**1.3 Changes in renal anatomy and physiology in normal pregnancy:**

To understand the pathophysiology and proper management of renal problems in pregnancy it is important that we are familiar with the anatomical and physiological changes that occur during normal pregnancy.

#### **1.3.1 Renal tract anatomy**

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

Pregnancy-specific conditions such as preeclampsia, HELLP syndrome, acute fatty liver of pregnancy (AFLP), haemolytic uremic syndrome/ thrombotic thrombocytopenic purpura independently or in combination cause uterine bleeding ante-partum or post-partum haemorrhage. These conditions are frequently associated with complications like abruptioplacentae, hepatic infarction, hepatic rupture, intra-abdominal bleeding, and puerperal sepsis all of which can be further complicated by AKI. This occurs frequently in third trimester (Krane, 1988; Maynard et al, 2007; Prakash, 2010). Preeclampsia is a multi-system disorder unique to human pregnancy characterised by hypertension and involvement of one or more other organ systems and/or the foetus. American College of Obstetrics and Gynaecology, requires blood pressures >140/90 mm Hg on two occasions combined with urinary protein excretion >300 mg/d for the diagnosis of preeclampsia. Preeclampsia occurs in 3-5% of pregnancies and is associated with increased maternal and fetal mortality especially in developing countries. It is a leading cause of premature deliveries in developed countries thus increases the neonatal morbidity (Society of Obstetric Medicine of Australia

Abruptio placentae and puerperal sepsis; may also occur independent of these conditions and can be complicated by AKI. Obstetric complications such as septic abortion and placental abruption are associated with severe acute tubular necrosis (ATN) and bilateral cortical necrosis. Acute cortical necrosis, usually involves bilateral renal cortex, may occur as a consequence of irreversible or severe ATN. It has been found to be associated with poor renal outcome in longer term. Bilateral cortical necrosis is most often a complication of abruptio-placentae (36 per cent in the series of Chugh); while in other studies it was associated with disseminated intravascular coagulation. It presents as acute renal failure in other conditions too but, unlike acute tubular necrosis, total and persistent anuria is almost constant (Kleinknecht et al, 1973; Chugh, 1976). The diagnosis can be established either by renal biopsy or, better, by selective renal angiography. Other imaging studies (plain radiograph, ultrasound scan, CT-scan of abdomen and nuclear renal scan) may also be helpful. Renal cortical necrosis which occurs as a consequence of AKI in pregnancy continues sporadically (Naqvi et al, 1996; Prakash et al, 2007). With overall decrease in the incidence of AKI in pregnancy and improved overall management; incidence of cortical necrosis is decreasing even in the developing countries. Whenever present it is associated with irreversible renal failure (Khanal, 2010). Sepsis is still a major cause including septic abortions and puerperal sepsis in several studies published from India over last decades

Obstructive uropathy; obstruction may occur in gravidas due to polyhydramnios, incarcerated gravid uterus, or can occur even in women with otherwise uncomplicated gestation due to retroverted uterus. Rarely, acute urinary tract obstruction in pregnancy is induced by a kidney stone, and it seldom causes renal failure (Strothers & Lee, 1992; Scarpa

Amniotic fluid embolism which occurs primarily in multi-para after prolonged labour can cause AKI. Those with underlying renal parenchymal disease even without advanced chronic kidney disease are more prone to develop acute tubular necrosis (ATN) especially due to super imposed pre-eclampsia (Pertuiset & Grunfeld, 1994). Thrombotic thrombocytopenic purpura-haemolytic uremic syndrome (TTP-HUS) can easily be confused

and New Zealand [SOMANZ], 2009).

(Sivakumar, 2011).

et al, 1996).

Less common and miscellaneous causes of obstetric AKI include:

The kidneys enlarge during normal pregnancy, increasing by 1 to 2 cm in length and in volume by up to 70% towards term, due to tissue hypertrophy and expansion of both interstitial and vascular compartments. More important from a clinical perspective is the increase in size of the renal pelvices and ureters. By third trimester about 80% of the pregnant women have hydronephrosis which is easily evident by ultrasound, more on the right than on the left (Baylis & Davison , 2010; Brown et al, 2010). A number of factors are thought to be important in this change. Progesterone, a smooth muscle relaxant, reduces ureteric tone and peristalsis. The asymmetric dilation of the pelvicalyceal system suggests extrinsic compression by the enlarging uterus at the pelvic brim, hypertrophy of surrounding connective tissue (Waldeyer's sheath) and kinking due to ligaments or compression by iliac blood vessels (Brown et al, 2010). The clinical consequence of these changes can be urinary stasis; increasing the risk of bacterial growth and asymptomatic bacteriuria of pregnancy. If the changes are in extreme and precipitate the over distention syndrome, with massive dilation they may present with symptoms like recurrent severe flank pain, increasing serum creatinine, hypertension, or even reversible acute kidney injury (Khanna & Nguyen, 2001). In case of presentation with over distension symptoms that suggest renal colic but no stone detectable by ultrasound or by radiographic imaging; it is imperative to exclude urinary tract infection and to avoid the temptation to drain the system using nephrostomy tubes. Furthermore it is important to remember that acute renal failure as a consequence of ureteric obstruction in pregnancy is uncommon; and that ureteric dilation is part of normal pregnancy and it is not usually possible to distinguish between this and pathologic dilation (Brown et al, 2010).
