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Coronary Slow Flow Phenomenon (CSFP) is characterized by the slow flow of contrast in one or more epicardial coronary vessels without evidence of coronary artery stenosis during coronary angiography procedures. CSFP is fairly common at the time of elective angiography with an incidence of around 7% and accounts for about 4% of hospitalized unstable angina cases. Coronary angiography is currently still the only effective way to detect CSFP, but this procedure is an invasive procedure with high costs, there is a risk of allergy to contrast. Electrocardiography (ECG), as a widely available, inexpensive, and simple modality is felt to be an attractive alternative in early detection of this abnormality. The ECG parameters on CSFP discussed in this study include; p-wave dispersion, QT interval dispersion, QRS intrinsic (Tpeak-Tenddeflection duration), and QRS fragmentation. Further studies are needed on the ECG image in CSFP so that in the future ECG can be a cheaper and non-invasive diagnostic modality for CSFP compared to coronary angiography.

Background. Acute kidney injury (AKI) is a common and serious medical condition associated with significant increases in morbidity, mortality, cost of care and non recovery of kidney function that leads to progression to chronic kidney disease. Cell cycle arrest is implicated in the pathogenesis and repair process following AKI. The urinary cell-cycle arrest markers tissue inhibitor of metalloproteinase-2 (TIMP-2) and insulin-like growth factor binding protein 7 (IGFBP-7) have been utilized to predict the risk of AKI in many studies from specific population with good performance. However, their use in predicting recovery is still lacking. The aim of this study was to determine the association between two novel AKI biomarkers, urinary TIMP2 and IGFBP7 and renal recovery after 7 days of treatment in AKI patients at Dr. Mohammad Hoesin Hospital Palembang. Method. This was a prospective cohort study conducted in dr. Mohammad Hoesin Hospital Palembang from January 2021 until March 2021. Subjects enrolled in this study were patients whom diagnosed AKI based on KDIGO 2012 criteria. Urine samples were collected upon patients’ enrollment within 24 hours of AKI diagnosis. We utilized Sandwich Enzyme Linked Immunosorbant Assay (ELISA) method to detect urinary TIMP-2 and IGFBP-7 levels. The primary outcome is recovery from AKI after 7 days of treatment. Chi square test is used to analyze the association between urinary TIMP-2 and IGFBP-7 levels and renal recovery. Results. There were 70 subjects, only 22 of them were recovered after 7 days (31%). Median of urinary TIMP-2 and IGFBP-7 was 0,0047(0,0001-0,1439) [(ng/ml)2/1000]. There was significant association between urinary TIMP2 and IGFBP7 and renal recovery (p=0,027; OR 3,19; 95% CI 1,116-9,128). Conclusion. There was significant association between urinary TIMP2 and IGFBP7 and renal recovery in AKI patients.

Background: Eclampsia and severe preeclampsia is of the most frequent cause of maternal death. We usually find the case like this in our daily practice. The case most likely could be prevented. Eclampsia defined as a generalized seizure following preeclampsia in pregnancy. Eclampsia/Preeclampsia (EPH-Gestosis) cause a multisystem dysfunction such as HELLP syndrome, microangiopathy hemolytic anemia, liver dysfunction, and thrombocytopenia. Eclampsia and HELLP syndrome lead to maternal mortality, which happened mostly during third trimester. Most of the patient came to the hospital in a bad condition where the multi organs failure were exist. EPH-Gestosis are due to maternal death in 43,75%. Even the case usually severe, it’s a preventable death. A proper strategy is needed to reduce or to avoid the maternal death.Objective: To analyse a maternal death with eclampsia and how to prevent this recurrent death.Case Report: A woman, 30 years old, G2P1A0 32 weeks pregnant not in labor with antepartum eclampsia was admitted to Mohammad Hoesin General Hospital (MHGH) Palembang, a referral case. Patient experienced generalized seizure six times before coming to MHGH which every seizure duration is less than five minutes and unconscious. On physical examination, patient was conscious, with blood pressure of 160/100 mmHg, pale, and cold extremities. By ultrasound examination, it showed 34 weeks pregnancy with single life fetus. Laboratory examination showed leukocytosis (25.000/mm3), thrombocytopenia (58.000/mm3), hyperbilirubinemia, elevated SGOT and SGPT (1691 and 861 U/L), elevated creatinine serum (2,46 mg/dl), and elevated LDH (3629 U/L). The patient was treated based on the protocol for stabilization with intramuscular injection of MgSO4 40%, nifedipin 10 mg per oral, intravenous injection of dexamethasone 12 mg, and plan to terminate the pregnancy by caesarean procedure. The male baby was born, 2000 g weight and APGAR score 4/6/8. After the cesarean the consciousness not so well. Collaborating therapy to handle the case, with the anesthesiologist, internist and neurologist. Maternal death occurred in 3 days hospitalized …caused by multi organ failure (MOF). Conclusion: The maternal death caused by antepartum eclampsia and the complication. The diagnosis of antepartum eclampsia and HELLP syndrome was decided based on history taking, physical examination, and supporting examination. Multiple organ failure exist in this case when the patient came to MHGH. Patient already treated and tried to overcome the complication but maternal death still occurred. This maternal death has a likely same story of previous death pattern. It is needed a strategy to prevent or to reduce the maternal death and how to make a good effort to cease the case become severe or worst.

