**1. Introduction**

88 Basic Nephrology and Acute Kidney Injury

Tsukahara, H, Fujii, Y, Tsuchida, S, Hiraoka, M, Morikawa, K, Haruki, S & Sudo, M. (1994).

Tsukahara, H, Yoshimoto, M, Saito, M, Sakaguchi, T, Mitsuyoshi, I, Hayashi, S, Nakamura,

Tucker, J & McGuire, W. (2004). Epidemiology of preterm birth. *BMJ*, Vol. 329, No. 7467,

Ueda, N & Shah, SV. (2000). Tubular cell damage in acute renal failure-apoptosis, necrosis,

van Venrooij, NA, Junewick, JJ, Gelfand, SL, Davis, AT, Crumb, TL & Bunchman, TE. (2010).

Vidaeff, AC, Doyle, NM & Gilstrap, LC, 3rd. (2003). Antenatal corticosteroids for fetal

Vieux, R, Hascoet, JM, Merdariu, D, Fresson, J & Guillemin, F. (2010). Glomerular filtration

Wilkins, BH. (1992). Renal function in sick very low birthweight infants: 1. Glomerular

Zaffanello, M, Brugnara, M, Bruno, C, Franchi, B, Talamini, G, Guidi, G, Cataldi, L, Biban, P,

Zimanyi, MA, Bertram, JF & Black, MJ. (2004). Does a nephron deficit in rats predispose to

Zimanyi, MA, Denton, KM, Forbes, JM, Thallas-Bonke, V, Thomas, MC, Poon, F & Black,

*Diabetologia*, Vol. 49, No. 4, (Apr 2006), pp. 801-810, 0012-186X (Print) Zohdi, V, Moritz, KM, Bubb, KJ, Cock, ML, Wreford, N, Harding, R & Black, MJ. (2007).

*Physiol*, Vol. 293, No. 3, (Sep 2007), pp. R1267-1273, 0363-6119 (Print)

*Radiol*, Vol. 40, No. 9, (Sep 2010), pp. 1505-1508, 1432-1998 (Electronic) Vanpee, M, Blennow, M, Linne, T, Herin, P & Aperia, A. (1992). Renal function in very low

Vol. 121, No. 5 Pt 1, (Nov 1992), pp. 784-788, 0022-3476 (Print)

No. 2, 1994), pp. 212-216, 0028-2766 (Print)

(Sep 18 2004), pp. 675-678, 1468-5833 (Electronic)

(Dec 2003), pp. 825-840, vii, 0095-5108 (Print)

(Aug 2010), pp. 1192-1198, 1651-2227 (Electronic)

pp. e1186-1192, 1098-4275 (Electronic)

1468-2044 (Electronic)

247, 1420-4096 (Print)

0931-041X (Print)

(Print)

Renal handling of albumin and beta-2-microglobulin in neonates. *Nephron*, Vol. 68,

K, Kikuchi, K & Sudo, M. (1990). Assessment of tubular function in neonates using urinary beta 2-microglobulin. *Pediatr Nephrol*, Vol. 4, No. 5, (Sep 1990), pp. 512-514,

or both. *Nephrol Dial Transplant*, Vol. 15, No. 3, (Mar 2000), pp. 318-323, 0931-0509

Sonographic assessment of renal size and growth in premature infants. *Pediatr* 

birth weight infants: normal maturity reached during early childhood. *J Pediatr*,

maturation in women at risk for preterm delivery. *Clin Perinatol*, Vol. 30, No. 4,

rate reference values in very preterm infants. *Pediatrics*, Vol. 125, No. 5, (May 2010),

filtration rate. *Arch Dis Child*, Vol. 67, No. 10 Spec No, (Oct 1992), pp. 1140-1145,

Mella, R & Fanos, V. (2010). Renal function and volume of infants born with a very low birth-weight: a preliminary cross-sectional study. *Acta Paediatr*, Vol. 99, No. 8,

salt-sensitive hypertension? *Kidney Blood Press Res*, Vol. 27, No. 4, 2004), pp. 239-

MJ. (2006). A developmental nephron deficit in rats is associated with increased susceptibility to a secondary renal injury due to advanced glycation end-products.

Nephrogenesis and the renal renin-angiotensin system in fetal sheep: effects of intrauterine growth restriction during late gestation. *Am J Physiol Regul Integr Comp*  Regulation of intracellular and extracellular potassium concentration is a fundamental process vital for cellular metabolism. Potassium intake, from the diet, is carefully balanced with excretion of potassium via the renal tract and gastrointestinal losses. Following a potassium load, extra-renal buffering of potassium occurs in peripheral tissues prior to its excretion. Thus potassium regulation is achieved by both short term and long term mechanisms. It has become clear that a series of potassium ion channels and transporter proteins have physiologically important roles throughout the length of the nephron. Our knowledge of normal physiological mechanisms has been increased by studying molecular defects responsible for variety of disorders associated with potassium transport. Studying renal tubular epithelial cell proteins and their regulation has improved the understanding of inherited tubular disorders which may cause hypokalemia.

Here, we review the normal renal tubular handling of potassium and discuss the molecular basis of clinical syndromes associated with hypokalemic alkalosis and hypokalemic forms of hypertension.
