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This chapter gives a broad overview of nephrology as it affects hospitalists while also hoping to answer a few of the essential questions hospitalists may ask their nephrology colleagues. Evaluation and treatment of both acute and chronic kidney disease is constantly evolving as the small but tight-knit community of hospital-nephrologists continue to collect, review, and research data. The majority of the chapter will be focused on discussing a few new updates in the field of nephrology and how these updates could potentially change hospital care. © The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Switzerland AG 2022.
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Background: FSGS is a histologic pattern of glomerular injury with numerous causes, frequently associated with kidney disease progression and kidney failure. Although CVD events are known to be associated with end stage kidney disease (ESKD), there is a paucity of research examining this relationship in the FSGS population. We assessed the impact of baseline proteinuria and eGFR decline to ESKD on CVD event incidence and all-cause mortality. Method(s): A descriptive, retrospective analysis using Optum de-identified Market Clarity and proprietary Natural Language Processed (NLP) Data (2007-2020). Inclusion criteria: Patients (>=18yo) with >=2 FSGS ICD-10 codes (N031, N041, N051, N061, N071) and/or >=2 FSGS NLP terms within 180 days and >=30 days apart without associated negation terms, >6mo pre-index activity (exclusion: COVID-19). Post-index CVD events included myocardial infarction (MI), ischemic stroke/transient ischemic attack (TIA), unstable angina, congestive heart failure (CHF), percutaneous coronary intervention (PCI), or coronary artery bypass graft (CABG). All-cause mortality included patients with a death date post-index. Result(s): Overall (n=7,974), 11.7% of patients with FSGS experienced a CVD event. Post-ESKD, and among patients with higher baseline proteinuria, CVD events and mortality were significantly elevated (p<.001;Table 1). Conclusion(s): A significant increase in CVD events and death was associated with elevated proteinuria and progression to ESKD in patients with FSGS. New therapies for FSGS that reduce proteinuria may reduce CVD events and improve overall survival. (Table Presented).
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Background: COVID-19-associated nephropathy (COVAN) is a type of collapsing glomerulopathy that leads to acute kidney injury (AKI) and overt proteinuria in individuals with apolipoprotein L1 (APOL1) polymorphism infected with SARS-CoV-2. Although the severity of the acute presentation of COVAN is well described, the long-term renal prognosis has not been clearly established. Method(s): We retrospectively identified native kidney biopsies from patients with diagnosis of COVAN discharged alive between January 2020 and March 2021. Time of biopsy pathological and clinical data were collected. We performed APOL1 genotyping for G1/G2 risk alleles. We examined the rate of end-stage kidney disease (ESKD), de novo or progressive chronic kidney disease (CKD) and death. Factors associated with those outcomes were assessed by logistic regression. Result(s): A total of 43 patients with COVAN with median follow-up at 244 days were included. Mean age was 53 +/- 12 years (range 30-78), 49% women, and 85% were of African descent. High-risk APOL1 genotypes were found in 86%. Most presented with AKI (91%) and nephrotic-range proteinuria (81%). Sixteen patients required dialysis at presentation (AKI-RRT), 8 of which reached ESKD and dialysis dependence at followup. Additionally, 6 patients without AKI-RRT developed ESKD and required dialysis at follow-up. Forty patients (93%) either developed de novo CKD or progressed to advanced stage of CKD [mean serum creatinine (sCr) 3.1 +/- 1.9 mg/dL]. Overall, 35% reached the combined endpoint of ESKD, progressive CKD or death. Predictive factors of ESKD included older age (59.1 +/- 13.9 vs. 50.4 +/- 10.7 years, p=0.03), increased sCr at time of biopsy (9.4 +/- 3.2 vs. 6.0 +/- 4.9, p=0.03), increased glomerular obsolescence (52.8 +/- 21.3 vs. 25.0 +/- 23.2%, p=0.0005), and IFTA [moderate-severe vs. mild, OR 9.8 (CI: 1.1-85.2), p=0.03]. AKI-RRT, sex, proteinuria at the time of biopsy, and absence vs. presence of an APOL1 high-risk genotype were not predictive of ESKD. Conclusion(s): COVAN is associated with ominous long-term renal sequelae. Serum creatinine at time of biopsy, patient age, glomerular obsolescence, and IFTA are associated with greater risk of ESKD.
