Acute effects of Iodixanol on renal function after intra-arterial administration in patients with end-stage kidney disease

2019 ◽  
Vol 70 (4) ◽  
pp. 391-398 ◽  
Author(s):  
U. Gerk ◽  
R.P. Franke ◽  
A. Krüger-Genge ◽  
F. Jung
2010 ◽  
pp. 99-107
Author(s):  
Michael J. Field ◽  
David C. Harris ◽  
Carol A. Pollock

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Paraish S. Misra ◽  
Stephen G. Szeto ◽  
Adriana Krizova ◽  
Richard E. Gilbert ◽  
Darren A. Yuen

ESC CardioMed ◽  
2018 ◽  
pp. 981-984
Author(s):  
Thomas F. Mueller ◽  
Valerie Luyckx

Chronic kidney disease (CKD) encompasses a spectrum of diseases that are identified by a glomerular filtration rate below 90 mL/min/1.73m2 or the presence of proteinuria, or both of these, persisting for over 3 months. In population-based studies, mortality in patients with CKD is consistently several-fold higher than that in patients without CKD, and the risk increases as the severity of renal function worsens. Mortality risk is, not surprisingly, highest among those with end-stage kidney disease. In developed countries, patients with CKD and end-stage kidney disease do not die of renal disease, but die primarily of non-renal causes, the relative proportions of which change across the spectrum of renal function. In the early stages of CKD, malignancy tends to be the predominant case of death; however, as renal function worsens, the proportion of deaths related to cardiovascular disease increases. Coronary artery disease contributes to most cardiac deaths in those with milder CKD. The proportions of cardiac and overall deaths from heart failure and sudden cardiac death increase progressively as renal function declines. Sudden cardiac death is a major cause of death among patients with end-stage kidney disease. Multiple factors including underlying coronary artery disease, left ventricular hypertrophy, valvular heart disease, arrhythmias, volume and electrolyte abnormalities, uraemia, and inflammation all likely contribute to the increased risk of cardiovascular death. Much work is needed to understand the pathophysiology and develop strategies to prevent cardiovascular deaths especially in the CKD population.


Author(s):  
Rodolfo J Galindo ◽  
Francisco J Pasquel ◽  
Priyathama Vellanki ◽  
Cesar Zambrano ◽  
Bonnie Albury ◽  
...  

Abstract Introduction Differences in biochemical parameters of diabetic ketoacidosis in patients with end-stage kidney disease (ESKD) has not been established. Accordingly, we assessed the relationship between degree of metabolic acidosis and ß -hydroxybutyrate in patients ESKD (eGFR <15 mL/min/1.73 m 2), moderate renal failure (eGFR 15-60) or preserved renal function (eGFR >60). Methods This observational study included adults (18-80 years) with DKA, admitted to Emory University Hospitals between 01/01/2006 to 12/31/2016. DKA and renal stages were confirmed on admission laboratory values. Results Admission bicarbonate levels (13.9±5 vs 13.4±5.3 vs 13.8±4.2 mmol/L, p=0.7), and pH levels (7.2±0.3 vs 7.2±0.2 vs 7.2±0.2, p=0.8) were similar among groups. Patients with ESKD had lower mean ß -hydroxybutyrate (4.3±3.3 vs 5.6±2.9 vs 5.9±2.5 mmol/L, p=0.01), but higher admission glucose (852±340.4 vs 714.6±253.3 mg/dL vs 518±185.7 mg/dL, p <0.01), anion gap (23.4±7.6 vs 23±6.9 vs 19.5±4.7 mmol/L, p <0.01), and osmolality (306±20.6 vs 303.5± vs 293.1±3.1mOsm/kg, p<0.01), compared to patients with moderate renal failure and preserved renal function. The sensitivity of ß-hydroxybutyrate >3 mmol/L for diagnosing DKA by bicarbonate level <15 and <18 mmol/L was 86.9% and 72% in ESKD, 89.3% and 83.7% in moderate renal failure and 96.2% and 88.3% in preserved renal function. In patients with ESKD, the corresponding ß-hydroxybutyrate with bicarbonate levels <10, 10-15, <18 mmol/L were 5.5, 3.9, 3.0 mmol/L, respectively. Conclusions Significant metabolic differences were found among DKA patients with different levels of renal function. In patients with ESKD, a ß-hydroxybutyrate level > 3 mmol/L may assist with confirmation of DKA diagnosis.


2020 ◽  
Vol 20 (2) ◽  
pp. 89-95
Author(s):  
Apexa Kuverji ◽  
Kath Higgins ◽  
James O Burton ◽  
Andrew H Frankel ◽  
Chee Kay Cheung

The management of diabetes ketoacidosis (DKA) in people with normal renal function is well established. Although DKA is less common in people with end-stage kidney disease (ESKD), when it occurs, the management needs to be adapted to account for the different physiological state that these patients present with. This report presents two cases of DKA in people on maintenance haemodialysis for ESKD. Each case identifies learning points, when combined with a comprehensive literature review, generates key recommendations on the management of DKA in people on maintenance haemodialysis.


2021 ◽  
Vol 95 (1) ◽  
pp. 54-61
Author(s):  
Makoto Fukuda ◽  
Naoki Sawa ◽  
Junichi Hoshino ◽  
Kenichi Ohashi ◽  
Miyazono Motoaki ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-5
Author(s):  
Patrick Hamilton ◽  
Olumide Ogundare ◽  
Ammar Raza ◽  
Arvind Ponnusamy ◽  
Julie Gorton ◽  
...  

A 27-year-old man presented with a palpable purpuric skin rash and joint and abdominal pain in April 2010. He had acute kidney injury and his creatinine quickly deteriorated to 687 μmol/L, with associated nephrotic range proteinuria. Kidney biopsy showed crescentic Henoch-Schonlein nephritis. He was treated with intravenous cyclophosphamide and prednisolone despite which his renal function deteriorated; he required haemodialysis for a short duration and seven sessions of therapeutic plasma exchange (TPE). Renal function improved, but after discharge from hospital he suffered 2 further relapses, each with AKI, in 4 months. Cyclophosphamide was not effective and therefore Rituximab was introduced. He initially had a partial response but his renal function deteriorated despite continued therapy. TPE was the only treatment that prevented rapid renal functional deterioration. A novel long-term treatment strategy involving regular TPE every one to two weeks was initiated. This helped to slow his progression to end-stage kidney disease over a 3-year period and to prolong the need for renal replacement therapy over this time.


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