Search

Chronic kidney disease (CKD) has been recognized as a highly prevalent risk factor for both the severity of coronavirus disease 2019 (COVID-19) and COVID-19 associated adverse outcomes. In this multicenter observational cohort study, we aim to determine mortality and readmission rates of patients hospitalized for COVID-19 across varying CKD stages. We performed a multicenter cohort study among COVID-19 patients included in the Dutch COVIDPredict cohort. The cohort consists of hospitalized patients from March 2020 until July 2021 with PCR-confirmed SARS-CoV-2 infection or a highly suspected CT scan-based infection with a CORADS score ≥ 4. A total of 4151 hospitalized COVID-19 patients were included of who 389 had a history of CKD before admission. After adjusting for all confounding covariables, in patients with CKD stage 3a, stage 3b, stage 4 and patients with KTX (kidney transplantation), odds ratios of death and readmission compared to patients without CKD ranged from 1.96 to 8.94. We demonstrate an evident increased 12-week mortality and readmission rate in patients with chronic kidney disease. Besides justified concerns for kidney transplant patients, clinicians should also be aware of more severe COVID-19 outcomes and increased vulnerability in CKD patients., (© 2022. The Author(s).)

Background: By binding to negatively charged polysaccharides called glycosaminoglycans, sodium can be stored in the body-particularly in the skin-without concurrent water retention. Concordantly, individuals with changed glycosaminoglycan structure (e.g. type 1 diabetes (DM1) and hereditary multiple exostosis (HME) patients) may have altered sodium and water homeostasis., Methods: We investigated responses to acute (30-min infusion) and chronic (1-week diet) sodium loading in 8 DM1 patients and 7 HME patients in comparison to 12 healthy controls. Blood samples, urine samples, and skin biopsies were taken to investigate glycosaminoglycan sulfation patterns and both systemic and cellular osmoregulatory responses., Results: Hypertonic sodium infusion increased plasma sodium in all groups, but more in DM1 patients than in controls. High sodium diet increased expression of nuclear factor of activated t-cells 5 (NFAT5)-a transcription factor responsive to changes in osmolarity-and moderately sulfated heparan sulfate in skin of healthy controls. In HME patients, skin dermatan sulfate, rather than heparan sulfate, increased in response to high sodium diet, while in DM1 patients, no changes were observed., Conclusion: DM1 and HME patients show distinct osmoregulatory responses to sodium loading when comparing to controls with indications for reduced sodium storage capacity in DM1 patients, suggesting that intact glycosaminoglycan biosynthesis is important in sodium and water homeostasis. Trial registration These trials were registered with the Netherlands trial register with registration numbers: NTR4095 ( https://www.trialregister.nl/trial/3933 at 2013-07-29) and NTR4788 ( https://www.trialregister.nl/trial/4645 at 2014-09-12).

Purpose: Calcimimetics are currently indicated for severe secondary hyperparathyroidism (SHPT). However, the role of parathyroidectomy (PTX) for these patients is still under debate, and its impact on subsequent kidney transplantation (KTX) is unclear. In this study, we compare the outcomes of kidney transplantation after PTX or medical treatment., Methods: Patients who underwent KTX and had SHPT were analyzed retrospectively. Two groups were selected (patients who had either PTX or calcimimetics prior to KTX) using a propensity score for sex, age, donor type, and parathyroid hormone levels (PTH) during dialysis. The primary outcome was graft failure, and secondary outcomes were surgical KTX complications, survival, serum PTH, serum calcium, and serum phosphate levels post-KTX., Results: Matching succeeded for 92 patients. After PTX, PTH was significantly lower on the day of KTX as well as at 1 and 3 years post-KTX (14.00 pmol/L (3.80-34.00) vs. 71.30 pmol/L (30.70-108.30), p < 0.01, 10.10 pmol/L (2.00-21.00) vs. 32.35 pmol/L (21.58-51.76), p < 0.01 and 13.00 pmol/L (6.00-16.60) vs. 19.25 pmol/L (13.03-31.88), p = 0.027, respectively). No significant differences in post-KTX calcium and phosphate levels were noted between groups. Severe KTX complications were more common in the calcimimetics group (56.5% vs. 30.4%, p = 0.047). There were no differences in 10-year graft failure and overall survival., Conclusion: PTX resulted in lower PTH after KTX in comparison to patients who received calcimimetics. Severe complications were more common after calcimimetics, but graft failure and overall survival were similar.

