Introduction: In-hospital decline in renal function during the immediate post myocardial infarction (MI) period is known to predict poorer outcome; subsequent chronic change in renal function is less well reported. This study sought to track long-term change in renal function after MI, and assess its correlation with the outcome.
Methods And Results: Individuals who had sustained a first validated MI in the preceding 2.5-11.5 years were identified from the monitoring of trends and determinants in cardiovascular disease (MONICA) register and were invited to undergo a screening process in 1995, and again in 1998. All deaths were recorded up to the end of 2006. Change in renal function between 1995 and 1998 was available for 500 individuals (mean age 61.6+/-7.3 years, 74.8% men). Change in (Delta) calculated estimated glomerular filtration rate (eGFR) was normally distributed, with a mean crude fall in eGFR of 1.91+/-9.47 ml/min per 1.73 m. This corresponded to a -1.9+/-13.3% change in eGFR, or -0.8+/-3.6 ml/min/1.73 m2 per year. Delta eGFR correlated negatively with baseline eGFR (r=l-0.307, P<0.001). The first tertile (with the largest decline in eGFR) had an adjusted hazard ratios of 1.86 (1.14-3.03) for all cause mortality and 2.06 (1.13-3.74) for cardiovascular death, compared to the third tertile. A rise in creatinine of greater than 0.3 mg/dl carried adjusted hazard ratios of 2.27 (1.13-4.57) and 3.61 (1.73-7.54) for all cause mortality and cardiovascular death, respectively.
Conclusion: Chronic change in renal function after MI is predictive of long-term prognosis.
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http://dx.doi.org/10.1097/HJR.0b013e328332d48b | DOI Listing |
BMC Nephrol
January 2025
Department of Nephrology, Japan Community Healthcare Organization Sendai Hospital, 981-3281, Sendai, Miyagi, Japan.
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Sci Rep
January 2025
Department of Immunology, Genetics and Pathology, Uppsala University, Rudbeck Laboratory, C11, 75185, Uppsala, Sweden.
The existence of transmissible amyloid fibril strains has long intrigued the scientific community. The strain theory originates from prion disorders, but here, we provide evidence of strains in systemic amyloidosis. Human AA amyloidosis manifests as two distinct clinical phenotypes called common AA and vascular AA.
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January 2025
Division of Public Health, Hygiene and Epidemiology, Faculty of Medicine, Tohoku Medical and Pharmaceutical University, Sendai, Japan.
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View Article and Find Full Text PDFAm J Chin Med
January 2025
School of Integrated Chinese and Western Medicine, Nanjing University of Chinese Medicine (NJUCM), Nanjing, Jiangsu, P. R. China.
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View Article and Find Full Text PDFKeio J Med
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I.M. Sechenov First Moscow State Medical University, Moscow, Russian Federation.
We describe a case of sarcoidosis in a previously healthy 39-year-old man with the development of an acute kidney injury, requiring renal replacement therapy, as the first manifestation of the disease. The course of the disease was complicated by a сatheter-associated bloodstream infection. According to the histological examination of kidney biopsy samples, granulomatous interstitial nephritis was diagnosed.
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