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Saudi Journal of Kidney Diseases and Transplantation
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Table of Contents   
ORIGINAL ARTICLE  
Year : 2021  |  Volume : 32  |  Issue : 5  |  Page : 1356-1364
Impact of frailty and viral load on acute kidney injury evolution in patients affected by Coronavirus Disease 2019


1 Department of Health Science, Universidad Simón Bolivar; Department of Nephrology, Cost Clinic, Barranquilla, Colombia
2 Department of Health Science, Universidad Simón Bolivar, Barranquilla, Colombia; Department of Research, Hospital Italiano de Buenos Aires; Department of Physiology, Instituto Universitario del Hospital Italiano de Buenos Aires, Buenos Aires, Argentina
3 Department of Health Science, Universidad Simón Bolivar, Barranquilla, Colombia
4 Department of Health Science, Universidad Simón Bolivar, Barranquilla; Doctorate in Biomedical Science, Universidad del Valle, Cali, Colombia
5 Department of Health Science, Free University, Barranquilla, Colombia
6 Department of Internal Medicine, Division of Immunology, Alejandro Posadas National Hospital, Buenos Aires, Argentina

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Date of Web Publication4-May-2022
 

   Abstract 


This paper describes the main characteristics of coronavirus diseases 2019 (COVID-19) patients suffering from acute kidney injury (AKI) assisted at a high complexity clinic in Barranquilla, Colombia. The patients included in this study (n = 48) were those with a positive diagnosis of COVID-19 confirmed by polymerase chain reaction detection of severe acute respiratory syndrome coronavirus 2, who had developed AKI during their hospital stay. Serum and urine parameters, as well as patient’s viral load and clinical frailty scale (CFS) were recorded. A statistical analysis of the recorded parameters, such as comparisons, and correlations between variables of interest, were explored. The prevalence of COVID-19 induced AKI was 41%, being the majority of them classified as AKI network classification 3, with a renal replacement therapy requirement of 29%, and an associated mortality of 73%. AKI patients’ mortality showed a significant positive correlation (33%) with patients’ CFS score but not with their viral load. COVID-19 induced AKI significantly correlated with patients’ frailty status but not to their viral load.

How to cite this article:
Aroca-Martínez G, Musso CG, Avendaño-Echavez L, González-Torres HJ, Vélez-Verbel M, Chartouni-Narvaez S, Peña-Vargas W, Acosta-Hoyos A, Ferreyra L, Cadena-Bonfanti A. Impact of frailty and viral load on acute kidney injury evolution in patients affected by Coronavirus Disease 2019. Saudi J Kidney Dis Transpl 2021;32:1356-64

How to cite this URL:
Aroca-Martínez G, Musso CG, Avendaño-Echavez L, González-Torres HJ, Vélez-Verbel M, Chartouni-Narvaez S, Peña-Vargas W, Acosta-Hoyos A, Ferreyra L, Cadena-Bonfanti A. Impact of frailty and viral load on acute kidney injury evolution in patients affected by Coronavirus Disease 2019. Saudi J Kidney Dis Transpl [serial online] 2021 [cited 2022 May 25];32:1356-64. Available from: https://www.sjkdt.org/text.asp?2021/32/5/1356/344755



   Introduction Top


In December 2019, the first cases of a lung disease of unknown etiology began to be described in the province of Wuhan (China). These were later attributed to a new variety of coronavirus i.e., the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and the disease it causes i.e., coronavirus diseases 2019 (COVID-19).[1],[2]

COVID-19 can affect many other organs in addition to the respiratory system, particularly in the kidney, heart, digestive tract, blood, and nervous system.[3] As for the kidney alterations, preliminary reports indicated an incidence of 3%–9%. However, it has been proposed that this varies depending on the specific type of reported renal affectation: albuminuria (34%), proteinuria (63%), hematuria (27%), proteinuria with hematuria (44%), and/or increase in serum creatinine and urea levels (14%–27%).[4] Direct deleterious action of this virus on the kidney has been demonstrated by the histopathological analysis of samples of this organ collected from patients who died of COVID-19. Findings include loss of the brush border and non-isometric tubular vacuolation, microvascular luminal occlusions (glomerular and peritubular) consisting mainly of erythrocytes, endothelial damage, and pigmented casts detected in association with high serum levels of creatine phosphokinase (rhabdomyolysis).

