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Aims and objectives: The aim of the article was to study the safety profile of renin-angiotensin-aldosterone system (RAAS) inhibitor in COVID- 19-affected Indian patients. Introduction: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is responsible for COVID-19 infection. There has been uncertainty about use of RAAS inhibitors in COVID-19. The association of RAAS inhibitors with severity of infection and clinical outcomes was addressed in this study. Materials and methods: This is a single-center retrospective study from Indian intensive care unit (ICU). A total of 138 were included, who were divided into group A (RAAS inhibitor) and group B (non-RAAS inhibitor). They are followed up till ICU stay during which peak levels of ferritin, D dimer, interleukin-6 were noted (primary outcome). The number of ventilator days, ICU length of stay, and ICU outcome also compared. Results: Of 138 patients, 18 are included in group A and 120, in group B. There is no difference in peak levels (mean) D dimer [5,893 vs 7,710, p 0.46], ferritin [2,388 vs 3,635, p 0.56], interleukin-6 [9,597 vs 3,625, p 0.06]. There is no difference in number of ventilator days (2.2 vs 1.78, p 0.53) and ICU length of stay (6.5 vs 6.1, p 0.74). Conclusion: RAAS inhibitors can be safely continued in COVID-19 infection. It is not associated with an increase in severity of infection, ICU length of stay, and mortality. [ABSTRACT FROM AUTHOR]

Background: The renin-angiotensin system (RAS) is an important facet of blood pressure regulation physiology. Treatment of essential hypertension targets the RAS using Angiotensin Converting Enzyme Inhibitors (ACEIs). However, ACEIs are not uniformly effective and show inter-individual pharmacodynamic variations. Aim: To assess the correlation between genetic polymorphisms in the genes coding for RAS components (angiotensin converting enzyme (ACE I/D), α-adducin (ADD1) and β1-adrenoreceptor (β1-ADR)) and response to Ramipril. Materials and Methods: We recruited 120 patients with essential hypertension who were administered Ramipril monotherapy initially, followed by combination therapy, if needed, based on their responses. Relationship between genotypes of the three candidate genes and decrease in the blood pressure (BP) was analyzed. Results: One hundred and six patients were evaluable at the end of the study period and 21 different genotypes were observed among them. Seven of them were classified as responders after 8 weeks and at the end of 12 weeks, an additional 77 (72.64%) were deemed responders. 19/22 non-responders were treated with combination therapy and 7/19 (36.84%) showed a response to the same. There was a significant difference between the proportions of responders and non-responders among the genotypes of the ADD1 and β1-ADR genes (P = 0.005 and 0.003, respectively). The best predictors of response to Ramipril 5 mg daily were the II/GG/SS, II/TG/SS, II/GG/SG, ID/GG/SS, ID/GG/SG and ID/TT/SS and DD/GG/SS; II/GG/GG, II/TT/SG, ID/TG/SG, ID/TT/SG, DD/GG/SG and DD/GG/GG were moderately predictive and II/TT/SS, II/TG/GG, ID/TG/GG, DD/TG/SG and DD/TG/GG were poorly predictive of response. Discussion: Variable responses to Ramipril may be the result of genetic factors. Conclusion: Pre-prescription genotyping may help individualize treatment. [ABSTRACT FROM AUTHOR]

Aim: To study renin angiotensin system (RAS) activity after posterior urethral valve ablation and the role of early induction of angiotensin converting enzyme‑inhibitors (ACE‑I) on the outcome of renal function. Materials and Methods: Thirty four children underwent valve ablation in which therapy with ACE‑I was started 40.5 ± 4.1 (range 32‑47 months) formed the study group. Post‑ACE‑I data were collected after mean duration of 18.2 ± 4.0 (12‑28 months). Plasma renin activity (PRA), urinary micro albumin, glomerular filtration rate (GFR), and serum creatinine, before and after therapy were monitored. Results: Therapy with ACE‑I resulted in a fall in micro albuminuria by 45.7% and 42.0% in patients without and with vesico ureteral reflux, respectively, and improvement in split renal function by 6.6% and 5.9% GFR respectively. A similar response was noted in patients without and with renal scars. Conclusion: The decline in renal function after valve ablation is accompanied by activation of RAS reflected in a gradual rise in PRA. Therapy with ACE‑I stabilizes and then improves renal function, thereby, retarding the pace of renal damage. [ABSTRACT FROM AUTHOR]