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Abstract
The major targets of coronavirus disease 2019 (COVID-19) are the respiratory and immune systems. However, a significant proportion of hospitalized patients had kidney dysfunction. The histopathological surveys have principally focused on respiratory, hematopoietic, and immune systems, whereas histopathologic data of kidney injury are lacking. Our study aimed to summarize the renal histopathological findings in COVID-19 from the published case report and case series. We conducted a systematic searching of databases such as MEDLINE, EMBASE, and Cochrane Library for published reports of COVID-19 patients with renal histopathological changes from autopsy studies and from “for cause” indication biopsies. Included in our study are case reports and case series with extractable quantitative data on patient demographics such as age, sex, ethnicity, as well as data on renal function tests, their comorbidities, and biopsy to study the histopathological changes. Data were analyzed with Microsoft Excel. To evaluate the methodological quality, we chose the framework for appraisal, synthesis, and application of evidence suggested by Murad et al. Systematic searches of literature found 31 studies that fulfilled the eligibility criteria. These studies included a total of 139 cases, where individual case details including clinical and histopathological findings were available. The median age of the cases was 62 years with a male:female ratio of 2.5:1. Associated comorbidities were noted in 78.4% of cases. The majority of the cases had renal dysfunction with proteinuria which was documented in more than two-thirds of the cases. The histopathological findings observed the frequent tubular involvement manifested by acute tubular injury. Regarding glomerular pathology, collapsing glomerulopathy emerged as a distinct lesion in these patients and was noted among 46.8% of cases with glomerular lesions. A small subset of cases (4.3%) had thrombotic microangiopathy. Collapsing glomerulopathy emerged as a hallmark of glomerular changes among COVID-19 patients. Tubular damage is common and is linked to multiple factors including ischemia, sepsis among others. In the form of thrombotic microangiopathy seen in a subset of patients, vascular damage hints toward the hyper-coagulable state associated with the infection. The demonstration of viral particles in renal tissue remains debatable and requires further study.
Introduction 
Global pandemic caused by coronavirus disease 2019 (COVID-19) emerged from Wuhan, Hubei Province, China, in December 2019, affected more than 135 million individuals including more than 2.9 million deaths.[1] Coronavirus integrates with human cell by binding the Angiotensin-converting enzyme receptor 2 (ACE2). These receptors are highly expressed in the type II alveolar cells of lung, proximal tubule cells of the kidney, bladder urothelial cells, myocardial cells, ileum and esophagus epithelial cells, brain, heart, liver, blood vessels, etc., which is confirmed on the basis of single-cell RNA-seq (scRNA-seq) data analyses.[2],[3]
The lungs are the most affected organ due to the abundance of ACE2 receptors and clinical presentations range from asymptomatic to severe pulmonary involvements with diffuse alveolar damage and respiratory failure. However, the involvement of other organs especially the kidney has been also reported in a lot of studies associated with pulmonary involvement.[4],[5]
Initial reports showed during hospitalization acute kidney injury (AKI) occurred in up to 5.1% of patients with COVID-19 with proteinuria and hematuria observed at 43.9% and 26.7%, respectively.[6] However, in critically ill patients who were admitted to the intensive care unit (ICU) in Washington State, 19% of total patients developed AKI.[7] In another study conducted on 5449 patients admitted with COVID-19 in New York, 36.6% of hospitalized patients developed AKI. Among these patients, 53.5% had moderate or severe AKI while 14.3% required renal replacement therapy.[8]
The most common renal manifestation in COVID-19 patients is AKI, proteinuria, and hematuria. The etiology of AKI in COVID-19 patients is considered to be multifactorial. There have been several proposed mechanisms which includes: (1) direct cytopathic damage of kidney tubular and endothelial cells by the virus, as it has greater affinity for the ACE2 receptor; (2) indirect damage by virus-induced cytokine release, (IL2, 7, and 10, and granulocyte colony-stimulating factor), (3) by excessive activation of T lymphocytes, (4) renal hypoperfusion due to hypovolemia, (5) abnormal coagulation and (6) hyperventilation-relevant rhabdomyolysis.[4],[9],[10]
On the basis of various kidney biopsy and autopsy reports, acute tubular injury (ATI) is the most common pathological finding in COVID-19 patients. Besides ATI, Su et al[4] observed vasculitis and endothelial damage probably by obstruction of capillaries lumen by aggregation of erythrocyte. In another study, Golmai et al[11] observed ATI as the most common pathological finding but there was no confirmation of any vascular or capillary microthrombi and significant glomerular disease in the biopsy material.
