scholarly journals A Hospital Based Study of Pulmonary Arterial Hypertension in Various Stages of Chronic Kidney Disease and Associated Risk Factors among Patients Attending a Tertiary Care Hospital in Ujjain, Madhya Pradesh

2021 ◽  
Vol 8 (20) ◽  
pp. 1500-1504
Author(s):  
Rajesh Deshpande ◽  
Amit Kumar Yadav ◽  
Vipin Porwal

BACKGROUND Multiple mechanisms have been identified contributing to pulmonary arterial hypertension (PAH) in chronic kidney disease (CKD) patients and it is one of the important sequelae of CKD and needs early detection. We wanted to study PAH in various stages of CKD and its association with renal and cardiovascular parameters. METHODS This was an observational study. PAH was diagnosed if mean pulmonary artery pressure (MPAP) was ≥ 25 mmHg using 2D - Doppler echocardiography in 96 CKD patients. Staging of CKD was done as per Kidney Disease Improving Global Outcomes (KDIGO) stages 1 - 5. Age, gender, diabetes, hypertension, stages of CKD, corticomedullary differentiation (CMD), estimated glomerular filtration rate (EGFR), urinary albumin creatinine ratio (UACR), left ventricular ejection fraction (LVEF) and left ventricular hypertrophy (LVH) were included as risk factors. Data was analysed by calculating percentage, mean, standard deviation, chi square and t test. P value < 0.05 was taken as statistically significant. RESULTS PAH was detected in 37 (38.5 %) of CKD patients. Prevalence of PAH increased with stages of CKD being highest (59 %) in stage 5 and this was found to be statistically significant (P = 0.04). PAH was detected earliest in stage 2 (23.5 %). Lower mean eGFR ml / min / 1.733m2 (24.43 ± 17.8 vs 40.98 ± 25.7, P = 0.001) altered corticomedullary differentiation (50.9 % vs 20.5 % p = 0.003), reduced LVEF (81 % vs 26.7 % P = 0.000) and LVH (65 % vs 19.6 %, P = 0.000) were significantly associated with PAH in CKD patients. CONCLUSIONS PAH in CKD patients increases with CKD stages. Onset of PAH in CKD patients may be earlier and significantly associated with left ventricular dysfunction. KEYWORDS Pulmonary Arterial Hypertension, Chronic Kidney Disease, Left Ventricular Ejection Fraction, Left Ventricular Hypertrophy

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 2015-2015 ◽  
Author(s):  
Suporn Chuncharunee ◽  
Vichai Atichartakarn ◽  
Napaporn Archararit ◽  
Umaporn Udomsubpayakul ◽  
Atiporn Ingsathit ◽  
...  

Abstract Abstract 2015 Poster Board I-1037 Introduction: Pulmonary arterial hypertension (PAH) associated with thalassemia (Thal) hemoglobinopathy is now an accepted clinical entity. Most of the reports are in sickle cell disease and splenectomized β-Thal patients. Once manifested, it connotes poor prognosis. We herein present its prevalence and predictors in hemoglobin E/β-Thal (E/β-Thal) patients. Patients and Methods: One hundred and ten clinically stable E/β-Thal outpatients, on no medication aside from folic acid and who received no blood transfusion in the preceding 4 weeks were studied. All gave written informed consent, and study protocol was approved by the institution ethics committee on studies in humans (#0774/2548). Echocardiogram was used to estimate systolic PA pressure (SPAP). PAH was defined as an estimated SPAP ≥36 mmHg. Clinical features and laboratory data were stratified according to the presence or absence of PAH, and statistical analysis was done by STATA version 10 (Stata Corp, Texas), considering a P value <0.05 as statistically significant. Predictors of PAH were considered in univariate analysis. Results: There were 110 patients, 56 of whom were female and 61 were asplenic. PAH was present in 41 patients (37.3%), all of whom had normal left ventricular ejection fraction. There was no gender difference between the 2 groups (p=0.055). Selected statistically significant results are shown in the table. Conclusions: Prevalence of PAH in E/β-Thal patients is 37.3% without gender preponderance. Predictors are asplenia, more severe hemolysis, higher number of circulating (activated) platelets and nucleated RBCs, increased chronic low grade inflammation and increased cellular adhesion between blood and endothelial cells. These changes could facilitate development of thrombotic pulmonary arteriopathy, the underlying basis of PAH. Serum NT pro BNP assay can be utilized as a predictor or a screener of PAH in these patients. Disclosures: No relevant conflicts of interest to declare.


