Viable Podocyturia in Healthy Individuals: Implications for Podocytopathies

Maestroni, Silvia; Maestroni, Anna; Dell’Antonio, Giacomo; Gabellini, Daniela; Terzi, Simona; Spinello, Alice; Meregalli, Giancarla; Castoldi, Giovanna; Zerbini, Gianpaolo

doi:10.1053/j.ajkd.2014.08.016

Cited by 18 publications

(11 citation statements)

References 10 publications

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“…Therefore, it is particularly important to actively investigate the mechanism of diabetic proteinuria. In previous years, studies investigating the mechanism of proteinuria provided encouraging results, and it was confirmed that podocyte lesions are important in the development and progression of proteinuria (18). Lin et al (19) reported that two key factors of proteinuria progression were a reduced number of podocytes and decreased expression of nephrin in podocytes.…”

Section: Discussionmentioning

confidence: 88%

Protective effects of tacrolimus on podocytes in early diabetic nephropathy in rats

Peng

Chang

Wang

et al. 2017

Molecular Medicine Reports

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The aim of the present study was to investigate the protective effect of tacrolimus on early podocyte damage in rats with diabetic nephropathy (DN). A total of 38 normal male Sprague‑Dawley rats were randomly divided into four groups: Normal control group (group N; n=8), DN group (n=10), tacrolimus (FK506) treatment group (group F; n=10), benazepril (Lotensin) treatment group (group L; n=10). The rats in groups DN, F and L were administered with streptozotocin (STZ; 60 mg/kg) by intraperitoneal injection to establish the diabetic rat model. After 4 weeks, the diabetic rat model was established, and rats in the different groups were administered intragrastically with the respective drugs. Blood glucose (BS), body weight (BW) and 24‑h urine protein were detected every 4 weeks, serum creatinine (SCr), blood urea nitrogen (BUN) and kidney weight/body weight (KW/BW) were measured at the end of the 8 weeks of drug treatment. Renal pathological changes were observed under a light microscope and electron microscope. Expression of nephrin, which is a podocyte‑specific marker, was detected using western blot analysis. The results showed that the levels of SCr, BUN, KW/BW and 24‑h urine protein in groups D, F and L were significantly higher, compared with those in group N (P<0.05). No significant differences were found between groups F and L for the above indicators, with the exception of BS. However, all indices were significantly lower, compared with those in group DN (P<0.05). Renal pathological expression was normal in group N under light microscopy. There were significant increases in the glomerular volume, proliferative mesangial cells, width of the mesangial area and thickness of the basement membrane in group DN, however, all the above pathological characteristics were reduced in groups F and L, compared with group DN (P<0.05). No significant difference was found between groups F and L. A widened glomerular basement membrane, and disorder, widening and fusion of podocyte processes were observed under the electron microscope in group DN, however, these were reduced in groups F and L, compared with group DN (P<0.05). The results of the western blot analysis showed that the expression of nephrin decreased by 60.1% in group DN, compared with group N, and significant recovery in the expression of nephrin was observed in groups F and L (P<0.05). Tacrolimus reduced urinary protein and slowed the progression of DN, partially by recovering the protein expression of nephrin in the renal tissue of diabetic rats, and maintaining the integrity of the structure and function of podocytes.

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Section: Discussionmentioning

confidence: 88%

Protective effects of tacrolimus on podocytes in early diabetic nephropathy in rats

Peng

Chang

Wang

et al. 2017

Molecular Medicine Reports

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“…Urinary podocytes can be identified with colorimetric qualitative methods, as immunohistochemistry or with immunofluorescence[ 26 , 27 ] (Figure 2 ). Different podocyte proteins can be targeted with monoclonal antibodies and consequently identified with the proper microscopy method employed[ 28 ]. Podocytes can also be identified by polymerase chain reaction (PCR), employing primers that belong to the different podocyte proteins.…”