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Introduction: Immunizations have been previously described as potential triggering events for the development of certain glomerular diseases. However, there is paucity of reports of occurrence of glomerular diseases developing after exposure to a severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccine. Case Description: A 50-yearl-old man presented to a nephrology clinic for evaluation of persistent proteinuria. Six weeks prior to evaluation, the patient had reported developing a new rash approximately 2 weeks after receiving the first dose of a SARS-CoV-2 vaccine (Pfizer®). The rash was treated by his primary care provider with topical and oral corticosteroids, leading to partial improvement of the skin lesions. Three weeks after the first vaccine injection, the patient received his scheduled second vaccine injection. Within 2 days, the rash reappeared. This time, the lesions were more severe in nature, with a violaceous papular rash involving his lower legs and with some areas progressing to blisters. He also reported myalgias and arthralgias. A skin biopsy was performed and revealed IgA-dominant leukocytoclastic vasculitis. After completion of 2 weeks of oral corticosteroids, a urinalysis revealed proteinuria and a consultation to nephrology was requested. On examination, healing papules were noted on his legs but otherwise exam was normal. Serum creatinine was 0.9 mg/dL. Microscopic examination of the urinary sediment revealed acanthocytes. A urine protein-to-creatinine ratio (UPCR) was 1.1 g/g. Serum complements were normal and all pertinent serology was negative. A kidney biopsy was performed and light and immunofluorescence microscopy findings showed an IgA nephropathy. UPCR decreased to 0.7 g/g and rash completely subsided. Discussion: The clinical presentation and pathological findings in this case strongly suggest that SARS-CoV-2 vaccine (Pfizer®) can trigger a clinical syndrome compatible with Henoch-Schönlein purpura. The recurrence of the rash following re-exposure to the vaccine injection (second dose) argues for a definite causal association by Naranjo criteria.
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Background: There is paucity of data about post-hospital discharge kidney-related outcomes in individuals with COVID-19-associated acute kidney injury (CoV-AKI) during the pandemic. We hypothesized that patients who survive a hospital admission due to COVID-19 and AKI are at risk for acquiring residual chronic kidney disease (CKD) thereafter. Methods: We conducted a retrospective observational study examining records of patients hospitalized at Ochsner Medical Center over a 3-month period (March-May 2020) with COVID-19 and diagnosis of AKI by KDIGO. We examined the rate of full recovery of AKI (serum creatinine value back to within 10% of baseline or < 1.2 mg/dL) at 9 months post-hospital discharge. Factors associated with recovery were assessed. Results: Among 916 admissions due to COVID-19 within the study [220 (24%) to an intensive care unit], there were 226 (26%) cases of AKI, 98 of them (43%) with AKIrequiring dialysis (AKI-RRT). Patients with CoV-AKI had a median age of 67 (34-99) and 58% were men. Self-identified black race accounted for 65% of the cohort. Among those with CoV-AKI, there were 111 in-hospital deaths (49%). Of 115 patients with CoVAKI who were discharged alive, 9-month follow-up data were retrieved in 97 (missing data in 18). Full recovery of kidney function was achieved by 76 (78%). Among those who progressed to residual CKD, 11 (11%) patients were declared to have end-stage kidney disease (ESKD) requiring dialysis. Baseline CKD stages 3-5 was associated with lower rate of full renal recovery [23/76 (30%) vs. 14/23 (61%);RR: 2.01, p=0.004)]. Conclusions: Full recovery from CoV-AKI was observed in of those who remain alive post-hospital discharge. About 1/10th of patients with CoV-AKI reached ESKD at intermediate-term follow-up. Preexisting CKD is associated with lower rate of recovery in CoV-AKI. These data do not seem to suggest that CoV-AKI is associated with greater risk for development of CKD compared to other forms of in-hospital AKI.