2019 ◽  
Vol 8 (1) ◽  
pp. 24-31
Author(s):  
Balaram Shrestha ◽  
Dhiraj Gurung ◽  
Sanjib Dhungel

Background: Evaluation of cardiac diseases in chronic kidney disease has been rarely investigated in Nepal. Objectives: Objective of this study is to evaluate cardiac lesions in admitted chronic kidney disease patients. Methodology: It is a prospective observational study of echocardiography of chronic kidney disease patients from April, 2007 to April, 2013 in Nepal Medical College Teaching Hospital. Results: One hundred chronic kidney disease patients were evaluated. Male to Female ratio was 1.8:1 and age ± SD was 46.3 ± 17.2 years. Forty eight percent of the chronic kidney disease patients had left ventricular hypertrophy. Patients with chronic kidney disease with left ventricular hypertrophy group had interventricular septum of 1.5 ± 0.3 cm vs. 1.1 ± 0.1 cm (p<0.0001) and posterior wall of 1.1 ± 0.2cm vs. 1.0 ± 0.1cm (p< 0.01) in comparison to chronic kidney disease without left ventricular hypertrophy. Forty one percent had left ventricular systolic dysfunction with left ventricular ejection fraction of 39 ± 9.9 %. Pulmonary arterial hypertension was noticed in 39% patients. Valvular regurgitant lesions were quite common (24.1%) usually as multivalvular lesions (4.4 lesions per patient). Mitral regurgitation was the commonest regurgitant lesion (81%). Conclusion: Echocardiographic cardiac evaluation is useful to diagnose concomitant cardiac lesions for standard care of chronic kidney disease patients.


Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Valentina Raglianti ◽  
Alberto Giannoni ◽  
Annamaria Del Franco ◽  
Gianluca Mirizzi ◽  
Alberto Aimo ◽  
...  

Introduction: Pulmonary arterial hypertension (PAH) is an acknowledged independent prognostic factor in patients with heart failure (HF). Beyond a “passive” component due to the increased left ventricular pressure, an “active” component due to pulmonary vascular reactivity is frequently observed. However, the mechanism behind pulmonary vasoconstriction is not fully understood. Hypothesis: We hypothesized that central apneas (Cheyne-Stokes respiration [[Unable to Display Character: &#8211;]] CSR) through chemoreflex stimulation may contribute to PAH in HF. Methods: we studied 56 HF patients (left ventricular ejection fraction <50%), on stable optimal pharmacological treatment, without increased left ventriculare pressure (excluding patients with severe mitral disease and severe diastolic dysfunction). All patients underwent echocardiographic and neurohormonal assessment, 24-hour cardiorespiratory screening for CSR (patients with obstructive events were excluded) and chemoreflex test for hypoxic (HVR) and hypercapnic (HCVR) ventilatory responses (by rebreathing technique) . Results: Thirteen patients (23%) showed CSR, as defined by a 24 hour AHI > of 15. HF patients with CSR compared with patients with normal breathing, presented higher systolic arterial pulmonary pressure (SPAP: 40.1±7.6 vs 33.1±5.9, p<0.01) at echocardiography, despite similar systolic and diastolic function (data not shown). Furthermore, patients with central apneas also presented with enhanced HVR (median 0.78, interquartile range -IR 0.48-1.22 vs 0.43, IR 0.19-0.69 L/min/%, p<0.05) and HCVR (1.18, IR 0.98-1.35 vs 0.75, IR 0.51-0.95 L/min/mmHg, p<0.01) as well as increased plasma norepinephrine levels (546, IR 371-732 vs 393, IR 229-538 pg/mL, p<0.05). SPAP was indeed correlated with AHI (Spearman’s Rho, R=0.44, p<0.01), HCVR (R=0.48, p<0.001), HVR (R=0.33, p<0.05) and norepinephrine levels (R=0.31, p<0.05). Conclusions: In patients with systolic HF, the presence of diurnal-nocturnal CSR, likely via recurrent hypoxia and hypercapnia cycles, may determine a chemoreflex mediated adrenergic discharge and a consequent pulmonary vasoconstriction, responsible of the undesirable increase in pulmonary arterial pressure.


