Capillarosclerosis of the Renal Pelvis: Autopsy Study for Estimating
the Incidence of Phenacetin and Paracetamol Abuse

Schubert, Günther E.; Bethke, B.

doi:10.1159/000472648

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Histopathology Of Analgesic-induced Tubulointerstitial Nephritis1

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Cited by 3 publications

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“…The earliest lesion described in analgesic nephropathy is capillary sclerosis of the urinary tract mucosa [49,50]. A similar lesion consisting of peritubular capillary sclerosis is initially seen in the inner medulla and can be produced in experimental animals [51].…”

Section: Histopathology Of Analgesic-induced Tubulointerstitial Nephritismentioning

confidence: 99%

The clinical spectrum of tubulointerstitial nephritis

Rastegar

Kashgarian

1998

Kidney International

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Section: Histopathology Of Analgesic-induced Tubulointerstitial Nephritismentioning

confidence: 99%

The clinical spectrum of tubulointerstitial nephritis

Rastegar

Kashgarian

1998

Kidney International

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Habitual use of acetaminophen as a risk factor for chronic renal failure: A comparison with phenacetin

Buckalew

1996

American Journal of Kidney Diseases

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Pathogenesis of Tubular Interstitial Nephritis

Tanaka

Nangaku

2011

Contributions to Nephrology

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Injury to the interstitium of the kidney is regarded as a common pathway leading to end-stage renal insufficiency, regardless of etiology. Tubular interstitial nephritis is characterized histologically by inflammatory changes in the tubulointerstitial compartment, such as interstitial edema, leukocyte infiltration, accumulation of extracellular matrix proteins, tubular dilation and atrophy. Acute interstitial nephritis is often associated with use of drugs, such as β-lactam antibiotics and non-steroidal anti-inflammatory drugs, and is likely mediated through allergic mechanisms. On the other hand, chronic progressive tubular interstitial nephritis has a much more diverse etiology, ranging from infection and drugs to immune-mediated, hematologic, metabolic and hereditary disorders. Experimental studies in the past decade have focused mainly on common factors and mechanisms underlying chronic tubulointerstitial injury, such as activation of peritubular fibroblasts, leukocyte infiltration, release of inflammatory cytokines and growth factors at affected regions, epithelial-mesenchymal transition of tubular epithelium, and apoptosis. The execution of each is mediated by a number of local stimuli, such as filtered albumin, chronic hypoxia and oxidative stress, in addition to cytokines and growth factors. This chapter provides an overview of acute and chronic tubular interstitial nephritis, according to clinical manifestations of the disease. It also provides insight into common pathways underlying chronic tubular interstitial nephritis based on recent advances in translational and experimental research.

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Capillarosclerosis of the Renal Pelvis: Autopsy Study for Estimating the Incidence of Phenacetin and Paracetamol Abuse

Cited by 3 publications

References 6 publications

The clinical spectrum of tubulointerstitial nephritis

The clinical spectrum of tubulointerstitial nephritis

Habitual use of acetaminophen as a risk factor for chronic renal failure: A comparison with phenacetin

Pathogenesis of Tubular Interstitial Nephritis

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