Home About us Current issue Ahead of Print Back issues Submission Instructions Advertise Contact Login   

Search Article 
Advanced search 
Saudi Journal of Kidney Diseases and Transplantation
Users online: 2958 Home Bookmark this page Print this page Email this page Small font sizeDefault font size Increase font size 

Table of Contents   
Year : 2021  |  Volume : 32  |  Issue : 5  |  Page : 1220-1234
Coronavirus Disease 2019 and the Kidney

1 Department of Medicine, All India Institute of Medical Sciences, Bilaspur, Himachal Pradesh, India
2 Department of Nephrology, All India Institute of Medical Sciences, Bilaspur, Himachal Pradesh, India

Click here for correspondence address and email

Date of Web Publication4-May-2022


Coronaviruses are ubiquitous pathogens and have caused epidemics in the recent past. Coupled with globalization, they have the potential to transform into the pandemic, as is the case of coronavirus disease 2019 (COVID-19). Primarily to start as a respiratory illness, they are known to cause systemic disease and affect many organ systems. Due to the lack of, universally proven, specific anti-viral therapy, the mainstay of treatment is “supportive care” and some of the patients afflicted with it, require intensive care and organ support for lungs and/or kidneys. Patients with the diseases of the kidney, particularly those on dialysis and kidney transplant recipients, are predisposed to the worst outcomes with COVID-19. It also leads to acute kidney injury, which is an important and independent determinant of prognosis in these patients. It also creates a huge demand for the delivery of renal replacement therapy. COVID-19 is an emerging and evolving disease, and so, it is important to understand the mechanism and management of kidney diseases in COVID-19.

How to cite this article:
Jaryal A, Vikrant S. Coronavirus Disease 2019 and the Kidney. Saudi J Kidney Dis Transpl 2021;32:1220-34

How to cite this URL:
Jaryal A, Vikrant S. Coronavirus Disease 2019 and the Kidney. Saudi J Kidney Dis Transpl [serial online] 2021 [cited 2022 Dec 2];32:1220-34. Available from: https://www.sjkdt.org/text.asp?2021/32/5/1220/344741

   Introduction Top

Human coronaviruses (CoV) are zoonotic pathogens. They are usually known to cause respiratory infections in humans and intestinal infections in animals. Before the epidemic of severe acute respiratory syndrome (SARS), they were known to cause mild infections in immuno-competent people, but this perception changed with the discovery of the first epidemic of SARS in 2002.[1],[2] Subsequently the Middle East respiratory syndrome coronavirus (MERS-CoV) emerged in the Kingdom of Saudi Arabia in September 2012 and is still continuing.[3] Some authorities rightly consider SARS, to be the first emerging disease of the age of globalization, which was readily transmissible and where a contagion from one part of the world traveled to another part rapidly (with jet travel).[4] The current SARS CoV disease which started in China in December 2019, has already reached pandemic proportion and is still ensuing. It has been named as coronavirus disease 2019, (COVID-19) or the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).[5] Involvement of the kidney, with CoV, is quite common. What are CoV? And how they cause kidney injury? And how best such patients can be managed is reviewed here.

   What are Coronaviruses? Top

Human CoV were first characterized in the 1960s, by the efforts of many scientists, and were named so, because of their typical appearance on electron microscopy.[6] CoV belong to order Nidovirales, family Corona-viridae and subfamily Coronavirinae.[1] Based on their genomic structure and phylogenetic relationships the subfamily Coronavirinae is further divided into four genera namely–alphacoronavirus, betacoronavirus (infect only mammals), gammacoronavirus, and delta-coronavirus (usually infect birds, but some of them can also cause infection in mammals).[1],[2] Human CoV are enveloped single-stranded RNA viruses. They contain the largest known, positive-sense RNA genomes, ranging from 25.5 – nearly 32 Kb in length. The diameter of virus particles ranges from 70 to 120 nm and is surrounded by characteristic spike-shaped glycoprotein (180 kDa). The spike glycoprotein mediates the attachment and entry of the coronavirus utilizing virus and host-specific receptors.[5],[7] The receptor-binding domain (RBD) of the spike glycoprotein is poorly conserved among CoV, contributing to their broad host range and capability to breach tissue and host species barriers.[7] Bats are known to be a huge reservoir of coronavirus, and the diversity of coronavirus in bats and other species is not fully known. The origin of all the SARS CoV can be traced to bats. It is hypothesized that direct progenitors of SARS-CoV were produced by recombination in the bats or other animals (natural selection in the animal host before zoonotic transfer) which acted as intermediate hosts such as civets, Pangolins, and dromedary camel (in the case of MERS CoV), where it acquired more mutations and then spilled over to humans, or by natural selection in human-to-human transmission.[2],[7],[8]

   Pathogenesis of Coronavirus Diseases 2019 Top

The transmission, replication, and pathogenesis of coronavirus are determined by the viral genome and host receptors. Corona virion completes its life cycle in the host cells in the following steps, i.e., entry by utilizing viral and host receptors, expression of replicase, replication, and transcription of genome and release of progeny. It contains a few essential structural glycoproteins like–spike (S), membrane (M), envelope (E), and nucleocapsid (N), and many non-structural proteins like proteases, primase, RNA helicase and RNA dependent RNA polymerase (RdRp).[9] S protein is required for the initial attachment of the virus to the host cell and gives a characteristic appearance to the virus and hence the name “corona.” M protein maintains the structure of the virus and E protein is required for viral assembly and release. Many CoV bind to host cells through their S protein and host peptidases receptors. SARS-CoV2 shares 79% similarity with SARS-CoV, and 50% homology with MERS, however, it is more closely related to a few of the bat CoV.[5] SARS-CoV and SARS-CoV2 use angiotensin-converting enzyme type 2 (ACE2) and MERS-CoV uses Dipeptidyl peptidase (DPP4) as a receptor to bind to the host cell membrane. The fusion of the virus with the host membrane after attachment to ACE 2 receptors is mediated by proteases like transmembrane protein serine protease 2 (TMPRSS2) and furin.[9],[10],[11] Virus-infected cells release interferons (IFN), which are primary cytokines of defense against the virus. IFN is one of the constituents of the innate immune system. IFN I molecule binds to cell surface receptors and triggers Jak-Stat (Janus kinase/signal transducer and activator of transcription) signaling pathway which switches on many antiviral genes, which further are translated into various proteins, which inhibit viral replication. Cells of adaptive immunity like T-cells, memory B-cells and antibodies are also produced which have a protective role against infection, and reinfection. The kinetics of these cells of adaptive immunity in COVID-19 is variable, with the level of IgG to spike protein was found to be stable over six months, level of spike specific memory B-cells was more abundant at month 6 than on month 1, and level of SARS-CoV 2 specific CD4+ T cells and CD 8+ T cells declined with a half-life of 3–5 months after the onset of symptoms.[12] In patients who recovered from SARS-CoV infection, memory CD4 and CD8 T-cells have been found to last up to 11 years.[13]

