Dialysis and driving: an anonymous survey of patients receiving dialysis for end-stage kidney disease.

BACKGROUND: Driving is a complex task requiring multiple cognitive domains and the musculoskeletal system. Cognitive dysfunction is associated with driving impairment. Dialysis patients are known to have a high prevalence of cognitive impairment and other comorbidities, and may be at risk of driving impairment. No Australian guidelines address driving safety in dialysis patients. AIMS: To estimate the proportion of dialysis patients who were driving and those at risk of driving impairment, and to investigate the agreement between objective and subjective markers of risk. METHODS: This single-centre study involved dialysis patients voluntarily completing two questionnaires relating to risk of driving impairment; the first questionnaire focussed on objective markers, and the second questionnaire focussed on subjective markers. Risk of driving impairment was established using pre-determined criteria, and the agreement between objective and subjective markers was estimated using Cohen kappa. RESULTS: A total of 44.8% (99/221) of patients participated; 76.8% (76/99) of participants were driving, and 76.3% (58/76) of drivers were at risk of driving impairment. Factors associated with at-risk driving included post dialysis dizziness, leg weakness or numbness, falling asleep while driving and hypoglycaemia. Sixteen patients reported collisions since commencing dialysis. The questionnaires displayed slight agreement (Cohen kappa = 0.20) between objective and subjective markers. CONCLUSIONS: Dialysis patients are at risk of driving impairment based on self-reported questionnaire responses. Discrepancies between patients' perceptions and objective markers were apparent. Further research into appropriate risk assessments, as well as development of guidelines to aid in determining driving safety in dialysis patients, is needed.

Relationship between residual kidney function and symptom burden in haemodialysis patients.

BACKGROUND: Residual kidney function (RKF) has been associated with improved solute clearance and survival in haemodialysis (HD) patients. However, whether RKF impacts symptom burden in HD patients is unknown. AIMS: To determine the prevalence of RKF in HD patients and to explore associations between higher levels of RKF with symptom burden, as well as clinical and biochemical parameters. METHODS: This is a single-centre, retrospective, observational study. RKF was assessed as urea clearance (KRU) by interdialytic urine collection. Symptom burden was measured using the palliative care outcome scale renal questionnaire. RESULTS: A total of 90 maintenance HD patients was recruited; 31.9% had KRU ≥1 mL/min/1.73 m2 . Patients with KRU ≥1 mL/min/1.73 m2 reported fewer symptoms (5.3 ± 3.5 vs 7.7 ± 3.8) (P = 0.011), including less shortness of breath (15% vs 55%) (P = 0.0013) and vomiting (0% vs 30%) (P = 0.0016). Higher RKF was associated with lower ß2 -microglobilin (P < 0.0001), and lower serum potassium (P = 0.02), but no difference in phosphate, haemoglobin, C-reactive protein or serum albumin. CONCLUSION: Higher RKF was significantly associated with fewer symptoms, and lower serum ß2 -microglobulin and potassium, suggesting that strategies to preserve RKF may be beneficial.

Outcomes of patients commencing peritoneal dialysis with and without back-up arteriovenous fistulas.

BACKGROUND: Transitions from peritoneal dialysis (PD) to haemodialysis (HD) are often unpredictable and central venous catheters (CVCs) are frequently required. Early studies found few back-up arteriovenous fistulas (bAVFs) were ever used. The PD population's characteristics have changed over time which may have altered the likelihood of bAVFs being used. This study aimed to report use of, and outcomes associated with, bAVFs in a contemporary cohort of peritoneal dialysis patients. METHOD: A single-centre, retrospective study of PD patients commencing dialysis between 2006-2016, stratified according to presence/absence of bAVF. RESULTS: One hundred seventy-six patients were included-82 with bAVF, 94 without bAVF-of whom 156 transitioned off PD. Transitions were to HD (49%), transplantation (23%), death (15%) and renal-recovery (1%). 51% of bAVFs were successfully used and 82% of bAVFs were patent when required. Median time from creation to bAVF use was 2.5 years. More patients with a bAVF transitioned to HD (62 vs 38%, p < 0.005). However, CVC requirement at the time of transition to HD was much less common in the bAVF group (18 vs 83%, p < 0.0001), such that the overall risk of requiring a CVC was significantly lower in the bAVF group (11 vs 31%, p < 0.005). Rates of returning to PD amongst patients who transitioned to HD with a CVC or an AVF were similar (19 vs 26%, p = 0.16). CONCLUSIONS: In this cohort of PD patients, utilisation of back-up arteriovenous fistulas was higher than previously reported, and presence of a back-up arteriovenous fistula was associated with a lower rate of future CVC use.

Changes in Symptom Burden in Dialysis Patients Assessed Using a Symptom-Reporting Questionnaire in Clinic.