Purpose: Hyperparathyroidism (HPT) is a common abnormality in patients with end-stage renal disease (ESRD). Since the introduction of cinacalcet in 2004, a shift from surgery toward predominantly medical treatment has occurred. Surgery is thought to be associated with more complications than oral medication. The aim of this retrospective study was to evaluate 30-day outcomes and effectiveness of parathyroidectomy (PTx) in ESRD patients in the Netherlands., Methods: A national database containing data from four academic medical centers in the Netherlands of patients with ESRD-related HPT, who had undergone PTx and kidney transplantation between 1994 and 2015, was established. Primary endpoints were 30-day mortality and complication rate. Secondary endpoints were biochemical measurements., Results: We identified 187 HPT patients undergoing PTx, with a median age of 46 years. Median preoperative PTH level was 866 pg/mL (interquartile range [IQR] 407-1547 pg/mL). At 3 months, the median PTH drop from baseline was 93% (IQR, 71-98%) to a median of 61 pg/mL (IQR, 23-148 pg/mL, p < 0.001). Over the 25-year inclusion period, 13 patients (7.0%) required re-exploration for persistent or recurrent disease. Thirty-day mortality and complication rate were 0.0% and 7.9% respectively. Median serum calcium levels improved significantly postoperatively from 2.6 (2.4-2.8) mmol/L to 2.3 (2.1-2.5) mmol/L (p < 0.001)., Conclusions: PTx is a safe and effective procedure in the frail ESRD population. These data show that there should be no reluctance for surgical intervention and when indicated, nephrologists can safely refer these patients for PTx.

Background Isolated systolic hypertension (ISH) of the young has been associated with both normal and increased cardiovascular risk, which has been attributed to differences in central systolic blood pressure and arterial stiffness. Methods We assessed the prevalence of ISH of the young and compared differences in central systolic blood pressure and arterial stiffness between ISH and other hypertensive phenotypes in a multi-ethnic population of 3744 subjects (44% men), aged <40 years, participating in the HELIUS study. Results The overall prevalence of ISH was 2.7% (5.2% in men and 1.0% in women) with the highest prevalence in individuals of African descent. Subjects with ISH had lower central systolic blood pressure and pulse wave velocity compared with those with isolated diastolic or systolic-diastolic hypertension, resembling central systolic blood pressure and pulse wave velocity values observed in subjects with high-normal blood pressure. In addition, they had a lower augmentation index and larger stroke volume compared with all other hypertensive phenotypes. In subjects with ISH, increased systolic blood pressure amplification was associated with male gender, Dutch origin, lower age, taller stature, lower augmentation index and larger stroke volume. Conclusion ISH of the young is a heterogeneous condition with average central systolic blood pressure values comparable to individuals with high-normal blood pressure. On an individual level ISH was associated with both normal and raised central systolic blood pressure. In subjects with ISH of the young, measurement of central systolic blood pressure may aid in discriminating high from low cardiovascular risk.

Background: Evidence suggesting important ethnic differences in chronic kidney disease (CKD) prevalence comes mainly from the United States, and data among various ethnic groups in Europe are lacking. We therefore assessed differences in CKD in 6 ethnic groups living in the Netherlands and explored to what extent the observed differences could be accounted for by differences in conventional cardiovascular risk factors (smoking, physical activity, obesity, hypertension, diabetes, and hypercholesterolemia)., Study Design: Cross-sectional analysis of baseline data from the Healthy Life in an Urban Setting (HELIUS) cohort study., Setting & Participants: A random sample of 12,888 adults (2,129 Dutch, 2,273 South Asian Surinamese, 2,159 African Surinamese, 1,853 Ghanaians, 2,255 Turks, and 2,219 Moroccans) aged 18 to 70 years living in Amsterdam, the Netherlands., Predictors: Ethnicity., Outcomes & Measurements: CKD status was defined using the 2012 KDIGO (Kidney Disease: Improving Global Outcomes) severity of CKD classification. CKD was defined as albumin-creatinine ratio ≥ 3mg/mmol (category ≥ A2) or glomerular filtration rate < 60mL/min/1.73m(2) (category ≥ G3). Comparisons among groups were made using prevalence ratios (PRs)., Results: The age-standardized prevalence of CKD was higher in all ethnic minority groups, ranging from 4.6% (95% CI, 3.8%-5.5%) in African Surinamese to 8.0% (95% CI, 6.7%-9.4%) in Turks, compared with 3.0% (95% CI, 2.3%-3.7%) in Dutch. Adjustment for conventional risk factors reduced the PR substantially, but ethnic differences remained for all ethnic minority groups except African Surinamese, with the PR ranging from 1.48 (95% CI, 1.12-1.97) in Ghanaians to 1.75 (95% CI, 1.33-2.30) in Turks compared with Dutch. Similar findings were found when CKD was stratified into a moderately increased and a combined high/very high risk group. Among the combined high/very high CKD risk group, conventional risk factors accounted for most of the ethnic differences in CKD except for South Asian Surinamese (PR, 2.60; 95% CI, 1.26-5.34) and Moroccans (PR, 2.33; 95% CI, 1.05-5.18)., Limitations: Cross-sectional design., Conclusions: These findings suggest ethnic inequalities in CKD for most groups even after adjustment for conventional risk factors. These findings highlight the need for further research to identify other potential factors contributing to the ethnic inequalities in CKD., (Copyright © 2016 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.)