   Angiotensin-converting Enzyme Type 2: A Central Molecule in the Coronavirus Disease Pathogenesis Top

The renin-angiotensin system (RAS) is a complex system of various bioactive components and has not been fully elucidated yet. ACE and its homolog ACE2 play an important role in the renin-angiotensin-aldosterone axis, which regulates vascular tone, fluid and electrolyte hemostasis, cell growth, and inflammation. ACE and ACE2 usually have an opposite action to each other. ACE converts angiotensin 1 (AG I) to angiotensin II (AG II), which increases blood pressure. AG1 and AGII are also acted upon by ACE 2 and hydrolyzed to form angiotensin 1-7, which has vasodilator properties and lowers blood pressure.[14] Drugs that inhibit ACE (ACEI), upregulate ACE2 [Figure 1]. Hence, the people on ACEI would have increased expression of ACE 2, and ACE2 also acts as a cellular receptor for SARS CoV 2. Hence, it is hypothesized that people on ACEI might have increased susceptibility to infection with SARS-CoV 2 and may have even severe infection, however, ACE2 is also known to have anti-inflammatory effects.[15] A meta-analysis previously has shown that people on ACEI have significantly less risk of pneumonia and may even have less mortality.[16] It may be related to upregulation of ACE2 level which has vasodilatory effects and protect pneumocytes from injury by improving pulmonary blood flow and surfactant properties.[17] Similarly in the case of COVID-19 also studies did not find any association with the use of ACEI/angiotensin receptor blocker (ARB) and COVID-19 positivity and even found lower all-cause mortality in the patients who were hospitalized with COVID-19 and using ACEI/ARB versus nonusers.[18],[19] A large prospective cohort study also found a decreased risk of COVID-19, and no increased or decreased need of intensive care unit (ICU) care in patients on ACEI/ARB, although it may not hold true across all the ethnicities.[20] ACE2 is more avidly expressed in type II alveolar epithelial cells than epithelial cells of the upper respiratory tract and that may be a plausible cause of predominant lower respiratory tract symptoms. It is also extensively expressed in kidneys especially apical cells of proximal convoluted tubules (PCT), myocardial cells, enterocytes, urothelial cells, and in many other organs, and viral sequences have been isolated from urine and feces.[21] Infection of cells with SARS-CoV2 leads to downregulation of ACE2 and alters AG II/AG 1-7 and ACE/ACE2 balance in favor of increased vascular permeability, inflammation, coagulation, and microcirculatory disturbance.[21]
Figure 1: Interaction of renin-angiotensin system and coronavirus disease 2019.
RAS: Renin angiotensin system, ACE: Angitensin-converting enzyme, SARS CoV-2: Severe acute respiratory syndrome coronavirus 2.

Click here to view

   Cytokine Release Syndrome Top

The outcome of coronavirus infection depends on the interplay of viral and host factors including age, sex, and comorbidities. Beside it, the other important determinant is a balance between protective host immune response and devastating effects of immune dysregulation. Hyper-immune response, characterized by markedly elevated cytokines and systemic upset, can be given an umbrella term as “cytokine release syndrome or cytokine storm (CRS)”, and is known to occur after various therapies, cancers, pathogens, and autoimmune disorders. There is no uniformly accepted definition for CRS and its distinction from the normal immune response is also blurry, however, it is uniformly characterized by markedly elevated cytokines, systemic inflammation, constitutional symptoms, and multiorgan dysfunction.[22] In some severe cases of CRS, a combination of renal dysfunction, endothelial cell dysfunction, and acute hypoalbuminemia can occur leading to capillary leak syndrome and anasarca. Laboratory investigations are nonspecific and are influenced by the underlying cause. However, the level of CRP (almost uniformly elevated and correlate with disease severity),[23] erythrocyte sedimentation rate, triglyceride, ferritin, lactate dehydrogenase, interleukin (IL)-6, IL-10, tumor necrosis factor-alpha, IFN gamma, and D-dimer are usually elevated. Hemogram may show leukocytosis, lymphopenia, leukopenia, pancytopenia, anemia, and thrombocytopenia. Some people with dysregulated IFN response to COVID-19 may have severe disease. CRS has been implicated in the pathogenesis and is a determinant of disease outcome in SARS, MERS, and SARS-CoV 2.[24] It is important to differentiate CRS from normal immune response, as the institution of immunosuppressive therapy may prove to be counterproductive in the later situation.

   Kidney Pathology in Coronavirus Disease 2019 Top

Autopsy studies in patients with SARS and SARS-CoV 2 have shown diffuse alveolar damage in the lungs, with hyaline membrane formation.[25],[26] Viral particles have been demonstrated in the pneumocytes. Lungs in a patient infected with COVID-19 also showed microthrombi in pulmonary microcirculation, deep vein thrombosis, and pulmonary embolism.[26] Although the major brunt of the disease pathology is borne by the lungs, kidneys showed focal necrosis, monocytic infiltration, and vasculitis of small veins in the renal interstitium and acute tubular necrosis (ATN). Viral particles have been demonstrated in renal tubular epithelial cells in SARS-CoV.[25] In patients with COVID-19 autopsy studies showed changes in kidneys varying from acute tubular injury, congestion of peritubular capillaries, and hemosiderin deposits in the tubular lumen and viral particles have been also demonstrated in the kidney tissue.[26],[27] COVID-19 affects all the compartments of the kidney, i.e., glomerulus, tubulointerstitial and vascular. In a multi-centric study analyzing, 17 kidney biopsies in COVID-19 patients (14 native and 3 transplant) found that only three had severe COVID-19 disease at presentation. Indications for performing kidney biopsies were acute kidney injury (AKI) (n = 15) and proteinuria (n = 11), developing concurrently or within one week of COVID-19 symptoms in all the patients. The most common findings were acute tubular injury (n = 14), collapsing glomerulopathy (n = 7), and endothelial injury/thrombotic microangiopathy (n = 6). Two of the three transplant recipients developed active antibody-mediated rejection weeks after COVID-19. Eight patients required dialysis, and it highlights that many patients may present with exclusive renal dysfunction.[28] COVID-19 associated viral microangiopathy may be an important mechanism for COVID-19 associated renal involvement.[29] Proximal tubule dysfunctions, with transmission electron microscopy showing viral particles, has also been shown with COVID-19.[30] In one study collapsing glomerulopathy was the commonest biopsy findings, however evidence of SARS-CoV 2 in kidney tissue was not demonstrated.[31] In another kidney biopsy study of 10 patients, ATN was the commonest finding, with no evidence of SARS-CoV 2 in biopsied kidney tissue.[32] So kidney involvement in SARS-CoV 2 occurs by direct viral cytopathic effects and is also mediated by systemic effects of COVID-19 infection.

