The new coronavirus infection / disease 2019 (COVID-19) has become a global world health pandemic disease which has been regarded a health emergency in every country. COVID-19 infection has predominantly affected individuals whose ages have ranged between 30 years and 79 years old and out of these infections it has been documented that about 81% of the COVID-19 infection cases had been considered to be mild disease. Even though majority of individuals who develop COVID-19 infection do manifest with symptoms and signs that simulate the common cold, COVID-19 infection has also emanated in the development of alveolar damage which has been ensued by the development of alveolar damage which has resulted in the development of progressive respiratory failure in which fatalities had resulted in in 6.4% of the COVID-19 infection cases. The COVID-19 infection cases. It has been iterated that direct viral injury, uncontrolled inflammation, activation of coagulation, as well as complement cascades are conjectured to form part of the pathogenesis of COVID-19 infection. COVID-19 infection does affect not only the respiratory tract but it does also affect various organs of the body including the kidney. Individual patients who have been affected by COVID-19 infection have developed features of kidney damage through acute kidney injury, and they tend to manifest with mild proteinuria, haematuria, or slightly raised serum levels of creatinine which has been considered to have ensued from kidney tropism of the virus as well as from multi-organ failure. The impact of COVID-19 infection upon patients who have already pre-existing renal impairment, with the inclusion of individuals who already have chronic kidney disease (CKD), renal transplant recipients, as well as individuals who are undergoing haemodialysis (HD) have not yet been fully studied. Nevertheless, it could be envisaged that individuals have already been having some form of kidney disease could have more severe impairment of renal function and they would need renal support.  There is no consensus opinion most effective specific treatment options for COVID-19 infection in general and infection of the kidney yet to be ratified. Results of research studies had documented many agents which might be potential efficacious against COVID-19 infection, and many of these molecules have depicted preliminary efficacy against COVID-19 infection and they are at the moment being tested in clinical trials. It is important to check the renal function of all COVID-19 infected patients who do not have pre-existing renal disease as well as those who already have known renal disease so that based upon the results of the initial renal function test results and follow-up renal function results, clinicians can plan effective renal support management for all patients including rehydration and avoidance of renal toxic medicaments. 

It has been iterated that the coronavirus disease (COVID-19) outbreak had resulted in swift efforts to learn about the clinical course, prognostic markers, and complications of coronavirus disease and that as a consequence there has been a lot of scattered information available relating to severe acute respiratory syndrome coronavirus-2 infection; nevertheless, its pathophysiology has been poorly understood virus [1]. It has also been stated that macroscopic and microscopic findings of COVID-19 infected organs are pertinent for the understanding of any disease, including COVID-19 infection [1]. It has been documented that in the large number of original studies that are available to be read and studied on COVID-19 infection, it could be difficult to ascertain a full picture of the effect of COVID-19 infection has upon the body as a whole, in view of the fact that many studies had reported conflicting results [1]. The ensuing article on COVID-19 infection in general and in association with acute kidney injury (AKI) which has been divided into two parts: (A) Overview of COVID-19 infection generally and (B) Miscellaneous narrations and discussions related to some case reports, case series and studies related to COVID-19 infection kidney injury. 

Internet data bases were searched including: Google, Google Scholar, Yahoo, and PUBMED. Search words that were used included: COVID-19 infection, Coronavirus infection, and COVID-19 infection of kidney, COVID-19 Renal infection, Acute Kidney Injury in COVID-19 infection, renal failure in covid-19 infection, and kidney failure in coronavirus infection. Two hundred and thirty nine (239) references were identified which were used in writing the review and update of the literature on COVID-19 infection in general and in association with acute kidney injury (AKI) which has been divided into two parts: (A) Overview of COVID-19 infection generally and (B) Miscellaneous narrations and discussions related to some case reports, case series and studies related to COVID-19 infection kidney injury.   