2019 ◽  
Vol 9 (3) ◽  
pp. 204589401986862 ◽  
Author(s):  
Valentina Mercurio ◽  
Teresa Pellegrino ◽  
Giorgio Bosso ◽  
Giacomo Campi ◽  
Paolo Parrella ◽  
...  

Sympathetic nervous system hyperactivity has a well-recognized role in the pathophysiology of heart failure with reduced left ventricular ejection fraction. Alterations in sympathetic nervous system have been related to the pathophysiology of pulmonary arterial hypertension, but it is unclear whether cardiac sympathetic nervous system is impaired and how sympathetic dysfunction correlates with hemodynamics and clinical status in pulmonary arterial hypertension patients. The aim of this study was to evaluate the cardiac sympathetic nervous system activity by means of123Iodine-metaiodobenzylguanidine nuclear imaging in pulmonary arterial hypertension patients and to explore its possible correlation with markers of disease severity. Twelve consecutive pulmonary arterial hypertension patients (nine women, median age 56.5 (17.8), eight idiopathic and four connective tissue-associated pulmonary arterial hypertension) underwent cardiac123Iodine-metaiodobenzylguanidine scintigraphy. The results were compared with those of 12 subjects with a negative history of cardiovascular or pulmonary disease who underwent the same nuclear imaging test because of a suspected paraganglioma or pheochromocytoma, with a negative result (controls), and 12 patients with heart failure with reduced left ventricular ejection fraction. Hemodynamics, echocardiography, six-minute walking distance, cardiopulmonary exercise testing, and N-terminal pro brain natriuretic peptide were collected in pulmonary arterial hypertension patients within one week from123Iodine-metaiodobenzylguanidine scintigraphy. Cardiac123Iodine-metaiodobenzylguanidine uptake, assessed as early and late heart-to-mediastinum ratio, was significantly lower in pulmonary arterial hypertension compared to controls (p = 0.001), but similar to heart failure with reduced left ventricular ejection fraction. Myocardial123Iodine-metaiodobenzylguanidine turnover, expressed as washout rate, was similar in pulmonary arterial hypertension and heart failure with reduced left ventricular ejection fraction and significantly higher compared to controls (p = 0.016). In the pulmonary arterial hypertension group, both early and late heart-to-mediastinum ratios and washout rate correlated with parameters of pulmonary arterial hypertension severity including pulmonary vascular resistance, right atrial pressure, tricuspid annular plane systolic excursion, N-terminal pro brain natriuretic peptide, and peak VO2. Although we evaluated a small number of subjects, our study showed a significant impairment in cardiac sympathetic nervous system in pulmonary arterial hypertension, similarly to that observed in heart failure with reduced left ventricular ejection fraction. This impairment correlated with indices of pulmonary arterial hypertension severity. Cardiac sympathetic dysfunction may be a contributing factor to the development of right-sided heart failure in pulmonary arterial hypertension.


