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The effects of hypertension and diabetes on new-onset chronic kidney disease: A prospective cohort study.

ABSTRACT: The study aimed to determine the different status of hypertension and diabetes on the risk of new-onset chronic kidney disease (CKD) events in Kailuan Study. A total of 21 905 individuals were enrolled in the study. The new-onset incidents of CKD, hypertension, and diabetes were collected in the follow-ups. All the individuals were divided into five groups according to baseline and follow-up hypertension and diabetes status: baseline hypertension (BH), baseline hypertension and incidence of diabetes (BHID), baseline diabetes (BD), baseline diabetes and incidence of hypertension (BDIH), and baseline hypertension and diabetes (BHD). The risk of new-onset CKD of the five groups was calculated using the Cox regression analysis. In the median follow-up of 7.05 ± 2.59 years, the prevalence of new-onset CKD in the group of BH, BHID, BD, BDIH, and BHD were 27.1, 43.79, 25.4, 36.6, and 45.1 per 1000 years, respectively. When adjusted possible confounders, the hazard ratios (HRs) and 95% confidence intervals (CIs) of new-onset CKD were 1.50 (95% CI: 1.38-1.63), 1.25(95% CI: 1.07-1.47), and 1.52 (95% CI: 1.35-1.7) in the group of BHID, BDIH, and BHD, respectively, as referred to the BH group (P < .001). No obvious difference was observed in the group of BH and BD for the incidence of new-onset CKD. Sensitivity analysis still showed the similar results among the five groups. The study showed that the effect of simple hypertension or simple diabetes on new-onset CKD was not significantly different, but the incidence of new-onset hypertension or diabetes increased the risk of new-onset CKD. Hypertension and diabetes had a synergistic influence on the risk of new-onset CKD.

SUBMITTER: Wang M

PROVIDER: S-EPMC8030069 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:The incidence rates of diabetes mellitus (DM) and chronic kidney disease (CKD) are increasing worldwide and their coexistence can have a large negative impact on clinical outcomes. However, it is unclear how incident DM affects CKD patients. Incident CKD patients between 2000 and 2013 were identified from the National Health Insurance Research Database of Taiwan; they were classified as non-DM (n = 10,356), pre-existing DM (n = 6982), and incident DM (n = 1103). Non-DM cases were patients who did not develop DM before the end of the observation period. The outcomes of interest were end-stage renal disease (ESRD), mortality, and composite outcome (ESRD or death). The association between the DM groups and clinical outcomes was estimated using the inverse probability of group-weighted (IPW) multivariate-adjusted time-dependent Cox regression models. During the study period of 14 years, 1735 (16.6%) patients in the non-DM group reached ESRD compared with 2168 (31.05%) in the pre-existing DM group and 111 (11.03%) in the incident DM group (p < 0.001). Moreover, 2219 (21.43%) patients in the non-DM group died compared with 1895 (27.14%) in the pre-existing DM group and 303 (27.47%) in the incident DM group (p < 0.001). Compared with the non-DM group, the pre-existing DM group was associated with a higher risk of ESRD [hazard ratio (HR) 2.54; 95% confidence interval (CI 2.43⁻2.65), death (HR 2.23; 95% CI 2.14⁻2.33), and a composite outcome (HR 2.29; 95% CI 2.21⁻2.36). Similarly, incident DM was also associated with a higher risk of ESRD (HR 1.12; 95% CI 1.06⁻1.19), death (HR 2.48; 95% CI 2.37⁻2.60), and a composite outcome (HR 1.77; 95% CI 1.70⁻1.84) compared with the non-DM group. Factors contributing to incident DM included old age, low monthly income, and having hypertension, hyperlipidemia, and ischemic heart disease, while pentoxifylline reduced the risk of incident DM. Similarly to pre-existing DM, CKD patients with incident DM carried a higher risk of ESRD, mortality, and a composite outcome compared with those with non-DM. For those at risk of incident DM, strict monitoring and intervention strategies must be adopted to help improve their clinical outcomes.

Project description:Early?onset cardiovascular and renal diseases have a strong genetic component. In the present study, exome?wide association studies (EWASs) were performed to identify genetic variants that confer susceptibility to early?onset myocardial infarction (MI), hypertension, or chronic kidney disease (CKD) in Japanese individuals. A total of 8,093 individuals aged ?65 years was enrolled in the study. The EWASs for MI, hypertension, and CKD were performed in 6,926 subjects (1,152 cases, 5,774 controls), 8,080 subjects (3,444 cases, 4,636 controls), and 2,556 subjects (1,051 cases, 1,505 controls), respectively. Genotyping of single nucleotide polymorphisms (SNPs) was performed with Illumina Human Exome?12 DNA Analysis BeadChip or Infinium Exome?24 BeadChip arrays. The associations of allele frequencies for 31,245, 31,276, or 31,514 SNPs that passed quality control to MI, hypertension, and CKD, respectively, was examined with Fisher's exact test. Bonferroni's correction for statistical significance of association was applied to compensate for multiple comparisons of genotypes with MI, hypertension, or CKD. The EWASs of allele frequencies revealed that 25, 11, and 11 SNPs were significantly associated with MI (P<1.60x10?6), hypertension (P<1.60x10?6), or CKD (P<1.59x10?6), respectively. Multivariable logistic regression analysis with adjustment for covariates showed that all 25, 11, and 11 SNPs were significantly associated with MI (P<0.0005), hypertension (P<0.0011), or CKD (P<0.0011), respectively. On examination of the results from previous genome?wide association studies and linkage disequilibrium of the identified SNPs, 11 loci (TMOD4, COL6A3, ADGRL3?CXCL8?MARCH1, OR52E4, TCHP?GIT2, CCDC63, 12q24.1, OAS3, PLCB2?VPS33B, GOSR2, ZNF77), six loci (MOB3C?TMOD4, COL6A3, COL6A5, CXCL8?MARCH1, NFKBIL1?6p21.3?NCR3, PLCB2?VPS33B), and seven loci (MOB3C?TMOD4, COL6A3, COL6A5, ADGRL3?CXCL8?MARCH1, MUC17, PLCB2?VPS33B, ZNF77) were identified as novel loci significantly associated with MI, hypertension, and CKD, respectively. Furthermore, six genes (TMOD4, COL6A3, CXCL8, MARCH1, PLCB2, VPS33B) were significantly associated with MI, hypertension and CKD; two genes (ADGRL3, ZNF77) with MI and CKD; and two genes (COL6A5, MOB3C) with hypertension and CKD. Therefore, 13 novel loci (MOB3C?TMOD4, COL6A3, ADGRL3?CXCL8?MARCH1, OR52E4, TCHP?GIT2, CCDC63, 12q24.1, OAS3, PLCB2?VPS33B, ZNF77, COL6A5, NFKBIL1?NCR3, MUC17) were identified that confer susceptibility to early?onset MI, hypertension, or CKD. The determination of genotypes for the SNPs at these loci may provide informative for assessment of the genetic risk for MI, hypertension, or CKD.

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The effects of hypertension and diabetes on new-onset chronic kidney disease: A prospective cohort study.

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