A variant of focal segmental glomerulosclerosis (FSGS) and collapsing glomerulopathy (CG) were also found in some European and USA COVID-19 patients.[12],[13]
However, there is no clear observation as regards which type of renal failure most commonly affected COVID-19 patients. Furthermore, no study has been conducted to show the association of ethnicity, age, sex, and comorbidities with the renal involvement in COVID-19 patients.
To analyze the above lacunae, we conducted a systemic review of primary literature for recognizing the most common renal histo-pathological changes in COVID-19 patients with the help of renal biopsies.
Materials and Methods Data source and searches
To identify the case reports and case series on COVID-19-related renal changes, we systematically screened the PubMed/Medline and EMBASE database for medical literature. The articles were screened by using the search descriptor such terms as “[COVID” or “COVID-19” or “Severe acute respiratory syndrome coronavirus-2 (SARS-COV-2)] and (“renal disease” OR “kidney disease”) with filters for case reports in humans with English language. The search was limited to case reports or case series published between December 1, 2019, and December 31, 2020, with full text available in English.
Study selection and data extraction
All human studies published in full-text or abstract forms were initially screened for eligibility to assess the qualitative and quantitative analysis. From studies which are included, studies on specialized populations such as pediatric, or pregnant, or transplant, or autoimmune diseases were excluded. The articles published in languages other than English language or study designs such as prospective studies, cross-sectional studies, reviews, and randomized controlled trials for drug therapies were also excluded. The full texts of the remaining studies were then assessed for the following inclusion criteria: case reports and case series of renal tissue from autopsies as well as “for cause’ indication biopsies. Biopsies with extractable quantitative data on patient demographics such as age, sex, ethnicity, as well as data on renal function tests, their comorbidities, and biopsy to study the histopathological changes of a reverse transcriptase-polymerase chain reaction (RT-PCR) positive COVID-19 patient were also assessed. The study selection conducted by two authors (SBV, HK) independently was based on predefined selection criteria. Any differences between two authors about studies were resolved after discussions with all review authors. From the eligible case reports and case series, we extracted information like study characteristics, including author name, publication year, type of study, number of patients, patient demographics (e.g., age, gender, and ethnicity), comorbidities, details of renal function test and its biomarkers, and biopsy findings including histopathological changes, immunohistochemistry (IHC), and electron microscopic changes. The data were extracted by two authors (SBV, VV) independently from the selected studies. The data was collected, disagreements were discussed, and differences were resolved between review authors.
Quality assessment
Case reports and case series are uncontrolled study designs known for increased risk of bias. To evaluate the methodological quality, we chose the framework for appraisal, synthesis, and application of evidence suggested by Murad et al.[14] Domains included in the risk of bias assessment were selection, ascertainment, casualty, and reporting. Within each domain, a series of questions (“signaling questions”) to elicit information about features of the trial that are relevant to risk of bias were framed. Under selection “signaling question” was “Does the patient(s) represent(s) the whole experience of the investigator (center) or is the selection method unclear to the extent that other patients with similar presentation may not have been reported? Under the ascertainment, it was “Was the exposure adequately ascertained? And was the outcome adequately ascertained? Under the causality “Were other alternative causes that may explain the observation ruled out? And was follow-up long enough for outcomes to occur? Under the reporting “signaling question” framed was “Is the case(s) described with sufficient details to allow other investigators to replicate the research or to allow practitioners make inferences related to their own practice? Two authors (SBV, HK) read all papers and assessed the methodological quality. Discrepancies were resolved by consensus. This systematic review did not have a “standalone” study protocol. The study results were reported by following the guidelines of the “Preferred Reporting Items for Systematic Reviews and Meta-Analyses” (PRISMA) statement.[15]
Statistical Analyses Statistical analysis was done with IBM SPSS Statistics version 25.0 (IBM Corp., Armonk, NY, USA). Continuous variables were expressed as mean with standard deviation. Categorical variables were expressed as number of cases and percentages (%).
