Tubular atrophy in the end-stage kidney: A lectin and immunohistochemical study

Nádasdy, Tibor; Lászik, Zoltán; Blick, Kenneth E.; Johnson, Debbie L.; Silva, Fred G.

doi:10.1016/0046-8177(94)90166-x

Cited by 105 publications

(80 citation statements)

References 13 publications

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“…Endocrine-type tubular atrophy was scored when the atrophic tubule was small with narrow or absent lumen and clear regular epithelial cells. 15 Microcystic tubular dilatation was defined as dilatation of a tubular lumen to at least three times the diameter of a normal tubular profile with a large intraluminal PAS-positive hyaline cast.…”

Section: Study Design and Histologic Grading Of Renal Biopsiesmentioning

confidence: 99%

Histopathologic findings associated with APOL1 risk variants in chronic kidney disease

et al. 2015

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The effects of nephropathy risk variants in the apolipoprotein L1 gene (APOL1) on renal histopathology in African Americans with arterionephrosclerosis or putative 'hypertension-associated' nephropathy are unknown. APOL1 genotype-phenotype correlations were performed in a blinded manner from renal biopsies in 196 self-reported African Americans with arterionephrosclerosis on kidney biopsy at a large national nephropathology practice. Subjects had chronic kidney disease without nephrotic syndrome. A discovery analysis compared histopathologic changes in the glomerular and tubulointerstitial compartments in 58 subjects with 2 versus 56 subjects with 0 APOL1 risk variants. Validation was performed in biopsies from 82 additional subjects with 0, 1, and 2 risk variants. Two risk variant versus zero risk variant group genotype associations and subphenotypes were assessed by v 2 analyses. ANOVA compared means of continuous variables. In discovery analyses, significantly less obsolescent glomerulosclerosis, more (solidified and disappearing) glomerulosclerosis, more thyroidization-type tubular atrophy, and more microcystic tubular dilatation were seen in patients with two versus zero APOL1 risk alleles. Greater degrees of arteriosclerosis were present in those with zero risk alleles. Segmental glomerulosclerosis did not differ significantly between groups. Presence of two of the following discriminatory histopathologic findings from discovery, that is, o50% obsolescent glomerulosclerosis, thyroidization-type tubular atrophy, and microcystic tubular dilatation, was specific for the presence of two APOL1 risk alleles in the validation phase. African Americans with arterionephrosclerosis who possess two APOL1 risk variants more often lack obsolescent glomerulosclerosis and have greater degrees of (solidified and disappearing) glomerulosclerosis, thyroidization-type tubular atrophy, and microcystic tubular dilation than patients with fewer than two risk variants. These findings support involvement of multiple cell types in subnephrotic forms of APOL1-associated nephropathy, particularly renal tubule cells with resultant tubulointerstitial disease.

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Section: Study Design and Histologic Grading Of Renal Biopsiesmentioning

confidence: 99%

Histopathologic findings associated with APOL1 risk variants in chronic kidney disease

et al. 2015

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“…20,21 Briefly, kidney sections from three mice at each time point were stained with periodic acid-Schiff, and images of random fields were acquired at ϫ200 magnification. In each sample, at least 1000 proximal tubules were identified and scored.…”

Section: Evaluation Of Tubular Atrophy and Tubular Cell Apoptosismentioning

confidence: 99%

Autophagy Is a Component of Epithelial Cell Fate in Obstructive Uropathy

Zepeda‐Orozco

Black

et al. 2010

The American Journal of Pathology

178

162

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Epithelial cell fate and nephron loss in obstructive uropathy are not fully understood. We produced transgenic mice in which epithelial cells in the nephrons and collecting ducts were labeled with enhanced yellow fluorescent protein, and tracked the fate of these cells following unilateral ureteral obstruction (UUO). UUO led to a decrease in the number of enhanced yellow fluorescent protein-expressing cells and down-regulation of epithelial markers, Ecadherin, and hepatocyte nuclear factor-1␤. Following UUO, enhanced yellow fluorescent protein-positive cells were confined within the tubular basement membrane, were not found in the renal interstitium, and did not express ␣-smooth muscle actin or S100A4, markers of myofibroblasts and fibroblasts. Moreover, when proximal tubules were labeled with dextran before UUO, dextran-retaining cells did not migrate into the interstitium or express ␣-smooth muscle actin. These results indicate that UUO leads to tubular epithelial loss but does not cause epithelial-tomesenchymal transition that has been shown by others to be responsible for nephron loss and interstitial fibrosis. For the first time, we found evidence of enhanced autophagy in obstructed tubules, including accumulation of autophagosomes, increased expression of Beclin 1, and increased conversion of microtubular-associated protein 1 light chain 3-I to -II. Increased autophagy may represent a mechanism of tubular survival or may contribute to excessive cell death and tubular atrophy after obstructive injury.

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“…Proximal and distal tubular cells were identified primarily by morphologic criteria, including the presence of a brush border, the cell size, and nuclearcytoplasmic ratio. Lectin histochemistry with Phaseolus vulgaris erythroagglutinin (Sigma, St. Louis, MO) and Arachis hypogaea (AH; Sigma) was used as a confirmatory assay to identify proximal and distal tubules, respectively, as described previously (26,27). Briefly, serial sections were deparaffinized, treated with 1.25% H 2 O 2 in methanol for 30 min, incubated with either Phaseolus vulgaris erythroagglutinin (1 g/ml) or AH (10 g/ml) for 60 min, and developed with diaminobenzidine.…”

Section: Apoptosis Assay In Kidney Biopsy Samplesmentioning

confidence: 99%

Induction of Renal Tubular Cell Apoptosis in Focal Segmental Glomerulosclerosis

Erkan¹,

Garcia²,

Patterson³

et al. 2005

Journal of the American Society of Nephrology

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The hypothesis that apoptosis represents a proximate mechanism by which tubule cells are damaged in FSGS was tested. Thirty kidney biopsy specimens from children with idiopathic early FSGS were studied retrospectively. Unexpected, apoptosis was evident in both proximal and distal tubule cells. There was a significant correlation between the degree of proteinuria and the number of apoptotic cells. Fas protein was detected predominantly in the tubule cells that underwent apoptosis. When compared with patients with other chronic proteinuric states, those with FSGS displayed a proliferation/ apoptosis ratio in favor of proliferation in the glomerulus but dramatically in favor of apoptosis in the tubules. When both proteinuria and apoptosis were included in a stepwise logistic regression procedure, only apoptosis was found to predict independently the development of ESRD. Prolonged incubation of cultured Madin-Darby canine kidney (distal/collecting) cells with albumin also resulted in a dose-and duration-dependent induction of apoptosis and activation of the Fas pathway, lending support to the novel finding of distal tubule cell apoptosis in patients with FSGS. The results indicate that an elevated tubule cell apoptosis rate at the time of initial biopsy represents an independent predictor of progression to ESRD in patients with early FSGS.

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Tubular atrophy in the end-stage kidney: A lectin and immunohistochemical study

Cited by 105 publications

References 13 publications

Histopathologic findings associated with APOL1 risk variants in chronic kidney disease

Histopathologic findings associated with APOL1 risk variants in chronic kidney disease

Autophagy Is a Component of Epithelial Cell Fate in Obstructive Uropathy

Induction of Renal Tubular Cell Apoptosis in Focal Segmental Glomerulosclerosis

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