Home About us Editorial board Search Ahead of print Current issue Archives Submit article Instructions Subscribe Contacts Login 
Journal of Obstrectic Anaesthesia and Critical Care
Search articles
Home Print this page Email this page Small font size Default font size Increase font size Users Online: 173

 Table of Contents  
Year : 2013  |  Volume : 3  |  Issue : 1  |  Page : 7-15

Renal diseases during pregnancy: Critical and current perspectives

1 Department of Anesthesiology and Intensive Care, Gian Sagar Medical College and Hospital, Ram Nagar, Banur, Punjab, India
2 Department of Medicine, Gian Sagar Medical College and Hospital, Ram Nagar, Banur, Punjab, India
3 Department of Obstetrics and Gynaecology, Gian Sagar Medical College and Hospital, Ram Nagar, Banur, Punjab, India

Date of Web Publication1-Jul-2013

Correspondence Address:
Sukhminder Jit Singh Bajwa
Department of Anesthesiology and Intensive Care, Gian Sagar Medical College and Hospital, Ram Nagar, Banur, House No-27-A, Ratan Nagar, Tripuri, Patiala, Punjab - 147 001
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2249-4472.114257

Rights and Permissions

The advancements in medicine have made early detection and management of medical diseases possible especially during the pregnancy. The physiologic alterations of pregnancy have important implications for renal structure and functions, which may possibly lead to diagnostic dilemmas and wrong interpretation of various investigations carried out during the gestational period. Renal diseases are extremely challenging to treat during pregnancy as various drugs can have adverse effect on the pregnancy outcome. In general, these patients may either progress to normal delivery or may have to undergo surgical delivery under anesthesia. Apart from these anticipated challenges, many other renal problems can develop during the pregnancy in patients with normal renal functions such as urinary tract infections, acute kidney injury or renal trauma. Planning of pregnancy in renal diseases is also associated with increased potential risks especially in patients on dialysis as well as in patients who had undergone renal transplantation.

Keywords: Acute renal failure, hemodialysis, pregnancy, renal diseases

How to cite this article:
Bajwa SJ, Kwatra IS, Bajwa SK, Kaur M. Renal diseases during pregnancy: Critical and current perspectives. J Obstet Anaesth Crit Care 2013;3:7-15

How to cite this URL:
Bajwa SJ, Kwatra IS, Bajwa SK, Kaur M. Renal diseases during pregnancy: Critical and current perspectives. J Obstet Anaesth Crit Care [serial online] 2013 [cited 2021 May 18];3:7-15. Available from: https://www.joacc.com/text.asp?2013/3/1/7/114257

  Introduction Top

Pregnancy is a state of altered hormonal and hemodynamic milieu. These physiologic alterations have important implications for renal structure and functions, which may possibly lead to diagnostic dilemmas and incorrect interpretation of various investigations carried out during the gestational period. Patients having underlying renal diseases attributed to different etiologies need to be monitored carefully during the pregnancy so as to achieve successful maternal and fetal outcomes. Large numbers of patients with chronic kidney disease (CKD) undergo renal transplant surgery and the resultant improved survival and quality of life gives opportunities to many of these patients to become pregnant and experience motherhood. Management of such patients requires a multidisciplinary approach and close co-operation between urologist, physician, gynecologist and anesthesiologist. In general, these patients may either progress to normal delivery or may have to undergo surgical delivery under anesthesia. [1]

Apart from these anticipated challenges many other renal problems can develop during the pregnancy in patients with normal renal function such as urinary tract infections, acute kidney injury or renal trauma during pregnancy. [2] A basic understanding of renal molecular genetics can be extremely helpful in identification of patients who are at risk of developing deranged renal functions during the pregnancy. [3] Pregnancy induced hypertension (PIH) can also affect renal functions and the research related to its pathophysiology has revealed the role of newer molecules. The present review analyzes the current status of the various renal disease states and their implications for the obstetrician, urologist, nephrologist, and anesthesiologist [Table 1].
Table 1: The comparative clinical and laboratory features of different critical illnesses related to renal
pathologies during the pregnancy

Click here to view

  Structural Changes During the Pregnancy Top

The length of both kidneys increases by approximately 1 cm during gestational period. [4] Major changes can be seen in the collecting system as there is dilatation of calyces, renal pelvis, and ureters, which are usually more prominent on the right side. The smooth muscles and connective tissue in the renal system show hypertrophy and hyperplasia as well as increase in the tone of tissues. Though the exact cause of obstruction is not clear, both hormonal and obstructive pathophysiologies are the proposed mechanisms. [5],[6],[7] These physiologic changes may mimic the picture of obstructive uropathy during investigations.

These changes have some important clinical implications as well. These physiologic alterations can cause collection errors in tests (because of stasis of urine in the renal system leading to falsely low urinary volume in 24 h) based on timed collections such as creatinine clearance and 24 h urinary proteins estimation. Patients should have a good hydration and lie down on their side for an hour before and after finishing of the sample collection. The increase of 1 cm in kidney size until 16 weeks postpartum is an accepted physiological norm and should not be considered as pathological. However, these changes are permanent in approximately 11% of patients. [5] Hence, intravenous urography should be deferred until 16 weeks postpartum if any renal pathology is suspected on the basis of enlarged size as physiological dilatation persists until 16 weeks postpartum and can lead to wrong diagnosis of hydronephrosis/obstruction) All these changes lead to an increased propensity for frank pyelonephritis.

