Analgesic-associated nephropathy

Schwarz, Anke

doi:10.1007/bf01785520

Cited by 33 publications

(13 citation statements)

References 174 publications

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“…The progression of renal failure in analgesic-associated nephropathy has been well documented (13,32,47,78,96,142,170,171,203,204). Analgesic nephropathy is a degenerative condition leading to renal failure following long-term analgesic abuse.…”

Section: Analgesic Nephropathymentioning

confidence: 99%

“…There are few clinical symptoms associated with the early development of analgesicassociated RF" (13,32,78,171,203,204). The progression of renal damage is insidious and renal function may be severely compromised before the condition becomes obvious (13,32,78,171,203,204). 2 141 microscopic hematuria, ureteral colic, and lower back pains.…”

Section: Analgesic Nephropathymentioning

confidence: 99%

“…It is also apparent that the problem of excessive use of analgesics continues today (13,46,56,87,96,171,185,200,201) and this healthcare cost is probably preventable (46,47,59). Analgesic abuse is a frequent cause of analgesic nephropathy that leads to end-stage renal disease and upper urothelial carcinoma throughout Europe (46, 47, 58-64, 179,180,203,204), Australia (149-150, 171, 216), and other parts of the world (206)(207)(208)(209)(210). Interestingly, there are apparently only few cases in the USA (21,29,56,96,184,200,201,226).…”

Section: Introduchonmentioning

confidence: 99%

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Renal Papillary Necrosis—40 Years On

Bach

Thanh

1998

Toxicol Pathol

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Analgesics and nonsteroidal anti-inflammatory drugs (NSAIDs) are well recognized as a major class of therapeutic agent that causes renal papillary necrosis (RPN). Over the last decade a broad spectrum of other therapeutic agents and many chemicals have also been rcportcd that have the potential to cause this lesion in animals and man. There is consensus that RPN is the primary lesion that can progress to cortical degeneration; and it is only at this stage that the lesion is easily diagnoscd. In the absence of sensitive and selective noninvasive biomarkers of RPN there is still no clear indication of which compound, under what circumstances, has the greatest potential to cause this lesion in man. Attempts to mimic RPN in rodents using analgesics and NSAIDs have not provided robust models of the lesion. Thus, much of the research has concentrated on those compounds that cause an acute or subacute RPN as the basis by which to study the pathogenesis of the lesion. Based on the mechanistic understanding gleaned from these model compounds it has been possible to transpose an understanding of the underlying processes to the analgesics and NSAIDs. The mechanism of RPN is still controversial. There are data that support microvascular changes and local ischemic injury as the underlying cause. Alternatively, several model papillotoxins, some analgesics, and NSAIDs target selectively for the medullary interstitial cells, which is the earliest reported aberration, after which there are a series of degenerative processes affecting other renal cell types. Many papillotoxins have the potential to undergo prostaglandin hydroperoxidase-mediated metabolic activation, specifically in the renal medullary interstitial cells. These reactive intermediates, in the presence of large quantities of polyunsaturated lipid droplets, result in localized and selective injury of the medullary interstitial cells. These highly differentiated cells do not repair, and it is generally accepted that continuing insult to these cells will result in their progressive erosion. The loss of these cells is thought to be central to the degenerative cascade that affects the cortex. There is still a need to understand better the primary mechanism and the secondary consequences of RPN so that the risk of chemical agents in use and novel molecules can be fully assessed.

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Section: Analgesic Nephropathymentioning

confidence: 99%

Section: Analgesic Nephropathymentioning

confidence: 99%

Section: Introduchonmentioning

confidence: 99%

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Renal Papillary Necrosis—40 Years On

Bach

Thanh

1998

Toxicol Pathol

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“…Animal experiments have failed to provide conclu sive evidence [7], and epidemiologic studies have not explained why only 1-7% of analgesic abusers develop renal problems or whether analgesics are a predisposing or a causal factor for nephropathy [8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Progression of Renal Failure in Analgesic-Associated Nephropathy

Schwarz¹,

Kunzendorf²,

Keller³

et al. 1989

Nephron

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The factors that influence the progression of renal failure in analgesic-associated nephropathy (AAN) still remain to be clarified. In this study, the actual analgesic intake (N-acetyl-p-aminophenol, NAPAP, i.e. acetaminophen in urine) and progression of renal failure (1/crea method) in 127 outpatients with various renal diseases were investigated over a period of 7–150 months. AAN was diagnosed in 57 of the 127 patients (44%). The NAPAP test was positive in 21% of the 57 AAN patients and in 3% of the 70 control patients with other renal diseases (p = 0.0001). The AAN patients presented with more advanced renal insufficiency, lost more weight, and had more severe hypertension as well as a higher mortality rate than the control patients (univariate analysis). Progression of renal insufficiency, as measured by regression analysis of the reciprocal of serum creatinine versus time and expressed as clearance loss per year, was more rapid in the AAN patients who were found positive for NAPAP (6.9 ± 5.5 ml/min/year) than in the AAN patients who were found negative (4.1 ± 11.0 ml/min/year) or in control patients with other renal diseases (5.1 ± 14.9 ml/min/year). Multivariate analysis showed the more rapid clearance loss to be the most discriminating factor between the AAN patients who continued analgesic abuse of phenacetin- or acetaminophen-containing drugs and AAN patients who stopped. We therefore conclude that continued analgesic abuse promotes renal insufficiency in AAN. The progression of renal failure in AAN patients who stopped abusing analgesics, however, cannot be explained within the parameters investigated, i.e. urinary tract infection, hypertension, hyperalimentation, or papillary necrosis.

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“…In metaanalyses, it was shown that only 25-27% of the patients had a benefit from daily aspirin intake [2]. On the other hand, a number of side-effects that may lead to severe malfunctions, even to death, is of considerable medical interest [3][4][5][6][7][8].…”

Section: Introductionmentioning

confidence: 99%

From Aspirin to Aspirin Resistance – History, Biochemical Background, Diagnostics and Clinical Relevance

Nowak¹

2007

Transfus Med Hemother

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The story of success of aspirin has lasted for more than 100 years. Initially used as an analgetic with anti-inflammatory, antirheumatic as well as antipyretic effects, aspirin has been widely used as antithrombotic drug since the 1970s, too, due to its more recently discovered platelet inhibitory efficacy. Primary and secondary prophylaxis of cardiovascular events by long-term intake of aspirin has been performed million-fold worldwide, even without any medical attendance. In spite of a clear positive effect on the incidence of coagulation disorders, a residual risk remains for the aspirin user - the aspirin resistance. In this review a short historical survey is given, and the biochemical background of the aspirin effect on blood platelets as well as aspirin resistance with the possible causes and the clinical relevance are described. Different laboratory methods for detection of aspirin resistance are discussed with respect to validity and limitations. Not until both the predisposition for aspirin resistance and the presence of acute aspirin resistance can be clearly detected using reliable methods, the patient will receive adequate treatment.

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Analgesic-associated nephropathy

Cited by 33 publications

References 174 publications

Renal Papillary Necrosis—40 Years On

Renal Papillary Necrosis—40 Years On

Progression of Renal Failure in Analgesic-Associated Nephropathy

From Aspirin to Aspirin Resistance – History, Biochemical Background, Diagnostics and Clinical Relevance

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