[(A)] Overview 

Definition / general statements 

Some of the summations made related to the definition and some general aspects of COVID-19 infection include the following: [2] 

1. Coronavirus disease 2019 (COVID-19) is a terminology that is utilized for an infectious respiratory disease which is caused by novel coronavirus SARS-CoV-2 which had emerged in Wuhan, China at the end of 2019, emanating in a global pandemic

2. Infection control guidance for healthcare professionals have been made related to COVI-19 infection and could be found as follows:

                CDC [3] 
                Personal protective equipment (PPE) basics [4]

3. COVID-19 represents a viral infection which is caused by coronavirus SARS-CoV-2 which can progress to severe acute respiratory syndrome with pneumonia and acute respiratory distress syndrome [2]
4. COVID-19 infection did spread rapidly and became a pandemic with more than 100 million confirmed cases of CIVID-19 infection and over 2 million deaths related to COVID-19 infection globally by end of January 2021 [2]
5. Histologically, COVID-19 does show upon microscopy examination of the infected tissue of the lung in cases of COVID-19 infection of the lung diffuse alveolar damage corresponding to the phase of the disease  ranging from the acute to the fibrotic phase that is, divided into 3 main injury patterns: epithelial, vascular and fibrotic [2]
6. A  definite diagnosis of CIVID-19 infection tends to be based upon the detection of viral RNA by RT-PCR [2]

Terminology

•  It has been iterated that COVID-19 is also referred to as novel coronavirus pneumonia [2] 
• It has additionally been iterated that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is also referred to as 2019 novel coronavirus (2019-nCoV) [2] [pathologyoutlines.co]
• It is important to know that COVID-19 infection does affect various organs of the body and not the lung alone. [2] 

Epidemiology of COVID-19 in General 

• COVID-19 pandemic [2] 
  • It has been iterated that in December 2019, cases of pneumonia that were associated with unknown aetiology had been reported from Wuhan, Hubei Province, China to WHO [2] [5] 
  • It has also been documented that in January 2020, the Chinese authorities had identified a novel type of coronavirus, which was subsequently named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) [2] 
  • It has been reported that at the beginning of February 2020, almost 10,000 cases of COVID-19 were confirmed in China and more than 100 cases of COVID-19 infection had been identified outside of China  [2, 6] 
  • It has been iterated that the COIVID-19 disease did spread rapidly and that it became a pandemic with more than 100 million confirmed cases and over 2 million deaths globally by end of January 2021 [2] 
  • It has been iterated that the United States of America now has the most confirmed cases of COVID-19 infection with more than 25 million reported cases and confirmed deaths that amounted to more than 400,000 throughout the world.  [2, 7]
• Person to person transmission of COVID-19 infection is suspected to occur through respiratory droplets including coughing and sneezing. [2] 
• The key to slowing the spread of COVID-19 infection is through widespread testing for COVID-19 infection so that patients could be quickly identified and isolated from the public. [2] 
• More than 120 SARS-CoV-2 vaccines are under development [8]

Sites affected by COVID-19 infection

• It has been iterated that the upper respiratory tract tends to be affected by COVID-19 infection  in mild disease of the respiratory tract [2] 
• It has also been iterated that bilateral lobes of the lung tend to be affected in more severe COVID-19 disease [2] 
• It is important to note that COVID-19 infection does affect various organs of the body including the kidney and the urinary tract [2]. 

Pathophysiology

• It has been iterated that with regard to the pathophysiology of COVID-19 infection a spike surface glycoprotein of the virus does bind onto the host through receptor binding domains of the angiotensin converting enzyme 2 (ACE2), that is most abundant in type II alveolar cells [2] [9] 
  • In COVID-19 infection there tends to be10 times to 20 times higher binding affinity in comparison with the SARS-CoV-1 virus [2] [10] 
• It has been explained that after a SARS-CoV-2 has attached to a target cell, the virion does release RNA into the cell, that initiates replication of the virus which then further disseminates to infect more cells [2] [11] 
• It has been documented that SARS-CoV-2 does produce many virulence factors which promote shedding of new virions from host cells as well as inhibit immune response [2] 
• It has been iterated that there tends to be virus independent immunopathology in fatal COVID-19  [2] [12]
  • It has been documented that organ injury and death in COVID-19 tends to be immune mediated rather than pathogen mediated [2] 
  • It has also been stated that tissue inflammation as well as organ dysfunction in fatal COVID-19 do not correlate with the tissue and cellular distribution of SARS-CoV-2 [2] 