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Background: Early reports of acute kidney injury (AKI) associated with COVID-19 have claimed high incidence of proteinuria. If so, it may suggest an AKI pathogenesis not solely related to ischemic acute tubular injury (ATI). We hypothesized that those claims result from observation bias. Therefore, we sought to investigate the rate of De novo proteinuria in AKI associated with COVID-19 (CoV-AKI) compared to that of AKI in the pre-COVID-19 era (non-CoV-AKI). Methods: Hospitalized patients with CoV-AKI entered the cohort (n=161). As a control non-CoV-AKI group (n=186), we accessed a database of patients with AKI who underwent urinary sediment microscopy due to suspicion of an intrinsic cause of AKI (Sedi-AKI cohort, 2017-2019). We examined the incidence of proteinuria of any degree (1+ dipstick), significant [urine protein-to-creatinine ratio (UPCR) ≥ 0.5-3.0 g/g or 2+ dipstick] or overt [UPCR ≥ 3.0 g/g + 3+ dipstick]. Results: Median age were similar: 65 (34-95) and 60 (20-88) years for CoV-AKI and non-CoV-AKI, respectively. Women were 62% and 63% (p=0.86). Black race was more common in CoV-AKI (75% vs. 35%;p=<0.0001). ATI (ischemic and/or toxic) was the presumed cause of AKI in 75% and 71% of CoV-AKI and non-CoV-AKI, respectively. Incidence of any, significant or overt proteinuria were 123/148 (83%) vs. 127/184 (69%) (p=0.003), 98/148 (66%) vs. 81/184 (44%) (p=0.0001) and 14/148 (10%) vs. 23/184 (13%) (p=0.39), for CoV-AKI and non-CoV-AKI, respectively. Among those with significant proteinuria, no difference in median UPCR was found [0.69 vs. 0.69 g/g (p=0.23)]. Using baseline UPCR when available, rates of De novo significant and overt proteinuria were similar [57/124 (46%) vs 57/123 (46%) (p=1.00) and 6/124 (5%) vs 7/123 (7%) (p=0.75)]. Among overt cases who underwent kidney biopsy, collapsing glomerulopathy was found in 3/4 (75%) in the CoV-AKI group compared to 0/11 (0%) in the control (p=0.002). Conclusions: The incidence rate of new onset proteinuria was not found to be increased in CoV-AKI and is consistent with that of other forms of ATI. An observed overall greater incidence in significant proteinuria in CoV-AKI may be driven by preexisting proteinuria. While the rate of overt proteinuria is not greater in CoV-AKI, the primary cause of De novo glomerular disease may vary.
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Background: Patients with end-stage kidney disease (ESKD) comprise a vulnerable population to infections. COVID-19 has been responsible for high mortality worldwide. To-date, there is limited data regarding the impact of COVID-19 in the ESKD population. We report clinical outcomes of ESKD patients with COVID-19 admitted to an academic hospital in New Orleans. Methods: We conducted an observational study in patients with ESKD and COVID-19 hospitalized at Ochsner Medical Center over a 7-week period. We compared rates of need for mechanical ventilation, shock, need for intensive care (ICU) and inhospital mortality as outcome measures between patients with and without ESKD. Results: Among 851 admissions (67% black) with COVID-19, 49 (6%) patients had diagnosis of ESKD. Patients with ESKD were mostly male [61% vs 49% in non-ESKD (n = 806), p = 0.10] with a median age of 64 (38 - 90) years. Median body mass index (BMI) were 32 vs 27 kg/m2 (p = 0.11) for those admitted to ICU vs wards, respectively. Thirteen of them (27%) vs 293 (37%) in the non-ESKD group, p=0.16) were admitted to an intensive care unit (ICU). In-hospital mortality rate for the ESKD cohort was 32% compared to 24% for non-ESKD (p = 0.21). Compared to a subset with 161 patients with acute kidney injury (AKI) with 50% mortality, the 32% mortality rate in ESKD was significantly lower (p = 0.027). Shock and/or mechanical ventilation requirement were comparable between groups [12 (24%) of those with ESKD vs 213 (26%) of non-ESKD, p = 0.65]. Median serum ferritin level was significantly more elevated in ESKD compared to non-ESKD [2125 vs 633 ng/mL, p = 0.0019). Conclusions: Clinical outcomes in individuals with ESKD with COVID19 appear to be grossly similar to that of non-ESKD population with COVID19. The similar mortality rate was seen despite higher levels of ferritin, suggesting that the interpretation of the significance of serum ferritin in ESKD has to be done with caution. Furthermore, the mortality in ESKD patients with COVID19 is lower than that observed in AKI. The observed lack of increased mortality in ESKD does not align with the outcomes of this patient population in other critical illnesses. The ability to mount and exaggerated inflammatory response in COVID19 might be somewhat restricted in ESKD.
