scholarly journals Perspectives on the relationship of renal disease and coronavirus disease 2019

2020 ◽  
Vol 9 (2) ◽  
pp. e22-e22 ◽  
Author(s):  
Banafsheh Yalameha ◽  
Bijan Roshan ◽  
Lakkakula VKS Bhaskar ◽  
Leila Mohmoodnia

Coronavirus disease 2019 (COVID-19) is now a pandemic and its death toll is rocketing up. Patients with acute kidney injury (AKI) and chronic kidney disease (CKD) are at high risk of developing COVID-19 complications and COVID-19 infection can also lead to renal dysfunction. Considering the importance of kidney function in COVID-19 patients, the present review is aimed to dig into the available evidence about kidney and COVID-19. We summarize the mechanisms underlying the renal injury in COVID-19 patients, and treatment strategies in dialysis and kidney transplant patients. We conclude, it is imperative to highlight the early monitoring of patients with AKI and carefully control kidney function during severe acute respiratory syndrome coronavirus 2 (SARSCoV-2) infection.

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Sara Núñez Delgado ◽  
Miren Iriarte-Abril ◽  
Júlia Farrera-Núñez ◽  
Sergi Pascual-Sánchez ◽  
Laia Sans-Atxer ◽  
...  

Abstract Background and Aims Acute renal failure (AKI) associated to rhabdomyolysis conditions a worse prognosis in short-term, its implication in the long-term renal function has been less evaluated. Method Retrospective analysis of patients diagnosed with rhabdomyolysis defined by creatinine kinase > 5000 IU/L between 2015-2019. Basal and 12-month renal function was evaluated. AKI was classified as either non-severe (AKI-KDIGO 1/2) or severe (AKI-KDIGO 3). Results Eighty-seven patients were included, 25 (28.74%) had some degree of chronic kidney disease (CKD) on admission. 56 (64.37%) had AKI on admission, 17 of which were severe (6 required hemodialysis). The patients with AKI had more cardiovascular disease (CVD) and worse analytical parameters on admission (table). Patients with severe AKI showed no difference in CVD from those with non-severe AKI but were younger and had more hyperkalemia. There were no significant differences between patients with severe AKI who required hemodialysis and those who did not. Inpatient mortality was 8%, higher in patients with AKI but without differences according to severity. In 45 patients kidney function was available 12 months after the episode, loss of eGF was -4.90 ± 14.35 ml/min-1.73m2 (p=0.007). There was no difference between patients who developed AKI and those who did not (-4.10 ± 14.4 vs. -5.39 ± 14.57 ml/min-1.73m2; p=0.67), nor between non-severe and severe AKI (-5.50 ± 14.76 vs. -5.12 ± 15.08ml/min-1.73m2; p=0.98). Of the 33 patients without previous CKD, 5 developed CKD, with greater decrease in eGF than those who did not (-22.69 ± 6.04 vs. -2.63 ± 13.92 ml/min-1.73m2; p=0.003). Female sex (60% vs. 12%; p=0.031) and previous basal eGF (72.22 ± 4.37 vs. 95.6±19.97 ml/min-1.72m2; p=0.016) were related to this deterioration. Conclusion After an episode of rhabdomyolysis, the loss of eGF is similar in patients who develop AKI compared to those who do not.


2020 ◽  
Vol 51 (3) ◽  
pp. 172-181 ◽  
Author(s):  
Carl P. Walther ◽  
Wolfgang C. Winkelmayer ◽  
Anita Deswal ◽  
Jingbo Niu ◽  
Sankar D. Navaneethan

