Clinical Pediatric Nephrology, Second Edition by Kanwal Kher, H. William Schnaper, Sudesh Paul Makker

By Kanwal Kher, H. William Schnaper, Sudesh Paul Makker

The second one variation of this scientific source for nephrologists and condominium officials in perform and nephrology fellows in education has been revised according to suggestions from clients of the 1st variation. The case histories with dialogue on the topic of prognosis and administration of a medical situation were vastly multiplied all through as a distinct and significant characteristic of the book's charm.

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48. Bohn S, Thomas H, Turan G, et al. Distinct molecular and morphogenetic properties of mutations in the human HNF1beta gene that lead to defective kidney development. J Am Soc Nephrol 14:2033, 2003. 49. Pilia G, Hughes-Benzie RM, MacKenzie A et al. Mutations in GPC3, a glypican gene, cause the Simpson–Golabi–Behmel overgrowth syndrome. Nat Genet 12:241, 1996. 50. Salerno A, Kohlhase J, Kaplan BS. Townes–Brocks syndrome and renal dysplasia: a novel mutation in the SALL1 gene. Pediatr Nephrol 14:25, 2000.

16 The peritubular capillary hydrostatic pressure opposes net proximal tubular sodium reabsorption, whereas the peritubular capillary oncotic pressure promotes proximal tubular sodium reabsorption. Therefore, following volume expansion, the peritubular capillary protein concentration falls, while the hydrostatic pressure rises, both of which reduce proximal tubular sodium reabsorption. With volume contraction, however, peritubular capillary protein concentration rises and peritubular capillary hydrostatic pressure falls, both of which increase tubular sodium reabsorption.

Sall1 Sall1, a transcription factor, is expressed in the metanephric mesenchyme at the time of induction by the ureteric bud. Mutations in Sall1 exist in patients with Townes–Brock syndrome (OMIM # 107480). In Sall1-deficient mice, ureteric bud outgrowth occurs, but the bud fails to invade the metanephric blastema, resulting in renal agenesis. 34 Gli3 The gene encoding Gli3 is mutated in patients with Pallister–Hall syndrome (OMIM # 146510) and renal dysplasia. GLI3 is one member among a family of GLI proteins that control gene transcription.

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