A Case of Lupus Nephritis Showing Good Clinical Course and Apoptosis in Glomerular Cells Detected by the Nick End Labeling Method

Kodera, Sanki; Tashiro, Kyouichi; Ohmuro, Hiroyuki; Shirato, Isao; Tomino, Yasuhiko

doi:10.1159/000169143

Cited by 3 publications

(3 citation statements)

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“…Apoptotic bodies in the proliferated glomerular cells were detected at the third renal biopsy but not at the second biopsy. We concluded that apoptosis might control glomerular cell proliferation and also influence the clinical course of lupus nephritis 14 . In patients with IgA nephropathy, we also reported that 5 out of 11 patients with apoptotic cells in the glomeruli using TUNEL were in the severe glomerular damage group, and only 1 out of 12 patients was in the mild glomerular damage group 15 …”

Section: Discussionmentioning

confidence: 70%

“…Gavrieli et al 12 developed the method of terminal deoxynucleotidyl transferase (TdT)‐mediated dUTP–biotin nick end labelling (TUNEL) for detecting apoptosis of proliferated cells. The authors reported an adult patient with lupus nephritis who had a good clinical course under long‐term observation 14 . Apoptotic bodies in the proliferated glomerular cells were detected at the third renal biopsy but not at the second biopsy.…”

Section: Discussionmentioning

confidence: 99%

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Apoptotic cells in six patients with IgA nephropathy in repeat biopsies

et al. 2001

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SUMMARY: Programmed cell death is a selective process of physiological cell deletion and is known as apoptosis. The purpose of the present study was to determine the relationship between the existence of apoptotic cells in glomeruli and the clinical or histopathological findings obtained in repeat renal biopsies of patients with IgA nephropathy. Repeat renal biopsy specimens were obtained from six patients with IgA nephropathy. The nick end labelling method (TUNEL) was used for the detection of apoptotic cells. Clinical laboratory data, i.e. urinary protein excretion, creatinine clearance (Ccr), blood urea nitrogen (BUN) and serum creatinine, (s‐Cr) were obtained from these patients. At the first renal biopsy, apoptotic cells in the glomeruli were observed in three out of six patients using TUNEL. These patients were classified as the severe glomerular damage group. The other three patients without apoptotic cells were in the mild glomerular damage group. Mean levels of urinary protein excretion at the first renal biopsy in the patients with apoptotic cells were slightly higher than those in patients without apoptotic cells. Levels of Ccr in patients with apoptotic cells were lower than those in patients without apoptotic cells. There were no significant differences in the levels of BUN and s‐Cr in patients with or without apoptotic cells. Two patients with apoptotic cells in glomeruli at the first renal biopsy did not show apoptotic cells at the second renal biopsy. These two patients showed improvement not only in clinical laboratory findings but also in histological findings at the second biopsy. Only one patient with apoptotic cells at the first and second biopsies exhibited deterioration at the second biopsy. All three patients without apoptotic cells at the first renal biopsy also showed deterioration of the clinical laboratory and histopathological findings. It is postulated that various factors other than apoptosis might induce progression of renal injuries in such patients. It appears that the clinical laboratory data, i.e. proteinuria, renal function and histopathological findings, might be influenced by apoptosis in patients with IgA nephropathy. It is postulated that apoptosis may induce reduction of excess proliferative glomerular mesangial cells and/or infiltrating cells and tissue repair.

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Section: Discussionmentioning

confidence: 70%

Section: Discussionmentioning

confidence: 99%

Apoptotic cells in six patients with IgA nephropathy in repeat biopsies

et al. 2001

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“…Lupus nephritis may serve as a good example for the association of apoptosis with prothrombotic states in human renal disease. Systemic lupus is characterized by a general tendency of accelerated cell senescence and apoptotic cell death, and in this disease apoptotic cells have been described within the glomerulus (Berden & van Bruggen, 1997; Kodera et al ., 1997; Pickering et al ., 2000). Of special interest, particularly in lupus nephritis microthrombi formation in the glomerular capillaries is a histological hallmark together with or without other prothrombotic factors such as antiphospholipid antibodies (Hughson et al ., 2001).…”

Section: Discussionmentioning

confidence: 99%

Protein kinase C (PKC) dependent induction of tissue factor (TF) by mesangial cells in response to inflammatory mediators and release during apoptosis

Lang

Terstesse

Dohle

et al. 2002

British J Pharmacology

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1 In in¯ammatory kidney diseases procoagulatory activity (PCA) becomes evident. Glomerular ®brin deposits and capillary microthrombi are histopathological hallmarks in most forms of glomerulonephritis. 2 Therefore in this study the expression of tissue factor (TF) as the main inducer of thrombogenesis was examined in cultured human mesangial cells (MC) in response to proin¯ammatory stimuli such as interleukin-1 (IL-1b), tumour necrosis factor alpha (TNF-a) and lipopolysaccharide (LPS). Also main signalling pathways were investigated. 3 IL-1b, TNF-a and LPS induced TF in MC in a time and dose dependent manner on mRNA and protein levels. Highest activity was found after 12 h of stimulation. Induction of TF was completely blockable by BAPTA-AM, a chelator of intracellular [Ca 2+ ] i as well as calphostin, a protein kinase C (PKC) inhibitor. Activation of the protein kinase A (PKA) pathway had no in¯uence on basal TF expression, but down-regulated cytokine-induced TF. The PKA blocker, KT5720, increased TF formation signi®cantly. Since TF exerts its activity primarily on the surface of cells and after release of encrypted receptors we further tested TF activity in MC supernatants. IL-1b did not signi®cantly increase TF activity in supernatants of intact cells. However, when MC were rendered apoptotic by oxidative metabolites, IL-1b treated MC released highly stimulated TF activity into the supernatants, suggesting that a paracrine activation of the coagulatory cascade can take place under such conditions. 4 In¯ammatory mediators up-regulate TF expression in MC by a PKC dependent pathway whereas PKA can serve as a negative feed-back link. Apoptosis of in¯ammatory MC may trigger to spread PCA.

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