Aetiology

•  It has been iterated that in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a positive sense, single stranded RNA virus having close genetic similarity to bat coronaviruses tends to be found. [2] [13] 

Clinical features of COVID-19 in general

• It has been iterated that the average time from exposure COVID-19 to the onset of symptom is 5 days [2] [14] 
  • It has also been stated that 97.5% of people who develop symptoms related to COVID-19 infection do so within 11.5 days [2] [8] 
• It has been iterated that the asymptomatic COVID-19 infection rate 46% [2] [15] 
• It has been documented that COVID-19 infection is rare in children, and this does amount to about 2% to 5% of confirmed cases of COVID-19 infection and children tend to have milder symptoms and very low hospitalization rate of less than 7%  [2] [8]
• It has been iterated that the common symptoms of COVID-19 infection in hospitalized patients do include the following: [2] [8]
  • Fever in 70% to 90% of cases
  • Dry cough in 60% to 86% of cases
  • Shortness of breath in 53% to 80% of cases
  • Fatigue in 38% of cases
  • Myalgias in15% to 44% of cases
  • Nausea / vomiting or diarrhoea in15% to 39% of cases
  • Headache, weakness in 25% of cases
• It has been iterated that patients who have COVID-19 infection could manifest with nonclassical symptoms [2] [8] which could include:
  • Isolated gastrointestinal symptoms
  • Isolated anosmia or ageusia in 3% of cases
• It has been iterated that COVID-19 infection could emanate in progress to severe acute respiratory syndrome as well as its major clinicopathological phenotypes that include pneumonia and acute respiratory syndrome. [2] 
  • The distribution of severity of COVID-19 infection has been summated as follows: [2] [16] :
    • Mild or no disease in 81% of cases
    • Severe disease in 14% of cases
    • Critical disease in 5% of cases
    • Overall case fatality rate in 2.3% of cases
  • It has been documented that 20% to 42% of hospitalized patients who had COVID-19 infection developed acute respiratory distress syndrome [2] [17] [18] 
• It has been reported that patients who required intensive care support (ICU) supportive care had manifested with acute respiratory distress syndrome, acute cardiac injury, acute kidney injury and shock as well as up to 15% of them had fatal outcomes [2] [19] 
• The documented common complications that ensued COVID-19 infection among hospitalized patients were summarized as follows: [2]  [8] 
  • Pneumonia in 75% of cases
  • Acute respiratory distress syndrome in15% of cases
  • Acute liver injury in19% of cases
  • Cardiac injury in 7% to 17% of cases with troponin elevation, acute heart failure, dysrhythmias, myocarditis [2] [8] 
  • Prothrombotic coagulopathy resulting in venous and arterial thromboembolic events in10% to 25% of cases
  • Acute kidney injury in 9% of cases
  • Acute cerebrovascular disease in 3% of cases
  • Shock in 6% of cases
• It has additionally been iterated that a rare multi-system inflammatory syndrome which is similar to Kawasaki disease has recently been described in children which amounted to 2 cases per 100,000 persons aged who were less 21 years old. [2] [8] 

Diagnosis

Summations related to diagnostic testing of SARS-CoV-2 (COVID-19) that have been documented include: [2] 

It has been iterated that nasopharyngeal swab has been recommended for the specimen; oropharyngeal swab, sputum and bronchoalveolar lavage could be utilized alternatively [2] [20] 

