Analgesic abuse is a major public health hazard in Australia, and analgesic nephropathy with consequent terminal renal failure is the underlying cause in 20% of the patients requiring dialysis and transplantation. Analgesics are invariably taken in the form of compounds and mixtures. In the aspirin-phenacetin-caffeine (APC) mixture, aspirin appears to be the major nephrotoxic agent and phenacetin appears to play a secondary and synergistic role. The renal disease associated with abuse of analgesics is characteristic and is part of a much wider clinical syndrome, the analgesic syndrome, which includes peptic ulcer disease (35%), anemia (60 to 90%), hypertension (15 to 70%), ischemic heart disease (35%), psychological and psychiatric manifestations, pigmentation, and possible gonadal- and pregnancy-related effects. The primary lesion in analgesic nephropathy is renal papillary necrosis (RPN), and this is a nephrotoxic effect common to all nonsteroid antiinflammatory agents. The most important factor in the management of patients with analgesic nephropathy is the cessation of analgesic abuse, and this leads to improvement and stabilization of renal function. A small proportion of patients will, however, deteriorate in relation to accelerated hypertension, persistent proteinuria, ischemic heart disease, and complications leading to nephrectomy. Patients with analgesic nephropathy are poor risk patients and have a poor prognosis, even after dialysis and transplantation.

AimsThe aim of the present study was to explore the level of risk associated with community use of non-steroidal anti-inflammatory drugs (NSAIDs). Methods We carried out a matched case-control study of the relationship between recent use of NSAIDs and the presence of functional renal impairment present at the time of hospitalisation with a range of clinical problems. Cases (n=110) were consecutive patients admitted acutely to hospital who had serum creatinine levels greater than or equal to 0.15 mmol l −1 , which improved by 20% or more within the next 14 days, or prior to discharge from hospital. Controls (n=189) were subjects of the same sex and age (to within 5 years) as the cases, who were admitted to the same hospital, who had normal serum creatinine levels (<0.12 mmol l −1 ) throughout their hospital stay. Information on a number of study factors, including recent use of aspirin and other NSAIDs, was obtained by structured interview. Results Overall, there was a weak association between consumption of NSAIDs (including non-prophylactic aspirin) and the development of functional renal impairment-adjusted odds ratios (OR) with use of NSAIDs in the previous week or in the previous month: OR 1.5 (95% CI 0.80, 2.9) and 1.8 (95% CI 0.97, 3.4) respectively. In subjects with a previous history of renal disease the adjusted OR was 6.6 (0.75, 57.8) and in those with a history of gout or hyperuricaemia the OR was 7.2 (1.3, 40.2). There was a weak positive relationship between the dose of drug consumed in the previous week and the odds of functional renal impairment. The relationship between risk and published figures for drug half-lives (t D ) was stronger. The odds ratio increased from 1.2 (95% CI 0.61, 2.4) with a t D ≤4 h, to 4.8 (1.5, 15.8) with a t D of ≤12 h ( P=0.012, test for trend). This relationship remained statistically significant after adjustment for a number of clinical variables and the dose of drug ingested. Conclusions NSAIDs are an important cause of functional renal impairment in subjects with renal disease or a history of gout or hyperuricemia. The half-life of the drug is more important than the ingested dose in determining the risk of this outcome. Long half-life drugs should be avoided in individuals who are at risk of developing renal impairment.

The objective of this study was to re-evaluate the effect of arm position on blood pressure (BP) measurement with auscultatory and oscillometric methods including ambulatory blood pressure monitoring (ABPM). The setting was the hospital outpatient department and the subjects chosen were normotensive and hypertensive. The effect of lowering the arm from heart level on indirect systolic BP (SBP) and diastolic BP (DBP) measurement as well as the importance of supporting the horizontal arm were measured. In the sitting position, lowering the supported horizontal arm to the dependent position increased BP measured by a mercury device from 103 7 10/60 7 7 to 111 7 14/ 67 7 10 mmHg in normotensive subjects, a mean increase of 8/7 mmHg (Po0.01). In hypertensive subjects, a similar manoeuvre increased BP from 143 7 21/78 7 17 to 166 7 29/88 7 20 mmHg, an increase of 23/10 mmHg (Po0.01). Combined results from normotensive and hypertensive subjects demonstrate a direct and proportional association between BP (SBP and DBP) and the increase produced by arm dependency. Similar changes and associations were noted with oscillometric devices in the clinic situation. However, supporting the horizontal arm did not alter BP. Of particular interest, analysis of 13 hypertensive subjects who underwent ABPM on two occasions, once with the arm in the 'usual' position and once with the arm held horizontally for BP measurement during waking hours, demonstrated changes comparable to the other devices. The mean 12-hour BP was 154 7 19/82 7 10 mmHg during the former period and significantly decreased to 141 7 18/74 7 9 mmHg during the latter period (Po0.01). Regression analysis of the change in SBP and DBP with arm position change again demonstrated a close correlation (r 2 ¼ 0.8113 and 0.7273; Po0.001) with the artefact being larger with higher systolic and diastolic pressures. In conclusion, arm movements lead to significant artefacts in BP measurement, which are greater, the higher the systolic or diastolic pressure. These systematic errors occur when using both auscultatory and oscillometric (clinic and ABPM) devices and might lead to an erroneous diagnosis of hypertension and unnecessary medication, particularly in individuals with high normal BP levels. Since clinical interpretations of heart level vary, the horizontal arm position should be the unambiguous standard for all sitting and standing BP auscultatory and oscillometric measurements.

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