Background: Acute kidney injury (AKI) frequently complicates hospitalizations for left ventricular assist device (LVAD) implantation. Little is known about the relationship of AKI with subsequent readmissions, and we investigated the relationship of AKI during LVAD implantation hospitalization with all-cause and cause-specific 30-day readmissions. Methods: We used a United States (US) nationwide all-payer administrative database, identifying patients who underwent implantable LVAD placement 2010–2015. Patients were classified into 3 mutually exclusive groups based on presence and severity of AKI during the LVAD placement hospitalization: no AKI, AKI, and AKI requiring dialysis (AKI-D). Outcomes were all-cause and cause-specific 30-day readmissions. Results: Within 30 days after discharge 25.4% of patients were readmitted. Of those without AKI, 23.9% were readmitted, compared to 25.5% of those with AKI and 42.2% of those with AKI-D. Compared to no AKI (adjusted for demographics, index hospitalization and chronic comorbidity factors, and year), odds of 30-day readmission were 2.18 (95% CI 1.37–3.49) times higher for those with AKI-D, whereas those with AKI not requiring dialysis had similar 30-day readmission risk (OR 1.03 [95% CI 0.89–1.20]). Those with AKI-D had higher risk of 30-day readmission for infection (OR 2.02 [95% CI 1.13–3.61]), gastrointestinal (GI) bleed (2.32 [95% CI 1.24–4.34]), and kidney disease (13.9 [95% CI 4.0–48]). There was no increased risk for stroke readmission with AKI or AKI-D. Conclusion: AKI-D was associated with highest ­30-day readmission risk, possibly related to negatively synergistic effects of LVAD, kidney dysfunction, and dialysis related factors on infection and GI bleeding risks. AKI alone was not associated with increased readmission risk.


2018 ◽  
Vol 314 (1) ◽  
pp. F1-F8 ◽  
Author(s):  
Matthew R. Lynch ◽  
Mei T. Tran ◽  
Samir M. Parikh

Acute kidney injury (AKI) arising from diverse etiologies is characterized by mitochondrial dysfunction. The peroxisome proliferator-activated receptor γ coactivator-1alpha (PGC1α), a master regulator of mitochondrial biogenesis, has been shown to be protective in AKI. Interestingly, reduction of PGC1α has also been implicated in the development of diabetic kidney disease and renal fibrosis. The beneficial renal effects of PGC1α make it a prime target for therapeutics aimed at ameliorating AKI, forms of chronic kidney disease (CKD), and their intersection. This review summarizes the current literature on the relationship between renal health and PGC1α and proposes areas of future interest.


Author(s):  
Dr Andrew Davenport

Chapter 11 discusses diseases and emergencies involving renal medicine, including investigation of the renal tract, acute kidney injury (AKI), haematuria and proteinuria, urinary tract infection (UTI), urinary tract obstruction, tumours of the renal tract, chronic kidney disease (CKD), and renal transplant patients.


2019 ◽  
Vol 17 (1) ◽  
Author(s):  
Qi Wang ◽  
Yi Tang ◽  
Jiaojiao Zhou ◽  
Wei Qin

Abstract Background Acute kidney injury (AKI) has high morbidity and mortality in intensive care units (ICU). It can also lead to chronic kidney disease (CKD), more costs and longer hospital stay. Early identification of AKI is important. Methods We conducted this monocenter prospective observational study at West China Hospital, Sichuan University, China. We recorded information of each patient in the ICU within 24 h after admission and updated every two days. Patients who reached the primary outcome were accepted into the AKI group. Of all patients, we randomly drew 70% as the development cohort and the remaining 30% as the validation cohort. Using binary logistic regression we got a risk prediction model of the development cohort. In the validation cohort, we validated its discrimination by the area under the receiver operator curve (AUROC) and calibration by a calibration curve. Results There were 656 patients in the development cohorts and 280 in the validation cohort. Independent predictors of AKI in the risk prediction model including hypertension, chronic kidney disease, acute pancreatitis, cardiac failure, shock, pH ≤ 7.30, CK > 1000 U/L, hypoproteinemia, nephrotoxin exposure, and male. In the validation cohort, the AUROC is 0.783 (95% CI 0.730–0.836) and the calibration curve shows good calibration of this prediction model. The optimal cut-off value to distinguish high-risk and low-risk patients is 4.5 points (sensitivity is 78.4%, specificity is 73.2% and Youden’s index is 0.516). Conclusions This risk prediction model can help to identify high-risk patients of AKI in ICU to prevent the development of AKI and treat it at the early stages. Trial registration TCTR, TCTR20170531001. Registered 30 May 2017, http://www.clinicaltrials.in.th/index.php?tp=regtrials&menu=trialsearch&smenu=fulltext&task=search&task2=view1&id=2573


2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Alan S. Go ◽  
Thida C. Tan ◽  
Rishi V. Parikh ◽  
Andrew P. Ambrosy ◽  
Leonid V. Pravoverov ◽  
...  

