Case control study / 926 newly diagnosed chronic kidney disease patients were interviewed and logistic-regression models were used to estimate the relative risks of disease-specific types of chronic renal failure associated with the use of various analgesics (aspirin, acetaminophen)
Use of either of the drug was associated with a 2.5 times increase risk of chronic kidney disease.
Case control studies / Five hundred and eighty-three cases and 1190 controls were included in the analysis.
Long-term use of any analgesic was associated with an overall odds ratio of 1.22 (95% CI, 0.89-1.66). Risks for aspirin was 1.56 (1.05-2.30). The risk of chronic kidney diasesae stage V associated with aspirin was related to the cumulated dose and duration of use, and it was particularly high among the subset of patients with vascular nephropathy as underlying disease [2.35 (1.17-4.72)].
Case control of study of 716 Chronic Kidney Disaese –V. Control were of similar from Maryland, Virginia, West Virginia, and Washington, D.C.
Authors found increased risk of chronic kidney disease-V in a dose-dependent fashion with acetaminophin. A cumulative dose of 5000 or more pills containing NSAIDs was also associated with an increased odds of ESRD (odds ratio, 8.8). Aspirin was not associated with increased risk of chronic kidney disease.
Multicenter case-control study to examine the use of analgesic as cause of chronic kidney disease. A total of 554 adults with newly diagnosed kidney disease and 516 matched control subjects selected randomly from the same area of North Carolina.
The risk of renal disease was highest in daily users of phenacetin (odds ratio, 5.11; confidence interval, 1.76 to 14.9, after adjustment for the effects of other analgesics). The risk of renal disease was also increased in daily users of acetaminophen; after adjustment for the use of aspirin and phenacetin, the odds ratio was 3.21 (confidence interval, 1.05 to 9.80). There was no increased risk in daily aspirin users (adjusted odds ratio, 1.32; confidence interval, 0.69 to 2.51).
Prospective cohort study of healthy male physicians. Self-reported use of aspirin, acetaminophen, and other nonsteroidal anti-inflammatory drugs (NSAIDs) was classified as never (<12 pills during the study period), 12 to 1,499 pills, 1,500 to 2,499 pills, and 2,500 or greater pills during the study period.
Authors concluded that occasional to moderate analgesic intake of aspirin, acetaminophen, or NSAIDs does not appear to increase the risk for decline in kidney function during a period of 14 years in healthy physicians.
Prospective cohort study / Data was taken from the Physicians’ Health Study, which lasted 14 years from September 1982 to December 1995 with annual follow-up.
Multivariable analyses adjusted for age; body mass index; history of hypertension, elevated cholesterol, and diabetes; occurrence of cardiovascular disease; physical activity; and use of other analgesics, the relative risks of elevated creatinine level associated with intake of 2500 or more pills were 0.83 (95% confidence interval [CI], 0.50-1.39; P for trend =.05) for acetaminophen, 0.98 (95% CI, 0.53-1.81; P for trend =.96) for aspirin, and 1.07 (95% CI, 0.71-1.64; P for trend =.86) for other nonsteroidal anti-inflammatory drugs. No association was observed between analgesic use and reduced creatinine clearance.
Cross-sectional analysis of National Health and Nutrition Examination Survey conducted in 1999-2002. Age-standardized prevalence in habitual analgesic users and non-habitual analgesic users and multivariable-adjusted odds ratios (ORs) were measured.
Habitual analgesic use of single or multiple products was not associated with increased prevalence of albuminuria or reduced eGFR as compared to non-habitual analgesic user.
Prospective Health Nurse Study. Informations were gatherered via a mailed questionnaire in 1999 about lifetime use of acetaminophen, aspirin, and NSAIDs and provided blood samples in 1989 and 2000.
Acetaminophen use was associated with an increased risk of a GFR decline of at least 30 mL/min per 1.73 m(2) (P trend =.01) and a GFR decline of 30% or greater (P trend<.001), but aspirin and NSAID use were not.
Randomized controlled trial (RCT), the Japanese Primary Prevention of Atherosclerosis with Aspirin for Diabetes (JPAD) trial, to evaluate low-dose aspirin as primary prevention for CVD in patients with type 2 diabetes. Patients with negative urine dipstick albumin of the JPAD trial in were followed in a cohort study after the RCT period was completed.
Low-dose aspirin did not increase the risk of positive urine dipstick albumin. There were no significant differences in annual changes in eGFR between the groups (aspirin, -0.8±2.9; no aspirin, -0.9±2.5 ml/min/1.73 m(2)/year).
Randomized double-blind crossover trial of 17 type 1 diabetic patients with microalbuminuria to study the effect of aspirin on proteinuria
Use of 150 mg ASA daily does not have any impact on albumin excretion rate or glomerulofilteration rate in type 1 diabetic patients with microalbuminuria.
Randomized, double-blind, crossover trial, of 31 type 2 diabetic patients with elevated levels of AER (>30 mg/24 h) were, in random order, given ASA (150 mg/day) for 4 weeks followed by placebo for 4 weeks with a 2 week washout period or vice versa.
Low-dose treatment with 150 mg aspirin daily does not have any impact on albumin excretion rate or GFR in type 2 diabetic patients with micro- or macroalbuminuria.
Double-blind crossover pilot study to study the effect of administration of aspirin-dipyridamole and reduction of proteinuria in diabetic nephropathy.
24 hour urinary protein excretion significantly reduced during aspirin-dipyridamole administration from a geometric mean (range) of 1.9 (0.4-7.7) g/24 h to 1.4 (0.5-9.9) g/24 h (P vaslue less than 0.05).
Retrospective, multivariate analysis toassess the effect of low-dose aspirin treatment (100 mg/day) on allograft function and survival of 830 renal transplant recipients.
Allograft survival was significantly longer in patients receiving low-dose aspirin therapy compared with patients receiving no aspirin treatment (n=205, 13.8 +/- 2.6 vs. 7.8 +/- 0.3 years, n=625; adjusted relative risk=0.443, 95% confidence interval , P<0.0001).
Aspirin reduced the risk of allograft failure (4 studies; RR: 0.57, 95% CI: 0.33 to 0.99), allograft thrombosis (2 studies; RR: 0.11, 95% CI: 0.02 to 0.53), and major adverse cardiac events (MACEs) or mortality (2 studies; RR: 0.72, 95% CI: 0.59 to 0.88), but not allograft rejection (3 studies; RR: 0.86, 95% CI: 0.45 to 1.65) or delayed graft function (DGF) (2 studies; RR: 1.00, 95% CI: 0.58 to 1.72) In KTR. Data on risk of major or minor bleeding were limited.
Retrospective analysis of 82 patients on low-dose aspirin 75 mg once daily who underwent renal transplant between 1 January 2000 and 31 December 2010 from a single center with 65 patients not taking aspirin.
Aspirin use was not significantly associated with creatinine levels (P = .59) after adjusting for other relevant variables.
A prospective consecutive series of 105 cadaveric renal transplants treated with aspirin 150 mg daily for the first 3 months after transplantation was compared with an untreated historical control group (n = 121). Needle protocol core biopsies were performed.
Rate of significant primary allograft thrombosis in patients treated with aspirin (none of 105) compared with that in the control group (six (5 per cent) of 121; P = 0.03) was found. No differences in renal function or 2-year allograft survival between the two groups was found. Aspirin-treated patients had a lower incidence of chronic allograft nephropathy at 1 year than controls, however P value was not significant.