INTRODUCTION: To determine the prevalence, severity, and change in symptoms experienced by dialysis patients following the introduction of use of a symptom-reporting questionnaire in nephrology clinic. METHODS: This is an observational study of 160 prevalent dialysis patients. Palliative care Outcome Scale symptom (POS-renal) questionnaires modified for patients with end-stage kidney disease were completed at baseline and follow-up (median 3 months), with results available to nephrologists at clinic appointments. FINDINGS: The baseline prevalence of individual symptoms ranged from 15% to 66%. The most common symptoms were lack of energy (66%) and poor mobility (58%). The median number of symptoms was 7/17 (interquartile range [IQR]: 4-10). Forty-nine percent of patients rated at least 1 symptom as severe or overwhelming. At follow-up, the median number of symptoms experienced was unchanged at 7/17 (IQR: 3-10). However, there was considerable flux in symptom severity. On average, individual symptoms that were present at baseline improved in 56% of patients and worsened in 18%; only 26% had stable symptom severity. Individual symptoms newly occurred in 8% to 20% of patients between time points, with 77% of patients experiencing at least 1 new symptom. The percent of patients rating at least 1 symptom as severe or overwhelming was reduced from 49% to 39% (P = .040). CONCLUSIONS: Use of the POS-renal questionnaire identified a high symptom burden. The presence and severity of symptoms changed dramatically over a short follow-up period, highlighting the need for regular surveillance of symptoms in the dialysis population. Routine use of a symptom questionnaire in clinic may be useful for the identification and management of symptoms in dialysis patients.

Phosphate nephropathy: an avoidable complication of bowel preparation for colonoscopy.

It is known that oral sodium phosphate, used as bowel preparation for colonoscopy, can cause acute phosphate nephropathy, a potentially severe and irreversible form of acute kidney injury. Due to these safety concerns, guidelines have advised against the routine use of this agent for a decade. We present a case report and biopsy series that demonstrate that oral sodium phosphate is still being used and that cases of APN are still occurring, in Australia.

The Thiazide-Sensitive Co-Transporter Promotes the Development of Sodium Retention in Mice with Diet-Induced Obesity.

BACKGROUND/AIMS: Intravascular volume expansion due to sodium retention is involved in the pathogenesis of obesity-related hypertension. Institution of high fat diet (HFD) feeding leads to an initial state of positive sodium balance due to enhanced tubular reabsorption of sodium, but which tubular sodium transporters are responsible for this remains undefined. METHODS: C57/Bl6 mice were fed control or HFD for 3 weeks. Blood pressures were recorded by tail cuff method. Sodium transporter expression and phosphorylation were determined by Western blotting. In vivo activity of NCC was determined using natriuretic responses to hydrochlorothiazide. Expression of NCC mRNA was determined using qPCR. RESULTS: At 3 weeks HFD mice had significant weight gains compared to control mice, but blood pressures were not yet elevated. There were no changes in expression or phosphorylation of the bumetanide-sensitive cotransporter, NKCC2, or in expression of subunits of the amiloride-sensitive ion channel, ENaC. However, there were significant increases in mRNA and protein expression of the thiazide-sensitive co-transporter, NCC, in kidneys from HFD mice. Consistent with this, HFD mice had increased in vivo activity of NCC. CONCLUSIONS: Increased expression of NCC promotes the sodium loading response to institution of HFD feeding before onset of hypertension.

AMPK couples plasma renin to cellular metabolism by phosphorylation of ACC1.

Salt reabsorption is the major energy-requiring process in the kidney, and AMP-activated protein kinase (AMPK) is an important regulator of cellular metabolism. Mice with targeted deletion of the ß1-subunit of AMPK (AMPK-ß1(-/-) mice) had significantly increased urinary Na(+) excretion on a normal salt diet. This was associated with reduced expression of the ß-subunit of the epithelial Na(+) channel (ENaC) and increased subapical tubular expression of kidney-specific Na(+)-K(+)-2Cl(-) cotransporter 2 (NKCC2) in the medullary thick ascending limb of Henle. AMPK-ß1(-/-) mice fed a salt-deficient diet were able to conserve Na(+), but renin secretion increased 180% compared with control mice. Cyclooxygenase-2 mRNA also increased in the kidney cortex, indicating greater signaling through the macula densa tubular salt-sensing pathway. To determine whether the increase in renin secretion was due to a change in regulation of fatty acid metabolism by AMPK, mice with a mutation of the inhibitory AMPK phosphosite in acetyl-CoA carboxylase 1 [ACC1-knockin (KI)(S79A) mice] were examined. ACC1-KI(S79A) mice on a normal salt diet had no increase in salt loss or renin secretion, and expression of NKCC2, Na(+)-Cl(-) cotransporter, and ENaC-ß were similar to those in control mice. When mice were placed on a salt-deficient diet, however, renin secretion and cortical expression of cyclooxygenase-2 mRNA increased significantly in ACC1-KI(S79A) mice compared with control mice. In summary, our data suggest that renin synthesis and secretion are regulated by AMPK and coupled to metabolism by phosphorylation of ACC1.