Results In this study, a total of 284 articles were screened for admissibility, out of which 208 article seems to be relevant for analysis after removing duplicates. From 208 articles, 96 were excluded for various reasons and 112 articles were screened for eligibility. Among 112 articles, 31 articles were included for final qualitative and quantitative analysis and 81 articles were excluded because in 33 articles studies included transplant kidney, 40 articles did not have biopsy report and 8 articles were published in other languages. A total of 31 studies were included, which together included 139 cases. [Figure 1] shows the PRISMA flow chart depicting the study selection process along with reasons for their ineligibility or exclusion.[4],[10],[11],[13],[16],[17],[18],[19],[20],[21],[22],[23],[24],[25],[26],[27],[28],[29],[30],[31],[32],[33],[34],[35],[36],[37],[38],[39],[40],[41],[42] All these cases were selected on the basis of the availability of demographic data, renal function tests, urinalysis, and histopathological findings.
Figure 1. Preferred Reporting Items for Systematic Reviews and Meta-Analyses flow chart.The median age of the cases was 62 years (25-92 years). Male to female ratio was 2.5:1. Details of race were available in 98 cases, of which the majority were black (42/98, 42.8%). Single (44, 40.7%) and multiple (64, 59.3%) comorbidities were noted in 78.4% (108/139) cases. Hypertension and diabetes mellitus were the two most common comorbidities. Serum creatinine value was available in 129 (92.8%) cases. The mean serum creatinine is 5.7 and median value is 4.9 mg/dL (range 0.4−20 mg/dL). A total of 81.4% (105/129) cases had serum creatinine value of more than 1.5 mg/dL. Proteinuria was assessed in 77% (107/139) cases. The proteinuria was moderate to heavy in 74.3% (78/107) cases. Hematuria is noted in 58.2% (53/91) cases. The most common renal presentation was AKI, with or without accompanying nephrotic range protei-nuria/nephrotic syndrome.
Summary of characteristics of individual patient data is described in [Table 1] and details of the individual studies are summarized in Supplementary Table 1[Additional file 1].
Table 1. Baseline characteristics and histopathological changes of included studies.
Glomerular pathology
Glomerular pathology was noted in 67.6% (94/139) cases. CG was noted in 46.8% (44/94) cases. Other glomerular changes were noted in 31 cases [diabetic nephropathy (DN) - 9, FSGS other than CG - 6, membranous glomerulonephritis (MGN) - 4, anti-neutrophil cytoplasmic antibodies (ANCA) associated glomerulonephritis - 4, postinfectious GN (PIGN), IgA nephropathy (IgAN) and Henoch-Schönlein purpura (HSP) nephritis, each in two cases while anti-glomerular basement membrane (anti-GBM) disease, lupus nephritis with PIGN, each in one case]. These changes probably are not associated with COVID-19.
Thrombi in glomerular capillary loops were observed in 10.6% (10/94) cases; of these six were labeled as thrombotic microangiopathy (TMA) and two had extensive renal cortical necrosis. Non-specific glomerular lesions were described in 20.2% (19/94) cases. Among these, mesangial changes were noted in nine cases (minimal mesangial expansion - 3, mild mesangial expansion - 4, moderate mesangial expansion - 1 and mesangial sclerosing glomerulopathy - 1), non-specific glomerular sclerosis in five cases, glomerular hypertrophy in two cases, mild hypoperfusion, endothelial swelling, glomerular RBCs congestion and segmental inflammatory cells in GCL, each in one case. A large number of these cohorts had hypertension and/or diabetes, so we compared the frequencies (using Fischer’s exact test) of CG between two groups-cases with hypertension and/or diabetes versus cases without hypertension and/or diabetes. Similar comparisons were also done for tubulointerstitial pathology and vascular lesions. We could not observe any significant difference for any of these histopathological parameters between these two groups.
Tubulointerstitial pathology
The acute tubular injury was noted in 86.3% (120/139) cases, which was graded in 81.7% (98/120) cases as mild, moderate, and severe. In 22.4% (22/98) cases, it was mild or focal, in 23.4% (23/98) cases as moderate and severe in 54% (53/98) cases. Tubular casts were noted in 7.9% (11/139) cases, of which pigmented casts in 5 cases (1 myoglobin casts), muddy brown casts in three cases, RBCs casts in one case, and unspecified in two cases. Interstitial fibrosis and tubular atrophy (IFTA) were assessed in 46.7% (65/139) cases only, where it was graded as mild in 66.1% (43/65) cases, moderate in 21.5% (14/65) cases, and severe in 12.3% (8/65) cases. Variable degree of interstitial inflammation was noted in 28% (39/139) cases. Tubular microcysts were noted in 13.7% (19/139) cases. Oxalate crystals were noted in 2.9% (4/139) cases, of which two cases it was significant to label it as oxalate nephropathy. Acute interstitial nephritis was noted in 3.6% (5/139) cases while tubulitis was noted in 2.1% (3/139) cases.