  Renal Hemodynamic Changes in Pregnancy Top

Glomerular filtration rate (GFR) and renal plasma flow increases by 35-50% during the pregnancy. GFR starts increasing after conception and reaches a peak during the last phase of the first trimester. However, renal plasma flow is greatest at mid gestation and declines during the last 4 weeks of pregnancy. Filtration fraction decreases during early pregnancy. As a result, serum creatinine and urea nitrogen values decrease in normal pregnancy. [8] Therefore, in a pregnant women a serum creatinine > 0.8 mg/dl and urea > 13 mg/dl suggests need for additional evaluation. Excretion of Glucose, majority of the amino acids, proteins, and water soluble vitamins have higher excretion rate during pregnancy. [9] The modification of diet in renal disease formula for estimating GFR, which has become a standard clinical method to estimate renal function in patients with CKD has not been validated for use in the pregnant women. Creatinine-based formulas developed in non-pregnant populations are likely to be inaccurate when applied to pregnant women because the fall in the serum creatinine during the pregnancy is due to both pregnancy-induced increase in real GFR and hemodilution. The inherent inaccuracy of creatinine based methods is more pronounced at the high GFR of pregnancy. Weight-based formulas, like as Cockroft-Gault also overestimates GFR because the increased body weight of pregnancy does not typically reflect increased muscle mass or creatinine production. Given these issues, 24-h urine collection for creatinine clearance is the gold standard for GFR estimation in pregnancy. [10]

  Renal Metabolic Profile During Pregnancy Top

The excretion of renal bicarbonate threshold decreases during pregnancy. Serum bicarbonate is 4-5 mmol/l lower than that of non-pregnant levels striking an approximate average of about 22 mmol/l and early morning urine samples exhibit alkaline nature. These physiologic alterations are usually in response to the hyperventilation, which occurs as a normal compensatory phenomenon during the pregnancy. During the pregnancy, the most significant biochemical problems related to severe uncorrected renal disease are hyperkalemia and acidosis. In spite of all these changes, patients exhibit normal physiologic response to any acid base disturbance. If acidosis is severe, it should best be treated by dialysis. Attempts to correct the low pH with administration of bicarbonate solution should only be considered if the pH is <7.2. Side-effects of bicarbonate solutions include hypernatremia and volume overload. If pregnant patient is suffering from any respiratory disorder, a PCO 2 ≥ 40 mm indicates significant CO 2 retention. [11]

  Renal Endocrine Osmoregulation and Hemodynamic Stabilization Top

Pregnancy is a state of altered osmoregulation and serum osmolality decreases by 10 mOsm/l. Osmotic threshold for thirst and arginine vasopressin (AVP) release are also decreased. Metabolic clearance of AVP increases almost fourfold during mid-gestation as compared to normal physiological values. This occurs due to higher levels of vasopressinase circulating in the blood the source of origin of which is usually placenta. The resultant increase in metabolic clearance of AVP leads to the possible development of two unusual syndromes: unapparent-partial central diabetes insipidus which is responsive to both AVP and dAVP and partial diabetes insipidus, which does not respond to AVP - vasopressinase, but responds to dAVP. [12],[13]

  • Pregnancy is accompanied by an increase in body weight to the extent of 10-12 kg and the total body water increases by 6-8 l. [14] Plasma volume increases to the extent of 50% by mid pregnancy. There is a cumulative sodium gain of 900 meq/l. Though, there is apparent hyervolemia, but body receptors sense it as normal therefore salt reduction or diuretics should be used carefully in pregnancy. The increase in aldosterone levels causes a marked stimulation of renin angiotensin axis and that occurs in spite of normal blood pressure (BP) and normal potassium levels. [14] This is thought to be a compensatory mechanism to retain sodium, relative arterial under filling, and to balance natriuretic effects of progesterone.
Mean BP starts decreasing during the early gestational period and increases again near term. Early in pregnancy, systemic vascular resistance decreases and arterial compliance increases. These changes are evident by the 6 th week of gestation. Mean arterial BP decreases approximately 10 mm Hg below the baseline during second trimester. The vascular tone is hormonally mediated and these physiologic changes occur due to synergistic effects of estrogen, progestin and possibly nitric oxide. In spite of low BP, plasma levels of all components of renin angiotensin system are elevated. [14]

  Renal Diseases Complicating Normal Pregnancy Top

Acute renal failure (ARF)

Incidence of ARF in pregnancy is about 1/20,000 births. [15] Mortality varies from 10% to 56% but the incidence has decreased tenfold during the last 30 years. [16] This decrease is most likely due to liberalization of abortion laws, availability of more aggressive and effective antibiotic therapy and improved prenatal care. Maternal mortality associated with ARF has decreased due to early diagnosis and improved care. Etiology is varied ranging from functional causes to a variety of other causes.

Functional renal failure

It is rare cause of renal failure accounting for 2-3% cases of renal failure in pregnancy. Plasma volume expansion is essential and critically important for successful outcome of pregnancy. Severe hyper-emesis gravidarum can lead to water and electrolyte disturbance resulting in pre-renal renal failure. Other possible etiologies include excessive blood loss due to any cause, diarrhea and the use of diuretics. [17] Absolute or relative hypovolemia can also occur in PIH but the incidence of renal failure is rare in such clinical states.