   Epidemiology of Kidney Disease in Coronavirus Disease 2019 Top

Kidneys are affected in systemic viral infections by various mechanisms namely: direct viral effects on glomeruli, vasculature and renal tubular cells, immune-mediated effects on glomeruli and tubulointerstitial, toxic effects of drugs and endogenous toxins like myoglobin and hemoglobin, generalized endothelial dysfunction, renal hypoperfusion, hypoxia, and cytokine release [Figure 2]. Kidneys play an important role in maintaining blood pressure, fluid, electrolyte, and acid-base hemostasis. RAS axis is also orchestrated in the kidneys and besides this, there is abundant expression of ACE 2 in kidney tissue.[33] AKI is also recognized to be the most common complication in a patient with acute respiratory distress syndrome (ARDS), occurring in almost 50% of the patients and is also an independent determinant of mortality in ARDS.[34] ARDS per se is a leading cause of death in a patient with COVID-19. All these factors predispose kidneys to be affected with COVID-19 leading to either AKI or acute on chronic kidney disease (CKD).
Figure 3: Delivery of maintenance hemodialysis (in-center) during coronavirus disease 2019.
ILI: Influenza like illness, COVID-19: Coronavirus disease 2019, PPE: Personal protective equipment.

Click here to view

   Acute Kidney Injury in Coronavirus Disease 2019 Top

The incidence of AKI was around 9.6% in patients with SARS with mortality around 98.9%, and the incidence of AKI was 42% in patient with MERS with 100% mortality. CKD, end-stage renal disease (ESRD), and the need for urgent renal replacement therapy (RRT) are also associated with increased mortality in SARS, MERS, and SARS-CoV 2.[35] The incidence of AKI in COVID-19 varies from (5.1% to 56.9%). An early study in the pandemic emanating from patients admitted to a teaching hospital with COVID-19 showed that 43.9% of patients had proteinuria, and 26.7% had hematuria at the time of admission in hospital with COVID-19. AKI developed in 5.1% of the patients during the hospital stay. Elevated baseline creatinine, blood urea nitrogen, proteinuria, hematuria, and AKI were independent risk factors for in-hospital death.[36] A retrospective study found a higher incidence of AKI in patient admitted with COVID vs non-COVID (56.9% vs. 25.1%). Patients with COVID-19 were more likely to need RRT (less likely to recover renal function), ICU support, mechanical ventilation and also had more in-hospital death.[37] One study showed an incidence of AKI to be 36.6% in patients infected with COVID 19. The risk factors for AKI in this study were old age, diabetes mellitus, cardiovascular disease, blacks, hypertension, need for ventilatory support, and need of vasopressors drugs. 35% of the patients with AKI died. Authors found AKI to occur early and in temporal relation with respiratory failure and a marker of poor prognosis.[38] In another multicenter cohort of study of 3099 critically ill adults with COVID-19, it was found that a total of 637 of 3099 patients (20.6%) developed RRT requiring AKI (AKI-RRT) within 14 days of ICU admission, and 350 of whom (54.9%) died within 28 days of ICU admission. At the end of a median follow-up of 17 days (range, 1–123 days), 403 of the 637 patients (63.3%) with AKI-RRT had died, 216 (33.9%) were discharged, and 18 (2.8%) remained hospitalized. Of the 216 patients discharged, 73 (33.8%) remained RRT dependent at discharge, and 39 (18.1%) remained RRT dependent 60 days after ICU admission. It implies poor immediate and long-term outcomes for the patients who develop AKI-RRT with COVID-19.[39] Hence, all these diverse studies inform us that, there is a high incidence of AKI in COVID-19, and it is associated with the increased need for ICU care, RRT, and mortality, and is in itself an independent determinant of outcomes.

   Coronavirus Disease 2019 in Dialysis and Kidney Transplant Recipients Top

Uremia leads to immune dysfunction in the form of immunodepression and inflammation, and so the patients of ESRD on hemodialysis (HD) or peritoneal dialysis (PD) are predisposed to infections.[40] The incidence of COVID-19 is around 8% in patients on maintenance HD (MHD) which is the same as in the general population but mortality is around 25.7%, which is almost the same as SARS but lower than MERS.[35] Patient on home-based PD may have the theoretical advantage of getting less infected with COVID-19 over in-center HD if proper infection control measures are used. In a study of 818 patients on PD, eight patients were diagnosed with COVID-19 during the studied period (January 1, 2020, to April 12, 2020), two of whom died and six survived. In this study incidence of symptomatic COVID-19 in patients on PD was close to that of the general population of the same city.[41] In another study of 11 patients on chronic PD with COVID-19, three patients required mechanical ventilation, two of whom died and nine of the 11 patients (82%) were discharged alive.[42] Kidney transplant recipients (KTRs) are predisposed to various viral infections due to the use of immunosuppressant medications, and hence there is worry about them getting infected with COVID-19. In an observational cohort study, high mortality of 26.7% in the dialysis patients and 29.2% in the transplant patients were found.[43] In another study of 20 KTRs, six patients developed AKI, with one requiring HD, and five KTRs died after a median period of 15 days, from symptom onset.[44] So, patients of ESRD on MHD and PD, and KTR have uniformly adverse outcomes once they contract COVID-19.

   Management of Coronavirus Disease 2019 patients with Kidney Involvement Top

General principles

It is well-known that patients with COVID-19 can develop various types of kidney injury, and patients with underlying kidney diseases such as CKD, MHD, and KTR have adverse outcomes, which are more than the general population, once they contract COVID-19. The kidney is precariously predisposed to adverse effects of systemic inflammation, hypoxia, and hypotension, and it is also a seat of excretion and handling of many drugs. Important aspects of handling COVID-19 disease with kidney disease are:

  1. Prevention of COVID-19 in patients of CKD, MHD and KTR:

    1. Routine screening of patients on MHD (in-centre) for COVID 19 and their isolation if positive for COVID-19.
    2. Vaccination.