Vascular pathology
Vascular changes in form of arteriosclerosis or arteriolosclerosis were assessed in 79.1% (110/139) cases, and were present in 89.1% (98/110) cases. Among these 98 cases, these changes were graded in 92.8% (91/98) cases. It was mild in 28.6% (26/91) cases, moderate in 37.4% (34/91) cases, and severe in 34% (31/91) cases. Changes of vascular thrombotic microangiopathy with arteriolar thrombi were noted in 4.3% (6/139) cases, of which 4 cases had also glomerular TMA while the remaining two cases had isolated arteriolar TMA.
Electron microscopy
Electron microscopy findings were available in 67.6% (94/139) cases, of which coronavirus (CoV) like viral particles were noted in 11.7% (11/94) cases. Among these 11 cases, seven cases reported the presence of viral particles in both podocytes and tubular epithelial cells, two cases in podocytes only while two cases in tubular epithelial cells only. Additional specific findings were described as: variable foot process effacement in 60.6% (57/94) cases, endothelial injury in the form of swelling and subendothelial lucent expansion in 17.0% (16/94) cases, tubule-reticular inclusions (TRIs)/ aggregates in 24.5% (23/94) cases and electron-dense deposits in 7.4% (7/94) cases.
Immunohistochemistry and in-situ hybridization
IHC was performed in four studies with a total of 9.3% (13/139) cases and was positive in 23% (3/13) cases. In situ hybridization testing for COVID-19 was also performed in four studies with a total of 9.3% (13/139) cases and was negative in all cases.
Risk of bias
Risk of bias of each study was done based on selection, ascertainment, casualty, and reporting. The various outcomes of quality assessment of individual case study are summarized in Supplementary [Table 2]. Risk of bias was low, but the study design of case reports or case series constitutes for low quality of evidence. Therefore, the certainty of the evidence was low for included studies. However, considering total number of case reports and case series and cumulative analysis of their changes makes reliable data for histological changes of kidney among COVID-19 patients.
Discussion SARS-CoV-2 causes infection resulting in a varied clinical spectrum ranging from asymptomatic cases to life-threatening illnesses. The major brunt of the disease is faced by the pulmonary parenchyma, where the classical morphological change of acute respiratory distress syndrome is described. The damage to the lung tissue can occur via direct cytotoxic insult by the virus or can be a result of generalized inflammatory response.[43],[44]
Early studies of COVID-19 revealed a low frequency of AKI ranging from 0.5% to 1.5%. However, later studies showed a much higher incidence of AKI, over 20% in hospitalized patients and over 50% in ICU patients.[45] AKI in COVID-19 patients can be attributed a number of etiologies that can range from prerenal insult to acute tubular injury resulting from ischemia, drugs or intrinsic toxin, to CG.[24] Hemodynamic factors, cytokine storm, imbalances in cell-mediated immunity, tropism of virus toward renal tissue and endothelial injury leading to the development of microthrombi are the different postulated mechanism that can lead to AKI.[39] We have reviewed the kidney pathological findings from both, autopsy studies as well as “for cause” biopsies in COVID-19 cases. Four-fifth of these cases had renal dysfunction, with serum creatinine value of more than 1.5 mg/dL.
