What is the impact of blood pressure on neurological symptoms and the risk of ESKD in primary and secondary thrombotic microangiopathies based on clinical presentation: a retrospective study.
Blood pressure
ESKD
epidemiology
hypertension
neurological symptoms
posterior reversible encephalopathy syndrome
thrombotic microangiopathy
Journal
BMC nephrology
ISSN: 1471-2369
Titre abrégé: BMC Nephrol
Pays: England
ID NLM: 100967793
Informations de publication
Date de publication:
20 01 2022
20 01 2022
Historique:
received:
15
04
2021
accepted:
05
01
2022
entrez:
21
1
2022
pubmed:
22
1
2022
medline:
11
3
2022
Statut:
epublish
Résumé
The impact of blood pressure on neurological symptoms and risk of end-stage kidney disease (ESKD) is unknown in primary and secondary thrombotic microangiopathies (TMAs). We measured baseline systolic (SBP) and diastolic (DBP) BP in consecutive 563 patients with adjudicated primary and secondary TMAs, and assessed its association with the risk of ESKD. Normal BP, grade 1, 2 and 3 hypertension were present in 243 (43.1%), 132 (23.4%), 101 (17.9%) and 88 (15.6%), respectively. Significant BP differences were noted in relation to the cause of TMA: highest BP values were found in patients with atypical hemolytic-uremic syndrome (aHUS), pregnancy, transplantation and auto-immune-related TMAs. Normal BP or grade 1 hypertension was found in 17/18 (94.4%) patients with thrombotic thrombocytopenic patients (only 1/18 (5.6%) had a SBP value>150 mmHg). In contrast, BP values could not differentiate isolated "essential" malignant hypertension (MH) from MH associated with aHUS (isolated MH (n=15): BP (median (IQR)): 220 (182-249)/132 (101-150) mmHg; MH with aHUS (n=5): BP: 223 (196-245)/131 (111-144) mmHg). The risk of vigilance disturbances (6.9%, 15.0%, 25.0%, respectively), epileptic seizures (1.5%, 4.0%, 12.5%, respectively) and posterior reversible encephalopathy syndrome (0.76%, 2.97%, 6.82%, respectively) increased with increasing baseline BP values from grade 1 to grade 3 hypertension. ESKD occurred in 35/563 (6.2%) patients (1.23%, 2.27%, 11.9% and 19.3% of patients with normal BP, grade 1, 2 and 3 hypertension, respectively). As compared to patients with normal BP (<120/139 mmHg), grade 1, grade 2 and grade 3 hypertension were associated with a greater risk of ESKD in univariate (OR: 1.91 [0.83-4.40], 13.2 [3.56-48.9] and 34.8 [9.31-130], respectively) and multivariate (OR: 0.89 [0.30-2.69], 7.00 [1.57-31.3] and 19.7 [4.53-85.2], respectively) analyses. The association between BP and the risk of ESRD was unchanged after adjustment on eculizumab use (OR: 3.46 [1.41-8.49], 17.7 [4.44-70.0] and 70.6 [8.61-579], respectively). Patients with MH, regardless of its cause, had a greater risk of ESKD (OR: 26.4 [10.0-69.8] vs other patients). Baseline BP differs in primary and secondary TMAs. High BP reduces the neurological tolerance of TMAs and is a powerful independent risk factor of ESKD, even after adjustment on TMA's cause.
Sections du résumé
BACKGROUND
The impact of blood pressure on neurological symptoms and risk of end-stage kidney disease (ESKD) is unknown in primary and secondary thrombotic microangiopathies (TMAs).
METHODS
We measured baseline systolic (SBP) and diastolic (DBP) BP in consecutive 563 patients with adjudicated primary and secondary TMAs, and assessed its association with the risk of ESKD.
