Objective: This study aimed to verify the impact of predialysis systolic pressure (PDSP) on patients’ mortality. Design and method: We reviewed files of incident patients, in one reference center of hemodialysis, between January 2009 and June 2010. Arterial pressure was measured by sphygmomanometer before initiating the patient's first dialysis session. We considered: as “high PDSP” a SP equals or over 180 mmHg; as “low PDSP” a PS equals or less than 100 mmHg. Univariate and multivariate analysis were performed to study PDSP association with absolute mortality at five years. Odds ratio (OR) was subject to a 95% confidence interval. We used Kaplan Meier method for survival curves. Results: One hundred eleven patients were included. Sex ratio was 1.7 M/W. At dialysis initiation: mean age was 55 ± 14.9 years. Sixty nine patients (62%) were hypertensive; all of them were under antihypertensive agents. MAP, SP and DP were respectively 98.8 ± 16.3 mmHg, 139.4 ± 25.4 mmHg and 79.1 ± 14 mmHg. Mean urinary output was 1156 ± 542 ml/day and initial serum creatinine 887 ± 271 μmol/l. In univariate analysis, absolute mortality at five years was associated with low PDSP (p = 0.001, OR = 4.8). This association was pronounced among orderlies (p = 0.001) and diabetic patients (p = 0.001). High PDSP was also associated with absolute mortality at five years (p = 0.03; OR = 1.67). In multivariate study, neither low nor high PDSP were associated to mortality. Survival was decreased for patients with low PDSP (log-rank p = 0.001) (Figure 1) and high PDSP (log-rank p = 0.03) (Figure 2). Conclusions: These results suggest the presence of a “U” curve relationship between PDSP and mortality. Further studies, with larger populations, are needed to determine the potential use of low PDSP as a mortality risk factor.
Objective: This study aimed to establish clinical particularities of patients with primitive IgA nephropathy (IgAN) in case of associated thrombotic microangiopathy (TMA); comparatively with patients without TMA. Design and method: We compared two groups of patients diagnosed with primitive IgAN, from 1995 to 2017. The group1 (G1) comprised all patients with at least one TMA lesion in their renal biopsy. The group 2 (G2) was a randomly chosen sample of patients without TMA. Inclusion criteria were: patients older than 16, and followed up by our team. Exclusion criteria were: secondary IgAN or IgA vascularites, incomplete files and inconclusive IF results. We collected the initial clinical parameters. Then, using the “U” test of Mann-Witney test, we compared the two groups. Results: We selected 50 patients for G1 and 74 patients for G2. Baseline characters of all subjects were: mean age 33, men to women ratio 1.95, mean BMI 24.6 [17–38], mean albuminemia 33 [8–53] g/l, median serum creatinine (SCr) 207 [49–1800]μmol/l, mean eGFR 47 [2–156] ml/min and mean proteinuria 2.9 [0–11] g/day. Mean systolic and diastolic pressure were 139 [90–200] and 85 [50–120] mmHg. Seventy two patients (58%) had hypertension: grade 1, grade 2 and grade 3 for 23.4%, 23.4% and 11.3%. Comparing the two groups (G1 vs G2) the difference was significant for: systolic pressure (p = 0.000, 155 vs 128 mmHg), diastolic pressure (p = 0.000, 93 vs 79 mmHg), hypertension frequency (p = 0.000, 96% vs 32%), grade 2 hypertension (p = 0.000, 38% vs 13.5%), grade 3 hypertension (p = 0.000, 24% vs 2.7%) and SCr (p = 0.000, 501 vs 231 μmol/l). There was no significant difference forage (p = 0.10), BMI (p = 0.26), albuminemia (p = 0.14) and proteinuria (p = 0.059). Conclusions: Founding a TMA lesion in our patients’ biopsies should alert us to a more severe form of IgAN, with a more frequent hypertension and more advanced renal failure.
Objective: Our study aimed to describe blood pressure (BP) in case of thrombotic microangiopathy (TMA) associated with primitive IgA nephropathy (IgAN), its correlation with histological lesions and its prognostic impact. Design and method: We reviewed files of IgAN patients admitted and followed-up in our department between 1980 and 2017. We included adults showing at least one TMA lesion at their biopsy. Patients with IgA vasculitis or secondary IgAN were excluded. Results: Fifty files were studied. IgAN was revealed by malignant hypertension (MH) in 42% of cases. At admission, 68% of patients were under antihypertensive treatment. Mean arterial pressure (MAP), systolic pressure (SP) and diastolic pressure (DP) were respectively 113, 155 and 93 mmHg. Hypertension was found in 96% of patients, and was graded 1, 2 and 3 in 32%, 40% and 28% of cases. Only 30 patients had initial cardiac ultrasound and eye fundus revealing hypertensive cardiopathy in 53% and hypertensive retinopathy in 47% of cases. Mean proteinuria was 3.2 g/day ± 1.8. Median serum creatinine was 310 μmol/L. SP was correlated to C2 crescents (p = 0.015); DP to M1 mésangial hypercellularity (p = 0.033) and PAM to S1 glomerulosclerosis and C2 crescents (p = 0.045; p = 0.023). Those lesions were associated with more severe hypertension. After biopsy, all patients received antihypertensive agents (2.22 drugs per person): 80% had calcic inhibitors and 62% had renin angiotensin system inhibitors. At six months, among the 26 patients not on dialysis, only three had controlled BP. Dialysis risk was associated with initial MAP > = 100 mmHg (p = 0.027; OR = 12) and initial MH (p = 0.007; OR = 7.7). This risk was correlated with a higher SP at six months: 146 mmHg if dialysis versus 132 mmHg if not (p = 0.043). Renal survival was significantly reduced for patients with initial grade 3 hypertension (log Rank p = 0.043). Conclusions: Hypertension is frequent and severe in IgAN associated with TMA. Renal prognosis would be poorer in case of malignant, severe or persistent hypertension.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.