Background: Chronic kidney disease (CKD) is an important comorbidity during human immunodeficiency virus (HIV) infection. Historically, HIV-associated nephropathy has been the predominant cause of CKD and has primarily been observed in people of African ancestry. This study aims to investigate the role of ethnicity in relation to CKD risk in recent years., Methods: Analyses were performed including 16 836 patients from the Dutch AIDS Therapy Evaluation in the Netherlands (ATHENA) cohort. Baseline was defined as the first available creatinine level measurement after 1 January 2007; CKD was defined as a glomerular filtration rate of <60 mL/min/1.73 m(2). The associations between ethnicity and both prevalent CKD at baseline and incident CKD during follow-up were analyzed., Results: The prevalence of baseline CKD was 2.7% (460 of 16 836 patients). Birth in a sub-Saharan African country (hereafter, "SSA origin") was significantly associated with baseline CKD (adjusted odds ratio 1.49; 95% confidence interval [CI], 1.04-2.13). During follow-up (median duration, 4.7 years; interquartile range, 2.4-5.2), the rate of incident CKD was 6.0 events per 1000 person-years. The risk of newly developing CKD was similar between patients of SSA origin and those born in Western Europe, Australia, or New Zealand (adjusted hazard ratio, 1.00; 95% CI, .63-1.59)., Conclusions: Among HIV-infected patients in the Netherlands, being of SSA origin was associated with a higher baseline CKD prevalence but had no impact on newly developing CKD over time. This suggests a shift in the etiology of CKD from HIV-associated nephropathy toward other etiologies., (© The Author 2015. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.)

Objective: Acute kidney injury (AKI) is a serious complication after repair of a ruptured abdominal aortic aneurysm (RAAA). In the present Society for Vascular Surgery (SVS)/International Society for CardioVascular Surgery (ISCVS) reporting standards patients are classified as no dialysis (grade I), as temporary dialysis (grade II), and as permanent dialysis or fatal outcome (grade III). However, AKI is a broad clinical syndrome including more than the requirement for renal replacement therapy. The recently introduced 'Risk,' 'Injury,' 'Failure,' 'Loss,' and 'End-stage' (RIFLE) classification for AKI comprises three severity categories based on serum creatinine and urine output ('Risk,' 'Injury,' and 'Failure'). The objective of the present study was to assess the incidence of AKI using the RIFLE criteria (AKIRIFLE). Secondary objectives were to assess the incidence of AKI as defined using the SVS/ISCVS reporting standards (AKISVS/ISCVS) and the association between AKIRIFLE and death., Methods: This was an observational cohort study in 362 consecutive patients with an RAAA in three hospitals in Amsterdam (The Netherlands) between 2004 and 2011. The end points were the incidence of AKIRIFLE, of AKISVS/ISCVS, and the combined 30-day or in-hospital death rate. A multivariable logistic regression model was made to assess the association between AKIRIFLE and death after adjustment for preoperative shock profile (Glasgow Aneurysm Score) and postoperative shock profile (Acute Physiology and Chronic Health Evaluation [APACHE] II score, use of vasopressors, and fluid balance during the first 24 hours after intervention)., Results: AKIRIFLE occurred in 74% (267/362; 95% confidence interval [CI], 69%-78%), with 27% of these patients categorized as 'Risk' (71/267; 95% CI, 22%-32%), 39% categorized as 'Injury' (104/267, 95% CI, 33%-45%), and 34% categorized as 'Failure' (92/267; 95% CI, 29%-40%). AKISVS/ISCVS occurred in 48% (175/362; 95% CI, 43%-53%), with 53% of these categorized as 'grade I' (92/175; 95% CI, 45%-60%), 19% as 'grade II' (34/175; 95% CI, 14%-26%), and 28% as 'grade III' (49/175; 95% CI, 22%-35%). After multivariable adjustment for shock profiles the risk of dying in patients categorized as AKIRIFLE 'Failure' was greater than in patients without AKIRIFLE (adjusted odds ratio, 6.360; 95% CI, 2.231-18.130)., Conclusions: The incidence of AKI defined according to the RIFLE criteria (74%) was greater than defined using the SVS/ISCVS reporting standards (48%) and patients categorized as 'Failure' using the RIFLE criteria had a greater risk of dying than patients without AKI. These results indicate that the problem of AKI is much bigger than previously anticipated and that minimizing injury to the kidney could be an important focus of future research on reducing the death rate after RAAA repair., (Copyright © 2014 Society for Vascular Surgery. Published by Elsevier Inc. All rights reserved.)

