A National audit of the care of patients with acute kidney injury in England and Wales in 2019 and the association with patient outcomes.

BACKGROUND: Acute kidney injury (AKI) is a common complication of hospitalisations. This national audit assessed the care received by patients with AKI in hospital Trusts in England and Wales. METHODS: Twenty four hospital Trusts across England and Wales took part. Patients with AKI stage2/3 were identified using the UK Renal Registry AKI master patient index. Data was returned through a secure portal with linkage to hospital episode statistic mortality and hospitalisation data. Completion rates of AKI care standards and regional variations in care were established. RESULTS: 989 AKI episodes were included in the analyses. In-hospital 30-day mortality was 31-33.1% (AKI 2/3). Standard AKI interventions were completed in >80% of episodes. Significant inter-hospital variation remained in attainment of AKI care standards after adjustment for age and sex. Recording of urinalysis (41.9%) and timely imaging (37.2%) were low. Information on discharge summaries relating to medication changes/re-commencement and follow-up blood tests associated with reduced mortality. No quality indicators relating to clinical management associated with mortality. Better communication on discharge summaries associated with reduced mortality. CONCLUSIONS: Outcomes for patients with AKI in hospital remain poor. Regional variation in care exists. Work is needed to assess whether improving and standardising care improves patient outcomes.

Incidence, care quality and outcomes of patients with acute kidney injury in admitted hospital care.

BACKGROUND/INTRODUCTION: Acute kidney injury (AKI) is common in acute hospital admission and associated with worse patient outcomes. AIM: To measure incidence, care quality and outcome of AKI in admitted hospital care. DESIGN: Forty-six of 168 acute NHS healthcare trusts in UK caring for 2 million acute hospital admissions per annum collected information on adults identified with AKI stage 3 (3-fold rise in serum creatinine or creatinine >354 µmol/l) through routine biochemical testing over a 5-month period in 2012. METHODS: Information was collected on patient and care characteristics. Primary outcomes were survival and recovery of kidney function at 1 month. RESULTS: A total of 15 647 patients were identified with biochemical AKI stage 3. Case note reviews were available for 7726 patients. In 80%, biochemical AKI stage 3 was confirmed clinically. Among this group, median age was 75 years, median length of stay was 12 days and the overall mortality within 1 month was 38%. Significant factors in a multivariable model predicting survival included age and some causes of AKI. Dipstick urinalysis, medication review, discussion with a nephrologist and acceptance for transfer to a renal unit were also associated with higher survival, but not early review by a senior doctor, acceptance for transfer to critical care or requirement for renal replacement therapy. Eighteen percent of people did not have their kidney function checked 1 month after the episode had resolved. DISCUSSION/CONCLUSIONS: This large study of in-hospital AKI supports the efficacy of biochemical detection of AKI in common usage. AKI mortality remains substantial, length of stay comparable with single-centre studies, and much of the variation is poorly explained (model Cox and Snell R2 = 0.131) from current predictors.

Poorer graft survival in ethnic minorities: results from a multi-centre UK study of kidney transplant outcomes.

BACKGROUND: The STEPP group was established to investigate factors that affect long-term transplant outcomes including quality of life and other patient-reported outcomes between different transplant centers and patients. METHODS: Data were collected for 2,650 patients whose first renal transplant took place between 1992 and 2003 in five UK centers. Univariable and multivariable survival analyses were performed using eleven candidate explanatory variables. RESULTS: Graft survival was worse in Black (B) patients (HR B v W 1.57 95% CI 1.10, 2.24), and in South Asian (A) patients (HR A v W 1.39 95% CI 1.03, 1.85) compared to Whites (W) after adjusting for other factors including HLA mismatch, and time on dialysis. Time spent on dialysis pre-transplantation was non-linearly associated with patient, but not death-censored graft survival. Losing a functioning graft was a strong predictor of patient death. One site had both the best graft and the worst patient survival. CONCLUSIONS: Differences in patient and graft survival between ethnic groups cannot be explained by currently recognized factors. These, and the complex balance between optimum patient and graft survival which differs between sites in this study require further investigation.

Sleep disorders in dialysis patients.

Poor sleep and sleep-related breathing disorders are common in patients with end-stage renal disease (ESRD) but are often unrecognized and undertreated. Sleep disorders are known negative prognostic factors for morbidity and mortality. The most frequent sleep disorders seen in patients with ESRD are conditioned insomnia, excessive daytime sleepiness, obstructive or central sleep apnea (SA), as well as restless legs syndrome (RLS) and periodic limb movement disorder (PLMD). Several uremic and nonuremic factors are thought to participate in the pathogenesis of sleep disorders in patients with ESRD. The therapy of sleeping disorders includes nonpharmacological and pharmacological measures that can improve the functionality and quality of life in patients with ESRD.

Effects of glucose dialysate on extracellular matrix production by human peritoneal mesothelial cells (HPMC): the role of TGF-beta.