Acute pyelonephritis

Incidence of pyelonephritis increases during pregnancy as compared to non-pregnant state. About 1-2% patients develop pyelonephritis even without laboratory evidence of bacteriuria and about 40% of parturients with untreated bacteriuria develop pyelonephritis. [18] Non-pregnant patients suffering from pyelonephritis usually do not develop renal failure, but significant decline in renal functions during the pregnancy in such patients possibly leads to multi organ involvement and subsequent renal failure.

Obstructive component

It is a rare cause of ARF during the pregnancy. Nephrolithiasis can lead to obstruction and ARF although its incidence is same as in non-pregnant state. [19] Other possible causes include but are not limited to ureteric obstruction by the gravid uterus, which is more common in primi-gravida, twin pregnancy and polyhydramnios, but such obstructive symptoms usually resolves after delivery. [20] Though, extremely rare, renal tubular obstruction by uric acid has also been reported in the literature. [21] In this clinical scenario, symptomatic relief can be obtained by ureteric stenting and definitive intervention should be postponed until completion of pregnancy.

Acute tubular necrosis (ATN)

It is one of the major causes of ARF in developing countries. It usually occurs after septic abortion procedures, and clostridia species are thought to be the pathogenic organism in majority of these cases. Clinically, the patient may presents with varied clinical features such as hyperthermia, myalgias, vomiting, diarrhea, and multi organ dysfunction. ARF may last for 3 weeks or more and treatment involves administration of antibiotics and dialysis support if required. [22] It has also been reported after drug ingestion (aminoglycosides, diuretics), incompatible blood transfusions, various nephritides, collagen disorders or rarely in sarcoidosis or lymphoma. No specific drugs are implicated, but diuretics can cause renal failure because expanded intravascular volume is critical in pregnancy. Pre-eclampsia and HELLP syndrome: Over the years it has emerged as the main cause of renal failure both in the developing and developed nations. In a recently reported series, it has been observed that this clinical entity accounts for 50% of all cases of ARF during the pregnancy. [23],[24] Renal biopsy carried out in these parturients showed ATN in majority of the cases. However, pathognomonic renal histological features of glomerular endotheliosis were seen only in few of the patients. HELLP syndrome was originally thought to be a rare complication of severe ­pre-eclampsia having elevated liver enzymes, low platelet count, hypertension and proteinuria. [25],[26] However, it can occur independently of eclampsia. Clinically, it is characterized by epigastric or right upper quadrant pain, nausea, vomiting, headache, visual changes, bleeding, jaundice, and diarrhea. Laboratory investigations may reveal mild hemolytic anemia, thrombocytopenia, moderate increase of transaminases and lactic dehydrogenase while alkaline phosphatase and bilirubin levels are usually normal. ARF occurs in most severe cases and is associated with multiorgan involvement, obstetric complications such as abruptio placentae and disseminated intravascular coagulation (DIC). Most of these cases show an evidence of ATN on histological examination. Pre-eclampsia factor Search is an area of intense investigation. It has been seen that circulating agonist antibodies to angiotensin 1 receptor is increased in pre-eclampsia. Various antiangiogenic factors are implicated such as:

  • sFlt-1 - (soluble FMS like tyrosine kinase 1) - production is increased in pre-eclampsia
  • Secreted protein-splice variant of vascular endothelial growth factor 9 (VGEF) receptor Flt1
  • Circulating antagonist to VGEF and placental growth factor (PIGF)
  • VGEF and PIGF - made by placenta and circulate in high levels during the pregnancy
  • VGEF - glomerular podocytes and vascular endothelial cells.
Acute fatty liver

It usually occurs in third trimester and is common in nulliparous women and it is characterized by abdominal pain, vomiting, fever, progressive jaundice, and hepatic failure. Hypertension occurs in approximately 20-30% of such cases. The clinical investigation profile may show marked hyperbilirubinemia with mild elevation of enzymes, which helps to differentiate this clinical entity from HELLP syndrome. It can also occur in patients with pre-eclampsia and there is an increase likelihood of clinical features being getting overlapped and posing diagnostic challenges in these two clinic-pathologic states. Renal failure is mild and there is no urgent need for dialysis as the recovery usually occurs by 1 week. [27],[28],[29] The incidence of this clinical entity is usually seen between 28 and 39 weeks of gestation and do not recur in subsequent pregnancies. Histological changes may show micro vacuolar fatty infiltrates in centrilobular areas of liver. Histopathological picture of renal tissue may exhibit varied findings ranging from normal histology, changes of ATN and/or hemolytic uremic syndrome (HUS). Exact etiopathogenesis is not known, but most probably, the hemodynamic changes are largely responsible as similar changes are encountered in hepato-renal syndrome.

