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The Interstitium of the Cystic Kidney. Models of Cysts and Cystic Kidneys. Pathogenesis of Cysts and Cystic Kidneys. The Genetics of Renal Cystic Disease. A Classification of Renal Cysts. Radiology of Cystic Kidneys. Systemic Manifestations of Renal Cystic Disease.

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Management of Cystic Kidney Disease. Bennett, L. Elzinga, J. Ethical Issues and Cystic Kidneys. Autosomal Dominant Polycystic Kidney Disease. Unique vimentin-positive tubules with simplified morphology in both groups were mainly located in the vicinity of glomeruli, suggesting that these tubules represent the convoluted portion of proximal tubules, which must be exposed to abnormally filtered massive protein from a glomerulus. Proteinuria could induce apoptosis in proximal tubular cells [ 12 , 13 ], and urinary protein from MCNS patients induces cellular injuries and apoptosis in a human proximal tubular cell line [ 14 ].

In addition, the straight portion of proximal tubules is more vulnerable to ischaemic changes compared with the convoluted portion of proximal tubules [ 27 ]. Thus, it is conceivable that proximal tubular injuries in the non-AKI group may be caused primarily by toxicity due to massive proteinuria but not by altered intrarenal haemodynamics. In the present study, the percentage of the vimentin-positive tubular area was correlated with uNAG in all patients and the non-AKI group, separately.

On the other hand, the percentage of the vimentin-positive tubular area was correlated with uA1MG in all patients but not in each group. The percentage of the vimentin-positive tubular area was not correlated with urinary protein excretion but was correlated inversely with serum albumin in all patients and the non-AKI group probably because levels of urinary protein excretion at kidney biopsy do not necessarily reflect the degree of accumulated protein toxicity to tubular cells.

Increased uNAG levels and reduced serum albumin may indicate the presence of unique tubular cell injuries in MCNS patients without renal dysfunction. In this study, the tubular injuries at kidney biopsy were not intense even in the AKI group. In this context, renal blood flow is thought to be sufficient to prevent ATN but not sufficient to maintain GFR [ 28 ]. However, vimentin-positive tubular injuries might make patients susceptible to coexisting haemodynamic alterations.

If severe haemodynamic alterations persist together with acute toxic tubular injuries, the kidney cannot sacrifice GFR to preserve tubular integrity and tubular regeneration, resulting in severe AKI with intense ATN. In this study, two patients in the AKI group exhibited relatively severe vimentin-positive tubular injuries followed by increased serum Cr. Thus, we postulated that severe persistent intrarenal haemodynamic changes might be superimposed on acute toxic tubular injuries in these patients.

Some limitations of the present study should be noted. First, the study design was a retrospective, single-centre investigation with a small number of patients. Second, there was a lack of repetitive kidney biopsy to evaluate the alteration of vimentin expression. Despite these limitations, the present study clearly demonstrated the significance of vimentin expression in proximal tubular cells in association with the development of AKI observed in MCNS. Toxic tubular cell injuries with superimposition of altered intrarenal haemodynamics might contribute to the development of severe AKI in adult MCNS patients.

We thank Ms. Hiromi Yamaguchi and Ms. We are also grateful to all physicians in Teikyo University Hospital who took care of the MCNS patients and collected clinical and laboratory data used in this article. FY designed the study. FY and TY performed the statistical analyses. FY and US wrote the manuscript.

JaypeeDigital | Nephrology

All authors read and approved the final manuscript. Written informed consent was waived after IRB approval. Instead, a detailed disclosure of this study contents was published on the research ethics committee website. Patient records and information were anonymized and de-identified prior to analysis.

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Yoshihide Fujigaki, Email: pj. Yoshifuru Tamura, Email: moc. Michito Nagura, Email: moc. Shigeyuki Arai, Email: moc. Tatsuru Ota, Email: pj.

Shigeru Shibata, Email: pj. Fukuo Kondo, Email: pj. Yutaka Yamaguchi, Email: pj.

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This may be because the snippet appears in a figure legend, contains special characters or spans different sections of the article. BMC Nephrol. Published online Nov PMID: Corresponding author. Received Jul 13; Accepted Nov This article has been cited by other articles in PMC. Methods We performed a retrospective analysis of clinical data and tubular cell changes using the immunohistochemical expression of vimentin as a marker of tubular injury and dedifferentiation at kidney biopsy in 37 adult MCNS patients. Results Thirteen patients Histological characteristics Kidney biopsy tissue specimens including at least 10 glomeruli were examined by light microscopy, immunofluorescence and electron microscopy, and all the patients were diagnosed with MCNS [ 15 ].

Table 1 Comparison of the clinical characteristics in patients with and without AKI. Open in a separate window. Table 3 Comparison of renal pathological data in patients with and without AKI. Vimentin expression in tubular cells and its comparison with clinical parameters Vimentin is observed in mesangium and blood vessels but not in tubule cells in normal human adult kidneys.

Acknowledgements We thank Ms. Funding None. Consent for publication Not applicable. Competing interests The authors declare that they have no competing interests.

Contributor Information Yoshihide Fujigaki, Email: pj. References 1. Adult minimal-change disease: clinical characteristics, treatment, and outcomes. Guidelines for Perinatal Care , 8th ed. Dietary Guidelines for Americans , 8th ed. Occupational Health. Environmental and Occupational Medicine , 4th ed. Diseases of the Orbit: A Multidisciplinary Approach , 2nd ed. Shields Textbook of Glaucoma , 6th ed.

Handbook of Fractures , 5th ed. Lovell and Winter's Pediatric Orthopaedics , 7th ed. Master Techniques in Orthopaedic Surgery: Fractures , 2nd ed. Master Techniques in Orthopaedic Surgery: Pediatrics , 2nd ed.