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Background: There have been anecdotal accounts of an unusual incidence of persistent hyperkalemia (hyperK) and hyperphosphatemia (hyperP) in patients with COVID-19 and acute kidney injury (AKI) (CoV-AKI) despite renal replacement therapy (RRT). However, an observation bias could not be discarded. Thus, we examined the rate and severity of hyperK and hyperP in patients with CoV-AKI actively treated with RRT. Methods: Among 161 patients with CoV-AKI, we selected those who underwent RRT by sustained low efficiency dialysis (SLED) for ≥2 days (n=64). A database of patients with AKI on SLED who underwent urinary sediment microscopy (Sedi-AKI cohort, 2017-2019, n=60) served as control (non-CoV-AKI). We examined the rate of hyperK [serum potassium (sK) ≥ 5.5 mEq/L], severe hyperK [sK ≥ 6.5 mEq/L], hyperP [serum phosphate (sP) ≥ 4.5 mg/dL], moderate hyperP [sP ≥ 7.0-10.0 mg/dL] and severe hyperP [sP >;10.0 mg/dL] as % SLED-days with an event. Results: Median age were similar: 60 (39-84) and 58 (22-88) years for CoV-AKI and non-CoV-AKI, respectively. Black race (77% vs. 30%;p<0.0001) and male sex (78% vs. 61%;p=0.04) were more common in CoV-AKI. Ischemic ATI was the presumed cause of AKI in 85% and 82% of the CoV-AKI and non-CoV-AKI, respectively. Along the duration of SLED, the incidence of hyperK was greater in CoV-AKI [mean 19 ± 2% vs. 14 ± 3% SLED-days, p=0.002]. The proportion of patients with ≥1 event of severe hyperK was greater in CoV-AKI [33% vs. 7%, p=0.0004]. The incidence of hyperP were similar between groups [mean 56 ± 4% vs. 53 ± 5% SLED-days, p=0.49]. However, the proportion of patients with ≥1 event of moderate and severe hyperP were greater in CoV-AKI [86% vs. 60% (p=0.001) and 50% vs. 18%, (p=0.0002)]. In CoV-AKI, sK and sP correlated with lactate dehydrogenase (LDH) [R=0.305 (p=0.044) and R=0.307 (p=0.043), respectively] but not with creatine kinase;and hyperP events correlated with shorter SLED runs (hours/run) (R=-0.268, p=0.055). Conclusions: HyperK and hyperP refractory to RRT (by SLED) were more frequent in CoV-AKI compared to other forms of AKI in the pre-COVID-19 era. Because of the correlation of sK and sP with higher LDH and shorter SLED runs, intracellular ion release from cell injury due to cytokine 'storm' and RRT interruptions may play a role.
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Background: Infections are an important cause of morbidity and mortality among kidney transplant recipients. The novel Coronavirus Disease 2019 (COVID-19) has affected all kinds of populations world-wide. However, the role of immunosuppression in the outcomes of these patients is not well understood. Methods: We conducted a retrospective study in kidney transplant recipients from a single health system that were diagnosed with COVID-19 based on a positive real-time reverse transcription polymerase chain reaction test for SARS-CoV-2 RNA between 03/01/2020 and 04/30/2020. We compared them with affected patients without a kidney transplant and without any kind of immunosuppressive medication (control). We examined the rates of hospitalization, intensive-care unit (ICU) admission, acute kidney injury (AKI) and mortality as outcome measures. Results: A total of 8473 patients were diagnosed with COVID-19 within our Health System within the study period. Thirty-three (0.4%) were kidney transplant recipients. Sixteen of the 33 (48%) were admitted to the hospital (median age of 56, 68% males, 93% African American) vs 2201 admissions (25%) for the control group (median age 66, 48% males, 65% African-American), i.e., a significantly greater risk for hospitalization for transplant recipients (p = 0.002). Percentage of patients with hypertension in the transplant group was numerically higher (93% vs 80%, p = 0.06), as well as the number of ICU admissions (43% vs 28%, p = 0.055). AKI was more common in transplant patients (81% vs 33.8% p<0.0001). No difference in mortality was observed (31 vs 24%, p = 0.34). Among transplant patients, those hospitalized were more likely to be on prednisone (75% vs 35%, p = 0.025) and had a post-transplant graft life of 7.9 years compared to 5.5 years for those not hospitalized, p 0.08). Conclusions: Kidney transplant recipients affected with COVID-19 exhibited a greater incidence of hospitalization, AKI and a trend for more ICU admissions. Use of immunosuppression with prednisone was associated with greater risk for hospitalization.