  2. Prevention of Kidney injury in patients with COVID-19:

    1. Periodic measurement of hemodynamic parameters, volume status, urine output, and serum creatinine.
    2. Identify patients at risk of AKI, identify new-onset AKI, establish the cause of AKI and treat the cause of AKI.
    3. Prevent further worsening of AKI:

      1. Avoiding/omitting potential nephrotoxic drugs.
      2. Dosage modification of drugs in patients with reduced GFR.
      3. Prevention of hypotension, hypoxia, dehydration, fluid overload, and systemic inflammation.

    4. Nutritional support, control of blood pressure, and glycemic control.

  3. Institution of specific drugs:

    1. Anti-viral-Likely to be effective in the initial stages of viral infection.
    2. Immunomodulators-Appropriate use during the phase of the abnormal hyperimmune response.
    3. Optimal supportive care.

  4. Institution of RRT as per expertise and clinical context of the patient:

    1. Medical measures to manage complications of AKI:

      1. Fluid overload: Fluid restriction, Diuretics if pulmonary edema.
      2. Hyperkalemia: Omit drugs likely to cause hyperkalemia like potassium-sparing diuretics, trimethoprim, ACEI/ARB, β blockers, digoxin. Medical measures to treat hyperkalemia.

    2. Appropriate and complementary use of: PD, HD, sustained low-efficiency dialysis (SLED), prolonged intermittent renal replacement therapy (PIRRT) or continuous renal replacement therapy (CRRT).

  5. Follow up:

    1. For the resolution of kidney injury.
    2. Biopsy to look for other causes, if kidney disease remains unexplained.
    3. To provide reno-protective and cardiovascular protective care to patients with AKI.

   Coronavirus Disease 2019 and Delivery of Maintenance Hemodialysis Top

Worldwide, around 2.5 million people are on various modes of life-sustaining RRT.[45] HD is the commonest mode of RRT and Over two million people are dependent on it,[46] and majority of them are on in-center HD. Delivery of MHD to these patients in the pandemic of COVID-19 is challenging. It not only involves adherence to infection control measures to prevent disease in the staff and patient, but also extends to ensuring logistics like travel, consultation, medication adherence, and maintenance of dialysis supplies [Figure 3]. As COVID-19 is an evolving and ongoing pandemic, it is important for renal physicians to stay abreast with the policies developed by national and international scientific bodies and local public health authorities to ensure optimal delivery of in-center MHD.{Figure 3}

   Drugs in the Management of Coronavirus Disease 2019 Top

The diagnosis of COVID-19 is based on the nucleic acid amplification test, and this also holds true for patients with diseases of the kidney. Effective and safe drug for the treatment of any infectious agent is the cornerstone of managing any contagion, be it bacterial, fungal, or viral. This safe and effective drug is still elusive for COVID-19. Some of the drugs already in use have been repurposed for the treatment of COVID-19 like: hydroxychloroquine, azithromycin, protease inhibitors, and ivermectin. However, currently, NIH recommends against the use of chloroquine, hydroxychloroquine alone or in combination with azithromycin, or HIV protease inhibitor like lopinavir/ritonavir in the management of COVID-19, of any severity.[45] Specific antiviral drugs currently in various phases of development and approval are recombinant human monoclonal antibodies like casirivimab plus imdevimab and bamlanivimab that bind to spike protein RBD of SARS-CoV-2, and have neutralizing effect on the virus.[47]


Remdesivir is one of the most widely used, specific antiviral drugs against COVID-19. It has a broad-spectrum activity against corona-viruses. It is an intravenous nucleotide prodrug that is metabolized to its active triphosphate, that binds to the viral RdRp, and inhibits viral replication through premature termination of RNA transcription. It has a short plasma half-life of 1 h but has a prolonged intra-cellular t1/2 of 40 h.[48],[49] It is rapidly metabolized by plasma hydrolases, and has less than 10% renal excretion, however, some of its metabolites may have higher renal excretion.[48],[49] In vitro studies show, that it is a weak inhibitor of cytochrome 450, but due to its rapid in vivo degradation, it may not lead to clinically significant drug interaction.[49] Its formulation contains sulfobutylether-beta-cyclodextrin sodium (SBECD) which is cleared through kidneys, and hence there is concern about its accumulation in patient with reduced estimated GFR (eGFR). It was not used in the people with eGFR <30 mL/min, in the trials, so it is not recommended for use in the people with eGFR <30 mL/min.[47] However, it is also known that SBECD is rapidly and extensively eliminated by HD and hemodiafiltration.[50] Some authors have successfully used Remdesivir in patients on dialysis and eGFR <30 mL/min without any infusion-related adverse effects and any clinically significant ALT elevation.[51]

Immunosuppressant drugs

The use of immunomodulating/immuno-suppressants drugs is helpful in the management of COVID-19. They should be used at the right stage of the disease when there is dysregulated immune response inimical to the host. Dexamethasone is effective in lowering the mortality in the patient with severe to critical COVID-19, who required supplemental oxygen therapy or ventilatory support. Baricitinib (an inhibitor of oral JAK) along with remdesivir is another drug in various stages of development and approval in the management of COVID-19. NIH is neither for nor against, the use of baricitinib plus remdesivir in patients with COVID-19.[47] There has been a surge in the use of biologicals in the management of COVID-19, and it may be of concern in patients with reduced GFR. However, these monoclonal antibodies are relatively large molecules and are hence confined to vascular space. They are eliminated by proteolytic degradation at the site of absorption, and during transportation, target mediated drug disposition and intracellular catabolism. Because of their large size, they are not filtered by the kidneys and hence are not eliminated in the urine, except in pathological conditions.[52] Tocilizumab is one such biological agent, which has been used in severe COVID-19. It is a recombinant humanized anti-IL-6-receptor monoclonal antibody. NIH recommends against the use of tocilizumab for the treatment of COVID-19, except in a clinical trial.[47]