Chen et al observed that men were more vulnerable to acquire COVID-19 than females. A similarity to this observation was reflected in this analysis, where male patients were twice more common than females.[46] Earlier studies suggested that the innate immune responses against majority of virus infections in females were greater than male and estrogen play a major role in these antiviral immune response.[46],[47],[48] Further SARS-CoV-2 binds to ACE2-positive cells and higher expression of ACE2 in men probably explains why male gender is considered as a risk factor for higher severity and poorer outcome in COVID 19 patients.[49],[50],[51] Although based on our study, it is difficult to infer that male patients are more vulnerable to COVID-19. In this study, more than half of the patients aged above 60 years. Aiello et al observed that as age advances, both innate and adaptive immune defense system disrupted due to immunosenescence.[52] Both expression and downstream signaling of TLRs appear to be impaired leading to an inadequate immune response.[52],[53]
The most common comorbidity associated with COVID-19 is hypertension. Hypertension induces an imbalance of cytokines, particularly it leads to increased levels of IL-6, interleukin-7, granulocyte-macrophage colony-stimulating factor, and tumor necrosis factor-α increased. Huang et al observed that the cytokine storms of above said cytokines results in deterioration of COVID-19 patients.[54] Patients with higher body mass index are more predisposed to COVID-19 by decreasing respiratory capacity and ventilation. Furthermore, abdominal obesity, surges inflammatory cytokines, and free radical species which are responsible for the development of hypertension, diabetes, and impaired lipid profile.[55] DM, a chronic inflammatory condition with various micro and macrovascular complications, may affect immune responses to various microbes.[56] Uncontrolled diabetes is responsible for impaired immune responses including impaired lymphocyte proliferation, monocyte/macrophage, and neutrophil actions against various harmful pathogens.[57],[58]
Among all the morphological findings analyzed in the present study, tubular compartment appeared to be the most significantly affected. Nearly all cases had a variable degree of tubular injury manifested by necrosis and sloughing of epithelial cells, cytoplasmic vacuolization, and attenuation of lining epithelium and luminal ectasia. Potential triggers for ATI in these cases included significant hemodynamic instability, sepsis, medications including antibiotics, ACE-2 inhibition, and rhabdomyolysis. Apart from these triggers, studies have shown that there is a temporal association with initiation of mechanical ventilation and vasopressor drugs to the evolution of AKI.[59] Rhabdomyolysis, one of the contributory factors for AKI, has been described in several studies.[43],[48] Sharma et al, described the pathological findings in 10 “for cause” kidney biopsies. The authors described tubular damage in all cases, and the tubular damage was attributed to hemodynamic instability, pigment nephropathy, and medications. In their study, two cases lacked these triggers.[35]
Variable degree of interstitial inflammation was described in more than one-fourth of cases. Although a number of viruses can cause interstitial inflammation, including parvovirus, cytomegalovirus, Epstein-Barr virus, among others.[45] Interstitial inflammation to a mild degree is often non-specific and may be accompanied by associated tubular damage, however, systemic inflammatory response to COVID-19 may also lead to accentuated inflammatory cells response in interstitial compartment.[60]
A spectrum of glomerular changes is noted in kidney tissue of COVID-19. CG has been described in 46.8% of cases. CG is a severe form of FSGS characterized histologically by hyperplasia and hypertrophy of visceral epithelial cells with underlying obliterated or narrowed glomerular capillaries and collapsed glomerular tufts. The collapsing lesions are also associated with significant degree of tubulointerstitial damage in the form of tubular microcysts and interstitial nephritis. A small subset of cases with COVID-19 associated CG had these features. In the mid-1980s, CG was first described in small series of six African-American subjects presenting with nephrotic syndrome and rapidly progressive renal failure. CG is the defining lesion in HIV-associated nephropathy (HIVAN). Apart from HIV/AIDS-associated CG, other conditions associated with CG include viral infections (such as parvovirus B19, cytomegalovirus, Epstein−Barr virus and influenza), drugs (such as interferon therapy and pamidronate), bacterial infections (such as tuberculosis), systemic lupus erythematosus (SLE), hemo-phagocytic syndrome and glomerular ischemia, among others.[61] Several of these triggers are postulated to cause podocyte cytotoxicity through inflammatory cytokines generation including interferons (type 1).[62] Except HIV and Parvovirus infections, CG associated with other viral infections lack the presence of viral particles in renal epithelial cells.[45] This point hints toward the role of additional pathogenic mechanism such as cytotoxic effects of interferons against podocytes. In Nasr et al’s study, collapsing GN was noted in 57% (8/14) cases of COVID-19. However, no definite viral particles were identified on ultrastructural examination.[31] Similarly, Kudose et al, found CG in 35.7% (5/14) cases and, no definite viral particles were identified in renal epithelial cells with the different orthogonal approaches used by the authors. However, both these studies showed the presence of TRIs on ultrastructural examination in a subset of their CG cases.