Section: Methods Of Diagnosis Of Podocyturiamentioning

confidence: 99%

Podocyturia: Potential applications and current limitations

Trimarchi

2017

WJN

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Chronic kidney disease is a prevalent condition that affects millions of people worldwide and is a major risk factor of cardiovascular morbidity and mortality. The main diseases that lead to chronic kidney disease are frequent entities as diabetes mellitus, hypertension and glomerulopathies. One of the clinical markers of kidney disease progression is proteinuria. Moreover, the histological hallmark of kidney disease is sclerosis, located both in the glomerular and in the interstitial compartments. Glomerulosclerosis underscores an irreversible lesion that is clinically accompanied by proteinuria. In this regard, proteinuria and glomerular sclerosis are linked by the cell that has been conserved phylogenetically not only to prevent the loss of proteins in the urine, but also to maintain the health of the glomerular filtration barrier: The podocyte. It can then be concluded that the link between proteinuria, kidney disease progression and chronic kidney disease is mainly related to the podocyte. What is this situation due to? The podocyte is unable to proliferate under normal conditions, and a complex molecular machinery exists to avoid its detachment and eventual loss. When the loss of podocytes in the urine, or podocyturia, is taking place and its glomerular absolute number decreased, glomerulosclerosis is the predominant histological feature in a kidney biopsy. Therefore, tissular podocyte shortage is the cause of proteinuria and chronic kidney disease. In this regard, podocyturia has been demonstrated to precede proteinuria, showing that the clinical management of proteinuria cannot be considered an early intervention. The identification of urinary podocytes could be an additional tool to be considered by nephrologists to assess the activity of glomerulopathies, for follow-up purposes and also to unravel the pathophysiology of podocyte detachment in order to tailor the therapy of glomerular diseases more appropriately.

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“…Therefore, the diagnosis of proteinuria is a late event. Podocyturia could be used as an early indicator of glomerular pathology (6,7). Podocyturia points to a dynamic injury, on the other hand, proteinuria, cannot differentiate between active and chronic glomerular damaging process (8).…”

Section: Introductionmentioning

confidence: 99%

Urinary podocin level as a predictor of diabetic kidney disease

et al. 2018

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Background: Albuminuria showed to be a deteriorating condition in diabetic kidney disease (DKD) associated with high morbidity and mortality. A need for a novel marker for early detection of DKD development and progression becomes mandating. Objective: To study the clinical value of urinary podocin as an early marker of diabetic kidney disease and its association with severity of the disease. Patients and Methods: This study included 45 individuals with type 2 DM whose GFR >60 mL/min/1.73 m2 , recruited from Ain Shams University Hospital, Cairo, Egypt. Patients were further divided into three groups according to urinary albumin/creatinine ratio (ACR). In addition to, ten healthy volunteers serving as the control group was enrolled in the study. Routine chemistry including serum creatinine, fasting blood glucose (FBG), HbA1c, albumin, lipid profile, urine analysis, ACR and urinary podocin quantification were conducted for all participants (by ELISA method). Results: Podocin was higher in patients with ACR <30 mg/g, ACR 30-299 mg/g and ACR ≥ 300 mg/g versus healthy controls, respectively (P<0.001). Both GFR and serum albumin showed highly significant negative correlations with urinary podocin. Significant positive correlations were detected between urinary podocin with blood urea nitrogen (BUN), serum creatinine, FBG, HbA1c, cholesterol, and triglyceride levels. Conclusions: Urinary podocin is assumed to be a promising marker for early DKD detection in type 2 DM patients.

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Viable Podocyturia in Healthy Individuals: Implications for Podocytopathies

Cited by 18 publications

References 10 publications

Protective effects of tacrolimus on podocytes in early diabetic nephropathy in rats

Protective effects of tacrolimus on podocytes in early diabetic nephropathy in rats

Podocyturia: Potential applications and current limitations

Urinary podocin level as a predictor of diabetic kidney disease

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