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Saudi Journal of Kidney Diseases and Transplantation
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ARTICLE Table of Contents   
Year : 1998  |  Volume : 9  |  Issue : 3  |  Page : 261-266
Acute Renal Failure in Pregnancy


Renal Section, Rush Presbyterian St. Luke's Medical Center, Chicago, Illinois, USA

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How to cite this article:
Hou S, Peano C. Acute Renal Failure in Pregnancy. Saudi J Kidney Dis Transpl 1998;9:261-6

How to cite this URL:
Hou S, Peano C. Acute Renal Failure in Pregnancy. Saudi J Kidney Dis Transpl [serial online] 1998 [cited 2019 May 21];9:261-6. Available from: http://www.sjkdt.org/text.asp?1998/9/3/261/39268
Acute renal failure in pregnancy is largely a preventable problem usually resulting from obstetric complications and not intrinsic renal disease. With this in mind, pregnancy related acute renal failure (AFR) can be viewed more as a public health problem than a nephrologic problem.

Historically, ARF in pregnancy once represented 20-40% of all cases of ARF and was responsible for 50% of cases in women. In 1958, the estimated incidence of ARF in pregnancy 'was as high as 1 in 1400. Today, in industrialized countries, the approximate incidence is 1 in 20,000 [1] . In pregnancy, ARF occurs with a bimodal distribution. A peak in early pregnancy is associated with infection, particularly septic abortion, while a third trimester peak is associated with late obstetric complications such as preeclampsia abruptio placentae, post partum hemorrhage, amniotic fluid embolism and retained dead fetus [2],[3] .

In industrialized countries where most women have access to high quality prenatal care and the frequency of illegal abortion has been reduced, there has been a marked decline in pregnancy related ARF with near elimination of the first peak [1] . The legalization of abortion in France was followed by a decrease in the percentage of cases of acute renal failure attributable to obstetric causes from 40% in 1966 to 4.5% in 1978 [1] . In Rumania, where illegal abortion was widely used as a form of birth control: from 1966 to 1989, complications of illegal abortion became a major cause of acute renal failure [4] .

In a report of 653 patients dialyzed for acute renal failure between 1966 and 1989, 131 (20%) of them resulted from compli­cations of illegal abortion [4] . Between 1990 and 1992, after the legalization of abortion, obstetric acute renal failure accounted for only 1.52% of the total.

In developing countries, obstetric ARF remains a serious problem. Randeree and colleagues described the changing picture of obstetric acute renal failure as the health system in South Africa improved [5] . Between 1978 and 1991 the frequency of acute renal failure in pregnancy in a hospital serving an impoverished community fell from one in every 450 pregnancies to one in every 900 pregnancies. With improvement in prenatal care, the proportion of obstetric acute renal failure secondary to septic abortion decreased from 65% to 19%, while percentage of obstetric ARF from preeclampsia increased from 10% in 1978 to 48% in 1991. With further improvement in obstetric care and early recognition of preeclampsia, the frequency of acute renal failure from this cause would be expected to decrease. Furthermore, the prevention of unwanted pregnancy and illegal abortion is a key to eliminate acute renal failure associated with infection early in pregnancy.

Acute renal failure can occur in the setting of sepsis from any organism following abortion, but is most common and most dramatic with infection by Clostridium welchii because of its production of a toxin which causes hemolysis and renal failure [6] . The infection may follow a fulminant course characterized by severe abdominal pain and vascular collapse. Clostridium welchii is difficult to culture and clostridia species exist as part of normal vaginal flora, but characteristic gas in the uterine wall on x-ray is highly suggestive. Care is supportive, aimed at fluid resuscitation and control of infection. The need for hyste­rectomy has been debated but can be often avoided with early aggressive conservative treatment [7],[8] .


   Acute Renal Failure in the Third Trimester Top


While improved public health and the widespread availability of good prenatal care have minimized acute renal failure from infection, a number of much less frequent causes of obstetric acute renal failure remain. The most pertinent of these will be summarized below.


