Abstract
Salt retention or salt deficit has a bearing on the body fluid volume. Both states are clinically difficult to recognize and quantitate. Salt deficit is particularly cumbersome in that regard since orthostatic blood pressure, heart rate changes, and simple physical inspection are inaccurate and unreliable. Salt deficit can be acute such as after hemorrhage or massive diarrhea, or more chronic as observed in Addison’s disease, failure of renal sodium chloride transporters, drug-related effects, or distal nephron disease. Molecular genetics has given us important new insights into salt deficit syndromes. Recent recognition of a novel sodium storage compartment involving sodium binding to proteoglycans adds to the overall complexity of these syndromes.
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Bandulik S, Schmidt K, Bockenhauer D, Zdebik AA, Humberg E, Kleta R, Warth R, Reichold M (2011) The salt-wasting phenotype of EAST syndrome, a disease with multifaceted symptoms linked to the KCNJ10 K+ channel. Pflugers Arch 461(4):423–435. doi:10.1007/s00424-010-0915-0
Berendes E, Walter M, Cullen P, Prien T, Van Aken H, Horsthemke J, Schulte M, von Wild K, Scherer R (1997) Secretion of brain natriuretic peptide in patients with aneurysmal subarachnoid haemorrhage. Lancet 349(9047):245–249
Chang SS, Grunder S, Hanukoglu A, Rosler A, Mathew PM, Hanukoglu I, Schild L, Lu Y, Shimkets RA, Nelson-Williams C, Rossier BC, Lifton RP (1996) Mutations in subunits of the epithelial sodium channel cause salt wasting with hyperkalaemic acidosis, pseudohypoaldosteronism type 1. Nat Genet 12(3):248–253. doi:10.1038/ng0396-248
De Nicola L, Gabbai FB, Liberti ME, Sagliocca A, Conte G, Minutolo R (2014) Sodium/glucose cotransporter 2 inhibitors and prevention of diabetic nephropathy: targeting the renal tubule in diabetes. Am J Kidney Dis. doi:10.1053/j.ajkd.2014.02.010
Geller DS, Rodriguez-Soriano J, Vallo Boado A, Schifter S, Bayer M, Chang SS, Lifton RP (1998) Mutations in the mineralocorticoid receptor gene cause autosomal dominant pseudohypoaldosteronism type I. Nat Genet 19(3):279–281. doi:10.1038/966
Grunder S, Firsov D, Chang SS, Jaeger NF, Gautschi I, Schild L, Lifton RP, Rossier BC (1997) A mutation causing pseudohypoaldosteronism type 1 identifies a conserved glycine that is involved in the gating of the epithelial sodium channel. EMBO J 16(5):899–907. doi:10.1093/emboj/16.5.899
Hamdi T, Latta S, Jallad B, Kheir F, Alhosaini MN, Patel A (2010) Cisplatin-induced renal salt wasting syndrome. South Med J 103(8):793–799. doi:10.1097/SMJ.0b013e3181e63682
Hildebrandt F, Omram H (2001) New insights: nephronophthisis-medullary cystic kidney disease. Pediatr Nephrol 16(2):168–176
Ji W, Foo JN, O’Roak BJ, Zhao H, Larson MG, Simon DB, Newton-Cheh C, State MW, Levy D, Lifton RP (2008) Rare independent mutations in renal salt handling genes contribute to blood pressure variation. Nat Genet 40(5):592–599. doi:10.1038/ng.118
Luft FC (2014) GABA the Hutt. J Mol Med (Berl). doi:10.1007/s00109-014-1153-2
Maesaka JK, Imbriano LJ, Ali NM, Ilamathi E (2009) Is it cerebral or renal salt wasting? Kidney Int 76(9):934–938. doi:10.1038/ki.2009.263
McGee S, Abernethy WB 3rd, Simel DL (1999) The rational clinical examination. Is this patient hypovolemic? JAMA 281(11):1022–1029
Pro CI, Yealy DM, Kellum JA, Huang DT, Barnato AE, Weissfeld LA, Pike F, Terndrup T, Wang HE, Hou PC, LoVecchio F, Filbin MR, Shapiro NI, Angus DC (2014) A randomized trial of protocol-based care for early septic shock. N Engl J Med 370(18):1683–1693. doi:10.1056/NEJMoa1401602
Rivers E, Nguyen B, Havstad S, Ressler J, Muzzin A, Knoblich B, Peterson E, Tomlanovich M, Early Goal-Directed Therapy Collaborative G (2001) Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 345(19):1368–1377. doi:10.1056/NEJMoa010307
Seyberth HW (2008) An improved terminology and classification of Bartter-like syndromes. Nat Clin Pract Nephrol 4(10):560–567. doi:10.1038/ncpneph0912
Silva Rdo C, Castro M, Kater CE, Cunha AA, Moraes AM, Alvarenga DB, Moreira AC, Elias LL (2004) Primary adrenal insufficiency in adults: 150 years after Addison. Arq Bras Endocrinol Metabol 48(5):724–738
Simon DB, Nelson-Williams C, Bia MJ, Ellison D, Karet FE, Molina AM, Vaara I, Iwata F, Cushner HM, Koolen M, Gainza FJ, Gitleman HJ, Lifton RP (1996) Gitelman’s variant of Bartter’s syndrome, inherited hypokalaemic alkalosis, is caused by mutations in the thiazide-sensitive Na-Cl cotransporter. Nat Genet 12(1):24–30. doi:10.1038/ng0196-24
Titze J, Dahlmann A, Lerchl K, Kopp C, Rakova N, Schroder A, Luft FC (2014) Spooky sodium balance. Kidney Int 85(4):759–767. doi:10.1038/ki.2013.367
White PC (2009) Neonatal screening for congenital adrenal hyperplasia. Nat Rev Endocrinol 5(9):490–498. doi:10.1038/nrendo.2009.148
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Luft, F.C. Clinical salt deficits. Pflugers Arch - Eur J Physiol 467, 559–563 (2015). https://doi.org/10.1007/s00424-014-1643-7
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DOI: https://doi.org/10.1007/s00424-014-1643-7