   Management of Acute Kidney Injury in Coronavirus Disease 2019 Top

AKI is a clinical syndrome characterized by an abrupt decline in GFR leading to the accumulation of metabolic waste products. The initial approach for COVID-19 associated AKI should be to use an evidence-based approach to prevent further progression of AKI, as is being done in other non-COVID scenarios. Hemodynamics, volume status, serum creatinine, and urine output should be periodically monitored. Maintenance of euvolemia is important, as both dehydration and fluid overload are associated with adverse outcomes. Medical measures should be adopted to manage fluid overload and hyperkalemia. Kidney Diseases Improving Global Outcomes (KDIGO), guidelines advise for initiation of RRT in AKI, when there are life-threatening changes in fluid, electrolyte, and acid-base balance.[53] Delivery of RRT in pandemic like COVID-19 is challenging, because of the acute increase in the need for such therapies, which is overwhelming for any health care system and there is a risk of transmission of contagion to Health Care Workers and patients. RRT in COVID-19 should be delivered by adhering to strict epidemic control measures. Various modalities of RRT are: Intermittent HD, SLED, PIRRT, acute PD and CRRT. The first two have the advantage of intermittent therapy and may be less labor intensive. The latter two offer advantages of continuous slow convective clearance with better hemodynamic tolerability but may need more expertise and labor. In CRRT the pore size of CRRT hemofilter is 7–10 nm,[54] which is much smaller than the size of SARS-CoV2 (100 nm) which implies that passage of virus in CRRT effluent would be quite low. While delivering CRRT through a cytokine-absorbing polymethyl methacrylate membrane hemofilter, very weak but positive RT-PCR result for COVID-19 was detected in three of five effluent specimens.[55] COVID-19 creates a thrombogenic milieu, so clotting of CRRT filter becomes a major hindrance in the delivery of efficient, safe, and cost-effective dialysis in these patients. In one study, 83% of patients lost at least one filter with a median filter life of only 6.5 h.[56] Hence, anticoagulation needs to be meticulously monitored and individualized in the patients on extracorporeal therapy with COVID-19. CRRT can be successfully and safely incorporated and delivered with other extracorporeal therapies like: Cytokine reduction and extra corporeal membrane oxygenation.[57],[58] The main determinant for the type of RRT to choose, depends upon institutional expertise, overall clinical goals to be achieved with the RRT, and overall clinical suitability of the patient for a particular mode of RRT. In resource-poor areas acute PD fairs same as CRRT.[59] Epidemics like COVID-19 put a lot of strain on resources, and as such even an advanced and resource-rich health-care system can become resource-poor. Acute PD is under utilized in the management of AKI, mainly because of a lack of trained manpower. It has been also utilized in COVID-19 with successful outcomes.[60] Acute PD is a helpful complement to other modes of acute RRT and can be successfully administered with good outcomes in pandemic situations like this.[61] KDIGO guidelines suggest using CRRT, rather than standard intermittent RRT, for hemodynamically unstable patients and those with raised intracranial pressure. RRT should be provided to achieve the overall goals of electrolyte, acid-base, solute, and fluid balance. For intermittent and extended RRT, it recommends a Kt/V target of 3.9 per week and for CRRT it recommends delivering an effluent volume of 20–25 mL/Kg/h.[53] However, a patient’s overall clinical context should be taken into consideration while delivering RRT. COVID 19 does not appear to be one-time illness. Survivors of COVID 19 infection have reported various multisystem symptoms which persist from few weeks to few months. The symptoms which persist beyond a conventional threshold of four weeks (replication competent COVID-19 is usually not isolated beyond this period), which cannot be attributed to any other etiology has been defined as post-acute COVID-19 syndrome. It is also known to affect kidneys.[62] COVID-19 patients with RRT requiring AKI, experience high mortality on long-term follow-up. In one Chinese study around 13% of patients, with documented normal renal functions during acute COVID-19, developed new-onset reduction of eGFR, on long-term follow-up.[62],[63] Such patients with persistent renal impairment should be followed up closely.[62]

   Management of Kidney Transplant Recipients with Coronavirus Disease 2019 Top

KTR are another vulnerable group of patients for COVID-19. It is traditional to reduce the intensity of immunosuppression during infectious illness in KTR. On the same analogy, antimetabolites are usually withdrawn in most of the KTR with COVID-19, and a dose of CNI is reduced or stopped if further reduction in immunosuppressant drugs is warranted. In one study dose of the antiproliferative drug was reduced in 86% of the patients, and in 21% of the critically ill COVID-19 patients, tacrolimus was withheld.[64] In another study, the intensity of immunosuppression and degree of reduction following COVID-19 diagnosis were not associated with either survival or acute allograft rejection.[65] Profound lymphopenia is one of the important features of COVID 19 and correlates with poor outcomes.[66] The absolute lymphocyte count is also used as a marker for a therapeutic effect of anti-thymocyte globulin, used during induction in transplant.[67] So, the patients of COVID 19 may not be at increased risk of rejection, especially if they are lymphopenic. In a study of 30 KTRs with COVID-19 where CNI and antimetabolites were withheld, and 40% of patients continued baseline corticosteroids, and standard of care, it was found that the mortality in the cohort was 20%, four had RRT requiring AKI and there was no increased risk of acute allograft rejection.[68] As per the current understanding of COVID-19 pathogenesis, the initial assault of the disease is led by direct viral cytotoxic effect and later by immune hyperresponsiveness.

Hence, immunosuppression in COVID-19 may be modified as per the duration of illness, concomitant use of other drugs, and severity of the disease. It needs to be individualized and tailored as per the overall clinical context.[69]

   Coronavirus Disease 2019 Vaccine Top

The development of vaccine is a long and challenging process. However, in the case of COVID-19 concerted international efforts led to the rapid development and roll-out of various vaccines against it. Patients with kidney diseases are known to have a compromised immune system, and so live microbial replicating vaccines should be avoided in them.[70] Because of this immunocompromised state many patients with kidney diseases, especially those with reduced eGFR, and those on immunosuppressant drugs, are not able to develop an optimal immune response to various vaccines like hepatitis B, and influenza.[71] Hence, this sub-group of patients, may not be able to develop a sufficient immune response to the COVID-19 vaccine also. In some of the studies, around 97% of PD, and 90% of dialysis patients were found to have demonstrable anti spike antibodies after receiving a complete dose of mRNA vaccine.[71],[72] Most of KTR are on immunosuppressant drugs and exhibit subdued immune response to the COVID-19 vaccine. In one study anti-spike antibodies could be demonstrated in only 25% of KTR, after receiving full dose of mRNA vaccine.[73] However, seroconversion is known to increase in solid organ transplant recipients after administration of the second dose,[74] and despite lack of neutralizing antibodies vaccinees might be protected from severe COVID-19 disease by cellular immune response.[75] It is conventional to give higher and extra doses of hepatitis B vaccine to patients with reduced eGFR, and the same can also be explored for the COVID-19 vaccine. In patients on active immunosuppressants drugs, it is likely to be wise to postpone COVID-19 vaccination until dose of steroids have been reduced to below 20 mg prednisone equivalent a day, and six months have passed since the last dose of rituximab.[75] The currently available and widely used COVID 19 vaccines like killed whole virus vaccine, replication-defective viral-vectored vaccines ChAdOx1 nCoV-19 (Oxford-AstraZeneca), and the mRNA vaccines BNT162b2 (Pfizer-BioNTech) and mRNA-1273 (Moderna) are safe to use in these subgroups of the patients.[70],[71] Considering the vulnerability of these patients, they should be prioritized to receive COVID-19 vaccine. With the available evidence, it is inferred that the currently approved COVID-19 vaccines (mRNA and inactivated), are safe and efficacious in patients with various stages of CKD, patients on maintenance dialysis, patients with autoimmune diseases of the kidney and KTR.[70],[75]

