Objective:The purpose of our study is to correlate renal echogenicity with serum creatinine in order to determine the significance of renal echogenicity when it comes to identifying the progression of chronic kidney disease (CKD) and for the sonographic grading of CKD.Materials and Methods:Sixty patients above 30 years of age who had been diagnosed with CKD according to the guidelines of the National Kidney Foundation were included in the study. Patients on kidney replacement therapy or with fatty liver findings on ultrasonography were excluded. Ultrasounds of kidneys were performed by two radiologists who were blind to the patients’ serum creatinine levels. Renal cortical echogenicity was compared with serum creatinine. Statistical analysis was performed using one-way ANOVA followed by Scheffe's test. The relationship between serum creatinine and sonographic features was assessed by correlation coefficient analysis. A P value less than 0.05 was considered statistically significant.Results:Mean serum creatinine was 2.80 mg/dl for Grade 1 (range: 0.9-9.2 mg/dl), 3.69 mg/dl for Grade 2 (range: 1.2-10.3 mg/dl), 3.86 mg/dl for Grade 3 (range: 1.1-6.5 mg/dl), and 7.90 mg/dl for Grade 4 (range: 3.1-11.4 mg/dl). The grades being determined by cortical echogenicity on imaging A statistically significant, positive correlation was observed between serum creatinine and grading based on cortical echogenicity (P = 0.004).Conclusion:Renal echogenicity and its grading correlates better with serum creatinine in CKD than other sonographic parameters such as longitudinal size, parenchymal thickness, and cortical thickness. Hence, renal echogenicity is a better parameter than serum creatinine for estimating renal function in CKD, and has the added advantage of irreversibility.

BackgroundABO and Rh blood group systems are associated with many diseases including cancerous, infectious, non-infectious, bacterial and viral diseases. Studies have shown association of blood groups A and O with higher and lower odds for coronavirus disease 2019 positivity, respectively.MethodsThis is a single-center, retrospective study conducted at Sir Ganga Ram Hospital, Delhi. We investigated the association of ABO and Rh blood groups with susceptibility to coronavirus disease 2019 infection, severity of disease, recovery period, and mortality of patients. Patients were enrolled from April 8, 2020 to October 4, 2020. A total of 2,586 real-time PCR (RT-PCR)-confirmed coronavirus disease 2019 (COVID-19) patients were recruited. Data was analyzed using chi-square test, odds ratio, and Mann–Whitney test to determine the association of blood groups.ResultsIn the 2,586 COVID-19-infected patients, the frequencies of A, B, O, and AB were 29.93%, 41.80%, 21.19%, and 7.98%, respectively. Of the patients, 98.07% were Rh positive. Blood group A (odds ratio, 1.53; CI, 1.40–1.66; p < 0.001) and B (odds ratio, 1.15; CI, 1.06–1.24; p < 0.001) is observed to be significantly associated with COVID-19 susceptibility, whereas blood group O (odds ratio, 0.65; CI, 0.59–0.71; p < 0.001) and AB (odds ratio, 0.66; CI, 0.59–0.71; p < 0.001) have low risk of COVID-19 infection.ConclusionA, B, and Rh+ are found to be more susceptible to COVID-19 infection, whereas blood groups O, AB, and Rh− are at a lower risk of COVID-19 infection. No association was found between blood groups and susceptibility to severity of disease and mortality.

Background Cytokine storm triggered by Severe Coronavirus Disease 2019 (COVID-19) is associated with high mortality. With high Interleukin -6 (IL-6) levels reported in COVID-19 related deaths in China, IL-6 is considered to be the key player in COVID-19 cytokine storm. Tocilizumab, a monoclonal antibody against IL-6 receptor, is used on compassionate grounds for treatment of COVID-19 cytokine storm. The aim of this study was to assess effect of tocilizumab on mortality due to COVID-19 cytokine storm. Method This retrospective, observational study included patients of severe COVID-19 pneumonia with persistent hypoxia (defined as saturation 94% or less on supplemental Oxygen of 15 L per minute through non-rebreathing mask or PaO2/FiO2 ratio of less than 200) who were admitted to a tertiary care center in Mumbai, India, between 31st March to 5th July 2020. In addition to standard care, single Inj. Tocilizumab 400 mg was given intravenously to 151 consecutive COVID-19 patients with persistent hypoxia, from 13th May to 5th July 2020. These 151 patients were retrospectively analysed and compared with historic controls, ie consecutive COVID-19 patients with persistent hypoxia, defined as stated above (N = 118, from our first COVID-19 admission on 31st March to 12th May 2020 i.e., till tocilizumab was available in hospital). Univariate and multivariate Cox regression analysis was performed for identifying predictors of survival. Statistical analysis was performed using IBM SPSS version 26. Results Out of 269 (151 in tocilizumab group and 118 historic controls) patients studied from 31st March to 5th July 2020, median survival in the tocilizumab group was significantly longer than in the control group; 18 days (95% CI, 11.3 to 24.7) versus 9 days (95% CI, 5.7 to 12.3); log rank p 0.007. On multivariate Cox regression analysis, independent predictors of survival were use of tocilizumab (HR 0.621, 95% CI 0.427–0.903, P 0.013) and higher oxygen saturation. Conclusion Tocilizumab may improve survival in severe COVID-19 pneumonia with persistent hypoxia. Randomised controlled trials on use of tocilizumab as rescue therapy in patients of severe COVID-19 pneumonia with hypoxia (PaO2/FiO2 less than 200) due to hyperinflammatory state, are warranted.

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Crizotinib, an orally active multi-targeted small-molecule anaplastic lymphoma kinase (ALK) inhibitor, is an effective treatment modality for advanced ALK-positive non-small-cell lung cancer (NSCLC). Most drug-related adverse events are mild to moderate; however, some patients may develop acute interstitial lung disease (ILD) which is sometimes fatal. We present a case of crizotinib-associated ILD in a 47-year-old woman treated with crizotinib for metastatic adenocarcinoma of the lung. The patient presented with acute breathlessness and hypoxaemia in the second month of crizotinib therapy; radiological and histopathological work-up was suggestive of acute interstitial pneumonia. The patient improved clinically with corticosteroid therapy and was successfully re-challenged with crizotinib. In conclusion, while treating NSCLC patients with crizotinib, it is important to promptly investigate and treat any new-onset respiratory symptoms, as the latter could represent an adverse effect related to therapy. Prompt discontinuation of the offending drug and initiation of corticosteroid therapy may prevent adverse outcomes.