• It was stated that positive rates of SARS-CoV-2 PCR testing by specimen types were reported as follows: bronchoalveolar lavage fluid 93%, sputum 72%, nasal swabs 63%, pharyngeal swabs 32% [8] 
• Definite diagnosis of COVID-19 infection is based upon the detection of viral RNA by real time RT-PCR through many available laboratory tests. [21] [22] 
• False negative COVID-19 test results could occur in up to 20% to 67% of patients depending upon the quality and timing of testing
  • A modelling study had estimated sensitivity at 33Mays pursuant to exposure, 62% on the day of the onset of the symptom and 80=ays pursuant to the onset of symptom [23]

Laboratory test results in COVID-19 infection 

• Summations related to routine haematology and biochemistry blood test meta-analysis data of patients who have COVID-19 infection do include: [2] [19] 
  • Evidence of decreased albumin
  • Evidence of high C reactive protein level
  • Evidence of high lactate dehydrogenase (LDH) level
  • Evidence of lymphopenia
  • Evidence of high erythrocyte sedimentation rate (ESR)
• D dimer elevation was also reported in COVID-19 infection [2] [10]

Radiology imaging description of chest imaging in COVID 19 pulmonary infected patients [2] 

• It has been iterated that chest radiographs of individuals who have COVID-19 infection of the lungs do demonstrate Ground glass opacities, crazy paving pattern and consolidation in bilateral lobes which tend to be common findings [2] [24] 
• It has been documented that in individuals who have COVID-19 infection of the lungs,15% of computed tomography (CT) scans of the thorax and 40% of chest radiograph findings tend to demonstrate normal features early in the disease [2]  [8]
• It has been iterated that evolution of abnormalities within the pulmonary system does occur within the first 2 weeks pursuant to the onset of COVID-19 infection. [2]

Factors of prognostication in COVID-19 pulmonary infection

Some of the risk-factors associated with COVID-19 pulmonary infections have been summated as follows; [2] 

• Risks for the development of acute respiratory syndrome do include an age greater than 65 years, underlying diseases including diabetes mellitus, as well as secondary infection. [2] [17], [25] 
• Risk factors for progression of COVID-19 infection / disease do include: male sex, old age of being older than 65 years of age, as well as smoking [2] [26] 
• Risk factors for critical / mortal states of COVID-19 infection, in order of strength of association have been summated to include: [2] [27]
  • Cardiovascular disease
  • Respiratory disease
  • Diabetes mellitus
  • Hypertension

Treatment of COVID-19 pulmonary infection [2] 

• It has been iterated that home management is recommended for patients who have mild COVID-19 infection symptoms
  • It has been stated that the optimal duration of home isolation is under investigation but the COVID-19 virus is shed for an average of about 20 days after the commencement of the COVID-19 infection in hospitalized patients [2] [27].
• It has been advised that patients who have severe COVID-19 disease should require hospital care
  • It has been iterated that patients who have severe COVID-19 disease may need oxygenation support, ranging from low dose oxygen supplement to invasive ventilation as well as extracorporeal membrane oxygenation (ECMO) [2].
• It has been iterated that among antiviral medicaments including ribavirin, favipiravir, and remdesivir which are undergoing clinical testing, remdesivir does seem to be most promising [2, 8].

It has been iterated that NIH COVID-19 Treatment Guidelines Panel has recommended utilization of dexamethasone in patients on ventilators and in those who do require supplemental oxygen but not in other COVID-19 infected patients [27-29]

Macroscopic examination features of COVID-19 pulmonary infected lung. 

It has been iterated that gross examination of the lung of individuals who are infected with pulmonary COVID-19 tend to demonstrate the ensuing features: [2] 

• Gross examination of the lung of individuals who have pulmonary COVID-19 infection does various features from pulmonary oedema to consolidation of the lung [2] [30]
• Gross examination of COVID-19 infected lung does demonstrate increased lung weight [2]
• Macroscopic examination of the lung of patients who have COVID-19 pulmonary infection does show haemorrhagic changes within the lung [2] [31]
• Gross examination of the lung of individuals who have COVID-19 pulmonary infection does demonstrate evidence of macroscopic pulmonary emboli [2] [31] 
• Macroscopy examination of lungs of individuals who have pulmonary COVID-12 infection may demonstrate evidence of pleurisy in which features of pleural inflammation may be seen [2]
• In cases of COVID-19 infection of the lung that is associated with superimposed secondary infection, there would be evidence of purulent inflammation. [2]