Abstract Introduction Acute kidney injury is a common complication of percutaneous coronary intervention and has been associated with an increased risk of death and progressive chronic kidney disease. However, whether the timing of acute kidney injury after urgent percutaneous coronary intervention could be used to improve patient risk stratification is not known. Methods We conducted a retrospective cohort study in adults surviving an urgent percutaneous coronary intervention between 2008 and 2013 within Kaiser Permanente Northern California, a large integrated healthcare delivery system, to evaluate the impact of acute kidney injury during hospitalization at 12 (±6), 24 (±6) and 48 (±6) hours after urgent percutaneous coronary intervention and subsequent risks of adverse outcomes within the first year after discharge. We used multivariable Cox proportional hazards models with adjustment for a high-dimensional propensity score for developing acute kidney injury after percutaneous coronary intervention to examine the associations between acute kidney injury timing and all-cause death and worsening chronic kidney disease. Results Among 7250 eligible adults undergoing urgent percutaneous coronary intervention, 306 (4.2%) had acute kidney injury at one or more of the examined time periods after percutaneous coronary intervention. After adjustment, acute kidney injury at 12 (±6) hours was independently associated with higher risks of death (adjusted hazard ratio [aHR] 3.55, 95% confidence interval [CI] 2.19–5.75) and worsening kidney function (aHR 2.40, 95% CI:1.24–4.63). Similar results were observed for acute kidney injury at 24 (±6) hours and death (aHR 3.90, 95% CI:2.29–6.66) and worsening chronic kidney disease (aHR 4.77, 95% CI:2.46–9.23). Acute kidney injury at 48 (±6) hours was associated with excess mortality (aHR 1.97, 95% CI:1.19–3.26) but was not significantly associated with worsening kidney function (aHR 0.91, 95% CI:0.42–1.98). Conclusions Timing of acute kidney injury after urgent percutaneous coronary intervention may be differentially associated with subsequent risk of worsening kidney function but not death.


2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Malgorzata Kepska ◽  
Inga Chomicka ◽  
Ewa Karakulska-Prystypiuk ◽  
Agnieszka Tomaszewska ◽  
Grzegorz Basak ◽  
...  

Abstract Background and Aims Chronic kidney disease (CKD) and acute kidney injury (AKI) are common complications of hematopoietic stem cell transplantation (HSCT) associated with increased morbidity and mortality. On the other hand, presence of CKD is often used as an exclusion criterion when selecting patients who undergo HSCT, especially when fludarabine in conditioning or GVHD prophylaxis with a calcineurin inhibitor is contemplated. There is also no threshold (CKD stage, level of serum creatinine etc) below which patients should not undergo allogeneic HSCT. Kidney function in patients undergoing HSCT is frequently worsened by previous chemotherapy and exposure to a variety of nephrotoxic drugs. Several biomarkers were widely investigated for early diagnosis of acute kidney injury, including neutrophil gelatinase associated lipocalin (NGAL), urinary liver-type fatty acid-binding protein (uL-FABP) and others, however, in patients undergoing HSCT, the published literature is exceptionally scarce. A few studies with inconclusive results stress the knowledge gap and need for further research. The aim of the study was to assess biomarkers of kidney injury in patients at least 3 months after HSCT (to avoid the effect of calcineurin inhibitors) under ambulatory care of Hematology, Oncology and Internal Medicine Department, University Teaching Hospital. Method We studied 80 prevalent patients after allogeneic HSCT and 32 healthy volunteers to obtained normal ranges for biomarkers. In this cross-sectional study following biomarkers of kidney injury in urine were evaluated: IGFBP-7/TIMP2 (insulin growth factor binding protein-7/, tissue inhibitor of metalloproteinases-2), netrin-1, semaphorin A2 using commercially available assays. Results All the biomarkers studied were significantly higher in patients after HSCT when compared to healthy volunteers (all p<0.001). When we divided patients according to kidney function (below and over 60 ml./min/1.72m2), we found that only concentration of IGFBP-7 was significantly higher in 23 patients with CKD stage 3 (i.e. eGFR below 60ml.min/1.72m2) relative to patients with eGFR over 60 ml.min.1.72m2. All biomarkers in both subgroups of patients with eGFR below and over 60 ml./min/1.72m2 were significantly higher relative to healthy volunteers. In univariate correlations sempahorinA2 was related to netrin 1 (r=0.47, p<0.001), IGFBP7 (r=0.35, p<0.01), TIMP2 (r=0.32, p<0.01), whereas IGFBP7 was positively related to serum creatinine (r=0.38, p<0.001) and inversely to eGFR (r=-0.36, p<0.001). Conclusion Concluding, patients after allogeneic HSCT despite normal or near normal kidney function show evidence of kidney injury, which might be due to comorbidities, previous chemotherapy, conditioning regimen,complement activation, calcineurin therapy after HSCT, other possible nephrotoxic drugs etc. Nephroprotective strategies are to be considered as chronic kidney disease is a risk factor for increased morbidity and mortality in this vulnerable population.