Thrombotic microangiopathy-HUS and idiopathic postpartum renal failure

It is a rare cause of renal failure with a little over 200 cases described in literature. It typically occurs within few hours of delivery to 8-10 weeks postpartum. Pregnancy and delivery remains uneventful and the condition is more common in multiparous women. Maternal mortality reaches up to 50% and complete or partial recovery occurs in approximately 30% of cases. Generalized endothelial dysfunction is the key pathological feature. Plasma exchange is treatment of choice for this clinical entity, which accounts for almost 6% cases of ARF in general population. [30],[31],[32]

The pathogenesis of atypical HUS is not as fully understood. It seems to be associated with a dysregulation of the alternative complement pathway that leads to lesions in multiple body cells, namely endothelial cells. Several regulatory factor H and I, membrane cofactor protein (or CD46) and decay-accelerating factor and activation factor (C3 and factor B) molecules are involved in this complement pathway. [30],[31],[32]

Bilateral cortical necrosis

It accounts for approximately 6% cases of ARF in general population while during pregnancy bilateral cortical necrosis is responsible for 20-30% cases of ARF. [33] It is a common complication of abruptio placenta and DIC. Clinically, the patients may present with features of complete cessation of micturition. Renal biopsy is not always diagnostic as the process is patchy and one can miss the diagnosis even in a diseased state. The cellular picture exhibits extensive arterial, arteriolar, and glomerular fibrinoid thrombi. [34] Selective renal arteriography is a more sensitive investigation as it allows quantification of lesions. Size of kidneys is normal or increased and characteristically interlobular arteries show delayed filling. Cortical nephrogram exhibit a heterogeneous picture, but its diagnostic utility remains inconclusive. The short term mortality in this diseased state is approximately 60% and usually occurs due to non-renal complications, but many patients finally require chronic dialysis.

A new concept of unifying pathophysiology of renal failure in pregnancy has emerged. [35] Basically it involves three pathological processes: ATN in severe pre-eclampsia and HELLP syndrome, Micro-angiopathic diseases and Bilateral renal cortical necrosis.

It is proposed that endothelial dysfunction is responsible for causing renal failure in pregnancy as all these entities show some form of underlying endothelial dysfunction.

Principles of management

Initially the efforts should always be directed towards a careful search and treatment of any concealed hemorrhage. Treatment of pre-renal or functional ARF in pregnancy is to correct the underlying cause that is replete the lost volume or blood and treat sepsis. With timely and appropriate treatment, progressive ARF (ATN) may be avoided with an excellent chance of complete recovery of kidney functions. Thereafter, the focus can be shifted to the possibility of immediate delivery depending on gestational age and treatment of underlying cause of renal failure. If required, both hemodialysis and peritoneal dialysis can be undertaken, but the emphasis should be on frequent dialysis of short duration and taking care to avoid any intra-vascular volume depletion during such procedures. [36]

  Pregnancy in Patients with Underlying Renal Disease Top

  • The challenges in planning the pregnancy with co-morbid renal diseases involve various considerations and implications. Among the three most important considerations, firstly it is questioned whether pregnancy is advisable at all and if yes, what complications can put mother and fetus in jeopardy. Last but not the least, it should self-introspected whether the pregnancy will affect underlying renal disease in the long run?
  • As discussed earlier, normal values of creatinine decrease during pregnancy; assessment of renal function during the pregnancy should be done by measuring creatinine clearance.
It has been observed that outcomes are good if patient is having only mild renal dysfunction (creatinine < 1.4 mg/dl), no nephrotic proteinuria and minimal or absent hypertension. [37] The impact on long term renal functions is minimal in this subset of patients. However, Scleroderma and polyarteritis nodosa defy this postulate and can be considered exceptions. Most nephrologists do not recommend pregnancy in these two conditions. Further, such patients can be clinically divided into moderate (1-4 mg/dl-2.5 mg/dl) and severe (>2.5 mg/dl) categories depending on serum creatinine value. As plasma creatinine increases, there is worsening of hypertension and proteinuria and rate of functional renal decline is also increased as a combined result of these changes. Most of the studies have shown a poor outcome at plasma creatinine values > 2.5 mg/dl. [38]

Antenatal monitoring

Patient should be assessed every 2 weeks until 32 weeks and thereafter every week. During these regular assessments, BP should be carefully monitored and PIH should be detected and treated early. Creatinine clearance and proteinuria should be measured and fetal growth monitoring should be done. Normally at term, a total of 15-20% decrease in renal function occurs. If renal functions decrease beyond these limits, then one should be vigilant for identification of reversible causes. However, if there is no evidence of any reversible cause, termination of pregnancy should also be considered at the earliest. If only proteinuria is increasing, but there is no evidence of intra-uterine growth retardation (IUGR), then pregnancy can be continued under strict monitoring of nephrologist and the obstetrician.

Role of renal biopsy in pregnancy

Renal biopsy is usually safe under ultrasound guidance even in pregnancy. It is required occasionally only if [39] [Table 2].
Table 2: Indications of renal biopsy during pregnancy

Click here to view

Pregnancy in patients on dialysis

Patients on hemodialysis may become pregnant but the incidence is very low and is about 1 in 200. It is difficult to diagnose and patient also usually do not suspect it because of irregular menstruation associated with chronic renal failure. It is not advisable to continue pregnancy because it usually leads to volume overload, severe exacerbation of hypertension and pre-eclampsia. If patient wishes to continue pregnancy, then frequency and duration of dialysis should be increased to >20 h/week and urea should be maintained below 60 mg/dl. Hypotension and rapid fluctuations in the blood volume should be avoided by limiting intradialytic weight gain to less than 1 kg and this may require daily dialysis. Adequate attention to management of anemia and daily nutritional intake should be given. Fetal growth monitoring should be done vigorously. Pre-term labor is very common and can occur during dialysis. Cesarean section is usually required for obstetric indications only. [40],[41]

In patients on chronic ambulatory peritoneal dialysis, only few pregnancies have been reported due to greater incidence of infertility in this subset of population as compared to hemodialysis patients. Usually, the outcome is similar to the patient on hemodialysis except for a high incidence of peritonitis, which is a unique problem associated with Continuous Ambulatory Peritoneal Dialysis (CAPD). [42]

Diagnosis of pregnancy in dialysis patients

High degree of suspicion is required because amenorrhea is common in dialysis patients. Soft signs of pregnancy include increased erythropoietin dosage requirements and difficulty in fluid removal. As β HCG (Human chorionic gonadotropin) is removed by kidneys, it may be elevated in non-pregnant states also. Therefore, definitive diagnosis of pregnancy is made by ultrasound only.