Microscopy examination features of COVID-19 infected lung

It has been iterated that pulmonary changes tend to be the most significant finding in COVID-19 pulmonary disease, even though the features are nonspecific [2, 32-35] 

• It has been documented that the findings of diffuse alveolar damage (DAD) that correspond to the phase of COVID-19 infection disease tend to be seen upon microscopy examination as follows:
  • In the exudative phase of COVID-19 pulmonary disease, microscopy examination of the lung does demonstrate hyaline membrane formation, desquamation of pneumocytes, cellular or proteinaceous exudates, alveolar haemorrhage, fibrinoid necrosis of small vessels [34] [35]
  • In the organizing phase of COVID-19 pulmonary infection, microscopy examination of the lung does demonstrate interstitial and intra-alveolar proliferation of fibroblasts, lymphocytic infiltration, type II pneumocyte hyperplasia, as well as fibrin deposition
  • In the fibrotic phase of COVID-19 pulmonary infection, microscopy examination of the lung does show dense collagenous fibrosis, and architectural remodelling [34, 35]
  • Lung injury patterns in COVID-19 disease [2] [31] [36]:

Lung injury patterns of COVID-19 disease include: 

• Epithelial pattern in 85% of cases in which DAD with varying degrees of organization, denudation, hyperplasia of pneumocytes are seen
• Vascular pattern of COVID-19 disease in 59% of cases in which can be found diffuse intra-alveolar fibrin, microvascular damage, (micro) thrombi, acute fibrinous as well as organizing pneumonia
• Fibrotic pattern of COVID-19 disease in 22% of cases in which can be found: fibrotic DAD, and interstitial fibrosis
  • Viral infection changes:
    • Multinucleated enlarged pneumocytes with large nuclei, amphophilic cytoplasm and prominent nucleoli in alveolar spaces
    • Intranuclear inclusions
  • Bacterial pneumonia may be superimposed upon the COVID-19 pulmonary disease
• Extra-pulmonary COVID-19 infection changes [2] [31]
  • Cardiovascular COVID-19 infection changes that tend to be visualized upon microscopy examination does include: mild pericardial oedema, some serosanguinous pericardial effusion, mild myocardial oedema, low grade interstitial infiltration of mononuclear cells, as well as endotheliitis
    • It has been iterated that widespread systemic vasculitis that is with associated thrombo-emboli tends not to bet as common as was initially thought [2] [37]
  • Hepatobiliary COVID-19 infection changes that tend to be visualized include: hepatic congestion, mild steatosis, patchy hepatic necrosis, Kupffer cell hyperplasia, increased number of lymphocyte predominant inflammatory cells in the portal tracts and sinusoids, as well as endotheliitis [2]
  • Renal COVID-19 infection changes that tend to be visualized do include: various degrees of acute tubular injury, lymphocytic tubule interstitial infiltration, fibrin or hyaline thrombi in blood vessel, glomerular capillary dilatation, as well as lymphocytic endotheliitis [2] [38]
  • Gastrointestinal COVID-19 changes that tend to be visualized include: epithelial damage, prominent endotheliitis, as well as ischemic enterocolitis [2]
  • Spleen COVID-19 changes that tend to be seen include: reduced number of lymphocytes with necrosis, atrophy, congestion, haemorrhage, as well as infarction [2]
  • Bone marrow COVID-19 infection changes that tend to be seen include: histiocytic hyperplasia, as well as hemophagocytosis [2] [39]
  • Other COVID-19 infection changes that tend to be found include: cutaneous manifestations, prostatic manifestations, inflammation as well as clots in placenta with funisitis [2]

Cytology examination features of COVID-19 infection of the lung

• It has been iterated that cytology examination of bronchoalveolar lavage (BAL) in COVID-19 infection of the lung does show the following: [2]
  • Abundant activated plasma cells, as per a single case report [2] [40]
  • Alveolar macrophages could feature nuclear clearing or intranuclear cytopathic inclusions [2]

Immunohistochemistry Positive stains

• It has been iterated that immunohistochemistry (IHC) positive staining for SARS-CoV-2 antigen was detected in pneumocytes, ciliated airway cells as well as upper airway epithelium in the acute phase [2] [41]

Electron microscopy examination features of COVID-19 pulmonary disease specimen. 