In addition, electron microscopy evidenced spherical viral particles characteristic of coronavirus in podocytes and the proximal tubular epithelium, which were associated with effacement of the pedicels, occasional vacuolation, and detachment of podocytes from the glomerular basal membrane, with the viral presence being confirmed by immuno-fluorescence.[5]

There is growing evidence that acute kidney injury (AKI) is prevalent in SARS-CoV-2 infection, with a reported incidence of 8%–17%, reaching 35% in critical patients, and that this condition is considered a poor prognostic factor.[6] In this sense, the development of AKI in the context of COVID-19 has an associated mortality of 91.7%.[7] Among the risk factors associated with its development, the following have been identified: presence of malignant pathology, sepsis, right heart failure, and disseminated intravascular coagulation (DIC).[8] It has been proposed that the mechanism by which the virus produces renal injury has multiple causes, including direct cytopathic effects mediated by viral binding to angiotensin-converting enzyme II receptors, as well as acute tubular necrosis triggered by factors such as volume depletion, cytokine storm, hypoxia, shock or rhabdomyolysis, and finally, immune complex deposition.[9]

This paper describes the main characteristics of patients with COVID-19 and AKI assisted at a high complexity clinic in Barranquilla, Colombia, including their particular features, and evaluates the impact of viral load and prior patient frailty on the clinical evolution of AKI.


   Methods Top


A complete review of the medical records of all patients admitted to the institution from April 1, 2020 to July 11, 2020 and suspected of having COVID-19 was performed. The patients included were those with a positive diagnosis of COVID-19 confirmed by polymerase chain reaction (PCR) detection of SARS-CoV-2, who had developed AKI during their hospital stay in the emergency room, general hospitalization room, and intensive care unit. Sample handling and processing for SARS-CoV-2 diagnosis were conducted in accordance with the reverse transcription realtime PCR (RT-PCR) guidelines (Diagnostic detection of 2019-nCoV by real-time RT-PCR Charité Virology, Berlin, Germany).[10] AKI was defined as an increase in creatininemia >0.3 mg/dL relative to the hospital admission value. In addition, each documented episode of AKI was classified according to the AKIN criteria [Table 1].[11] Additionally to creatininemia, the following patient parameters were recorded: serum urea values, blood urea nitrogen, serum electrolytes, blood count, liver function tests [bilirubin, transaminase, lactate dehydrogenase (LDH)], serum ferritin, D-dimer, coagulation parameters [partial thromboplastin time (PTT), prothrombin time (PT), and international normalized ratio (INR)], troponin, and viral load, as well as the presence of proteinuria, hematuria, and leukocyturia. Moreover, to establish the degree of preexisting frailty, the Clinical Frailty Scale (CFS) was used [Table 2].[12]
Table 1: Acute kidney injury stages (KDIGO 2012).

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Table 2: Clinical frailty scale.

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A statistical analysis of the recorded values (mean, standard deviation, minimum, maximum, range, among others) was performed (Student t test). Mean or median comparisons between levels of frailty or viral load value and clinical parameters of interest were made, and correlations between variables of interest were also explored. Finally, a correspondence analysis in R-CRAN was carried out among all the variables evaluated.

This study was approved by Ethical Committee of Clinica de la Costa, Barranquilla (Colombia), and informed consent was obtained from all patients.


   Results Top


From a population of 762 patients admitted to Clínica de la Costa (Barranquilla, Colombia) with COVID-19-compatible symptoms, 117 patients tested positive for SARS-CoV-2 confirmed by PCR at the time of evaluation (April 2020–July 2020), 48 developed AKI (41% prevalence). AKI was documented 4 ± 3.4 days after admission, and most of these patients were in the intensive care unit (75%). With respect to the subgroup that developed AKI, the mean age was 61 ± 15 years, with a clear predominance of males (79%), and average creatininemia and uremia values of 3.35 ± 1.74 mg/dL and 106.91 ± 26.9 mg/dL at diagnosis, respectively [Table 3]. The most common stage of AKI was AKI network (AKIN) classification 3 (46%), followed by AKIN 1 (40%) and AKIN 2 (14%). A total of 29% of patients required renal replacement therapy (RRT), predominantly intermittent hemodialysis (76%). In contrast, the AKIN stage correlated inversely and significantly with survival so that for each increase in AKIN stage, the patient’s survival decreased by 29% (R = −0.2956, P = 0.04). Approximately 18.8% (n = 9) and 12.5% (n = 6) patients regained their kidney function in whole or in part, respectively. Documented urinary abnormalities in association with AKI were, in decreasing order, proteinuria (35%), hematuria (31%), and leukocyturia (4%). Regarding signs and symptoms secondary to COVID-19, the following stood out in the AKI subgroup: fever (100%), dyspnea (85%), marked asthenia (48%), and myalgia (40%). Among the inflammatory biochemical and systemic compromise markers (direct and indirect) which changed (increased) the most, the following stood out: C-reactive protein, ferritin, and D-dimer [Table 4]. In relation to the background of the patients who developed AKI, 69% were robust (CFS: 1–3), 21% were frail (CFS: 4–5), and 10% were very frail (CFS: 6–7). In terms of the impact of the frailty condition prior to the development of AKI secondary to COVID-19, significantly higher white blood cell counts (P = 0.007), serum LDH levels (P = 0.003), and mortality (P = 0.006) were documented among frail patients when compared with those in robust ones. Mortality increased by 33% with each rise in the patient’s degree of frailty (0.33, P = 0.02). When the comorbidities were evaluated, the most prevalent in decreasing order of frequency were: high blood pressure (58%), obesity (40%), chronic kidney disease (CKD) (23%), diabetes mellitus (23%), chronic obstructive pulmonary disease (19%), and congestive heart failure (13%). As for the overall evolution of these patients, most required administration of inotropic drugs (87%) and ventilatory support (93%), mainly invasive ventilation (67%). Finally, the mortality of patients with AKI was 73%. When all the variables evaluated in these patients were correlated with the need for RRT, a significantly positive correlation was found with previous CKD (P = 0.04), serum leukocyte count (P = 0.04), hemoglobinemia (P = 0.03), troponin (P = 0.03), LDH (P = 0.05), bilirubinemia (P = 0.02), and INR (P = 0.01) [Table 5]. It should be noted that the viral load (3.12 ± 0.3) in our study did not correlate significantly with the degree of frailty, the need for RRT, or with patient mortality.
Table 3: Renal function markers.