2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
O Obertynska

Abstract Purpose Mineralocorticoid receptor antagonists (MRAs) remain underused in cases of heart failure with a reduced left ventricular ejection fraction (HFrEF) and chronic kidney disease (CKD), largely due to the fear of inducing worsening of renal function (RF) and hyperkalemia (HK), particularly in combination with renin angiotensin inhibitors. The aim was to investigate the safety use of spironolactone (SP) in patients with HFrEF (ejection fraction &lt;40%) and CKD and determine predictors of worsening of RF and developing HK. Methods 208 patients with HFrEF (on top of standard therapy including ACE-I or an ARB) and CKD (baseline eGFR between 30 and 60 ml/min) were included in the study. The potassium (K) and creatinine (C) levels, plasma aldosterone (AS) and NT-proBNP were estimated at baseline and at week 12. After biochemical evaluation, 101 patients started on SP treatment with a median dose of 23 mg daily (titrated). K and RF were checked at weeks 1, 2, 4, 6, 8, 12. Results K and C levels increased significantly after start of SP: mean K levels increased from 4.47±0.59 to 5.23±0.57 mEq/l, (P&lt;0.01) and was dose dependent. After 12 weeks of treatment the incidence of severe HK (K+ ≥6.0 mmol/L) was &lt;5%, K 5.5–5.9 mmol/L occurred in 13 patients (13%) and it was predicted by baseline eGFR≤35 ml/min/1.73 m2. and K ≥5.0 mmol/L/. Subsequently, these patients required a prescription of K binders. Mean eGFR on SP decreased from 48.34±2.23 to 42.19±2.65 ml/min/1.73 m2 (P&lt;0.01) and a significant decrease in GFR was observed only during the first month (P &lt;0.01) with not significant increasing to 6 and 12 weeks after the start of SP. Five patients (5%) on SP experienced significant decline of RF result in withdrew SP. Age, NT-proBNP concentration &gt;1550 ng/L and eGFR ≤35 ml/min/1.73 m2 at baseline had modest discriminative powers for predicting decline of RF (0.456, P&lt;0.01; 0.542, P&lt;0.001; 0.712, P&lt;0.001; respectively). At baseline in patients with HFrEF was an inverse correlation between GFR and NT-proBNP level (r=−0.298, p&lt;0.001). The SP treatment resulted in significantly reduced NT-proBNP and AS (P&lt;0.01; P&lt;0.05 respectively). By linear regression analysis in SP group the eGFR was associated with NT-proBNP change (0.362, P&lt;0.05). Conclusion In patient with HFrEF and CKD the risk-benefit ratio of spironolactone with respect to renal failure appears favourable due to improvement of the neurohumoral profile. Although the renal disfunction and hyperkalemia on spironolactone are common: approximately 18% patients required the prescription of K binders and 5% required the withdrew SP duo to decline RF, the occurrence of hyperkalemia was predicted by baseline potassium level and eGFR. Age, higher level of NT-proBNP and eGFR were identified as potential predictors of worsening of RF. So, caution should be advised when using spironolactone in HFrEF with CKD and potassium of ≥5.0 mmol/L and eGFR ≤35 ml/min/1.73 m2 and NT-proBNP concentration &gt;1550 ng/L for safety reasons. FUNDunding Acknowledgement Type of funding sources: Public Institution(s). Main funding source(s): National Medical University


2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Rafael Del Pozo Alvarez ◽  
Teresa Vázquez ◽  
Dolores Martínez Esteban ◽  
Daniel Gaitan Roman ◽  
Alicia Moreno Ortiz ◽  
...  