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Background: Acute kidney injury (AKI) is a reported manifestation of COVID-19 (CoV-AKI). Release of inflammatory cytokines has been recognized as a characteristic feature of COVID-19 and is linked to severity of illness. However, it has not been clearly determined if levels of serum markers of inflammation are associated with risk for development of AKI or its severity. Methods: We conducted an observational study in patients hospitalized at Ochsner Medical Center over 1-month period with COVID-19 and diagnosis of AKI. We examined the relationship between the blood level of ferritin, C-reactive protein (CRP), procalcitonin (proCal), D-dimer and lactate dehydrogenase (LDH) and the incidence of AKI, as well as AKI requiring renal replacement therapy (AKI-RRT), by assessing comparison of means and proportions and by logistic regression analysis. Results: Among 644 patients with COVID-19, we compared 161 (26%) with AKI vs 414 (64%) without AKI. Median serum creatinine on admission was higher in the AKI group (1.8 vs 1.1 mg/dL, p<0.0001). Preexisting chronic kidney disease rates were comparable (35% vs 28%, for AKI and no AKI groups). The median value of inflammatory markers on admission were higher in the AKI group [ferritin 1016 (516-2534) vs 680 (315-1416) ng/mL, p<0.0001;CRP 163 (93-243) vs 93 (46-165) mg/L, p<0.0001;proCal 0.37 (0.2-1.6) vs 0.12 (0.06-0.32) ng/mL, p<0.0001;D-dimer 1.57 (0.96-5.14) vs 1.13(0.68-2.57) mcg/mL, p=0.0004;and LDH 532 (365-804) vs 428 (309-548), p=0.0004]. On multivariate logistic regression analysis, CRP (p=0.003) and ferritin (p<0.035) were associated with greater risk for AKI. In addition, ferritin ≥ 1200 ng/mL and CRP ≥ 300 mg/L were independently associated with AKI [adjusted odds ratio: 2.3 (1.3-4), p=0.003, and 2.5 (1.0-6.3), p=0.05;respectively]. Furthermore, ferritin, CRP, proCal and LDH levels were significantly higher in those with AKI-RRT compared to those not requiring RRT (p=0.022 to p=0.009). Conclusions: Higher level of inflammatory markers were associated with CoV-AKI, and levels were even higher for those with CoV-AKI-RRT. In patients with COVID-19, magnitude of ferritin and CRP on admission could be used for AKI risk stratification.
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Background: Acute kidney injury (AKI) is a manifestation of COVID-19 (CoVAKI). However, there is paucity of data from United States, particularly in a predominantly African American (AA) population. We report the phenotype and outcomes of AKI at an academic hospital in New Orleans. Methods: We conducted an observational study in patients hospitalized at Ochsner Medical Center over 1-month period with COVID-19 and diagnosis of AKI by KDIGO. We examined the rates of renal replacement therapy (RRT) and in-hospital mortality as outcome measures. Adjudication of cause of AKI was independently performed via manual chart review by 3 study team members. Results: Of 644 admissions with COVID-19, 69 were excluded due to ESRD or kidney transplant. Thus, 575 patients entered the cohort [173 (28%) to an intensive care unit (ICU)]. Patients were predominantly AA (71%). AKI was diagnosed in 161 patients (28% overall, 61% of ICU admissions), median age 65 (34 - 96), predominantly male (62%) and hypertensive (83%). Median follow up was 25 (1 - 45) days. Vasopressors and/or mechanical ventilation was required in 105 (65%) of them. In-hospital mortality rate for those with AKI was 50% (80/181). De novo AKI was diagnosed in 65%, whereas AKI over preexisting chronic kidney disease occurred in 35% of the cohort. Ninetyone (57%) patients arrived with AKI, whereas the remaining 43% acquired AKI during the hospitalization [median hospital day of AKI onset: 4 (2 - 10)]. RRT was required in 89/161 (55%) and 77/105 (73%) patients for all AKI cases and the ICU subset, respectively. The mortality rate for those with AKI-RRT was 72% (64/89). Hemodynamic instability leading to ischemic acute tubular injury (ATI) and rhabdomyolysis accounted for 66% and 7% of the etiology, respectively. Reversible prerenal azotemia occurred in 9%. In 13%, no obvious cause of AKI was identified aside from the COVID-19 diagnosis. Three (1.8%) patients had De novo collapsing glomerulopathy. Conclusions: CoV-AKI is associated with high rates of RRT, ICU care and death. Hemodynamic instability leading to ischemic ATI is the predominant cause of AKI in this setting, but other etiologies contribute to the overall AKI burden.