2017 ◽  
Vol 61 (11) ◽  
Author(s):  
Alan Forrest ◽  
Samira M. Garonzik ◽  
Visanu Thamlikitkul ◽  
Evangelos J. Giamarellos-Bourboulis ◽  
David L. Paterson ◽  
...  

ABSTRACT Acute kidney injury (AKI) occurs in a substantial proportion of critically ill patients receiving intravenous colistin. In the pharmacokinetic/toxicodynamic analysis reported here, the relationship of the occurrence of AKI to exposure to colistin and a number of potential patient factors was explored in 153 critically ill patients, none of whom were receiving renal replacement therapy. Tree-based modeling revealed that the rates of AKI were substantially higher when the average steady-state plasma colistin concentration was greater than ∼2 mg/liter.


2016 ◽  
Vol 62 (6) ◽  
pp. 876-883 ◽  
Author(s):  
Joanne L Carter ◽  
Christopher T Parker ◽  
Paul E Stevens ◽  
Gillian Eaglestone ◽  
Sarah Knight ◽  
...  

Abstract BACKGROUND Identification of acute kidney injury (AKI) is predominantly based on changes in plasma creatinine concentration, an insensitive marker. Alternative biomarkers have been proposed. The reference change value (RCV), the point at which biomarker change can be inferred to have occurred with statistical certainty, provides an objective assessment of change in serial tests results in an individual. METHODS In 80 patients with chronic kidney disease, weekly measurements of blood and urinary biomarker concentrations were undertaken over 6 weeks. Variability was determined and compared before and after adjustment for urinary creatinine and across subgroups stratified by level of kidney function, proteinuria, and presence or absence of diabetes. RESULTS RCVs were determined for whole blood, plasma, and urinary neutrophil gelatinase-associated lipocalin (111%, 59%, and 693%, respectively), plasma cystatin C (14%), creatinine (17%), and urinary kidney injury molecule 1 (497%), tissue inhibitor of metalloproteinases 2 (454%), N-acetyl-β-d-glucosaminidase (361%), interleukin-18 (819%), albumin (430%), and α1-microglobulin (216%). Blood biomarkers exhibited lower variability than urinary biomarkers. Generally, adjusting urinary biomarker concentrations for creatinine reduced (P < 0.05) within-subject biological variability (CVI). For some markers, variation differed (P < 0.05) between subgroups. CONCLUSIONS These data can form a basis for application of these tests in clinical practice and research studies and are applicable across different levels of kidney function and proteinuria and in the presence or absence of diabetes. Most of the studied biomarkers have relatively high CVI (noise) but also have reported large concentration changes in response to renal insult (signal); thus progressive change should be detectable (high signal-to-noise ratio) when baseline data are available.


Sign in / Sign up

Export Citation Format

Share Document