Abstract Background and Aims Neprilysin inhibition (NEPi) combined with a renin-angiotensin system (RAS) blocker has been shown to play an important role among patients with heart failure (HF), whose main cause of inpatient admission is congestion, reducing effectively HF hospitalization and cardiovascular death. These benefits stem from NEPi being a natriuresis and diuresis factor while RAS, which activates subsequently, staying blocked. Thanks to this, sacubitril/valsartan is a promising tool targeting patients with chronic kidney disease (CKD) and HF, which frequently coexist and lead one to the other, challenging their management. There is evidence NEPi-RASb may be beneficial in this population but long-term outcome still lacks. The primary aim is to analyse potential improvement in HF and advanced CKD. Secondary, to evaluate the tolerability and safety profile in this population. Method A prospective observational study, conducted from October 2016 to December 2020. Twenty-five patients were included meeting the following criteria: diagnosis of HF plus reduced left ventricular ejection fraction (LVEF) and New York Heart Association (NYHA) functional class of II-IV with indication of sacubitril/valsartan, and CKD stages 3-4. All of them were followed periodically by a Nephrologist at our Department. Results The male:women ratio was 4:21, with a mean age of 73.2 ± 5.9 years. All patients had diagnosed hypertension, 32% type 2 diabetes, and 92% dyslipidemia. By December 2020, seven patients had completed three-year follow-up, whereas 17 were followed successfully through one year of treatment. Six patients died during the study (50% due to cardiovascular event, none due to renal malfunction), another discontinued treatment due to hypotension, and no patient started renal replacement therapy. The median of the studied time of treatment was 31 months (IQR 23.5 - 35). Cardiac and renal characteristics are listed in Table 1. At first year a significant improvement in LVEF was found (p=0.018). Although it is observed a tendency to this enhancement at second and third years, statistical analysis was not significative, arguably because a limited sample. Nonetheless, the number of visits to the Emergency Department (ED) regarding congestion symptoms were significantly reduced at these periods. More interesting, kidney function improved at first year when comparing serum creatinine (p=0.043) and eGFR (p=0.008), and this improvement stays in the long term at second and third years (p=0.019, p=0.046 respectively). There were no significant changes in potassium nor in blood pressure, still urine protein excretion was significantly higher at third year (p=0.043), understandable possibly due to hyperfiltration mechanisms and diabetic nephropathy progression. Conclusion Sacubitril/valsartan showed a long-term improvement in cardiac and kidney function, explaining a reduction in the number of visits to ED due to congestion and eventually a better quality of life. Besides, the improvement in kidney function cannot be totally understood in the context of enhanced LVEF at first year as this effect fades with time. Future research should explore this line.


2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Anna M. Price ◽  
Manvir K. Hayer ◽  
Ravi Vijapurapu ◽  
Saad A. Fyyaz ◽  
William E. Moody ◽  
...  

Abstract Background Late gadolinium enhancement (LGE) using cardiac magnetic resonance (CMR) characterizes myocardial disease and predicts an adverse cardiovascular (CV) prognosis. Myocardial abnormalities, are present in early chronic kidney disease (CKD). To date there are no data defining prevalence, pattern and clinical implications of LGE-CMR in CKD. Methods Patients with pre-dialysis CKD (stage 2–5) attending specialist renal clinics at University Hospital Birmingham (UK) who underwent gadolinium enhanced CMR (1.5 T) between 2005 and 2017 were included. The patterns and presence (LGEpos) / absence (LGEneg) of LGE were assessed by two blinded observers. Association between LGE and CV outcomes were assessed. Results In total, 159 patients received gadolinium (male 61%, mean age 55 years, mean left ventricular ejection fraction 69%, left ventricular hypertrophy 5%) with a median follow up period of 3.8 years [1.04–11.59]. LGEpos was present in 55 (34%) subjects; the patterns were: right ventricular insertion point n = 28 (51%), mid wall n = 18 (33%), sub-endocardial n = 5 (9%) and sub-epicardial n = 4 (7%). There were no differences in left ventricular structural or functional parameters with LGEpos. There were 12 adverse CV outcomes over follow up; 7 of 55 with LGEpos and 5 of 104 LGEneg. LGEpos was not predicted by age, gender, glomerular filtration rate or electrocardiographic abnormalities. Conclusions In a selected cohort of subjects with moderate CKD but low CV risk, LGE was present in approximately a third of patients. LGE was not associated with adverse CV outcomes. Further studies in high risk CKD cohorts are required to assess the role of LGE with multiplicative risk factors.


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