Cardiovascular disease (CVD) is a major cause of morbidity and mortality in chronic kidney disease (CKD) patients. This study aimed to determine the roles of CVD biomarkers in CKD patients. This was a case-control study which recruited consecutive patients with stage 2-4 CKD patients with and without CVD. Serum levels of highly-sensitive C reactive protein (hs-CRP), cystatin C (CysC), asymmetrical dimetylarginine (ADMA) and symmetrical dimethylarginine (SDMA) were measured. Sixty two stage 2-4 CKD patients with a mean age of 60.3 ± 10.4 years were recruited. Twenty three (37.1%) of them had CVD. Those CKD patients with CVD were older (64.1±8.0 vs 58.1± 1.1, p<0.05) and had significantly higher systolic blood pressure (139.4 ± 16.2 vs 129.4 ± 14.8 mmHg, p<0.05). Diabetic patients had 8 times (95% CI 1.25-51.77, p< 0.05) higher risk to develop CVD. CKD patients with CVD had a higher serum creatinine (185.0 ± 54.1 vs 154.1 ± 54.4 μmol/L, p<0.05), a lower estimated glomerular filtration rate (33.7 ± 12.2 vs 42.2 ± 14.5 mL/min/1.73m2 p<0.05) and a lower triglyceride levels (1.3 (1.1-1.7) vs 1.8 (1.4-2.3) mmol/L, p<0.05), compared to those without CVD. Fasting blood sugar was 7.1 ± 2.7 mmol/L in CVD group and 6.3 ± 1.6 mmol/L in non CVD group (p>0.05). There were no differences in their mean serum levels of hs-CRP, CysC, ADMA and SDMA. Risk factors including age, diabetes mellitus, hypertension and renal functions were still the most important CVD risk factors in CKD patients.
Acinetobacter baumannii is an aerobic Gram-negative coccobacillus that is associated with hospital acquired pneumonia. There is increased reporting of emergent cases of community acquired multidrug resistance (MDR) acinetobacter associated with a higher mortality due to antibiotic resistance. Community acquired MDR acinetobacter pneumonia has not been reported in Malaysia. Here we report a case of a 19-year-old army officer who presented with fever and respiratory symptoms for 5 days. He had no known medical illness before and no history of hospitalization. Upon arrival, he was in septicaemic shock, requiring invasive ventilator support and renal replacement therapy in intensive care unit. Chest radiograph showed bilateral lung consolidations and bronchoscopy revealed haemoserous and greenish bronchiole secretion. He was treated with broad spectrum antibiotics and oseltamivir. Unfortunately he died on day 3 of hospital admission. His bronchial lavage culture came back positive for MDR Acinetobacter baumannii. This case illustrates that clinicians need to be aware that MDR Acinetobacter baumannii can cause severe community acquired pneumonia. We may need to consider this diagnosis in patients who do not respond to standard therapy.
A 54 year old lady with underlying chronic lung disease on long term oxygen therapy and end stage renal disease of unknown aetiology on regular haemodialysis for two years started developing progressive shortness of breath during her routine haemodialysis. She was unable to tolerate her haemodialysis sessions which had to be terminated prematurely in view of her symptoms despite adjustment of her dry weight and treatment of anaemia. She was not in chronic fluid overload and her symptoms always worsened after initiation of haemodialysis and improved after termination of haemodialysis. She was admitted to hospital for further investigations and initially treated for a lung infection but her symptoms did not improve. A computed tomography pulmonary angiography did not reveal any evidence of pulmonary embolism, and was consistent with chronic fibrotic changes. Her hypoxemia was concluded to be due to her underlying chronic lung disease, worsened by alveolar hypoventilation during haemodialysis. Her symptoms improved slightly with supplemental oxygen during her routine haemodialysis but we had to shorten her haemodialysis duration to 3 hours.
Introduction: Hyperuricemia is associated with chronic kidney disease (CKD) progression and poor cardiovascular outcomes. We studied the effect of febuxostat on estimated glomerular filtration rate (eGFR), proteinuria and monitored the safety profile of the medication.
Material and Methods: This is a prospective open-label, randomized study in CKD stage 3 and 4 patients with diabetic nephropathy and asymptomatic hyperuricemia. Patients were randomized into febuxostat 40 mg daily and no treatment group using block randomization method and were followed up for 6 months. Their usual care for diabetes mellitus, hypertension and dyslipidemia were continued in the study. Blood and urine investigations were monitored at baseline, 3 months and 6 months.
Results: The eGFR in febuxostat group was stabilized at 6 months with no significant reduction [26.2 (IQR 14.30) at baseline to 26.3 (IQR 15.2) ml/min/1.73 m2]. Whereas, there was a significant reduction of the eGFR in no treatment group from 28.2 (IQR 17.9) to 27.6 (IQR 19.3) ml/min/1.73 m2 (p value < 0.01). We found the HbA1c (glycosylated hemoglobin) was significantly increased in febuxostat group from 7.2 ± 0.5 % at baseline to 7.6 ± 1.4 at 6 months (p value 0.04) but no significant change of HbA1c in the no treatment group. Proteinuria level was unchanged in both groups. The commonest adverse event was joint pain.
Conclusions: Febuxostat was able to preserve eGFR in CKD patients with diabetic nephropathy and this effect was beyond glycemic control. Increment of HbA1c level in febuxostat group needs further larger trials.
Study site: Chronic kidney disease clinic, Hospital Canselor Tuanku Muhriz, Pusat Perubatan Universiti Kebangsaan Malaysia (PPUKM), Kuala Lumpur, Malaysia