluated for podocyturia. Most of the Fabry patients and many healthy subjects had podocyturia. The number of podocytes per gram of urine creatinine (UPodo/g Cr) was 3.6 fold greater in Fabry patients (3,741 ± 2796; p = 0.001) than healthy subjects (1,040 ± 972). Fabry patients with normoalbuminuria and normoproteinuria had over 2-fold greater UPodo/g Cr than healthy subjects (p = 0.048). UPodo/gCr was inversely related to eGFR in male patients (r = -0.69, p = 0.003). UPodo/gCr was directly related to urine protein creatinine ratio (r = 0.33; p = 0.04) in all Fabry patients. These studies confirm increased podocyturia in Fabry disease, even when proteinuria and albuminuria are absent. Podocyturia correlates with clinical severity of Fabry nephropathy, and potentially may be of prognostic value.

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Section: Methodsmentioning

confidence: 99%

Urinary Podocyte Loss Is Increased in Patients with Fabry Disease and Correlates with Clinical Severity of Fabry Nephropathy

et al. 2016

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“…Urine sediment tests are inexpensive and safe, and positive findings with respect to casts and various cell types could be useful for the diagnosis of renal glomerular and tubular damage. Podocytes, which can be identified via podocalyxin expression in the urine, indicate the early stage of glomerular damage [8,9]. Round cells were negative for podocalyxin and the clinical stages of patients who are positive for round cells were different from those that have previously been associated with podocytes.…”

Section: Discussionmentioning

confidence: 97%

Novel round cells in urine sediment and their clinical implications

Shukuya

Ogura

Tokuhara

et al. 2016

Clinica Chimica Acta

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“…Podocyte injury is considered to be one of the most critical factors in the development of proteinuria caused by glomerular filtration barrier dysfunction and continuous injury may cause severe apoptosis, leading to proteinuria, glomerulosclerosis and renal impairment; the major reason is that podocytes are highly differentiated cells with specific structural and biological functions, which are not renewable after sustained injury (1,2). To date, a large number of studies have indicated that podocyte injury, loss and dysfunction have an important role in pathologies including focal segmental glomerulosclerosis and membranous nephropathy (3)(4)(5). Immunosuppressants (e.g., steroids or cyclosporine A) have been used based on anecdotal evidence to treat NS (6).…”

Section: Introductionmentioning

confidence: 99%

Protective effect of astragalosides from Radix Astragali on adriamycin-induced podocyte injury

et al. 2018

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Abstract. Nephrotic syndrome (NS) is the most common kidney disease in clinical practice and may lead to end-stage renal failure. Astragalosides (AST) have been clinically tested for the treatment of NS, but their mechanism of action has remained to be elucidated. The aim of the present study was to investigate the effect of AST on the structure and function of podocytes with adriamycin (ADR)-induced damage and to elucidate the underlying molecular mechanisms. The mouse podocyte clone 5 (MPC5) immortalized mouse podocyte cell line was treated with 0.5 µmol/l ADR to establish a podocyte injury model. The MPC5 podocytes were divided into a control group, a podocyte injury group and a low-, medium-and high-concentration AST treatment group. The results indicated that the survival rate of the podocyte injury group was significantly decreased compared with that in the control group and each AST-treated group had an increased survival rate compared with that in the podocyte injury group. Furthermore, each dose of AST significantly inhibited the ADR-associated increases the levels of lactate dehydrogenase and malondialdehyde and the decrease in the activity of superoxide dismutase in MPC5 podocytes. In addition, AST improved the migration ability of MPC5 podocytes and suppressed the cytoskeletal rearrangement associated with ADR-induced damage. Furthermore, matrix metalloproteinase (MMP)-2 and -9 were decreased in the podocyte injury group, which was inhibited by different concentrations of AST. Thus, AST was able to maintain the balance of oxidative stress in podocytes cultured with ADR and protect them from ADR-induced injury. The mechanism may be associated with the upregulation of MMPs.

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Urinary and glomerular podocytes in patients with chronic kidney diseases

Abstract: Urinary podocyte excretion reflects ongoing glomerular injury in various kidney diseases, and podocyte loss correlated with glomerulosclerosis and impaired selectivity of proteinuria.

Cited by 19 publications

References 39 publications

Urinary Podocyte Loss Is Increased in Patients with Fabry Disease and Correlates with Clinical Severity of Fabry Nephropathy

Urinary Podocyte Loss Is Increased in Patients with Fabry Disease and Correlates with Clinical Severity of Fabry Nephropathy

Novel round cells in urine sediment and their clinical implications

Protective effect of astragalosides from Radix Astragali on adriamycin-induced podocyte injury

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