It has been iterated that electron microscopy examination of COVID-19 infection pulmonary tissue does demonstrate the following: [2]

• Spherical particles that are sized 60 mm to 140 nm [2]
• Distinctive spikes upon the surface that measure 9 nm to 12 nm which give virions the appearance of a solar corona, that is consistent with the Coronaviridae family [2]
• Inclusion bodies that are filled with virus particles in membrane bound vesicles in cytoplasm of the respiratory epithelium [2] [42]

Molecular / cytogenetics description features of COVID-19 infection patients

• It has been iterated that ISH, including RISH and FISH positive testing for SARS-CoV-2 antigen tend to be detected in pneumocytes, ciliated airway cells as well as upper airway epithelium in the acute phase [2] [43] [44]
• It has been iterated that sample post-mortem examination pathology reports of COVID-19 infection usually tend to reveal the following: [2]
• Diffuse alveolar damage due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection
• Diffuse alveolar damage with changes that are       compatible with viral infection

Differential diagnoses

Some of the documented differential diagnoses of COVID-19 pulmonary disease include the following: [2]

• Diffuse alveolar damage due to COVID-19 is stated to be morphologically indistinguishable from other DAD causes [45], including other viral pneumonias: cytomegalovirus, respiratory syncytial virus as well as herpes simplex virus.
• Severe acute respiration distress syndrome in which detection of SARS virus needs to be undertaken to confirm the diagnosis.[2]
• Acute respiratory distress syndrome of other aetiological causes [2]
• Idiopathic acute interstitial pneumonia. [2]

Epidemiology of Acute Kidney Injury in COVID-19 Infection

• It has been iterated that there is increasing evidence to demonstrate that there is a high prevalence of acute kidney injury (AKI) in COVID-19 patients [46] [47] [48]
• It has been documented that the presentations of acute kidney injury are many and they do tend to include: proteinuria, haematuria, raised serum levels of serum creatinine (SCR), or blood urea nitrogen (BUN), to acute renal failure. [46] 
• It has been intimated that a metanalysis of data related to COVID-19 infected patients had shown that more than half of the patients that constituted fifty seven percent (57%) of the patients who had COVID-19 infection had developed proteinuria, which was followed by raised serum levels of serum creatinine (Scr) that ranged between 9.6% and 15.5% and blood urea nitrogen (BUN) levels that ranged between 13.7% and 14.1% [46] [47] [49] 
•  It has been stated that computed tomography (CT) that is undertaken in cases of cases of COVID-19 infection with kidney injury also demonstrates inflammation of kidney as well as oedema of kidney. [46] [50]
• It has been documented that pathology examination of specimens of kidney of patients who have COVID-19 infection associated with acute kidney injury (AKI) does tend to show diffuse proximal convoluted tubule injury with loss of brush border as well as frank necrosis. [38] [46]. [51]. 
• It has been iterated that in comparison with patients who have Severe Acute Respiratory Syndrome (SARS) and Middle East Respiratory Syndrome (MERS), the incidence of acute kidney injury (AKI) was 6.7% and 42% respectively. [46] [52] [53].
• It has been documented that the incidence of acute kidney injury (AKI) related to COVID-19 infected patients was highly variable and that in the early cases that had been reported from China, COVID-19 patients who had acute kidney injury (AKI) was uncommon [46] [54-56],  and the incidence subsequently more severe with incidence rates that had varied from 25% to 29% in  patients who had been admitted to the intensive care unit (ICU) [46, 56, 57] . 
• It has been stated that large cohort studies related to COVID-19 infection that had been undertaken within the western countries did reveal that the incidence of acute kidney injury (AKI) had ranged between 27% and 37% [46] [58] [59], as well as the incidence subsequently became more severe which had amounted to 68% with regard to critically ill COVID-19 patients who had been admitted into the intensive care unit (ICU) within the New York city [60]. However, it is now clearly understood that the incidence of acute kidney injury (AKI) related to COVID-19 infected patients tends to be associated with the age of the patient, the smoking status of the patient, the cytokine storm, the severity of the COVID-19 disease, the ethnicity of the patient, and the history of diabetes mellitus, as well as hypertension, and cardiovascular disease of the patient [46] [48].
• It has also been iterated that acute kidney injury (AKI) is an independent risk factor for the poor long-term renal outcome and mortality in critically ill COVID-19 infected patients [46] [60] [61].
• It has been stated that during a follow-up study acute kidney injury (AKI) was found to be a major cause of in-hospital mortality. Furthermore, the complete kidney recovery rate of AKI in COVID-19 infection patients was found to be only about 30% to 4 [46]
• 5