   Bilateral Cortical Necrosis Top


In a majority of instances, acute renal failure secondary to preeclampsia or peripartum hemorrhage follows a course typical of acute tubular necrosis with recovery. In obstetric acute renal failure, however, a substantial minority of patients develop bilateral cortical necrosis in which renal function may fail to recover or recovery may be partial with later progression to end stage renal disease. Bilateral cortical necrosis may occur in any type of ischemic acute renal failure, but a disproportionate number of cases occur in obstetric patients. In a report of 3 8 instances of cortical necrosis, which occurred at Necker Hospital between 1953 and 1972, obstetric patients accounted for 68% [9] . The incidence of cortical necrosis was 2% in the non pregnant adults with acute renal failure, and 21 % of obstetric patients with acute renal failure. Cortical necrosis can be diagnosed by computed tomography (CT) scan or angiography [10] . The diagnosis is made primarily for prognostic purposes.


   Acute Renal Failure in Preeclampsia Top


Decreased glomerular filtration rate and decreased sodium excretion are characteristic of preeclampsia, but frank renal failure is unusual. Acute renal failure in preeclamptic women occurs most often when another obstetric complication such as abruptio placentae is present, or when preeclampsia has progressed to hemolysis, elevated liver enzymes and low platelet syndrome (HELLP) [11],[12],[13] . In the largest series of patients with HELLP, 7.7% suffered from acute renal failure [14] . When acute renal failure follows preeclampsia, the maternal mortality rate is high; 9.6% in one series [15] . Pulmonary edema occurs in over 50% of women with acute renal failure secondary to preeclampsia, emphasizing the need for judicious fluid administration in women with this syndrome. Women, who do not have underlying renal disease or essential hypertension, usually recover once they secondary to preeclampsia. When acute renal failure occurs in women with underlying chronic renal disease and renal insufficiency, as many as 80% eventually become dialysis dependent.


   Acute Fatty Liver of Pregnancy Top


Acute fatty liver of pregnancy is an obstetric emergency, which if untreated may progress to a fulminant hepatic failure, a life threatening condition for both the mother and fetus. The disease most often presents in the third trimester with complaints of headache, fatigue, malaise, nausea and abdominal pain. Late signs include jaundice, bleeding, seizures and hepatic encephalopathy. Liver biopsy shows microvesicular fatty infiltration of hepatocytes in a centrillobular distribution [16] . The maternal mortality rate for the disease has improved from 80­-85% in the 1970's to less than 20% in recent series, with the lowest mortality rate reported being 6.6% [17],[18],[19] . Improvement in the outcome of fulminant hepatic failure can be attributed to early recognition of even milder cases and better supportive care. The etiology of the syndrome is unknown but recent investigations have found a familial genetic defect in fatty acid metabolism [20],[21] .

Some degree of acute renal failure occurs in up to 90% of women with acute fatty liver of pregnancy. The renal biopsy findings include acute tubular necrosis, fatty vacuolization of tubular cells and occlusion of capillary lumens by fibrin-like material. Clinically, the acute renal failure in this syndrome may resemble hepatorenal syndrome with low fractional excretion of sodium and benign sediment. Treatment includes delivery of the baby and supportive care. Acute renal failure usually resolves postpartum, as does the liver failure. The availability of orthotopic liver women who do not recover. The timing of liver transplantation is difficult since temporizing may result in deterioration of the patient to the point where liver transplant carries a high mortality. On the other hand, a premature transplant may commit a woman, who might have had a complete recovery, to life-long immunosuppression.


   Postpartum Hemolytic Uremic Syndrome (HUS) Top


Initially described in children with antecedent diarrheal illness and in association with verotoxin, HUS is characterized by a micro­angiopathic hemolytic anemia, thrombo­cytopenia, and renal failure. It is also recognized in adults in association with diarrheal illnesses, certain forms of adenocarcinoma, medications and pregnancy. Although HUS, referred to in early reports as postpartum renal failure, usually occurs between one day and three months postpartum, it may occur prior to delivery as well [22],[23] . Renal failure in HUS is often severe enough to require temporary dialysis. Furthermore, patients frequently suffer residual renal damage, to the extent that some require chronic dialysis or transplant [24] .