Regarding outcome of pregnancy, about 23-40% patients had surviving infants as is evident from literature and among those that survived 30% to 40% were premature. [43] On long-term follow- up, it was later observed that 4.4% of these infants developed cerebral palsy.

  Pregnancy after Renal Transplant Top

Normally end stage renal disease (ESRD) disrupts normal gonadal function and leads to infertility. After successful renal transplantation, fertility improves within months and pregnancy occurs in approximately 12% women of childbearing age. [44] First successful pregnancy was reported in recipient of kidney transplant from identical twin sister in 1958. National Transplantation pregnancy registry (NTPR) data from United States have reported about 1500 successful outcomes in females and 1000 successful outcomes in male transplant recipients. [45]

Optimal contraception

Contraception should be initiated before transplant as pregnancies have been reported in peri-transplant period. According to American Society of Transplant Consensus Conference, progestin only or estrogen/progesterone oral contraceptives are drug of choice for contraception. Barrier methods and intrauterine devices (IUCD) are not optimal because IUCD requires intact immune system for its effective action. [46],[47]

Optimal timing of pregnancy

Traditionally, it was advised to wait for 2 years after successful transplant to conceive. However, recent guidelines indicate that as long as graft function is stable and immunosuppressive drugs are at maintenance levels, pregnancy can be contemplated. So, pregnancy can be considered even as early as 6 months post-transplant. Stable graft function is indicated by serum creatinine < 1.5 mg/dl, protein excretion < 500 mg/24 h, no recent acute rejection episodes, BP < 140/90 mmHg controlled on medications and a stable requirement for maintenance dosage of following medications-Prednisolone ≤ 15 mg/day, Azathioprine ≤ 2 mg/kg/day, Cyclosporine ≤ 4 mg/kg/day. [46],[48]

Risk of pregnancy to mother

Progression to CKD is rare if serum creatinine is < 1.3 mg/dl. Above this level, a decline in renal functions has been observed and few of the patients have even progressed to ESRD. [8] Risk of acute rejection is similar to that in non-pregnant patients. Owing to changes in blood volume and hyper filtration during pregnancy, detection of rejection is difficult. If acute rejection occurs, it should be treated with corticosteroids. Incidence of hypertension and superimposed pre-eclampsia is increased to 15-25% as compared to 5% in normal women and it usually requires aggressive treatment. Mode of delivery should be vaginal and lower segment caesarean section (LSCS) is indicated only for obstetric indications. [49]

Risk of pregnancy to fetus

There is high-risk of pre-term delivery and low birth weight (50-65%), premature rupture of membranes and IUGR (30-50%). A long-term impact on neurodevelopment of children is not exactly known. However, some developmental delay is seen after 5 years of age in about 26% of children born to these mothers. [50]

Immunosuppressive medications

All immunosuppressive medications pass through maternal fetal circulation. None of the immunosuppressive medications is safe as none is categorized as a category drug. [51]

Risks of pregnancy to female kidney donors

This issue is important as number of living donor transplants is increasing and about 60% of these donors are females. First women to become pregnant after transplant received kidney from identical twin sister. Later, the donor also became pregnant with successful outcome. Usually, there are no complications, but until date no long-term studies are available. Some reports have suggested increased incidence of pre-eclampsia. [52],[53]

  Renal Trauma During Pregnancy Top

The incidence of roadside accidents has increased tremendously in the last one decade and so is the incidence of trauma during pregnancy. [54] A pregnant female may suffer a generalized trauma pattern or it can affect any organ system. Renal tissue is liable to get affected either directly or indirectly as a result of these trauma changes. Renal trauma during the pregnancy can be extremely deleterious for the expectant mother and the fetus in utero depending upon the severity of trauma and derangement in hemodynamic functions. [2] Invariably these patients may require intensive care unit admission and therefore all the arrangements for delivery or operative interventions have to be planned with coordinated efforts of obstetrician, intensivist, anesthesiologist, and the nephrologist. [55]

  Anaesthetic Management of Operative Deliveries Top

Parturients with renal disease may present for operative deliveries for one indication or the other. The challenges for the attending anesthesiologists rise significantly if the patients have multi-organ involvement and advanced renal disease. [56] The choice of anesthesia is directed by the underlying critical illness as well as the comfort levels of the patient. Usually, regional anesthetic techniques such as epidural anesthesia is considered safe and effective provided the coagulation profile is normal. [57],[58] The general anesthesia may be required in few cases and the choice of drugs should be based on the renal metabolism. Total intravenous anesthetic techniques are considered safe compared to inhalational anesthetics as the latter are excreted through kidneys and can cause enhanced renal toxicity. [59]

Induction agents

All induction agents whether inhalational or intravenous have potential myocardial depressant effect and should be administered slowly by titration of the dose to the desired anesthetic effect. The dose of anesthetics and analgesics can be reduced by pre-operative administration of dexmedetomidine, which can enhance the safety of the anesthetics. Moreover, the attenuation of stress response during laryngoscopy and intubation with pre-operative administration of adjuvants such as lignocaine, fentanyl, and dexmedetomidine also helps in stabilization of hemodynamic status. [60] Inhalational agents can also precipitate renal failure as the fluoride ions produced during metabolism of these agents can worsen renal functions.