• Even though majority of individuals who have been afflicted by COVID-19 have manifested with symptoms that simulate common cold, COVID-19 infections has also induced alveolar damages which have which has emanated in the production of progressive respiratory failure and fatalities in 6.4% of COVID-19 infection cases.
• It is believed that direct viral injury, uncontrolled inflammation of coagulation, as well as complement cascades are postulated to participate in the pathogenesis of COVID-19 infection. 
• Some patients who have been afflicted by COVID-19 infection have depicted kidney damage through the process of acute kidney injury (AKI), development of mild proteinuria, visible and non-visible haematuria, or slight elevation in their serum creatinine levels, possibly as an emanation of kidney tropism of the COVID-19 VIRUS as well as multi-organ failure. 
• There reports of increasing clinical evidence which have indicated that acute kidney injury (AKI) does represent a common as well as severe complication which tends to develop with regard to patients with COVID-19 infection who are critically ill.   
• Some of the risk factors in COVID-19 infected patients that have tended to be linked with the development of acute kidney injury (AKI) do include: the older age group, the severity of the COVID-19 infection, the ethnicity of the patient, the history of diabetes mellitus, hypertension, as well cardiovascular disease. Out of the aforementioned factors, inflammation could represent a key player in the pathogenesis of acute kidney injury (AKI) in patients who have been afflicted with COVID-19 infection. 
• There is a postulated highly probability that SARS-COV-2 infection could trigger the activation of many inflammatory pathways that include: angiotensin II, cytokine storm such as interleukin-6, (IL-6), C-reactive protein (CRP), TGF-ß signaling, complement activation, as well as lung-kidney crosstalk to induce acute kidney injury (AKI). 
• It would hence be considered that therapies that target the aforementioned inflammatory molecules as well as pathways with utilization of a monoclonal antibody against IL-6 (Tacilizumab), C3 inhibitor AMY-101, anti-C5 antibody, anti-TGF-ß OT-101, as well as utilization of CRRT in patients with COVID-19 infection who are critically ill, could represent novel as well as specific treatment options for acute kidney injury (AKI) with regard to COVID-19 infected patients. 
• There is so far no consensus global opinion regarding any specific treatments for COVID-19 infection. 
• The results of some research studies related to COVID-19 infection have reported many agents which might have potential efficacy against COVID-19 infection, and many of these molecules have depicted preliminary efficacy against COVID-19 infection and these are currently being tested in some clinical trials. 
• Clinicians globally should be encouraged to report their experiences related to cases and case series of COVID-19 infections they managed so that more lessons would be learnt about COVID-19 infections and the biological behavior of COVID19. 

None 

Acknowledgements to all individuals and research groups that have reported their experiences related to COVID-19 infection through out the world which has provided pivots for the understanding of the pathogenesis and biological behavior of COVID-19 infection affecting various organs of the human body.