Increase in nephrology advanced trainee numbers in Australia and associated reduction in clinical exposure over the past decade.

BACKGROUND: Advanced training in nephrology should provide broad experience in all aspects of nephrology. In Australia, the Specialist Advisory Committee in Nephrology oversees nephrology training, and recent increases in advanced trainee numbers have led to concern about dilution of training experience. No study has examined variations in clinical exposure for nephrology trainees in Australia. AIM: To assess the changes in nephrology advanced training in Australia with respect to trainee numbers and exposure to patients and procedures over the past 10 years. METHODS: A retrospective study was performed by obtaining all available Royal Australasian College of Physician supervisor reports from 2000 to 2010 to determine differences in clinical exposure and procedures performed by nephrology trainees. RESULTS: Five hundred and forty-two reports were reviewed involving 208 nephrology trainees in Australia across 53 different training sites. In 2000, 22 trainees were undertaking a core clinical year of training. Trainee numbers have steadily risen from 33 in 2004 to 84 in 2010. The greatest increases have occurred in New South Wales, Victoria and Queensland (sixfold, threefold and fivefold increases respectively). Trainee exposure to dialysis patients has gradually decreased in the past decade. The average number per trainee per year in 2000 compared with 2010 were 66 versus 43 (P = 0.02) and 28 versus 16 (P = 0.01) for haemodialysis and peritoneal dialysis respectively. Acute kidney injury cases per trainee showed a gradual nonsignificant reduction over time and average procedural numbers per trainee decreased significantly from 2000 to 2010 with fewer temporary dialysis catheters inserted per year (39 vs 10, P < 0.01) and fewer renal biopsies performed per year (65 vs 41, P < 0.01). The proportion of trainees working in a hospital that does not provide exposure to acute transplantation has steadily increased from 15% in 2003 to 44% in 2010. CONCLUSIONS: There has been a dramatic and significant increase in nephrology advanced trainee numbers over the past decade at a more rapid rate than the growth in dialysis and transplant patient numbers. This study suggests that training experience has diminished over the past decade and supports a 3-year core clinical nephrology training programme in Australia.

Signal transducer and activation of transcription 6 (STAT6) regulates T helper type 1 (Th1) and Th17 nephritogenic immunity in experimental crescentic glomerulonephritis.

Experimental crescentic glomerulonephritis is driven by systemic cellular immune responses. A pathogenic role for T helper type 1 (Th1) and Th17 cells is well established. T-bet, a key transcription factor required for Th1 lineage commitment, and retinoic acid-related orphan receptor-γt (Rorγt), a key Th17 transcription factor, are required for full expression of disease. Similarly, several Th1- and Th17-associated cytokines have been implicated in disease augmentation. The role of Th2 cells in the disease is less clear, although Th2-associated cytokines, interleukin (IL)-4 and IL-10, are protective. We sought to determine the role of signal transducer and activation of transcription 6 (STAT6), a key regulator of Th2 responses, in experimental crescentic glomerulonephritis. Compared to wild-type mice, histological and functional renal injury was enhanced significantly in STAT6(-/-) mice 21 days after administration of sheep anti-mouse glomerular basement membrane globulin. Consistent with the enhanced renal injury, both Th1 and Th17 nephritogenic immune responses were increased in STAT6(-/-) mice. Conversely, production of IL-5, a key Th2-associated cytokine, was decreased significantly in STAT6(-/-) mice. Early in the disease process systemic mRNA expression of T-bet and Rorγ was increased in STAT6(-/-) mice. We conclude that STAT6 is required for attenuation of Th1 and Th17 nephritogenic immune responses and protection from crescentic glomerulonephritis.

Sensory nerve excitability and neuropathy in end stage kidney disease.

BACKGROUND: Peripheral neuropathy is present in 65% of patients with end stage kidney disease (ESKD) starting dialysis. Studies of membrane potential and axonal ion channel function may help explain the pathophysiology. OBJECTIVES: To follow changes in median sensory axon excitability in patients with ESKD treated with haemodialysis, and correlate them with clinical rating scales and serum levels of potential neurotoxins. METHODS: Sensory nerve action potentials were recorded from the second digit following stimulation of the median nerve in 12 ESKD patients. Stimulus-response behaviour using two stimulus durations, threshold electrotonus to 100 ms polarising currents, a current-threshold relation, and recovery of excitability following supramaximal stimulation were recorded before, during, and after haemodialysis. Serum concentrations of potential neurotoxins were measured. RESULTS: Before dialysis, there were changes in nerve excitability consistent with axonal depolarisation: refractoriness was increased; superexcitability and depolarising threshold electrotonus were reduced. Following dialysis there were improvements in all indices, with correlations between excitability abnormalities and serum potassium measurements. Neuropathic symptoms correlated with excitability changes. CONCLUSIONS: Nerves are depolarised before haemodialysis in ESKD patients. The correlation of excitability abnormalities with potassium indicates that the achievement of normokalaemia should be a priority in treating such patients.

The role of the hypothalamic-pituitary-adrenal (HPA) axis in the regulation of blood pressure.

The role of the HPA axis in blood pressure regulation was examined in 6 normal male volunteers by comparing haemodynamic and hormonal effects of placebo, captopril, and dexamethasone given in random order for two days. The average 24-hour systolic and mean arterial pressures on placebo (135 +/- 6 and 93 +/- 2 mmHg respectively) were significantly higher than on captopril (118 +/- 1 and 85 +/- 1 mmHg respectively, p < 0.05) but there were no significant changes on dexamethasone compared with placebo (128 +/- 3 and 89 +/- 3 mmHg respectively). There were no differences in the average 24-hour diastolic blood pressures or heart rates, nor the day-night differences, night:day ratios or percentage changes in blood pressure and heart rate between treatments. Captopril significantly increased active plasma renin concentration, whilst dexamethasone decreased cortisol concentration. These results confirm the role of the renin-angiotensin system in the regulation of blood pressure in normal subjects but suggest that the HPA axis does not play a major role in determining ambulatory blood pressure or day-night variability in the short term.