RESULTS
Normal BP, grade 1, 2 and 3 hypertension were present in 243 (43.1%), 132 (23.4%), 101 (17.9%) and 88 (15.6%), respectively. Significant BP differences were noted in relation to the cause of TMA: highest BP values were found in patients with atypical hemolytic-uremic syndrome (aHUS), pregnancy, transplantation and auto-immune-related TMAs. Normal BP or grade 1 hypertension was found in 17/18 (94.4%) patients with thrombotic thrombocytopenic patients (only 1/18 (5.6%) had a SBP value>150 mmHg). In contrast, BP values could not differentiate isolated "essential" malignant hypertension (MH) from MH associated with aHUS (isolated MH (n=15): BP (median (IQR)): 220 (182-249)/132 (101-150) mmHg; MH with aHUS (n=5): BP: 223 (196-245)/131 (111-144) mmHg). The risk of vigilance disturbances (6.9%, 15.0%, 25.0%, respectively), epileptic seizures (1.5%, 4.0%, 12.5%, respectively) and posterior reversible encephalopathy syndrome (0.76%, 2.97%, 6.82%, respectively) increased with increasing baseline BP values from grade 1 to grade 3 hypertension. ESKD occurred in 35/563 (6.2%) patients (1.23%, 2.27%, 11.9% and 19.3% of patients with normal BP, grade 1, 2 and 3 hypertension, respectively). As compared to patients with normal BP (<120/139 mmHg), grade 1, grade 2 and grade 3 hypertension were associated with a greater risk of ESKD in univariate (OR: 1.91 [0.83-4.40], 13.2 [3.56-48.9] and 34.8 [9.31-130], respectively) and multivariate (OR: 0.89 [0.30-2.69], 7.00 [1.57-31.3] and 19.7 [4.53-85.2], respectively) analyses. The association between BP and the risk of ESRD was unchanged after adjustment on eculizumab use (OR: 3.46 [1.41-8.49], 17.7 [4.44-70.0] and 70.6 [8.61-579], respectively). Patients with MH, regardless of its cause, had a greater risk of ESKD (OR: 26.4 [10.0-69.8] vs other patients).
CONCLUSIONS
Baseline BP differs in primary and secondary TMAs. High BP reduces the neurological tolerance of TMAs and is a powerful independent risk factor of ESKD, even after adjustment on TMA's cause.
Identifiants
pubmed: 35057750
doi: 10.1186/s12882-022-02672-3
pii: 10.1186/s12882-022-02672-3
pmc: PMC8781095
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
39Informations de copyright
© 2022. The Author(s).
Références
Clin J Am Soc Nephrol. 2019 Apr 5;14(4):557-566
pubmed: 30862697
Lancet. 2017 Aug 12;390(10095):681-696
pubmed: 28242109
Am J Physiol Heart Circ Physiol. 2017 Mar 1;312(3):H349-H354
pubmed: 27986662
Crit Care. 2013 Feb 04;17(1):204
pubmed: 23394211
Blood. 2013 Sep 19;122(12):2023-9; quiz 2142
pubmed: 23838348
Clin J Am Soc Nephrol. 2018 Feb 7;13(2):300-317
pubmed: 29042465
Am J Hematol. 2017 Apr;92(4):381-387
pubmed: 28133771
Nephrol Dial Transplant. 2020 Dec 10;:
pubmed: 33301026
J Hum Hypertens. 2016 Aug;30(8):463-6
pubmed: 26582411
Can J Cardiol. 2020 May;36(5):712-720
pubmed: 32389344
Hypertens Res. 2021 Jan;44(1):88-97
pubmed: 32719463
Am J Kidney Dis. 2017 Nov;70(5):715-721
pubmed: 28720207
PLoS One. 2012;7(1):e30886
pubmed: 22292070
Hypertension. 2008 Apr;51(4):862-6
pubmed: 18332284
Clin J Am Soc Nephrol. 2013 Apr;8(4):554-62
pubmed: 23307876
Eur Heart J. 2013 Jul;34(28):2159-219
pubmed: 23771844
Intern Med. 2010;49(1):7-15
pubmed: 20045995
J Am Soc Hypertens. 2016 Apr;10(4):352-9
pubmed: 26778772
Haematologica. 2019 Dec;104(12):2501-2511
pubmed: 30890598
Am J Hypertens. 2007 Aug;20(8):900-6
pubmed: 17679041
N Engl J Med. 2014 Aug 14;371(7):654-66
pubmed: 25119611
Kidney Int. 2017 Jun;91(6):1420-1425
pubmed: 28187980
Minerva Med. 2007 Dec;98(6):731-47
pubmed: 18299685
Can J Neurol Sci. 2003 Aug;30(3):210-4
pubmed: 12945943
Clin Exp Hypertens. 2011;33(2):77-83
pubmed: 21214403
PLoS One. 2017 May 18;12(5):e0177894
pubmed: 28542627
Arch Pathol Lab Med. 2003 Jul;127(7):834-9
pubmed: 12823037
Lancet Haematol. 2016 May;3(5):e237-45
pubmed: 27132698
J Hypertens. 2017 Nov;35(11):2310-2314
pubmed: 28622157
Kidney Int Suppl. 2009 Feb;(112):S8-S10
pubmed: 19180141
Br J Haematol. 2008 Sep;142(5):819-26
pubmed: 18637802
Eur J Neurol. 2013 Jan;20(1):153-9
pubmed: 22834894
Ann Hematol. 2017 Oct;96(10):1715-1726
pubmed: 28752391
Br Med J. 1964 Sep 5;2(5409):617-20
pubmed: 14171073