Muscle relaxants

Atracurium is a good choice for muscle relaxation as it gets metabolized in plasma and is independent of hepatic and renal metabolism. Succinylcholine should be avoided if evidence of hyperkalemia is present as it can cause fatal arrhythmias. Furthermore, gallamine should be avoided while vecuronium and mivacurium can be used as they are minimally excreted by the kidneys.


Long acting opioids such as morphine and pethidine should be avoided as they accumulate during renal failure while short acting opioids such as fentanyl and remifentanyl can be used for providing analgesia.


Short acting benzodiazepines such as alprazolam and midazolam can be safely used as sedative agents during anesthesia.

Whatever the techniques are used, the basic aim is to maintain normal renal milieu by adoption of renal protection strategies during the peri-op period. [61]

  Conclusion Top

The basic understanding of renal diseases and their impact on pregnancy can go a long way in decreasing the morbidity and mortality in pregnant patients. However, it is desired that all such deliveries should be referred to higher centers where all the facilities are available under one roof besides the availability of a good team of various disciplines to manage such complicated cases. The problems for the developing nations like India are multifold, which can be ascribed to multiple factors prevalent in the country. The early detection and management of renal diseases during pregnancy can have successful pregnancy outcome. The counseling for pregnancy in patients with underlying renal diseases and renal transplantation as well as regular antenatal monitoring will definitely decrease the maternal and infant morbidities and mortalities.

