Renal accumulation of salicylate and phenacetin: possible mechanisms in the nephropathy of analgesic abuse

Bluemle, Lewis W.; Goldberg, Martin

doi:10.1172/jci105932

Cited by 89 publications

(20 citation statements)

References 16 publications

(15 reference statements)

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“…Such distribution of lesions could be explained if the offending drugs were concentrated in the kidney tissue. Bluemle and Goldberg reported that they could find no difference in salicylate concentration between cortex and medulla in the dog kidney (33) in contradiction with our results. Salicylate in our studies was concentrated in the medulla by a factor of 1.5-3 with respect to the cortex.…”

Section: Discussioncontrasting

confidence: 99%

Direct Effects of Salicylate on Renal Function in the Dog

Quintanilla¹,

Kessler²

1973

J. Clin. Invest.

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Section: Discussioncontrasting

confidence: 99%

Direct Effects of Salicylate on Renal Function in the Dog

Quintanilla¹,

Kessler²

1973

J. Clin. Invest.

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“…When animals are fed phenacetin, it is para cetamol that is concentrated in the renal papilla [7], In the aspirin, phenacetin, caffein, mixture replacement of phenacetin by an equivalent dose of paracetamol does not alter the incidence and severity of RPN in animal studies [8][9][10]. Animal experiments have shown that para cetamol alone can cause RPN, although in high doses (3,000 mg/kgdaily) [8].…”

Section: Discussionmentioning

confidence: 99%

Paracetamol: A Cause for Analgesic Nephropathy and End-Stage Renal Disease

Segasothy

Ab²,

Puvaneswary³

et al. 1988

Nephron

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180 patients with end-stage renal disease (ESRD) on maintenance dialysis and those who had undergone renal transplantation were questioned retrospectively. 14 patients had consumed excessive quantities of analgesics ( > l kg) prior to the institution of long-term dialysis or transplantation. Sonographic examination done on these patients indicated that 7 had renal papillary necrosis (RPN). The sonographic features were renal papillary calcifications surrounding the central sinus in a complete or incomplete garland pattern. In 5 of these patients RPN is attibutable to the excessive consumption of paracetamol. We have earlier reported 10 cases of RPN due to excessive consumption of paracetamol. Thus 15 cases of RPN attributable to paracetamol consumption (1.0–15.3 kg over a period ranging from 3 to 23 years) have been documented. It is concluded that paracetamol may assume an increasingly important role in the causation of analgesic nephropathy (AN) and ESRD.

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“…49], Pre sumably. the papillary necroses are attributable to toxic effects of PH metabolites which are found in a high con centration within the papilla [6], Although the exact pathogenetic mechanisms are so far unknown, experi mental findings have implicated vascular damage [28].…”

Section: Discussionmentioning

confidence: 99%

Absence of a Complete Carcinogenic Effect of Phenacetin on the Quiescent and Proliferating Urothelium Stimulated by Partial Cystectomy

Kunze¹,

Wöltjen²,

Albrecht³

1983

Urol Int

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It was the object of the present animal experiments to test whether phenacetin (PH) exerts a complete solitary carcinogenic effect on the quiescent and rapidly proliferating urothelium of the lower urinary tract of the rat. In order to stimulate proliferative activity resection of one-third of the urinary bladder was performed which is known to induce intensive reparative regeneration in the stump. PH was administered either continuously with the diet or by gavage in three single doses when proliferative activity was highest. After an experimental period of 2 years 74–83% of the animals receiving PH continuously and 49–52% of the rats after limited gavage feeding had developed uni- and bilateral hyperplasia of the epithelium of the renal papilla. Histologically, the papillary hyperplasia exhibited urothelial differentiation and a typical endophytic growth pattern. It was always associated with healed or, rarely, fresh micronecroses of the subjacent papillary tissue. The urothelial hyperplasia of the renal papilla has to be considered not a true preneoplastic, but rather a reactive proliferative lesion in the sense of a reparative hyperregeneration due to toxic necroses. There was no evidence for a complete solitary carcinogenic action of PH on the urothelium of the entire lower urinary tract. It seems most likely that a metabolite of PH realizes tumor growth only as cocarcinogen with initiation-stimulating and/or initiation-promoting effects acting together with other causative factors during multifactorial multistage carcinogenesis. Based upon the experimental findings reported here, the concept of PH as a solitary complete urothelial carcinogen for man should be reassessed.

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Renal accumulation of salicylate and phenacetin: possible mechanisms in the nephropathy of analgesic abuse

Cited by 89 publications

References 16 publications

Direct Effects of Salicylate on Renal Function in the Dog

Direct Effects of Salicylate on Renal Function in the Dog

Paracetamol: A Cause for Analgesic Nephropathy and End-Stage Renal Disease

Absence of a Complete Carcinogenic Effect of Phenacetin on the Quiescent and Proliferating Urothelium Stimulated by Partial Cystectomy

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