[27] TRIs, also known as interferon footprints, are postulated to be caused by exposure of interferon-alpha. These structures are described mainly in HIVAN, however, it can be seen in SLE, following treatment with interferon-alpha and other viral infections as well.[63] One additional point noted was the association of COVID-19 related CG with black race and apolipoprotein L1 (APOL1) polymorphisms. In the study by Nasr et al, all cases with COVID-19 related CG had APOL1 risk alleles and all patients were of black race. Earlier, it was shown that 10%−15% of the African-Americans harbors highrisk APOL1 alleles (either G1/G1, G1/G2, or G2/G2). These alleles are overrepresented in cases of CG (both HIV-associated or non-HIV-associated) from African Americans.[31] Experimental studies using cell cultures and animal models suggest that the high-risk APOL1 alleles results in upregulation of APOL1 that confers podocyte damage with perturbed endosomal trafficking and autophagosome flux, resulting in depletion of podocytes and eventual glomerular scarring.[62]
In this analysis, 22% of cases had glomerular pathology other than collapsing variant of FSGS. Among these, DN and FSGS (other than CG) were the common glomerular lesions. These appear to be the incidental findings, rather than any pathogenic link with COVID-19. Three cases of ANCA-associated glomerulonephritis causing AKI were described in COVID-19.[39] Although a direct association between COVID-19 and ANCA-associated glomerulonephritis cannot be conclusively made, however, it might be speculated that COVID-19 might be the second hit event in these cases. Further, the role of neutrophil extracellular traps (TRAPs) in COVID-19 pathogenesis have been proposed, as observed in biopsy samples of ANCA-associated vasculitis.[39] Two cases of HSP nephritis associated with COVID-19 have been described in literature. The association of HSP nephritis with respiratory viruses is known. It might be possible that COVID-19, which targets lungs, is a triggering factor for this IgA vasculitis.[38]
Vascular changes in the form of TMA were noted in COVID-19. In this review, we found six cases of TMA. COVID-19 is a hyper-coagulable state.[64] Various theories have been proposed for the development of TMA, including direct viral attack to endothelial cells or indirect pathways through the activation of latent complement defect.[24] Endothelial cells express the ACE-2 receptor, a putative binding site for COVID-19 spike protein.[2] The invasion of endothelial cells by virus triggers a profound innate response leading to widespread activation of inflammatory cells, cytokine release, and activation of complement.[65] The presence of microthrombi in various microcirculation, as reported in various autopsy studies, suggests the presence of small vessel microangiopathy resembling TMA induced by complements defects.[66],[67]
In this analysis, the demonstration of viral particles within renal tissue was done in 12 cases (11 using electron microscopy and 3 using IHC; two had both IHC and electron microscopy done). Among the 25 studies describing electron microscopy findings, CoV-like particles in renal tissue were identified in only 20% (5/25) studies. However, several authors suspected the particles were multivesicular bodies or clathrin-coated vesicles, rather than true viral particles.[68],[69],[70] Without using additional orthogonal tools including IHC, ISH, or immunogold labeling, the confirmation of these viral particles is problematic. Su et al performed electron microscopic studies in nine cases, of which seven cases had viral particles in the podocytes and/or tubular epithelial cells. Further, the authors showed immunohistochemical staining against SARS-CoV nucleocapsid protein in three of these cases.[4] Findings SARS-CoV particles in these cases are intriguing and indicate the possible infection of podocytes and tubular epithelial cells by the virus. However, it is still debatable in the literature about the presence of viral particles in the renal parenchyma.
Strengths and Limitations In this study, renal histopathological changes among 139 COVID-19 patients across the world were analyzed. This pooled data may be helpful for the scientific community to guide the management of COVID-19 patients with renal dysfunction. CG observed to be a distinct glomerular change among COVID-19 patients. Acute tubular injury is common finding and is attributed to multifactorial etiology. Vascular changes in form of thrombotic microangiopathy, though seen in a minority of cases, support the hypercoagulable state associated with COVID-19. Ultrastructural findings hint toward the presence of viral particles in the podocytes and tubular epithelial cells. A major limitation of this study is that the lack of high-quality studies. Even though lack of high-quality studies, the inferences from these studies can be helpful in guiding decisionmaking in an individual with renal function abnormalities among COVID-19 patients. Another major limitation of this study was that only case reports/series published in English language were included.
Conclusion CG emerged as a hallmark glomerular change among COVID-19 patients. Tubular damage seems to be the most common pathology and is linked to multiple factors including ischemia, sepsis among others. Vascular damage, in the form of thrombotic microangiopathy seen in a subset of patients, hints toward the endothelial damage and hypercoagulable state associated with the infection. The demonstration of viral particles in renal tissue remains debatable and requires further studies.
Conflict of interest: None declared.
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