The mainstay of treatment for HUS, and the related syndrome thrombotic thrombo­cytopnic purpura (TTP), is plasma exchange. Prior to the advent of plasmapheresis, the maternal mortality rate was 90%. With this treatment, maternal survival has increased to 70-80%, with the most clear cut efficacy in TTP.

Plasma exchange during pregnancy has not shown adverse effects on the fetus [25],[26] . Plasma exchange is thought to work by removing factors that promote platelet aggregation and/or replacing inhibitory factors, which may be lacking in the serum of patients with HUS/TTP. The necessary ranging from 5 to 47 days in one series of 67 women [27] . The duration of treatment is determined by monitoring hematological, neurological and renal parameters. Other treatments, including prednisolone, aspirin, dipyridamole, heparin, immunoglobulin, vincristine and splenectomy, should be considered only as adjuncts to plasma exchange.

Recurrence of HUS has been described both in subsequent pregnancies and in response to other inciting factors including oral contraceptives, infections and drugs such as cyclosporine.

There is sometimes difficulty in distin­guishing HUS from severe preeclampsia accompanied by HELLP syndrome. Thrombo­cytopenia, microangiopathic hemolytic anemia, renal insufficiency, proteinuria and hypertension may occur in both. Some distinguishing features include isolated elevation of LDH in HUS as opposed to elevation of transminases in preeclampsia/ HELLP. Elevations of prothrombin time and partial thromboplastin time are unusual in HUS and suggest preeclampsia.

Preeclampsia generally improves following delivery, -although there may be transient worsening for 48 hours. HUS is not improved by termination of pregnancy. The distinction is important, as preeclampsia resolves with supportive care following delivery, whereas HUS is generally irreversible without plasma exchange.

Biopsy findings in HUS include glomerular capillary endothelial swelling and sub­endothelial deposition of fibrinoid material, which may cause occlusion of capillary [25] . Thrombi composed of fibrin and platelets are found within capillaries and arterioles [25] .

The pathophysiology of microthrombus formation in HUS is thought to involve endothelial injury along with other factors contributing to enhancement of platelet aggregation. Among those factors, abnormally large multimers of von Willebrand factor have been observed in TTP and these can cause aggregation of activated platelets.

Calpain, a cystine protease capable of causing aggregation of normal platelets and of exchanging platelet binding by von Willebrand factor, has been found in some patients with active TTP. Decreased fibrinolysis may play a role. Plasminogen activator inhibitor type-I, the major inhibitor of plasminogen activator, has been found to be increased in some cases of post diarrheal HUS. Decreased synthesis and increased degradation of prostacyclin has been suggested on the basis of studies using plasma from individuals with TTP [28] . There may also be some genetic pre­disposition to' HUS. There are known familial occurrences, and pregnancy associated HUS has been reported in sisters [29],[30],[31] .

While advances in treatment have dramatically increased patient survival in obstetric HUS, it still poses a significant threat to both mother and child, particularly if not diagnosed and treated promptly. Patients with pregnancy associated HUS should be aware of the possibility of recurrence in future pregnancies or with estrogen containing oral contraceptives. However, at present there is no method to identify those at risk.


   Other Renal Diseases Associated with Pregnancy Top


Acute renal failure can occasionally occur as a result of renal disease unrelated to pregnancy. Lupus nephritis occurs with increased frequency during pregnancy and a, woman with unexplained renal failure, active urine sediment or low serum complements should be evaluated for this disease. If lupus is excluded, other renal diseases, particularly glomerular diseases should be sought for. In some cases renal biopsy may be indicated.

In conclusion, historically, acute renal failure was a major cause of morbidity and mortality in pregnant women, contributing to the morbidity and mortality resulting from hemorrhage and infection. These causes of. renal failure are now largely preventable. Universally available good prenatal care and early recognition of the disease can minimize acute renal failure resulting from preeclampsia/eclampsia.