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Background: Acute kidney injury (AKI) is a reported manifestation of COVID-19 (CoV-AKI). However, there is paucity of data regarding risk factors for CoV-AKI. We examined the association of demographics and comorbidities with CoV-AKI risk and its severity at an academic hospital in New Orleans. Methods: We conducted an observational study in patients hospitalized at Ochsner Medical Center over 1-month period with COVID-19 and diagnosis of AKI. We assessed the relationship between baseline demographic and clinical characteristics and the incidence of AKI, as well as AKI requiring renal replacement therapy (AKI-RRT), by assessing comparison of means and proportions and by logistic regression analysis. Results: Among 644 patients with COVID-19, we compared 161 (26%) with AKI vs 414 (64%) without AKI. Male sex (62% vs 51%, p=0.02) and essential hypertension (HTN) (83% vs 70%, p=0.002) were more common in the AKI group. Median body mass index (BMI) was higher among those with AKI (34 vs 31 kg/m2, p<0.0001). No difference was found in age, race, presence of diabetes, chronic kidney disease or heart disease respect to AKI rate. On multivariate logistic regression analysis, HTN was strongly associated with greater risk for AKI [OR 1.96 (CI 1.2-3.2), p=0.009]. Male sex [OR 1.72 (CI 1.1-1.9), p=0.005] and higher BMI [OR 1.04 (CI 1.02-1.07), p<0.001] were also associated with AKI. RRT was required in 89 (55%) of the patients with AKI. Those with AKI requiring RRT (AKI-RRT) had higher median BMI (35 vs 33 kg/m2, p=0.048) and younger age (61 vs. 68, p=0.0003) compared to those with AKI not requiring RRT. Of note, higher BMI correlated with younger age (R=-0.53, p<0.0001). Conclusions: HTN, male sex and higher BMI were associated with greater incidence of AKI in patients hospitalized with COVID-19. Higher BMI was further associated with AKI-RRT. Hypertensive, male and obese patients are at higher risk for CoV-AKI and should be more closely monitored during the COVID-19 pandemic.
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Background: COVID-19 has caused an ominous healthcare toll in the United States. New Orleans rated among the top affected cities. Acute kidney injury (AKI) requiring renal replacement therapy (RRT) affected 16% of COVID-19-related hospitalizations, resulting in an exponential upsurge in resource utilization related to RRT. We report our single center experience providing metrics of overall utilization and workforce expansion. Methods: We conducted a prospective collection of data of daily census of hospitalized patients with COVID-19 and AKI or ESKD for 7 weeks (3/8-4/30, 2020) quantifying usage of RRT equipment and allocation of personnel. Two independent electronic health record databases were simultaneously used to track the data. Results: Within 1 month, in-hospital COVID-19 census peaked at 377 patients, with 97 (26%) of them receiving RRT at peak day. Starting from a mean of 65 patients on RRT per day in pre-COVID-19 era, the estimated RRT growth peaked at 49%. Four out of 10 newly purchased Fresenius K2 SLED machines (FKs) were utilized by week 5 (after delivery, assembly and negative culture). Starting from an average 80% usage of baseline capacity (31 of 38 FKs), usage of 42 K2s at peak revealed 35% growth. Four new reverse osmosis devices were obtained (growth: 25 to 29, 16%) by week 5. For CVVHDF, 4 PrismaFlex machines (PFs) were rented and 10 new PrisMax were bought. Starting from an average 33% usage of baseline capacity (2 of 6 FKs), use of 6 PFs at peak meant 400% growth. Up to 30 nurses were trained virtually on RRT. Eight agency nurses and 6 perfusionists were recruited, to increase the operator number from 21 to 35 (67% growth). Five of 21 (24%) RRT nurses were out of work at peak due to COVID19+ status. One attending physician, 1 nurse practitioner and 2 subspecialty residents were added to the inpatient service, increasing the number of providers from 9 to 13 (44% growth). Conclusions: The pandemic of COVID-19 resulted in substantial increase in inhospital RRT demand and resource utilization. Our experience may provide other centers a guide to optimize preparedness in the event of facing a 'second wave' of COVID-19 in the near future. Delay in implementation has to be accounted for during strategic planning.