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Table 4: Biochemical markers of inflammation and systemic compromise.

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Table 5: Main correlations with renal replacement therapy.

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In the correspondence analysis, only a significant correspondence was found between the “robust” condition and the serum ferritin level. Likewise, the D-dimer level was located at an intermediate point between the condition of “frail” and “very frail.”


   Discussion Top


This study found that the prevalence of AKI in the context of COVID-19 was 41%, ranging from 5% to 76% of the prevalence reported by other studies, a difference that possibly depends on whether inpatients in general are included in the study or only those admitted to the intensive care unit.[13],[14],[15],[16] Similar to other reports, the onset of AKI was within the 1st week of admission.[15] Likewise, the finding of a predominance for this condition in older adults (61 ± 15 years), particularly males, also coincides with what has been observed by other authors.[14] With respect to the AKI subtype (AKIN), based on our experience, the most common class was AKIN 3 and the least frequent was AKIN 2, a proportion that matches that of most previous reports, with the exception of some authors who reported that AKIN 1 was the most common class, followed by AKIN 3.[14],[15] It could be speculated that this difference in the AKIN type prevalence could be attributed to the evolution time at which AKI was diagnosed in each study. RRT was required in 29% of the patients affected by AKI due to COVID-19, a clinical picture that Meijers and Hilbrands have proposed to be designated as “COVAN.”[17] This percentage of patients receiving RRT is in line with what has been reported in the literature, where RRT use oscillates between 14% and 38%.[14],[15] In our study, the percentage of COVAN patients who recovered during internment, either totally or partially, was approximately 31%. The percentage of recovery described by other publications oscillates between 17.4% and 50%.[15] As for the urinary manifestations of COVAN, proteinuria was predominant (35%), followed by hematuria (31%), and to a lesser extent leukocyturia (4%). This order of frequency is commonly reported in scientific publications, with some variations depending on the various clinical contexts: proteinuria (44%–84%), hematuria (25%–81%), and leukocyturia (4%–60%).[9],[15],[18] The origin of these abnormalities has been attributed to the various mechanisms of kidney damage detailed below. However, it has been postulated that the clear preponderance of proteinuria, whose prevalence exceeds even the proportion of patients developing AKI, may be secondary to the febrile state inherent to this condition or to the activation of glomerular hyperfiltration in the context of a systemic inflammatory state.[15],[18],[19],[20] Mechanisms identified as a cause of COVID-19-related kidney injury or COVAN include[4],[9],[13],[14],[16],[17],[18],[19],[20],[21],[22],[23],[24],[25]

  1. Direct cytopathic action of the virus because studies have detected it in the urine and renal tissue (podocytes and proximal tubules), where angiotensin II-converting enzyme, considered the putative receptor of the virus mediating cell entry, is expressed in abundance. It is worth mentioning that some authors deny this mechanism.
  2. Acute tubular necrosis generated by various factors such as bacterial sepsis, cytokine storm, tissue hypoxia, rhabdomyolysis, and nephrotoxic drug use.
  3. Injury caused by immune complexes due to viral antigen deposition.