A B S T R A C TAnemia contributes to increased morbidity and mortality in chronic kidney diseasepatients. The pathogenesis of anemia in these patients is multifactorial, but thecontribution of erythropoietin deficiency becomes greater as glomerular filtrationrate declines which related to decreased nephron mass. The current standard ofcare includes supplemental iron, erythropoiesis-stimulating agents (ESA), and redblood cell transfusions, although each has drawbacks. Lately, concern has arisenfollowing randomized clinical trials showing that higher hemoglobin targets and/orhigh ESA doses may cause significant harm including increasing cardiovascular andthrombotic events, and even death. Recent experimental and clinical studies showthe promising efficacy of hypoxia inducible factor (HIF) stabilizer which stimulatesendogenous erythropoietin production and enhance iron availability.

Chronic kidney disease (CKD) is associated with high mortality rates related to cardiovascular complications. Atherosclerosis, arteriosclerosis and vascular calcification conditions are often found in CKD patients. Carotid intima media thickness (cIMT) thickening is one of the parameters of vascular disorders. A cross sectional study was conducted on patients with chronic kidney disease in the hospital. Mohammad Hoesin Palembang. Patients' blood samples were examined in the hospital laboratory. CIMT thickening was examined using echocardiography. A total of 55 patients with stage 3-5 chronic kidney disease were examined. The median cIMT is 0.8 (0.6-1.45) mm. Spearman's correlation analysis showed a significant correlation between triglyceride levels and thickening of cIMT (r = 0.303, p = 0.025). A significant correlation was also shown between phosphate levels and cIMT thickening (r = 0.290, p = 0.032). There is a significant correlation of triglyceride levels and phosphate levels to cIMT thickening in patients with chronic kidney disease in Palembang

BACKGROUND: The coronary slow flow phenomenon (CSFP) is believed to be affected by endothelial dysfunction ruled by renin, angiotensin, aldosterone, and the angiotensin-converting enzyme (ACE). The gene of ACE has been characterized in humans by a major insertion (I)/deletion (D) polymorphism. Serum ACE levels were associated with I/D polymorphism in the ACE-encoding gene. AIM: This study explored and analyzed the role of ACE gene polymorphism risk factors with the incidence of CSFP in the population of South Sumatra, Indonesia. METHODS: This study was a cross-sectional analytic observational study. A total of 112 CSFP and non- CSFP patients participated in this study. Blood was obtained from the study subjects then processed. Angiotensin I and aldosterone levels were examined using the enzyme-linked immunosorbent assay. The Judkins method was used in the assessment of coronary angiography, which was carried out through the femoral artery. For the examination of ACE I/D polymorphisms, genome deoxyribonucleic acid was extracted from blood cells (leukocytes), using the Wizard’s purification system and examined using the polymerase chain reaction method. All data were evaluated through the Chi-square test, two samples t-test, and Mann–Whitney U-test. All tests used two-sided significance and p < 0.05 was considered statistically significant. RESULTS: ACE I/D gene polymorphism possessed a significant effect in increasing the risk of CSFP. Genotype II polymorphism increased the risk of CSFP as much as 6.9 times compared to individuals with ID/DD genotype. The existence of allele I increased the risk of CSFP 5.7 times compared to allele D. Levels of angiotensin I and aldosterone were increased significantly in patients with CSFP. CONCLUSION: ACE I/D gene polymorphism possessed a significant effect in increasing the risk of CSFP. Genotype of II was the risk factor for the development of CSFP in population of South Sumatra, Indonesia.

Introduction. Chronic kidney disease (CKD) is associated with high mortality rates, mainly as a result of cardiovascular complications. Meanwhile, recent studies have suggested a role of a homodimer protein called activin A in chronic kidney disease-mineral and bone disorder (CKD-MBD) conditions that may exist in the vascular calcification and osteolytic process. Ultrasound examination of the carotid intima-media thickness (cIMT) is a noninvasive method to assess vascular calcification. This study aimed to analyze the relationship between the activin A serum level and cIMT in patients with CKD at Mohammad Hoesin Hospital, Palembang, Indonesia. Methods. We conducted a hospital-based, cross-sectional study of consecutive CKD patients at the Department of Internal Medicine, Mohammad Hoesin Hospital, from July to November 2019. The level of activin A was measured by enzyme-linked immunosorbent assay. Meanwhile, cIMT measurements were collected by B-mode ultrasound imaging. Results. A total of 55 patients with CKD were included in this investigation. The median serum activin A level in these patients was 236.17 (116.33–283) pg/mL, while the median cIMT was 0.8 (0.6–1.45) mm. A relationship between the serum activin A level and cIMT (r = 0.449; p = 0.001 ) was observed. During multivariate analysis with linear regression, triglyceride p = 0.049 , phosphate p = 0.005 , and activin A p = 0.020 serum levels were factors associated with cIMT. Conclusion. In this study, a relationship between the activin A serum level and cIMT in patients with CKD was identified. Vascular calcification should be screened for in all CKD patients by the measurement of cIMT.