BACKGROUND: Dialysate glucose has been implicated in the loss of peritoneal membrane function seen in long-term CAPD patients. METHODS: In order to investigate this in vitro, human peritoneal mesothelial cells (HPMC) were cultured in a 50:50 mix of dialysis solution and M199 for 12 h. The dialysate was laboratory manufactured and designed to be identical in composition to PD4 (LAB). The final glucose concentration ranged between 5 and 40 mmol/l. Experiments were conducted in the presence and absence of an anti-transforming growth factor-beta (TGF-beta) antibody. Cell viability was measured by lactate dehydrogenase (LDH) release. Fibronectin (FN) and TGF-beta protein were measured by ELISA, and FN gene expression was measured by Northern analysis. Separately, the effects of recombinant TGF-beta(1) added to M199: dialysate at 5 mmol/l glucose were investigated. RESULTS: Forty millimoles per litre d-glucose LAB caused a decrease in cell viability, as evidenced by an increase in LDH release (6.0+/-1.3 vs 2.6+/-0.7%). This effect was dependent on osmolality. Forty millimoles per litre d-glucose LAB stimulated a 15.4+/-4.6% increase in FN, a 46.5+/-18.3% increase in TGF-beta protein (both P<0.05), and 1.4+/-0.09-fold increase in FN mRNA compared with 5 mmol/l d-glucose LAB. Exogenous TGF-beta 0-1 ng/ml induced a dose-dependent increase in FN protein (280+/-45% increase at TGF-beta 1 ng/ml, P<0.0001), and FN mRNA levels (10.0+/-1.8-fold at TGF-beta 1 ng/ml). The increase in FN in response to 40 mmol/l glucose was significantly reduced by anti-TGF-beta antibody to levels not different from control (93.8+/-6.6%, P<0.05 vs no Ab). CONCLUSIONS: These data suggest that the pro-fibrotic effect of glucose dialysate on HPMC is mediated through stimulation of TGF-beta, which promotes FN gene expression and protein production.

Role of diuretics in the preservation of residual renal function in patients on continuous ambulatory peritoneal dialysis.

BACKGROUND: Patients on continuous ambulatory peritoneal dialysis (CAPD) are dependent on residual renal function for solute and water clearances, and this declines with time on dialysis. Loop diuretics have been postulated to slow this decline. METHODS: Sixty-one patients new to dialysis were randomly assigned to either furosemide 250 mg every day or no furosemide at the time of CAPD training and were followed prospectively. Urine volume (UV), urea clearance (C(Urea)), and creatinine clearance on cimetidine (C(Cr)) were measured at randomization at six months and at one year. Patients underwent a standard four-hour peritoneum equilibrium test, and total body water was measured by bioelectrical impedance. Results were expressed on an intention-to-treat basis. RESULTS: UV, C(Cr), and C(Urea) were similar at randomization (1020 +/- 104 vs. 1040 +/- 130 mL/24 hours, 4.95 +/- 0.51 vs. 4.07 +/- 0.40 mL/min/1.73 m2, 0.91 +/- 0.09 vs. 0.84 +/- 0.08, diuretic vs. control). UV in the diuretic-treated group increased, whereas in the control group, it declined (+176 vs. -200 mL/24 hours at 6 months and +48.8 vs. -305 mL/24 hours at 1 year, P < 0.05). C(Cr) and C(Urea) declined at a constant rate and were unaffected by diuretic administration (0.12 +/- 0.05 vs. 0.071 +/- 0.04 mL/min/1.73 m2/month, 0.020 +/- 0.01 vs. 0.019 +/- 0.01 per month). Urinary sodium excretion increased in the diuretic group and declined in the control group (+0.72 +/- 0.85 vs. -2.56 +/- 1.31 mmol/24 hours/month, P = 0.04). Body weight rose in both groups (4.3 vs. 3.0 kg), but the percentage of total body weight rose in the control group and remained constant in the diuretic group (52 +/- 2.4 vs. 64 +/- 6.6%, P = 0.10). CONCLUSIONS: Long-term furosemide produces a significant increase in UV over 12 months when on CAPD and may result in clinically significant improvement in fluid balance. However, furosemide has no effect on preserving residual renal function.

Haemodynamic responses to nonhypotensive central hypovolaemia induced by lower body negative pressure in men and women.

Haemodynamic responses to low levels of lower body negative pressure (LBNP) were investigated in two groups of healthy, normotensive volunteers (8 men and 8 women) during two repeated experimental runs on two occasions, the latter determined by the different phases of the menstrual cycle in the women. The data consisted of systolic blood pressure (SBP), diastolic blood pressure (DBP) and mean blood pressure (MBP), pulse rate (fc), forearm blood flow (FBF) and forearm vascular conductance (FC). The resting cardiovascular status was similar in men and women, except that women had a significantly higher fc than men. LBNP (1.3, 2.7 and 4 kPa) had no significant effect on any BP variable or on fc. However, FBF and FC were reduced at all levels of LBNP. Significant overshoots in FBF and FC were seen in all subjects following the release of LBNP of 2.7 and 4 kPa and, in most cases, after release of LBNP of 1.3 kPa. There were no significant gender differences in any of the responses to LBNP. Furthermore, none of the cardiovascular variables measured showed significant differences between the follicular and luteal phases of the menstrual cycle in women, either at rest or during exposure to LBNP, and the responses in the men on the two occasions were not different. These findings indicate that gender differences in responses to LBNP hypothesized previously are not apparent during and after exposure to low levels of LBNP.