It should be noted that the development of COVAN is a risk factor for admission to the intensive care unit, RRT requirement, and death.[15],[16] CKD (6%) and end-stage kidney disease (2%) have also been reported as COVAN sequelae.[18] Regarding the symptomatology characteristic of COVID-19, other reports have also described, as in our study, fever (100%) as well as respiratory (76%) and muscle (43%) symptoms.[21] As in other studies, among the inflammatory biochemical and systemic compromise markers (direct and indirect), C-reactive protein, ferritin, and D-dimer stood out. This reinforces the idea that the renal and systemic damage generated by COVID-19 is fundamentally reactive, induced by the patient’s own immune system and by a series of mediators (cytokines) released during the so-called “inflammatory storm”.[16],[22] When assessing the comorbidities of our patients, they coincided in type and proportion with those reported in other studies, the most significant ones being high blood pressure (60%), obesity (30%), CKD (34%), diabetes mellitus (30%), chronic obstructive pulmonary disease (14%), and oncological pathology.[13] In line with the literature, the vast majority of patients also required inotropic and ventilatory support (80%–90%). Nevertheless, mortality was very high (73%) when compared with previous reports, where it ranged between 16.1% and 62%.[13],[14],[15],[23] This phenomenon may be linked to the considerable proportion of frail patients reported in this population (31%), as discussed below. The homeostatic capacity of individuals allows them to successfully cope with clinical situations that jeopardize their body integrity. This capacity can be measured by applying a validated scale (the CFS) [Table 2]. To assess the impact of this clinical condition on the evolution of COVAN, the degree of frailty of the study population was determined and its relationship with the evolution of the disease was analyzed. The results showed that 69% of the patients who developed AKI were robust (CFS: 1–3), 21% were frail (CFS: 4–5), and 10% were very frail (CFS: 6–7). The degree of frailty was significantly correlated with mortality, with a 33% increase for each rise in the degree of frailty, which is reasonable given the effect that a reduced functional reserve has on the patient’s evolution.

Viral load (3.12 ± 0.3 copies/mL) was not significantly correlated with the degree of frailty, renal replacement requirement, or mortality. Although a previous report noted that viral load (6.2 copies /mL, RIC: 3.0–8.0) showed a significant independent association with mortality, the viral loads were much higher than in the population we studied.[23] It could also be hypothesized that the air way viral load did not correlate with AKI severity, since renal damage depends on the urine (tubular) viral load or, even probably more, on the sort of the patient’s immunological response.[25],[26],[27] Regarding the significant correspondence observed between the robust condition and the serum ferritin level, as well as between the frailty status and the D-dimer value, this could be interpreted as follows:[28],[29],[30],[31],[32],[33],[34],[35] Ferritin, transferrin, interleukin-6, D-dimer, fibrinogen, and C-reactive protein are among the parameters described as characteristic of the systemic inflammatory syndrome associated with acute infection by COVID 19. With respect to ferritin it is an intracellular iron storage protein. In moments of systemic stress, ferritin in the blood comes from the acute destruction of cells previously at rest such as hepatocytes, macrophages or cells of the bone marrow. By increasing suddenly in the blood, ferritin is responsible for the systemic stimulation of cells of innate immunity such as macrophages. The macrophage response is the secretion of cytokines generating the so-called cytokine storm, the activation of recruitment mechanisms of acute inflammatory mediators and subsequently the presentation of antigens.[29],[30],[31],[32],[33],[34],[35] Regarding the D-dimer in blood, it is a marker of thrombin generation and fibrinolysis. During coagulation, thrombin is generated that results in the conversion of fibrinogen to fibrin and degradation products, among them D-dimer. There is a constant interaction between the immune system and the coagulation system in response to infection by any microorganism to prevent its indiscriminate spread, causing the condition called DIC. This parameter is related to the presence of previously existing endothelial damage or activation, which can be acute or chronic. Differences in the host’s previous status at the time of SARS-CoV2 virus infection may be the factor that determines the degree of existing endothelial stress. The progression of the predominant biomarkers in the evolution of the systemic inflammatory syndrome would be the result of the combination of variables between the host and the virus. In a previously robust organism and without apparent prior pathology, the poor evolution of COVID-19 infection would depend on the way in which the immune system orchestrates its response. In this sense, an acute serum ferritin elevation as the predominant systemic inflammation mechanism will cause cytokine storm and organ damage. In contrast, in a fragile organism, previously chronically stressed, forms of severe endothelial inflammation occur. In this case, SARS-CoV-19 infection could potentiate the host frailty status, inducing an acute microthrombotic activity which significantly elevates dimer D levels in blood. This biomarker would also determine the poor clinical evolution due to micro-tromboembolic activity or DIC.[32]


   Conclusions Top


In this study, AKI secondary to COVID-19 (COVAN) showed a prevalence of 41% in a hospitalized population with a positive diagnosis of SARS-CoV2 by PCR. Most cases were AKIN 3, with a renal replacement requirement of 29%, and a mortality of 73%. The clinical frailty of patients was significantly correlated with COVAN mortality but not with the viral load.


   Ethical approval Top


All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards.


   Informed Consent Top


Informed consent was obtained from the patient.

Conflict of interest: None declared.



 
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Correspondence Address:
Carlos G Musso
Department of Physiology, Instituto Universitario del Hospital Italiano de Buenos Aires, Buenos Aires

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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1319-2442.344755

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    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]



 

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