**1. Introduction**

66 Novel Insights on Chronic Kidney Disease, Acute Kidney Injury and Polycystic Kidney Disease

Verbalis JG, Goldsmith SR, Greenberg A, Schrier RW, & Sterns RH. (2007) Hyponastremia

Wall BM, Crofton JT, & Share L. (1992) Chronic hyponatremia due to resetting of the osmostat in a patient with gastric carcinoma. *Am J Med* 1992,93,pp.223-228 Wall BM. (1993) Water loading test in the reset osmostat variant of SIADH*. Am J* 

Weinberger A, Santo M, Solomon F, Shalit M, Pinkhas J, & Sperling O. (1982) Abnormality

Welt LG, Seldin DW, Nelson WP, German WJ, & Peters JP. (1952) Role of the central nervous system in metabolism of electrolytes and water. *Arch Int Med*,90,pp.355-378) Wijdicks EF, Ropper AH, Hunnicutt EJ, Richardson GS, & Nathanson JA. (1991) Atrial

Wijdicks EF, Schievink WI,& Burnett JC Jr. (1997) Natriuretic peptide system and

Wijdicks EF, Vermeulen M, Haaf JA, Hijdra A, Bakker WH, van Gijn J. (1985) Volume

Wijdicks EF, Vermeulen M, Hijdra A, & van Gijn J. (1985) Hyponatremia and cerebral

Yamamoto T, Moriwaki Y, Takahashi S, Tsutsumi Z, & Hada T. (2000) Effect of losartan

Youmans S, & Maesaka JK.(2011) Urine of patients with cerebral/renal salt-wasting

Zerbe R, Stropes L, & Robertson G. (1980) Vasopressin function in the syndrome of

cellsAbst. *Annual Mtg Am Soc Nephrol*, Philadelphia, PA, USA

inappropriate antidiuresis*. Annu Rev Med*, 31,pp.315-327

Vogel JH. (1963) Aldosterone in the cerebral salt wasting. *Circulation*,l27,pp.44-50.

S21

*Med*.94,pp.343.

(ANP)

hormone. *Isr J Med*,18,pp.711-713.

harmful. *Ann Neurol,*17,PP.137-140

and purine bases. *J Rheumatol*, 27,pp. 2232-2236

*Stroke*,22(12),pp.1519-1524.

*Neurol,*18,pp.211-216

treatment guidelines 2007: Expert Panel Recommendations. *Am J Med,*120,pp.S1-

in renal urate handling in the syndrome of inappropriate secretion of antidiuretic

natriuretic factor and salt wasting after aneurysmal subarachnoid hemorrhage.

endothelin in aneurysmal subarachnoid hemorrhage. *J Neurosurg*, 87(2),pp.275-80

depletion and natriuresis in patients with a ruptured intracranial aneurysm*. Ann* 

infarction in patients with ruptured intracranial aneurysm: Is fluid restriction

potassium, an angiotensin II receptor antagonist, on renal excretion of oxypurinol

syndrome contains a substance that inhibits reabsorptive sodium flux in LLC-PK1

Acute kidney injury (AKI) is a clinical syndrome denoted by an abrupt decline in glomerular filtration rate (GFR) sufficient to decrease the elimination of nitrogenous waste products (urea and creatinine) and other uremic toxins (Jefferson et al, 2010). AKI is a not very common yet serious complication occurring in pregnancy. The incidence and the mortality rates associated with obstetric acute kidney injury (also known as pregnancy related acute renal failure; PRARF) have decreased over the last few decades especially in developed countries (Prakash et al, 2007; Stratta et al, 1996). There are several factors which lead to this improvement and will be discussed later in the chapter. Since the term AKI is now widely used in place of acute renal failure (Ricci et al, 2011); for the ease of description we have used obstetric AKI in place of PRARF in this chapter.

Obstetric AKI can occur at any stage of pregnancy; ante-partum or post-partum and may be AKI occurring as a coincidence during pregnancy or AKI due to causes specific to pregnancy.

Although obstetric AKI is vanishing from developed world (Stratta et al, 1996), it is still a frequent cause of maternal morbidity and mortality in the developing nations. Poverty, lack of awareness and difficulties (e.g. lack of transport) accessing obstetric care all are responsible for this additional burden (World Health Organization [WHO], 2009). This also increases the disparity in reported number of cases and its actual occurrence contributing to scarcity of literature even in recent time.