  References Top

1.Rasmussen PE, Nielsen FR. Hydronephrosis during pregnancy: A literature survey. Eur J Obstet Gynecol Reprod Biol 1988;27:249-59.  Back to cited text no. 1
2.Bajwa SJ, Kulshrestha A. Renal endocrine manifestations during polytrauma: A cause of concern for the anesthesiologist. Indian J Endocrinol Metab 2012;16:252-7.  Back to cited text no. 2
3.Bajwa SJ, Kwatra IS. Reno-endocrinal disorders: A basic understanding of the molecular genetics. Indian J Endocrinol Metab 2012;16:158-63.  Back to cited text no. 3
4.Brown MA. Urinary tract dilatation in pregnancy. Am J Obstet Gynecol 1991;164:642-3.  Back to cited text no. 4
5.Krane NK, Hamrahian M. Pregnancy: Kidney diseases and hypertension. Am J Kidney Dis 2007;49:336-45.  Back to cited text no. 5
6.Croce P, Signorelli P, Chiapparini I, Dedè A. Hydronephrosis in pregnancy. Ultrasonographic study. Minerva Ginecol 1994;46:147-53.  Back to cited text no. 6
7.Fried AM, Woodring JH, Thompson DJ. Hydronephrosis of pregnancy: A prospective sequential study of the course of dilatation. J Ultrasound Med 1983;2:255-9.  Back to cited text no. 7
8.Fischer MJ. Chronic kidney disease and pregnancy: Maternal and fetal outcomes. Adv Chronic Kidney Dis 2007;14:132-45.  Back to cited text no. 8
9.August P. The kidney in pregnancy. In: Greenberg A, Cheung A, Falk R, Coffman T, Jeannette J, editors. Primer on Kidney Diseases. 4 th ed. Philadephia, PA: National Kidney Foundation, National Kidney Foundation; 2005. p. 426-35.  Back to cited text no. 9
10.Maynard SE, Thadhani R. Pregnancy and the kidney. J Am Soc Nephrol 2009;20:14-22.  Back to cited text no. 10
11.August P. The patient with kidney disease and hypertension in pregnancy. In: Schrier RW, editor. Manual of Nephrology. 7 th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2009. p. 220-43.  Back to cited text no. 11
12.Lindheimer MD, Davison JM. Osmoregulation, the secretion of arginine vasopressin and its metabolism during pregnancy. Eur J Endocrinol 1995;132:133-43.  Back to cited text no. 12
13.Durr JA, Lindheimer MD. Control of volume and body tonicity. In: Lindheimer MD, Roberts JM, Cunningham FG, editors. Chesley's Hypertensive Disorders in Pregnancy. 2 nd ed. Stamford, CT: Appleton & Lange; 1999. p. 103.  Back to cited text no. 13
14.Lindheimer MD, Katz AI. Renal physiology and disease in pregnancy. In: Seldin DW, Giebisch G, editors. The Kidney: Physiology and Pathophysiology. 2 nd ed. New York: Raven Press; 1992. p. 3371.  Back to cited text no. 14
15.Gammill HS, Jeyabalan A. Acute renal failure in pregnancy. Crit Care Med 2005;33:S372-84.  Back to cited text no. 15
16.Prakash J, Kumar H, Sinha DK, Kedalaya PG, Pandey LK, Srivastava PK, et al. Acute renal failure in pregnancy in a developing country: Twenty years of experience. Ren Fail 2006;28:309-13.  Back to cited text no. 16
17.Dragun K, Haase M. Acute kidney failure during pregnancy and postpartum. In: Jörres A, Ronco C, Kellum J, editors. Management of Acute Kidney Problems. Berlin: Springer; 2010. p. 445-58.  Back to cited text no. 17
18.Ventura JE, Villa M, Mizraji R, Ferreiros R. Acute renal failure in pregnancy. Ren Fail 1997;19:217-20.  Back to cited text no. 18
19.Naqvi R, Akhtar F, Ahmed E, Shaikh R, Ahmed Z, Naqvi A, et al. Acute renal failure of obstetrical origin during 1994 at one center. Ren Fail 1996;18:681-3.  Back to cited text no. 19
20.Brandes JC, Fritsche C. Obstructive acute renal failure by a gravid uterus: A case report and review. Am J Kidney Dis 1991;18:398-401.  Back to cited text no. 20
21.Alexopoulos E, Tampakoudis P, Bili H, Mantalenakis S. Acute uric acid nephropathy in pregnancy. Obstet Gynecol 1992;80:488-9.  Back to cited text no. 21
22.Stubblefield PG, Grimes DA. Septic abortion. N Engl J Med 1994;331:310-4.  Back to cited text no. 22
23.Zamorski MA, Green LA. NHBPEP report on high blood pressure in pregnancy: A summary for family physicians. Am Fam Physician 2001;64:263-70, 216.  Back to cited text no. 23
24.Machado S, Figueiredo N, Borges A, São José Pais M, Freitas L, Moura P, et al. Acute kidney injury in pregnancy: A clinical challenge. J Nephrol 2012;25:19-30.  Back to cited text no. 24
25.Piccoli GB, Conijn A, Attini R, Biolcati M, Bossotti C, Consiglio V, et al. Pregnancy in chronic kidney disease: Need for a common language. J Nephrol 2011;24:282-99.  Back to cited text no. 25
26.Haram K, Svendsen E, Abildgaard U. The HELLP syndrome: Clinical issues and management. A review. BMC Pregnancy Childbirth 2009;9:8.  Back to cited text no. 26
27.Wei Q, Zhang L, Liu X. Clinical diagnosis and treatment of acute fatty liver of pregnancy: A literature review and 11 new cases. J Obstet Gynaecol Res 2010;36:751-6.  Back to cited text no. 27
28.Santana L, Hernández Medina E, O'Shanahan G, Sánchez-Palacios M. Acute renal failure in acute fatty liver of pregnancy: Apropos of a case. Nefrologia 2005;25:453-4.  Back to cited text no. 28
29.Koroshi A, Babameto A. Acute renal failure during acute fatty liver of pregnancy. Nephrol Dial Transplant 2002;17:1110-2.  Back to cited text no. 29
30.Martin JN Jr, Bailey AP, Rehberg JF, Owens MT, Keiser SD, May WL. Thrombotic thrombocytopenic purpura in 166 pregnancies: 1955-2006. Am J Obstet Gynecol 2008;199:98-104.  Back to cited text no. 30
31.George JN. The association of pregnancy with thrombotic thrombocytopenic purpura-hemolytic uremic syndrome. Curr Opin Hematol 2003;10:339-44.  Back to cited text no. 31
32.Ruggenenti P, Cravedi P, Remuzzi G. Thrombotic microangiopathies including hemolytic uremic syndrome. In: Floege J, Johnson R, Feehally J, editors. Comprehensive Clinical Nephrology. 4 th ed. Philadelphia, PA: Mosby; 2010. p. 344-55.  Back to cited text no. 32
33.Grünfeld JP, Ganeval D, Bournérias F. Acute renal failure in pregnancy. Kidney Int 1980;18:179-91.  Back to cited text no. 33
34.Prakash J, Tripathi K, Pandey LK, Gadela SR, Usha. Renal cortical necrosis in pregnancy-related acute renal failure. J Indian Med Assoc 1996;94:227-9.  Back to cited text no. 34
