Parathyroid hormone and phosphate homeostasis in patients with Bartter and Gitelman syndrome: an international cross-sectional study.

BACKGROUND: Small cohort studies have reported high parathyroid hormone (PTH) levels in patients with Bartter syndrome and lower serum phosphate levels have anecdotally been reported in patients with Gitelman syndrome. In this cross-sectional study, we assessed PTH and phosphate homeostasis in a large cohort of patients with salt-losing tubulopathies. METHODS: Clinical and laboratory data of 589 patients with Bartter and Gitelman syndrome were provided by members of the European Rare Kidney Diseases Reference Network (ERKNet) and the European Society for Paediatric Nephrology (ESPN). RESULTS: A total of 285 patients with Bartter syndrome and 304 patients with Gitelman syndrome were included for analysis. Patients with Bartter syndrome type I and II had the highest median PTH level (7.5 pmol/L) and 56% had hyperparathyroidism (PTH >7.0 pmol/L). Serum calcium was slightly lower in Bartter syndrome type I and II patients with hyperparathyroidism (2.42 versus 2.49 mmol/L; P = .038) compared to those with normal PTH levels and correlated inversely with PTH (rs -0.253; P = .009). Serum phosphate and urinary phosphate excretion did not correlate with PTH. Overall, 22% of patients had low serum phosphate levels (phosphate-standard deviation score < -2), with the highest prevalence in patients with Bartter syndrome type III (32%). Serum phosphate correlated with tubular maximum reabsorption of phosphate/glomerular filtration rate (TmP/GFR) (rs 0.699; P < .001), suggesting renal phosphate wasting. CONCLUSIONS: Hyperparathyroidism is frequent in patients with Bartter syndrome type I and II. Low serum phosphate is observed in a significant number of patients with Bartter and Gitelman syndrome and appears associated with renal phosphate wasting.

[Thiazides to prevent recurrence of kidney stones: is hydrochlorothiazide still indicated?] / Thiazidediuretica ter preventie van recidiverende nierstenen.

Thiazides are widely used to prevent recurrence of calcium-containing kidney stones. However, the recent NOSTONE trial reported no benefit of hydrochlorothiazide on the composite outcome of symptomatic or radiologic recurrence. Higher doses (25 and 50mg daily) resulted in a decrease of radiologic recurrence, but no difference in symptomatic stones. Current guidelines preserve the use of hydrochlorothiazide to patients with overt hypercalciuria, while NOSTONE also included patients without hypercalciuria. This might have underestimated the effect of hydrochlorothiazide. While patients received dietary counseling, results suggest adherence was poor e.g. with respect to oxalate and salt consumption, possibly mitigating a potential beneficial hypocalciuric effect of hydrochlorothiazide. Furthermore, previous studies that did show an effect of thiazides on stone recurrence used higher doses. Thus, while hydrochlorothiazide might not be effective in all patients with calcium-containing kidney stones, it should not be written off, as its efficacy in overt hypercalciuria needs to be further elucidated.

Kidney Injury in Patients Treated with Immune Checkpoint Inhibitors Does Not Meet KDIGO-AKI Criteria.

Kidney injury in patients treated with immune checkpoint inhibitors develops gradually and often does not meet the Kidney Disease Improving Global Outcomes criteria for AKI.Proper classification of kidney injury could prevent the development of CKD and improve continued oncologic treatment.