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Finally, we could not exclude that increased phosphorylation of NCC is mediated by arginine vasopressin, the hormone that primarily serves to control extracellular fluid homeostasis, via the WNK-SPAK/OSR1 pathway [49, 50]. In summary, this study showed that mice adapt to chronic furosemide treatment, by the upregulation of transporters distal to the furosemide target segment, including TRPM6, NCC and TRPV5. In this way, urinary wasting of especially Mg2+ and the subsequent development of hypomagnesaemia is prevented. Extrapolating these findings to patients on continuous furosemide treatment, with normal kidney function and consuming an adequate diet, suggests that it is unlikely that they develop hypomagnesaemia. Intriguing remains why patients AP24534 concentration with mutations in CLDN16 and CLDN19, tight junction proteins located in the TAL, develop hypomagnesaemia due to progressive renal Mg2+ wasting [51, 52], while blockade of NKCC2 does not result in hypomagnesaemia. It might be that the effect of mutations in CLDN16 and CLDN19 is more effective compared with blocking NKCC2 by furosemide. Another possible explanation is that CLDN16 and CLDN19 are expressed in more segments than only the TAL. Funding This research was financially supported by the Dutch Organization for Scientific Research (ZonMw 9120.8026; ALW 818.02.001), a European Young Investigator STI571 ic50 award from the European Science Foundation. Conflict of interest statement None declared.""A UNC2881 57-year-old man was referred from the Internal Medicine service at another hospital with presumed HSP. He presented with a 2-week history of fever, lethargy and night sweats, and 5 days of a widespread purpuric rash on the upper and lower extremities and new renal impairment, and a skin biopsy had shown a leukocytoclastic vasculitis. Apart from a history of malaria 20 years ago, for which he received prompt treatment, he was fit and healthy. A physical examination revealed an ill, febrile patient with palpable purpuric eruptions on all extremities (Figure 1). He was noted to have cervical lymphadenopathy and splenomegaly. His blood profile showed anaemia and thrombocytopaenia (haemoglobin 99 g/L, platelet count 113 �� 109/L, white cell count 10.5 �� 109/L, neutrophils 8.0 �� 109/L, monocytes 1.0 �� 109/L, lymphocytes 0.8 �� 109/L). He had renal impairment and an abnormal urinalysis (creatinine 119 ��mol/L, urine red cells 50 per high powered field, urine protein creatinine ratio 198 g/mol). He was noted to have elevated serum immmunoglobulins with a moderate polyclonal immune response (IgG 16.6 g/L, IgA 4.3 g/L, IgM 4.3 g/L). Rheumatoid factor, antinuclear antibodies, anti-neutrophil cytoplasmic antibody (ANCA) screen, antistreptolysin-O titers, hepatitis serology and cryoglobulins were all negative or within the normal limits. Tests for infection including malaria and tuberculosis were negative. Tests for immune-mediated haemolysis were positive (haptoglobins