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.