   Conclusion Top

COVID-19 affects kidneys, mainly as a part of systemic illness and ARDS, although rarely it can also involve kidneys, irrespective of the systemic disease. It can lead to AKI, with poor immediate and long-term outcomes. It is important to prevent AKI, timely diagnose and treat it, and prevent its further progression. Patients with CKD, ESRD, and KTR, have the worst outcomes with COVID-19. Delivery of RRT is challenging for any health care system in a pandemic of this magnitude. So, it becomes important to protect the vulnerable population and appropriately channelize resources and human expertise, in situations like this. Epidemic control measures, appropriate use of drugs like dexamethasone and remdesivir, supportive care, and now rapid deployment of vaccine would prove effective, in mitigating the pandemic of COVID 19. All modalities of RRT are complementary to each other and can be used effectively in the management of patients with COVID-19 who require RRT. Appropriate use of specific antiviral drugs, identification of abnormal hyperimmune response, and timely introduction of immunosuppressant can throw a light, on the management of viral diseases in the future. This unprecedented pandemic has also seen, unprecedented, concerted international efforts, which has led to the rapid transmission of research and knowledge across the globe.

Conflict of interest: None declared.

   References Top

Forni D, Cagliani R, Clerici M, Sironi M. Molecular evolution of human coronavirus genomes. Trends Microbiol 2017;25:35-48.  Back to cited text no. 1
Cui J, Li F, Shi ZL. Origin and evolution of pathogenic coronaviruses. Nat Rev Microbiol 2019;17:181-92.  Back to cited text no. 2
Sharif-Yakan A, Kanj SS. Emergence of MERS-CoV in the Middle East: Origins, transmission, treatment, and perspectives. PLoS Pathog 2014;10:e1004457.  Back to cited text no. 3
Chew SK. SARS: how a global epidemic was stopped. Bull World Health Organ 2007;85: 324.  Back to cited text no. 4
Ouassou H, Kharchoufa L, Bouhrim M, et al. The pathogenesis of coronavirus disease 2019 (COVID-19): Evaluation and prevention. J Immunol Res 2020;2020:1357983.  Back to cited text no. 5
Tyrrell DA, Almeida JD, Cunningham CH, et al. Coronaviridae. Intervirology 1975;5:76-82.  Back to cited text no. 6
Graham RL, Donaldson EF, Baric RS. A decade after SARS: Strategies for controlling emerging coronaviruses. Nat Rev Microbiol 2013;11:836-48.  Back to cited text no. 7
Andersen KG, Rambaut A, Lipkin WI, Holmes EC, Garry RF. The proximal origin of SARS-CoV-2. Nat Med 2020;26:450-2.  Back to cited text no. 8
Bergmann CC, Silverman RH. COVID-19: Coronavirus replication, pathogenesis, and therapeutic strategies. Cleve Clin J Med 2020; 87:321-7.  Back to cited text no. 9
Sawicki SG, Sawicki DL, Siddell SG. A contemporary view of coronavirus transcription. J Virol 2007;81:20-9.  Back to cited text no. 10
Banerjee A, Baid K, Mossman K. Molecular pathogenesis of Middle East Respiratory Syndrome (MERS) coronavirus. Curr Clin Microbiol Rep 2019;6:139-47.  Back to cited text no. 11
Dan JM, Mateus J, Kato Y, et al. Immunological memory to SARS-CoV-2 assessed for up to 8 months after infection. Science 2021; 371:eabf4063.  Back to cited text no. 12
Ng OW, Chia A, Tan AT, et al. Memory T cell responses targeting the SARS coronavirus persist up to 11 years post-infection. Vaccine 2016;34:2008-14.  Back to cited text no. 13
Donoghue M, Hsieh F, Baronas E, et al. A novel angiotensin-converting enzyme-related carboxypeptidase (ACE2) converts angiotensin I to angiotensin 1-9. Circ Res 2000;87:E1-9.  Back to cited text no. 14
Fang L, Karakiulakis G, Roth M. Are patients with hypertension and diabetes mellitus at increased risk for COVID-19 infection? Lancet Respir Med 2020;8:e21.  Back to cited text no. 15
Caldeira D, Alarcão J, Vaz-Carneiro A, Costa J. Risk of pneumonia associated with use of angiotensin converting enzyme inhibitors and angiotensin receptor blockers: Systematic review and meta-analysis. BMJ 2012;345: e4260.  Back to cited text no. 16
Khan A, Benthin C, Zeno B, et al. A pilot clinical trial of recombinant human angiotensin-converting enzyme 2 in acute respiratory distress syndrome. Crit Care 2017; 21:234.  Back to cited text no. 17
Mehta N, Kalra A, Nowacki AS, et al. Association of use of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers with testing positive for coronavirus disease 2019 (COVID-19). JAMA Cardiol 2020;5:1020-6.  Back to cited text no. 18
Zhang P, Zhu L, Cai J, et al. Association of inpatient use of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers with mortality among patients with hypertension hospitalized with COVID-19. Circ Res 2020;126:1671-81.  Back to cited text no. 19
Hippisley-Cox J, Young D, Coupland C, et al. Risk of severe COVID-19 disease with ACE inhibitors and angiotensin receptor blockers: Cohort study including 8.3 million people. Heart 2020;106:1503-11.  Back to cited text no. 20
Ni W, Yang X, Yang D, et al. Role of angiotensin-converting enzyme 2 (ACE2) in COVID-19. Crit Care 2020;24:422.  Back to cited text no. 21
Fajgenbaum DC, June CH. Cytokine storm. N Engl J Med 2020;383:2255-73.  Back to cited text no. 22
Lee DW, Gardner R, Porter DL, et al. Current concepts in the diagnosis and management of cytokine release syndrome. Blood 2014;124: 188-95.  Back to cited text no. 23
Gao YM, Xu G, Wang B, Liu BC. Cytokine storm syndrome in coronavirus disease 2019: A narrative review. J Intern Med 2021;289: 147-61.  Back to cited text no. 24
