Electron Microscopic Study of Pyelointerstitial Reflux Scars

Laberke, H. G.

doi:10.1016/s0344-0338(87)80073-0

Cited by 2 publications

(3 citation statements)

References 10 publications

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“…Our histopathology findings demonstrate interstitial inflammatory infiltration and tubulointerstitial fibrosis, which are well-described and essential features seen in all cases of RN (Morita et al, 1990; Weiss and Parker, 1939; Laberke, 1987; Risdon et al, 1993). In more severe cases of RN, secondary glomerular pathology is also seen with glomerular sclerosis and periglomerular fibrosis noted (Morita et al, 1990; Torres et al, 1980).…”

Section: Discussionsupporting

confidence: 70%

Interplay between vesicoureteric reflux and kidney infection in the development of reflux nephropathy in mice

Bowen

Watt

Murawski

et al. 2013

Disease Models &Amp; Mechanisms

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SUMMARYVesicoureteric reflux (VUR) is a common congenital defect of the urinary tract that is usually discovered after a child develops a urinary tract infection. It is associated with reflux nephropathy, a renal lesion characterized by the presence of chronic tubulointersitial inflammation and fibrosis. Most patients are diagnosed with reflux nephropathy after one or more febrile urinary tract infections, suggesting a potential role for infection in its development. We have recently shown that the C3H mouse has a 100% incidence of VUR. Here, we evaluate the roles of VUR and uropathogenic Escherichia coli infection in the development of reflux nephropathy in the C3H mouse. We find that VUR in combination with sustained kidney infection is crucial to the development of reflux nephropathy, whereas sterile reflux alone fails to induce reflux nephropathy. A single bout of kidney infection without reflux fails to induce reflux nephropathy. The host immune response to infection was examined in two refluxing C3H substrains, HeN and HeJ. HeJ mice, which have a defect in innate immunity and bacterial clearance, demonstrate more significant renal inflammation and reflux nephropathy compared with HeN mice. These studies demonstrate the crucial synergy between VUR, sustained kidney infection and the host immune response in the development of reflux nephropathy in a mouse model of VUR.

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Section: Discussionsupporting

confidence: 70%

Interplay between vesicoureteric reflux and kidney infection in the development of reflux nephropathy in mice

Bowen

Watt

Murawski

et al. 2013

Disease Models &Amp; Mechanisms

View full text Add to dashboard Cite

show abstract

“…3). Representative of renin granules were referred from a previous report [4]. But we could not identify them as extended JGA cells or not.…”

Section: Resultsmentioning

confidence: 99%

“…Although JGA looked normal in the first biopsy, areas of striking JGA hyperplasia containing increment of intracellular renin granules were ubiquitously recognized in the second biopsy. Previous report demonstrated renin-positive granules were observed in tubular epithelial cells, apparent atrophic and cell-rich glomeruli and walls of tortuous arterioles on reflux nephropathy [4]. Collecting duct was reported as a major source of prorenin in a diabetic animal model [5].…”

Section: Discussionmentioning

confidence: 99%

Prominent hyperplasia of renin-producing juxtaglomerular apparatus after chronic and complete blockade of the renin-angiotensin system in adult IgA nephropathy

et al. 2015

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Juxtaglomerular apparatus (JGA) hyperplasia rarely happened in renal biopsy and has been controversial clinically, because synthesis and secretion of renin were susceptible to the effect of clinical condition and medication. Here we present the case of a 39-year-old who got JGA hyperplasia of IgA nephropathy (IgAN) after long-term inhibition of the renin-angiotensin system (RAS) with an angiotensin receptor blocker (ARB), and a direct renin inhibitor (DRI) in combination with a diuretic. He was diagnosed with IgAN in his first renal biopsy, and was treated with supra-maximal dosages of ARB, DRI and a diuretic. In the second biopsy, because of the massive proteinuria and occurrence of steroid-induced diabetes, it was revealed that the area and the number of JGA cells were strikingly increased in observed glomeruli. Immunohistopathologically, the both specimens were stained by human renin antibody. The hyperplastic JG cells contained a large amount of renin granules. Putative renin granules were observed in some interstitial cells adjacent to an afferent arteriole by electron microscopy. The increasing response of renin granules co-localized in prominent JGA hyperplasia should be worried while physicians treat hypertensive patients with potent RAS inhibitors and diuretics even though they have diabetes. This is the first report showing a clinical course of forming prominent JGA hyperplasia directly after a full combination of RAS inhibitors and diuretics in adult IgA nephropathy.

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Electron Microscopic Study of Pyelointerstitial Reflux Scars

Cited by 2 publications

References 10 publications

Interplay between vesicoureteric reflux and kidney infection in the development of reflux nephropathy in mice

Interplay between vesicoureteric reflux and kidney infection in the development of reflux nephropathy in mice

Prominent hyperplasia of renin-producing juxtaglomerular apparatus after chronic and complete blockade of the renin-angiotensin system in adult IgA nephropathy

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