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Background: The global pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) leading to coronavirus disease 2019 (COVID-19) has predominantly resulted in a profound hypoxic respiratory disease with a significant subset of patients demonstrating abnormalities in renal function. Acute kidney injury (AKI) in these patients is an independent risk factor for mortality;however, the mechanism for injury is unknown and our understanding of the pathologic findings is limited. Methods: Kidney tissue from nine patients who died with COVID-19 was obtained at autopsy and evaluated by light, immunofluorescence, and electron microscopy. RNAScope technology was used to perform RNA in situ hybridization (RNA ISH) with probes to the SARS-CoV-2 virus (sense) and for human gene ACE2. Results: The cohort was comprised of 6 men and 3 women, 78% black, median age of 65 years (37 - 78) and median body mass index 29 (26 - 48) kg/m2, of which 6 (67%) had hypertension and 4 (44%) had diabetes. AKI was present in 7 of 9 (78%), 5 (55%) of them needed dialysis. One patient had creatine kinase about 5000 U/L suggestive of rhabdomyolysis. All but one expired while on mechanical ventilation. The predominant morphologic finding on postmortem biopsy was acute tubular injury. Three cases (33%) demonstrated endocapillary platelet aggregates with one demonstrating fibrin tactoids and loss of endothelial fenestrations by EM, consistent with early TMA;however, no overt thrombotic microangiopathy was present. Immunofluorescence in one case demonstrated mesangial C3 staining without deposits by EM. Background mild-to-moderate arterionephrosclerosis was present in 6 of 9 (67%) cases. In one patient with AKI at time of death, RNA-ISH detected SARS-CoV-2 in tubular epithelial cells which also express ACE2, the receptor for coronavirus cell entry. Conclusions: Among a cohort of 9 patients dying with COVID-19, postmortem evaluation of kidney samples predominantly revealed ATI without overt evidence of hypercoaguloability, complement dysregulation, or immune complex deposition. While the mechanism for AKI in most cases is not immediately apparent, this series suggests, but does not prove, direct renal infection with SARS-CoV-2 as the presence of viral RNA does not prove active viral infection.
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Background: Acute kidney injury (AKI) is a complication of COVID-19 that is not fully understood. Microscopic examination of the urinary sediment (MicrExUrSed) is a valuable diagnostic tool in AKI. Thus far, there has been scarcity of data about MicrExUrSed in COVID-19-associated AKI (CoV-AKI). We hypothesized that MicrExUrSed provides diagnostic clues in CoV-AKI. Methods: We conducted a prospective observational study in patients seen for inpatient nephrology consultation with KDIGO AKI stage ≥ 1 and COVID-19 over a 1-month period. Urine specimens were collected with personal protective equipment to perform MicrExUrSed. Slides were assessed for presence of white blood cells (WBC) [≥ 2+ dipstick, ≥ 6 per low power field (LPF)], red blood cells (RBC) (≥ 2+ dipstick, ≥ 8 per LPF), acanthocytes, granular casts (GC), renal tubular epithelial cell casts (RTECC) and waxy casts (WxC). Slides were assigned to a category of acute tubular injury (ATI) based on either a Perazella cast score ≥ 2 or a Chawla cast score ≥ 3. Results: Among 161 cases of AKI, MicrExUrSed was performed in 20 (12.4%). Anuria and contact precautions were barriers to obtain specimens. GC were found in 17 (85%) of which 16 (80%) had 'muddy' brown GC (MBGC). A median 5 MBGC per LPF (1-20) were found in a median 40% (10-95%) of LPFs. WxC were found in 10 (50%) cases with a median 2 (1-5) per LPF, all of whom had MBGC also present. RTECC were found in 3 (15%) cases with a median 1 (1-4) per LPF. Altogether, ATI score was assigned to 17 (85%) patients, of which 12 (60%) had AKI either after a hemodynamic/ischemic insult (9) or after a toxic insult (3) (rhabdomyolysis, vancomycin, contrast) and 3 (15%) had biopsy-proven ATI along with collapsing glomerulopathy;for a total of 15 (75%) patients with either clinical or histological evidence on ATI matching the MicrExUrSed findings. Ten (50%) and 5 (25%) had WBCs and RBCs, respectively. Acanthocytes were found in 1 (5%) patient with presumptive proliferative endocapillary glomerulonephritis. Conclusions: MicrExUrSed in most patients with CoV-AKI showed overt evidence of ATI with an abundance of MBGC and WxC, including in cases of coexisting glomerulopathy. Pyuria was observed in half. The diagnostic utility of MicrExUrSed in CoV-AKI was comparable to that demonstrated in other forms of AKI.