Background: Malignant hypertension is frequently complicated by renal insufficiency. Although the survival of this hypertensive emergency has improved, recent data on renal outcome and its predictors are lacking. We assessed renal outcome and its predictors in patients with malignant hypertension., Methods: Retrospective analysis of patients admitted with malignant hypertension in Amsterdam, the Netherlands between August 1992-January 2010. Follow-up data on vital status, renal function and blood pressure (BP) were obtained from the outpatient department and from general practitioners. The primary composite endpoint was end-stage renal disease (ESRD) defined as the start of kidney replacement therapy (KRT) or ≥ 50% decline of estimated glomerular filtration rate (eGFR). The secondary endpoint was all cause mortality., Results: A total of 120 patients admitted with malignant hypertension were included. After a median follow-up period of 67 months (IQR 28 to 108 months) the primary endpoint was reached by 37 (31%) patients, whereas 18 patients (15%) reached the secondary endpoint. Twenty-nine (24%) patients started KRT and 8 patients (7%) had an eGFR decline ≥ 50%. After the acute phase (> 3 months after admission), initial serum creatinine and follow-up BP were the main predictors of future ESRD with hazard ratios of 6.1 (95% CI, 2.2-17) for patients with initial serum creatinine ≥ 175 μmol /L and 4.3 (95% CI, 1.4-14) for patients with uncontrolled hypertension., Conclusions: Progressive renal function decline leading to ESRD remains a major threat to patients with malignant hypertension. BP control during follow-up was an important modifiable predictor of renal outcome.

Background and Objectives: Connective tissue growth factor (CTGF/CCN-2) is a key player in fibrosis. Plasma CTGF levels predict end-stage renal disease and mortality in diabetic chronic kidney disease (CKD), supporting roles in intra- and extrarenal fibrosis. Few data are available on CTGF in nondiabetic CKD. We investigated CTGF levels and effects of antiproteinuric interventions in nondiabetic proteinuric CKD., Design, Setting, Participants, & Measurements: In a crossover randomized controlled trial, 33 nondiabetic CKD patients (3.2 [2.5 to 4.0] g/24 h proteinuria) were treated during 6-week periods with placebo, ARB (100 mg/d losartan), and ARB plus diuretics (100 mg/d losartan plus 25 mg/d hydrochlorothiazide) combined with consecutively regular and low sodium diets (193 ± 62 versus 93 ± 52 mmol Na(+)/d)., Results: CTGF was elevated in plasma (464 [387 to 556] pmol/L) and urine (205 [135 to 311] pmol/24 h) of patients compared with healthy controls (n = 21; 96 [86 to 108] pmol/L and 73 [55 to 98] pmol/24 h). Urinary CTGF was lowered by antiproteinuric intervention, in proportion to the reduction of proteinuria, with normalization during triple therapy (CTGF 99 [67 to 146] in CKD versus 73 [55 to 98] pmol/24 h in controls). In contrast, plasma CTGF was not affected., Conclusions: Urinary and plasma CTGF are elevated in nondiabetic CKD. Only urinary CTGF is normalized by antiproteinuric intervention, consistent with amelioration of tubular dysfunction. The lack of effect on plasma CTGF suggests that its driving force might be independent of proteinuria and that short-term antiproteinuric interventions are not sufficient to correct the systemic profibrotic state in CKD.