RESUMO
BACKGROUND: More than one-third of US adults have prediabetes, which is typically accompanied by hypertension. METHODS: We examined whether prediabetes modified the effects of intensive systolic blood pressure (SBP) lowering on the incidence of chronic kidney disease (CKD) and acute kidney injury (AKI) events in a post-hoc analysis of the Systolic Blood Pressure Intervention Trial (SPRINT). Diabetes was a SPRINT exclusion criterion. We defined normoglycemia and prediabetes as fasting plasma glucose <100 mg/dl and ≥100 mg/dl, respectively. RESULTS: Of the 9,323 participants included in this analysis, 3,898 (41.8%) had prediabetes and the rest (5,425) had normoglycemia. In participants with baseline estimated glomerular filtration rate (eGFR) ≥60 ml/min/1.73 m2, incident CKD was defined as a ≥30% decline in eGFR to below 60 ml/min/1.73 m2 with repeat confirmation. AKI events were identified clinically. In the non-CKD participants (n = 6,678), there were 164 incident CKD events. The hazard ratios (HRs) for incident CKD for intensive SBP goal (<120 mm Hg) vs. standard SBP goal (<140 mm Hg) in the normoglycemia (HR: 3.25, 95% CI: 2.03, 5.19) and prediabetes (HR: 3.90, 95% CI: 2.17, 7.02) groups were similar (interaction P value 0.64). In the entire analytic cohort (N = 9,323), there were 310 AKI events. AKI HRs for intensive vs. standard SBP in the normoglycemia (HR: 1.59, 95% CI: 1.17, 2.15) and prediabetes (HR: 1.74, 95% CI: 1.22, 2.48) groups were also similar (interaction P value 0.71). CONCLUSIONS: Prediabetes was highly prevalent, but there was no evidence that prediabetes modified the effects of SPRINT intervention on kidney events.CLINICAL TRIALS REGISTRATIONNCT01206062.
Assuntos
Injúria Renal Aguda/epidemiologia , Anti-Hipertensivos/uso terapêutico , Pressão Sanguínea/efeitos dos fármacos , Taxa de Filtração Glomerular , Hipertensão/tratamento farmacológico , Hipertensão/epidemiologia , Rim/efeitos dos fármacos , Estado Pré-Diabético/epidemiologia , Insuficiência Renal Crônica/epidemiologia , Injúria Renal Aguda/diagnóstico , Injúria Renal Aguda/fisiopatologia , Idoso , Idoso de 80 Anos ou mais , Anti-Hipertensivos/efeitos adversos , Bases de Dados Factuais , Feminino , Humanos , Hipertensão/diagnóstico , Hipertensão/fisiopatologia , Incidência , Rim/fisiopatologia , Masculino , Pessoa de Meia-Idade , Estado Pré-Diabético/diagnóstico , Estado Pré-Diabético/fisiopatologia , Prevalência , Porto Rico/epidemiologia , Ensaios Clínicos Controlados Aleatórios como Assunto , Insuficiência Renal Crônica/diagnóstico , Insuficiência Renal Crônica/fisiopatologia , Medição de Risco , Fatores de Risco , Fatores de Tempo , Resultado do Tratamento , Estados Unidos/epidemiologiaRESUMO
Urate is a cause of gout, kidney stones, and acute kidney injury from tumor lysis syndrome, but its relationship to kidney disease, cardiovascular disease, and diabetes remains controversial. A scientific workshop organized by the National Kidney Foundation was held in September 2016 to review current evidence. Cell culture studies and animal models suggest that elevated serum urate concentrations can contribute to kidney disease, hypertension, and metabolic syndrome. Epidemiologic evidence also supports elevated serum urate concentrations as a risk factor for the development of kidney disease, hypertension, and diabetes, but differences in methodologies and inpacts on serum urate concentrations by even subtle changes in kidney function render conclusions uncertain. Mendelian randomization studies generally do not support a causal role of serum urate in kidney disease, hypertension, or diabetes, although interpretation is complicated by nonhomogeneous populations, a failure to consider environmental interactions, and a lack of understanding of how the genetic polymorphisms affect biological mechanisms related to urate. Although several small clinical trials suggest benefits of urate-lowering therapies on kidney function, blood pressure, and insulin resistance, others have been negative, with many trials having design limitations and insufficient power. Thus, whether uric acid has a causal role in kidney and cardiovascular diseases requires further study.
Assuntos
Injúria Renal Aguda/epidemiologia , Doenças Cardiovasculares/epidemiologia , Educação/organização & administração , Hipertensão/epidemiologia , Hiperuricemia/epidemiologia , Injúria Renal Aguda/sangue , Injúria Renal Aguda/fisiopatologia , Fatores Etários , Doenças Cardiovasculares/sangue , Doenças Cardiovasculares/fisiopatologia , Comorbidade , Feminino , Humanos , Hipertensão/sangue , Hipertensão/fisiopatologia , Hiperuricemia/sangue , Hiperuricemia/fisiopatologia , Masculino , Prevalência , Prognóstico , Ensaios Clínicos Controlados Aleatórios como Assunto , Medição de Risco , Índice de Gravidade de Doença , Fatores Sexuais , Análise de Sobrevida , Estados UnidosRESUMO
BACKGROUND: In individuals with a low diastolic blood pressure (DBP), the potential benefits or risks of intensive systolic blood pressure (SBP) lowering are unclear. METHODS: SPRINT (Systolic Blood Pressure Intervention Trial) was a randomized controlled trial that compared the effects of intensive (target <120 mm Hg) and standard (target <140 mm Hg) SBP control in 9361 older adults with high blood pressure at increased risk of cardiovascular disease. The primary outcome was a composite of cardiovascular disease events. All-cause death and incident chronic kidney disease were secondary outcomes. This post hoc analysis examined whether the effects of the SBP intervention differed by baseline DBP. RESULTS: Mean baseline SBP and DBP were 139.7±15.6 and 78.1±11.9 mm Hg, respectively. Regardless of the randomized treatment, baseline DBP had a U-shaped association with the hazard of the primary cardiovascular disease outcome. However, the effects of the intensive SBP intervention on the primary outcome were not influenced by baseline DBP level (P for interaction=0.83). The primary outcome hazard ratio for intensive versus standard treatment was 0.78 (95% confidence interval, 0.57-1.07) in the lowest DBP quintile (mean baseline DBP, 61±5 mm Hg) and 0.74 (95% confidence interval, 0.61-0.90) in the upper 4 DBP quintiles (mean baseline DBP, 82±9 mm Hg), with an interaction P value of 0.78. Results were similar for all-cause death and kidney events. CONCLUSIONS: Low baseline DBP was associated with increased risk of cardiovascular disease events, but there was no evidence that the benefit of the intensive SBP lowering differed by baseline DBP. CLINICAL TRIAL REGISTRATION: URL: https://www.clinicaltrials.gov. Unique identifier: NCT01206062.