Nonetheless, there remain a small number of instances of acute renal failure in the peripartum period, which continue to occur even with the best available obstetric care. These require accurate diagnosis and meticulous supportive care, and in some instances, such as HUS, specific treatment is indicated.

 
   References Top

1.Grunfeld JP, Ganeval D, Bournerias F. Acute renal failure in pregnancy. Kidney Int 1980; 18: 179-91.  Back to cited text no. 1    
2.Harkins JL, Wilson D R, Muggah HF. Acute renal failure in obstetrics. Am J Obstet GynecoI1974;1l8:331-6.  Back to cited text no. 2    
3.Krane NK. Acute renal failure in pregnancy. Arch Int Med 1988;148:2347­-57.  Back to cited text no. 3    
4.Vladutiu DS, Spanu C, Patiu IM, Neamtu C, Gherman M, Manasia M. Abortion prohibition and acute renal failure: the tragic Romanian experience. Ren Fail 1995;17:605-9.  Back to cited text no. 4  [PUBMED]  
5.Randeree IG, Czarnocki A, Moodley J, Seedat YK, Naiker IP. Acute renal failure in pregnancy in South Africa. Ren Fail 1995;17:147-53.  Back to cited text no. 5  [PUBMED]  
6.Hou SH. Acute renal failure in pregnancy. In: Clark SL, Cotton DB, Hawkins GD, Phelan JP (eds). Critical Care Obstetrics 2nd edition Blackwell Scientific Publications, Boston 1991.  Back to cited text no. 6    
7.Hawkins DF, Sevitt LH, Fairbrother PF, Tothill AD. Management of septic chemical abortion with renal failure. Use of a conservative regimen. N Engl J Med 1975;292:722-5.  Back to cited text no. 7    
8.Llorens AS, Grimes JH, Thompson JD. Maternal mortality at Grady Mc::morial Hospital. Am J Ob stet GynecoI1963;87: 386-93.  Back to cited text no. 8    
9.Kleinknecht D, Grunfeld JP, Gomez PC, Moreau JF, Garcia-Torres R. Diagnostic procedures and long-term prognosis in bilateral renal cortical necrosis. Kidney Int 1973;4:390-400.  Back to cited text no. 9    
10.Salloni DF, Yaqoob M, White E, Finn R. Case report: the diagnostic value of contrast enhanced computed tomography in acute bilateral renal cortical necrosis. Clin RadioI1995;50:126-7.  Back to cited text no. 10    
11.Sibai BM, Ramadan MK. Acute renal failure in pregnancies complicated by hemolysis, elevated liver enzymes and low platelets. Am J Ob stet Gynecol 1993; 168: 1682-90.  Back to cited text no. 11    
12.Stratta P, Canavese C, Colla L, et al. Acute renal failure in preec1ampsia-ec1ampsia. Gynecol Obstet Invest 1987;24:225-31.  Back to cited text no. 12  [PUBMED]  
13.Barton JR, Sibai BM. Acute life threatening emergencies in preec1ampsiaeclampsia. Clin Ob stet Gynecol 1992; 35:402-13.  Back to cited text no. 13    
14.Sibai BM, Ramadan MK, Usta I, Salama M, Mercer BM, Friedman SA. Maternal morbidity and mortality in 442 pregnancies with hemolysis, elevated liver enzymes and low platelets (HELLP syndrome). Am J Obstet GynecoI1993;169:1000-6.  Back to cited text no. 14    
15.Sibai BM, Villar MA, Mabie Bc. Acute renal failure in hypertensive disroders of pregnancy. Pregnancy outcome and remote prognosis in thirty-one consecutive cases. Am J Obstet GynecoI1990;162(3):777-83.  Back to cited text no. 15    
16.Bernuau J, Degott C, Nouel O, RueffB, Benhamou JP. Non-fatal acute fatty liver of pregnancy. Gut 1983;24:340-4.  Back to cited text no. 16    
