Zulkhair Ali
Division of Nephrology and Hypertension, Department of Internal Medicine, Faculty of Medicine, Universitas Sriwijaya/Dr. Mohammad Hoesin General Hospital, Palembang, Indonesia

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Recent Evidence on Acute Kidney Injury in COVID-19 Patients: A Narrative Review Herleni Kartika; Novadian Suhaimi; Zulkhair Ali; Suprapti; Ian Effendi; Harun Hudari; Mega Permata; Nelda Aprilia Salim; Eddy Yuristo
Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 6 No. 10 (2022): Bioscientia Medicina: Journal of Biomedicine & Translational Research
Publisher : HM Publisher

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.37275/bsm.v6i10.599

Abstract

The pandemic of coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). The clinical manifestation of COVID-19 is broad, ranging from an asymptomatic carrier state to severe disease leading to the death penalty. There is also emerging evidence that kidneys are affected early in COVID-19. Proteinuria and haematuria have been reported in 44% and 26.7% on admission, respectively. This literature review shows clinical manifestations of acute kidney injury (AKI) in a patient with COVID-19 infection. Literature reviews are carried out on various sources found on Google Scholar and Pubmed to search for articles, journal research, case reports, systematic reviews, meta-analyses, and textbooks. Various studies demonstrate the possibility of coronavirus infecting the kidney with several mechanisms such as cytokine storm syndrome (CSS), direct viral infection, and imbalance of renin-angiotensin-aldosterone (RAAS). Haematuria and proteinuria are associated with higher mortality and may signify aggressive disease early. Thus all patients should have a baseline urinalysis. There is a number of different causes of AKI in COVID-19, and some mechanisms by which COVID-19 affects kidneys remain unclear.
Recent Evidence on Acute Kidney Injury in COVID-19 Patients: A Narrative Review Herleni Kartika; Novadian Suhaimi; Zulkhair Ali; Suprapti; Ian Effendi; Harun Hudari; Mega Permata; Nelda Aprilia Salim; Eddy Yuristo
Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 6 No. 10 (2022): Bioscientia Medicina: Journal of Biomedicine & Translational Research
Publisher : HM Publisher

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.37275/bsm.v6i10.599

Abstract

The pandemic of coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). The clinical manifestation of COVID-19 is broad, ranging from an asymptomatic carrier state to severe disease leading to the death penalty. There is also emerging evidence that kidneys are affected early in COVID-19. Proteinuria and haematuria have been reported in 44% and 26.7% on admission, respectively. This literature review shows clinical manifestations of acute kidney injury (AKI) in a patient with COVID-19 infection. Literature reviews are carried out on various sources found on Google Scholar and Pubmed to search for articles, journal research, case reports, systematic reviews, meta-analyses, and textbooks. Various studies demonstrate the possibility of coronavirus infecting the kidney with several mechanisms such as cytokine storm syndrome (CSS), direct viral infection, and imbalance of renin-angiotensin-aldosterone (RAAS). Haematuria and proteinuria are associated with higher mortality and may signify aggressive disease early. Thus all patients should have a baseline urinalysis. There is a number of different causes of AKI in COVID-19, and some mechanisms by which COVID-19 affects kidneys remain unclear.
Renal Amyloidosis: A Narrative Literature Review Syahpri Putra Wangsa; Novadian Suhaimi; Zulkhair Ali; Suprapti Slamet; Ian Effendi; Kgs M Yusuf Arief Akbar; Deddy Primadona Mulia
Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 7 No. 11 (2023): Bioscientia Medicina: Journal of Biomedicine & Translational Research
Publisher : HM Publisher

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.37275/bsm.v7i11.889

Abstract

Amyloidosis is a disorder in which soluble proteins aggregate and are deposited extracellularly in tissues as insoluble fibrils, causing progressive organ dysfunction. Amyloid fibril formation begins with misfolding of amyloidogenic precursor proteins. The fibrils have a characteristic appearance by electron microscopy and produce double refraction under polarized light when stained with Congo red dye. Classification of amyloidosis is based on the precursor proteins that form amyloid fibrils and the distribution of amyloid deposition both systemically and locally. The main form of systemic amyloidosis; AL amyloid, AA amyloidosis, ATTR amyloid. The kidney is the organ most frequently involved in systemic amyloidosis. Systemic amyloidosis may originate from anomalous proteins, such as immunoglobulin light chains or serum amyloid protein in chronic inflammation or may arise from hereditary disorders. The clinical manifestations of renal amyloidosis vary with the type of amyloid protein and the location and extent of amyloid deposition. Treatment of amyloidosis should be a two-part process; managing symptoms and reducing or stabilizing amyloid protein. Treatment of amyloidosis is focused on reducing the production of amyloidogenic proteins and inhibiting their aggregation.
Diurnal Variation of Blood Pressure and Arterial Stiffness in Chronic Kidney Disease Kgs M Yusuf Arief Akbar; Novadian Suhaimi; Zulkhair Ali; Suprapti Slamet; Ian Effendi; Syahpri Putra Wangsa; Deddy Primadona Mulia
Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 7 No. 11 (2023): Bioscientia Medicina: Journal of Biomedicine & Translational Research
Publisher : HM Publisher

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.37275/bsm.v7i11.890

Abstract

Hypertension and chronic kidney disease (CKD) are interrelated public health problems throughout the world. Hypertension accompanied by CKD is mostly difficult to control. Difficulty in controlling blood pressure (BP) is known from changes in the diurnal variation of BP over 24 hours in CKD patients with a pattern of non-dipping and reverse dipping at night and an increase in pulse pressure due to arterial stiffness that occurs in CKD, resulting in a high incidence of nocturnal hypertension and masked hypertension. Nocturnal hypertension in CKD has a significant prognostic risk of increased risk of cardiovascular disease and cause of death. Therefore, guidelines for the management of hypertension strongly recommend that patients with hypertension have blood pressure well controlled at all times, especially to improve hypertension control at night in CKD patients.
The Role of Podocyte Cells in Diabetic Nephropathy: A Narrative Literature Review Fauzan Azhari; Novadian; Ian Effendi; Zulkhair Ali; Suprapti; Ratna Maila Dewi Anggraini; Yulianto Kusnadi; Alwi Shahab
Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 7 No. 12 (2023): Bioscientia Medicina: Journal of Biomedicine & Translational Research
Publisher : HM Publisher

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.37275/bsm.v7i12.893

Abstract

The main cells affected in diabetic nephropathy are podocytes and proximal tubular cells. One of the main functional proteins in the podocyte slit diaphragm is podocin which podocytes need to express together with several specific proteins in the correct way for their differentiation, as well as to maintain their complex anatomy. Podocytes are highly specialized epithelial cells. They line the urinary surface of the glomerular capillary bundles. Podocytes are part of the filtration barrier along with capillary endothelial cells and GBM. Podocytes ensure selective permeability of the glomerular capillary walls. Podocin is a membrane protein with a molecular weight of 42kD which is located in the foot processes, and also forms part of the SD with the nephrin protein. Urinary podocin levels more specifically indicate ongoing glomerular damage because they were significantly increased in the normoalbuminuria group compared with the control group.