35.Sibai BM, Kustermann L, Velasco J. Current understanding of severe preeclampsia, pregnancy-associated hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, hemolysis, elevated liver enzymes, and low platelet syndrome, and postpartum acute renal failure: Different clinical syndromes or just different names? Curr Opin Nephrol Hypertens 1994;3:436-45.  Back to cited text no. 35
36.Brown M, Mangos G, Peek M, Plaat F. Renal disease in pregnancy. In: Powrin R, Greene M, Camman W, editors. De Swiet's Medical Disorders in Obstetric Practice. 5 th ed. Oxford: Wiley-Blackwell; 2010.  Back to cited text no. 36
37.Baylis C. Impact of pregnancy on underlying renal disease. Adv Ren Replace Ther 2003;10:31-9.  Back to cited text no. 37
38.Jones DC, Hayslett JP. Outcome of pregnancy in women with moderate or severe renal insufficiency. N Engl J Med 1996;335:226-32.  Back to cited text no. 38
39.Brunskill N. Renal biopsy in pregnancy. In: Davison JM, Nelson-Piercy C, Kehoe S, Baker P, editors. Renal Disease in Pregnancy. London: RCOG Press; 2008. p. 201-6.  Back to cited text no. 39
40.Asamiya Y, Otsubo S, Matsuda Y, Kimata N, Kikuchi K, Miwa N, et al. The importance of low blood urea nitrogen levels in pregnant patients undergoing hemodialysis to optimize birth weight and gestational age. Kidney Int 2009;75:1217-22.  Back to cited text no. 40
41.Plant L. Pregnancy and dialysis. In: Davison JM, Nelson-Piercy C, Kehoe S, Baker P, editors. Renal Disease in Pregnancy. London: RCOG Press; 2008. p. 61-8.  Back to cited text no. 41
42.Okundaye I, Abrinko P, Hou S. Registry of pregnancy in dialysis patients. Am J Kidney Dis 1998;31:766-73.  Back to cited text no. 42
43.Imbasciati E, Gregorini G, Cabiddu G, Gammaro L, Ambroso G, Del Giudice A, et al. Pregnancy in CKD stages 3 to 5: Fetal and maternal outcomes. Am J Kidney Dis 2007;49:753-62.  Back to cited text no. 43
44.Sturgiss SN, Davison JM. Effect of pregnancy on long-term function of renal allografts. Am J Kidney Dis 1992;19:167-72.  Back to cited text no. 44
45.Armenti VT, Daller JA, Constantinescu S, Silva P, Radomski JS, Moritz MJ, et al. Report from the National transplantation pregnancy registry: Outcomes of pregnancy after transplantation. Clin Transpl 2006:57-70.  Back to cited text no. 45
46.McKay DB, Josephson MA, Armenti VT, August P, Coscia LA, Davis CL, et al. Reproduction and transplantation: Report on the AST consensus conference on reproductive issues and transplantation. Am J Transplant 2005;5:1592-9.  Back to cited text no. 46
47.Zerner J, Doil KL, Drewry J, Leeber DA. Intrauterine contraceptive device failures in renal transplant patients. J Reprod Med 1981;26:99-102.  Back to cited text no. 47
48.Josephson MA, McKay DB. Considerations in the medical management of pregnancy in transplant recipients. Adv Chronic Kidney Dis 2007;14:156-67.  Back to cited text no. 48
49.Davison JM. Pregnancy in renal allograft recipients: Problems, prognosis and practicalities. Baillieres Clin Obstet Gynaecol 1994;8:501-25.  Back to cited text no. 49
50.Cruz Lemini MC, Ibargüengoitia Ochoa F, Villanueva González MA. Perinatal outcome following renal transplantation. Int J Gynaecol Obstet 2007;96:76-9.  Back to cited text no. 50
51.Umans JG. Medications during pregnancy: Antihypertensives and immunosuppressives. Adv Chronic Kidney Dis 2007;14:191-8.  Back to cited text no. 51
52.Wrenshall LE, McHugh L, Felton P, Dunn DL, Matas AJ. Pregnancy after donor nephrectomy. Transplantation 1996;62:1934-6.  Back to cited text no. 52
53.Buszta C, Steinmuller DR, Novick AC, Schreiber MJ, Cunningham R, Popowniak KL, et al. Pregnancy after donor nephrectomy. Transplantation 1985;40:651-4.  Back to cited text no. 53
54.Bajwa SS, Kaur J, Bajwa SK, Kaur G, Singh A, Parmar SS, et al. Designing, managing and improving the operative and intensive care in polytrauma. J Emerg Trauma Shock 2011;4:494-500.  Back to cited text no. 54
[PUBMED]  Medknow Journal  
55.Bajwa SK, Bajwa SJ. Delivering obstetrical critical care in developing nations. Int J Crit Illn Inj Sci 2012;2:32-9.  Back to cited text no. 55
[PUBMED]  Medknow Journal  
56.Bajwa SK, Bajwa SJ, Kaur J, Singh K, Kaur J. Is intensive care the only answer for high risk pregnancies in developing nations? J Emerg Trauma Shock 2010;3:331-6.  Back to cited text no. 56
[PUBMED]  Medknow Journal  
57.Bajwa SJ, Bajwa SK, Kaur J, Singh A, Singh A, Parmar SS. Prevention of hypotension and prolongation of postoperative analgesia in emergency cesarean sections: A randomized study with intrathecal clonidine. Int J Crit Illn Inj Sci 2012;2:63-9.  Back to cited text no. 57
[PUBMED]  Medknow Journal  
58.Bajwa SJ, Bajwa SK, Kaur J. Comparison of epidural ropivacaine and ropivacaine clonidine combination for elective cesarean sections. Saudi J Anaesth 2010;4:47-54.  Back to cited text no. 58
[PUBMED]  Medknow Journal  
59.Bajwa SJ, Bajwa SK, Kaur J. Comparison of two drug combinations in total intravenous anesthesia: Propofol-ketamine and propofol-fentanyl.Saudi J Anaesth 2010;4:72-9.  Back to cited text no. 59
[PUBMED]  Medknow Journal  
60.Bajwa SJ, Kaur J, Singh A, Parmar S, Singh G, Kulshrestha A, et al. Attenuation of pressor response and dose sparing of opioids and anaesthetics with pre-operative dexmedetomidine. Indian J Anaesth 2012;56:123-8.  Back to cited text no. 60
[PUBMED]  Medknow Journal  
61.Bajwa SJ, Sharma V. Peri-operative renal protection: The strategies revisited. Indian J Urol 2012;28:248-55.  Back to cited text no. 61
[PUBMED]  Medknow Journal  


  [Table 1], [Table 2]


Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)  

  In this article
Structural Chang...
Renal Hemodynami...
Renal Metabolic ...
Renal Endocrine ...
Renal Diseases C...
Pregnancy in Pat...
Pregnancy after ...
Renal Trauma Dur...
Anaesthetic Mana...
Article Tables

 Article Access Statistics
    PDF Downloaded1398    
    Comments [Add]    

Recommend this journal