Ding Y, Wang H, Shen H, et al. The clinical pathology of severe acute respiratory syndrome (SARS): A report from China. J Pathol 2003;200:282-9.  Back to cited text no. 25
Maiese A, Manetti AC, La Russa R, et al. Autopsy findings in COVID-19-related deaths: A literature review. Forensic Sci Med Pathol 2021;17:279-96.  Back to cited text no. 26
Farkash EA, Wilson AM, Jentzen JM. Ultra-structural evidence for direct renal infection with SARS-CoV-2. J Am Soc Nephrol 2020; 31:1683-7.  Back to cited text no. 27
Akilesh S, Nast CC, Yamashita M, et al. Multicenterclinicopathologic correlation of kidney biopsies performed in COVID-19 patients presenting with acute kidney injury or proteinuria. Am J Kidney Dis 2021;77:82-93.e1.  Back to cited text no. 28
Fujimaru T, Shimada K, Hamada T, et al. Development of acute kidney injury with massive granular casts and microscopic hematuria in patients with COVID-19: Two case presentations with literature review. Ren Replace Ther 2020;6:59.  Back to cited text no. 29
Werion A, Belkhir L, Perrot M, et al. SARS-CoV-2 causes a specific dysfunction of the kidney proximal tubule. Kidney Int 2020; 98:1296-307.  Back to cited text no. 30
Kudose S, Batal I, Santoriello D, et al. Kidney biopsy findings in patients with COVID-19. J Am Soc Nephrol 2020;31:1959-68.  Back to cited text no. 31
Sharma P, Uppal NN, Wanchoo R, et al. COVID-19-associated kidney injury: A case series of kidney biopsy findings. J Am Soc Nephrol 2020;31:1948-58.  Back to cited text no. 32
Ahmadian E, Hosseiniyan Khatibi SM, Razi Soofiyani S, et al. Covid-19 and kidney injury: Pathophysiology and molecular mechanisms. Rev Med Virol 2021;31:e2176.  Back to cited text no. 33
Panitchote A, Mehkri O, Hastings A, et al. Factors associated with acute kidney injury in acute respiratory distress syndrome. Ann Intensive Care 2019;9:74.  Back to cited text no. 34
Zhou S, Xu J, Xue C, Yang B, Mao Z, Ong AC. Coronavirus-associated kidney outcomes in COVID-19, SARS, and MERS: A meta-analysis and systematic review. Ren Fail 2020;43:1-15.  Back to cited text no. 35
Cheng Y, Luo R, Wang K, et al. Kidney disease is associated with in-hospital death of patients with COVID-19. Kidney Int 2020; 97:829-38.  Back to cited text no. 36
Fisher M, Neugarten J, Bellin E, et al. AKI in hospitalized patients with and without COVID-19: A comparison study. J Am Soc Nephrol 2020;31:2145-57.  Back to cited text no. 37
Hirsch JS, Ng JH, Ross DW, et al. Acute kidney injury in patients hospitalized with COVID-19. Kidney Int 2020;98:209-18.  Back to cited text no. 38
Gupta S, Coca SG, Chan L, et al. AKI treated with renal replacement therapy in critically ill patients with COVID-19. J Am Soc Nephrol 2021;32:161-76.  Back to cited text no. 39
Kato S, Chmielewski M, Honda H, et al.  Back to cited text no. 40
Aspects of immune dysfunction in end-stage renal disease. Clin J Am Soc Nephrol 2008; 3:1526-33.  Back to cited text no. 41
Jiang HJ, Tang H, Xiong F, et al. COVID-19 in peritoneal dialysis patients. Clin J Am Soc Nephrol 2020;16:121-3.  Back to cited text no. 42
Sachdeva M, Uppal NN, Hirsch JS, et al. COVID-19 in hospitalized patients on chronic peritoneal dialysis: A case series. Am J Nephrol 2020;51:669-74.  Back to cited text no. 43
Bell S, Campbell J, McDonald J, et al. COVID-19 in patients undergoing chronic kidney replacement therapy and kidney transplant recipients in Scotland: Findings and experience from the Scottish renal registry. BMC Nephrol 2020;21:419.  Back to cited text no. 44
Alberici F, Delbarba E, Manenti C, et al. A single center observational study of the clinical characteristics and short-term outcome of 20 kidney transplant patients admitted for SARS-CoV2 pneumonia. Kidney Int 2020;97:1083-8.  Back to cited text no. 45
Liyanage T, Ninomiya T, Jha V, et al. Worldwide access to treatment for end-stage kidney disease: A systematic review. Lancet 2015;385:1975-82.  Back to cited text no. 46
Verma A, Patel AB, Tio MC, Waikar SS. Caring for Dialysis Patients in a Time of COVID-19. Kidney Med 2020;2:787-92.  Back to cited text no. 47
COVID-19 Treatment Guidelines Panel. Coronavirus Disease 2019 (COVID-19) Treatment Guidelines. National Institutes of Health. Available from: https://www.covid19treatment guidelines.nih.gov/. [Last accessed on 2021 Feb 03].  Back to cited text no. 48
Parang K, El-Sayed NS, Kazeminy AJ, Tiwari RK. Comparative antiviral activity of remdesivir and Anti-HIV nucleoside analogs against human coronavirus 229E (HCoV-229E). Molecules 2020;25:E2343.  Back to cited text no. 49
European Medicines Agency (EMA). Summary on compassionate use for Remdesivir Gilead [Internet]. Available from: https://www.ema.europa.eu/en/documents/othe r/summary-compassionate-use-remdesivir-gilead_en.pdf. [Last accessed on 2020 April 12].  Back to cited text no. 50
Hafner V, Czock D, Burhenne J, et al. Pharmacokinetics of sulfobutylether-beta-cyclodextrin and voriconazole in patients with end-stage renal failure during treatment with two hemodialysis systems and hemodia-filtration. Antimicrob Agents Chemother 2010; 54:2596-602.  Back to cited text no. 51
Thakare S, Gandhi C, Modi T, et al. Safety of remdesivir in patients with acute kidney injury or CKD. Kidney Int Rep 2021;6:206-10.  Back to cited text no. 52
Temrikar ZH, Suryawanshi S, Meibohm B. Pharmacokinetics and clinical pharmacology of monoclonal antibodies in pediatric patients. Paediatr Drugs 2020;22:199-216.  Back to cited text no. 53
Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO clinical practice guideline for acute kidney injury. Kidney Int Suppl 2012;2:1-138.  Back to cited text no. 54
Moriyama K, Soejima Y. Continuous hemodi-alfiltration using PMMA membrane: Clinical efficacy and its mechanisms. Contrib Nephrol 1999;125:222-32.  Back to cited text no. 55
Katagiri D, Ishikane M, Ogawa T, et al. Continuous renal replacement therapy for a patient with severe COVID-19. Blood Purif 2021;50:129-31.  Back to cited text no. 56
Endres P, Rosovsky R, Zhao S, et al. Filter clotting with continuous renal replacement therapy in COVID-19. J Thromb Thrombolysis 2021;51:966-70.  Back to cited text no. 57
Alharthy A, Faqihi F, Memish ZA, et al. Continuous renal replacement therapy with the addition of CytoSorb cartridge in critically ill patients with COVID-19 plus acute kidney injury: A case-series. Artif Organs 2021;45: E101-112.  Back to cited text no. 58
Chen H, Yu RG, Yin NN, Zhou JX. Combination of extracorporeal membrane oxygenation and continuous renal replacement therapy in critically ill patients: A systematic review. Crit Care 2014;18:675.  Back to cited text no. 59
Jaryal A, Vikrant S. A study of continuous renal replacement therapy and acute peritoneal dialysis in hemodynamic unstable patients. Indian J Crit Care Med 2017;21:346-9.  Back to cited text no. 60
[PUBMED]  [Full text]  
Al-Hwiesh AK, Mohammed AM, Elnokeety M, et al. Successfully treating three patients with acute kidney injury secondary to COVID-19 by peritoneal dialysis: Case report and literature review. Perit Dial Int 2020;40:496-8.  Back to cited text no. 61
El Shamy O, Patel N, Abdelbaset MH, et al. Acute start peritoneal dialysis during the COVID-19 pandemic: Outcomes and experiences. J Am Soc Nephrol 2020;31:1680-2.  Back to cited text no. 62
Nalbandian A, Sehgal K, Gupta A, et al. Post-acute COVID-19 syndrome. Nat Med 2021; 27:601-15.  Back to cited text no. 63
Huang C, Huang L, Wang Y, et al. 6-month consequences of COVID-19 in patients discharged from hospital: A cohort study. Lancet 2021;397:220-32.  Back to cited text no. 64
Akalin E, Azzi Y, Bartash R, et al. Covid-19 and kidney transplantation. N Engl J Med 2020;382:2475-7.  Back to cited text no. 65
Santeusanio AD, Menon MC, Liu C, et al. Influence of patient characteristics and immunosuppressant management on mortality in kidney transplant recipients hospitalized with coronavirus disease 2019 (COVID-19). Clin Transplant 2021;35:e14221.  Back to cited text no. 66
Huang I, Pranata R. Lymphopenia in severe coronavirus disease-2019 (COVID-19): Systematic review and meta-analysis. J Intensive Care 2020;8:36.  Back to cited text no. 67
Nanmoku K, Shinzato T, Kubo T, Shimizu T, Yagisawa T. Effect of rabbit antithymocyte globulin on acute and chronic active antibody-mediated rejection after kidney transplantation. Transplant Proc 2019;51:2602-5.  Back to cited text no. 68
Chen TY, Farghaly S, Cham S, Tatem LL, Sin JH, Rauda R, et al. COVID-19 pneumonia in kidney transplant recipients: Focus on immunosuppression management. Transpl Infect Dis 2020;22:e13378.  Back to cited text no. 69
Angelico R, Blasi F, Manzia TM, Toti L, Tisone G, Cacciola R. The management of immunosuppression in kidney transplant recipients with COVID-19 disease: An update and systematic review of the literature. Medicina (Kaunas) 2021;57:435.  Back to cited text no. 70
Windpessl M, Bruchfeld A, Anders HJ, et al. COVID-19 vaccines and kidney disease. Nat Rev Nephrol 2021;17:291-3.  Back to cited text no. 71
Rodríguez-Espinosa D, Broseta JJ, Maduell F, Bedini JL, Vera M. Humoral response of the mRNA-1273 SARS-CoV-2 vaccine in peritoneal dialysis patients. Kidney Int 2021;100: 476-7.  Back to cited text no. 72
Yanay NB, Freiman S, Shapira M, et al. Experience with SARS-CoV-2 BNT162b2 mRNA vaccine in dialysis patients. Kidney Int 2021;99:1496-8.  Back to cited text no. 73
Husain SA, Tsapepas D, Paget KF, et al. Postvaccine anti-SARS-CoV-2 spike protein antibody development in kidney transplant recipients. Kidney Int Rep 2021;6:1699-700.  Back to cited text no. 74
Boyarsky BJ, Werbel WA, Avery RK, et al. Antibody response to 2-Dose SARS-CoV-2 mRNA vaccine series in solid organ transplant recipients. JAMA 2021;325:2204-6.  Back to cited text no. 75
Kronbichler A, Anders HJ, Fernandez-Juárez GM, et al. Recommendations for the use of COVID-19 vaccines in patients with immune-mediated kidney diseases. Nephrol Dial Transplant 2021;36:1160-8.  Back to cited text no. 76

Correspondence Address:
Sanjay Vikrant
Department of Nephrology, All India Institute of Medical Sciences, Bilaspur - 174 001, Himachal Pradesh
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1319-2442.344741

Rights and Permissions


  [Figure 1], [Figure 2], [Figure 3]


    Similar in PUBMED
    Search Pubmed for
    Search in Google Scholar for
    Email Alert *
    Add to My List *
* Registration required (free)  

    What are Coronav...
    Pathogenesis of ...
    Cytokine Release...
    Kidney Pathology...
    Epidemiology of ...
    Acute Kidney Inj...
    Coronavirus Dise...
    Management of Co...
    Coronavirus Dise...
    Drugs in the Man...
    Management of Ac...
    Management of Ki...
    Coronavirus Dise...
    Article Figures

 Article Access Statistics
    PDF Downloaded161    
    Comments [Add]    

Recommend this journal