Heparin‐induced thrombocytopenia (HIT) is a potentially serious adverse drug reaction that can result in lethal vascular thrombosis. Dabigatran is a direct thrombin inhibitor that might be useful in the management of HIT. This study evaluated the efficacy and safety of dabigatran in patients with HIT. We included 43 patients in the study who received dabigatran for the management of suspected HIT, based on 4Ts (thrombocytopenia, timing of platelet count drop, thrombosis or other sequelae, and other causes of thrombocytopenia) scores. Three patients were excluded because they had received dabigatran with a creatinine clearance <15 mL/min. Patients’ records were analyzed longitudinally, with 12 months follow‐up from the time of initiation of dabigatran, for occurrence of thrombosis, dabigatran‐related complications, and outcome. Patients with chronic kidney disease, hepatic impairment, mechanical heart valves, active bleeding, and extremes of weights (<50 and >120 kg) were excluded from the study. Arterial thrombosis was not observed in any of our patients. The platelet counts normalized in all patients except for 2, which was attributed to the underlying comorbidities. We did not observe any hemorrhagic events or significant thrombosis during the follow‐up period. Eight patients died from nonthrombotic causes, which were unrelated to adverse effects of dabigatran. Based on our findings, dabigatran could be considered a safe and effective agent in the management of HIT, particularly in the developing countries, where there could be issues with the cost and availability of other agents recommended for this condition. Further studies are needed to validate our findings.

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 Pediatric Nephrology (ESPN). Results 285 patients with Bartter syndrome and 304 patients with Gitelman syndrome were included for analysis. Patients with Bartter syndrome type I & II had the highest median PTH level (7.5 pmol/l) and 56% had hyperparathyroidism (PTH &gt;7.0 pmol/l). Serum calcium was slightly lower in Bartter syndrome type I & II patients with hyperparathyroidism (2.42 vs. 2.49 mmol/l; p = 0.038) compared to those with normal PTH levels and correlated inversely with PTH (rs -0.253; p = 0.009). Serum phosphate and urinary phosphate excretion did not correlate with PTH. Overall, 22% of patients had low serum phosphate levels (phosphate – standard deviation score &lt; -2), with the highest prevalence in patients with Bartter syndrome type III (32%). Serum phosphate correlated with TmP/GFR (rs 0.699; p &lt; 0.001), suggesting renal phosphate wasting. Conclusions Hyperparathyroidism is frequent in patients with Bartter syndrome type I & II. Low serum phosphate is observed in a significant number of patients with Bartter and Gitelman syndrome and appears associated with renal phosphate wasting.

Kidney failure (KF) has become a major public health issue around the world and is associated with excess costs from kidney replacement therapy (KRT; dialysis and kidney transplantation), hospitalization, morbidity, and mortality. 1 Although several countries in the Middle East have an abundance of mineral resources, there are still several challenges in the region in the capacity to provide adequate kidney care for its people. Some of the challenges include