17.Usta IM, Barton JR, Amon EA, Gonzalez A, Sibai BM. Acute fatty liver of pregnancy: an experience in the diagnosis and management of fourteen cases. Am J Obstet GynecoI1994;171:1342-7.  Back to cited text no. 17    
18.Reyes H, Sandoval L, Wainstein A, et al. Acute fatty liver of pregnancy: a clinical study of 12 episodes in 11 patients. Gut 1994;35:101-6.  Back to cited text no. 18  [PUBMED]  [FULLTEXT]
19.Pockros PI, Peters RL, Reynolds TB. Idiopathic fatty liver of pregnancy: findings in, ten cases. Medicine Baltimore 1984; 63: 1-11.  Back to cited text no. 19    
20.Treem WR, Rinaldo P, Hale DE, et al. Acute fatty liver of pregnancy and long chain 3-hydroxyacyl-coenzyme A dehydrogenase deficiency. Hepatalogy 1994;19:339-4.  Back to cited text no. 20    
21.Sims HF, Brackett JC, Powell CK, et al. The molecular basis of pediatric long chain 3-hydroxyacyl-CoA dehydrogenase defi­ciency associated with maternal acute fatty liver of pregnancy. Proc Natl Acad Sci USA 1995; 92:841-5.  Back to cited text no. 21  [PUBMED]  [FULLTEXT]
22.Remuzzi G, Ruggenenti P. The hemolytic uremic syndrome. Kidney Int 1995;48:2-19.  Back to cited text no. 22  [PUBMED]  
23.Martinez RS, Gratacos E, Tom A, Torra R, Carmona F, Cararach V. Successful pregnancy in a woman with hemolyti.c uremic syndrome during the second trimester of pregnancy. J Reprod Med 1996;41:211-4.  Back to cited text no. 23    
24.Egerman RS, Witlin AG, Friedman SA, Sibai BM. Thrombotic thrombocytopenic purpura and hemolytic uremic syndrome in pregnancy: review of 11 cases. Am J Obstet GynecoI1996;175:950-6.  Back to cited text no. 24    
25.Conlon PI, Howell DN, Macik' G, Kovalik EC, Smith SR. The renal manifestations and outcome of thrombotic thrombocytop_nic purpura! hemolytic uremic syndrome in adults. Nephrol Dial Transplant 1995;10:118993.  Back to cited text no. 25    
26.Ezra Y, Rose M, Eldor A. Therapy and prevention of thrombotic thrombocytopenic purpura during pregnancy: a clinical study of 16 pregnancies. Am J Hemato11996; 51:16.  Back to cited text no. 26    
27.Rose M, Rowe JM, Eldor A. The changing course of thrombotic thrombocytopenic purpura and modern therapy. Blood Rev 1993;7:94-103.  Back to cited text no. 27    
28.Hayward CP, Sutton DM, Carter WH Jr,. et al. Treatment outcomes in patients with adult thrombotic thrombocytopenic purpura hemolytic uremic syndrome. Arch Intern Med 1994;154:982-7.  Back to cited text no. 28    
29.McCrae KR, ernes DB. Thrombotic micro­angiopathy during pregnancy. Semin HematoI1997;34:148-58.  Back to cited text no. 29    
30.Fuchs WE, George IN, Dotin LN, Sears DA. Thrombotic thrombocytopenic purpura. Occurrence two years apart during late pregnancy in two sisters. JAMA 1976;235: 2126-7.  Back to cited text no. 30    
31.Berns JS, Kaplan BS, Mackow RC, Hefter LG. Inherited hemolytic uremic syndrome in adults. Am J Kidney Dis 1992; 19:331-4.  Back to cited text no. 31  [PUBMED]  

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Correspondence Address:
Susan Hou
Renal Section, Rush Presbyterian St. Luke's Medical Center, 1653, West congress Parkway, Chicago, Illinois 60612
USA
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PMID: 18408298

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