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Saudi Journal of Kidney Diseases and Transplantation
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CASE REPORT Table of Contents   
Year : 2003  |  Volume : 14  |  Issue : 4  |  Page : 516-521
Anti-glomerular Basement Membrane Antibody Disease Presenting as Acute Renal Failure During Pregnancy

1 Division of Nephrology, Department of Internal Medicine, Security Forces Hospital Program, Riyadh, Saudi Arabia
2 Department of Pathology, King Faisal Specialist Hospital & Research Center, Riyadh, Saudi Arabia

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A 30-year-old seventh gravida presented with acute renal failure at 28 weeks of gestation. All her previous pregnancies were normal. With a differentional diagnosis of acute pyelonephritis, acute interstitial nephritis (cefuroxime induced) or rapidly progressive glomerulonephritis, treatment with antibiotics, intensive hemodialysis (HD) and pulse methylprednisolone followed by oral prednisolone was initiated. She was maintained on HD 5-6 times per week aiming at serum urea level of less than 15 mmol/L. After six weeks on HD, she underwent a cesarean section at 34 weeks of gestation with delivery of a baby weighing 1.6 kg. Percutaneous left renal biopsy performed one week post-delivery showed anti-glomerular basement membrane (GBM) antibody-mediated crescentic glomerulonephritis. The anti-GBM antibody, which was negative during pregnancy, was found to be positive at this juncture and remained so until ten months post-delivery while on HD. The patient continues to be on regular maintenance HD.

Keywords: Anti-GBM antibody glomerulonephritis, Acute renal failure, Pregnancy.

How to cite this article:
Al-Harbi A, Malik GH, Al-Mohaya SA, Akhtar M. Anti-glomerular Basement Membrane Antibody Disease Presenting as Acute Renal Failure During Pregnancy. Saudi J Kidney Dis Transpl 2003;14:516-21

How to cite this URL:
Al-Harbi A, Malik GH, Al-Mohaya SA, Akhtar M. Anti-glomerular Basement Membrane Antibody Disease Presenting as Acute Renal Failure During Pregnancy. Saudi J Kidney Dis Transpl [serial online] 2003 [cited 2022 Jan 26];14:516-21. Available from: https://www.sjkdt.org/text.asp?2003/14/4/516/32989

   Introduction Top

Acute renal failure (ARF) during pregnancy is an unusual but life threatening complication and is dialysis-requiring in less than 1 in 10,000 to 15,000 pregnancies [1] The greatest risk for developing pregnancy-related ARF is in the later months of pregnancy. Though uncommon, the recognized causes are pre苟clampsia, acute tubular necrosis/cortical necrosis following septic abortion, abruptio placentae, amniotic fluid embolism, thrombotic thrombocytopenic purpura/hemolytic-uremic syndrome, acute fatty liver of pregnancy and obstruction. [1] Acute pyelonephritis may cause ARF in some pregnant women. [2],[3] Rapidly progressive glomerulonephritis (GN) mediated by anti-glomerular basement membrane (anti胃BM) antibody disease is a distinctly rare cause of renal insufficiency during pregnancy. In one report a patient with Goodpasture's syndrome carried pregnancy successfully to term; [4] another case report describes Good計asture's syndrome following delivery of a stillborn infant. [5] Deubner et al described a case of rapidly progressive glomerulonephritis with anti-GBM antibody during pregnancy that caused precipitous renal failure post計artum. [6] However, none of these cases needed dialysis or had significant renal failure during pregnancy.

We describe a case of anti-GBM antibody GN in the last trimester of pregnancy maintained on hemodialysis (HD) for six weeks before successful delivery of a live fetus at 34 weeks.

   Case Report Top

A 30-year-old seventh gravida, at 28 weeks of gestation, presented to the emergency room with progressively increasing shortness of breath, bilateral loin pain and decreased urine output of three weeks' duration. There was no history of cough, hemoptysis, skin rash or joint pains. During antenatal checkup six weeks before presentation, she had fever, dysuria and loin pains. Urinalysis showed pyuria, urine culture grew E. coli and the patient was treated for urinary tract infection with cefuroxime for 10 days. Renal function tests were not performed at that time. There was no history of hypertension or pre苟clampsia in the previous pregnancies. A review of her past medical records revealed normal urinalysis and renal function. She was known to have sickle cell trait. On clinical exami-nation, the patient was tachypneic and pale, with respiratory rate of 28/minute, pulse rate of 96/minute which was regular, and blood pressure 145/45 mm Hg. There was no facial puffiness or pedal edema, and jugular venous pressure was 3 cm above the sternal angle. Rest of the systemic exami要ation was unremarkable.

Laboratory Investigations

Urine analysis revealed protein 2+, blood 3+ and microscopic examination showed red blood cells (RBC) >25/HPF, white blood cells (WBC) >25/HPF and no casts. Hemogram showed WBC 9.5 x 10 9 /L, neurophils 85%, hemoglobin 6.6 g/dL, platelets 510 x 10 9 /L, reticulocyte count 2% and ESR 136 mm. Serum creatinine was 1217 痠ol/L, urea 30.6 mmol/L, sodium 142 mmol/L, potassium 6.1 mmol/L, bicarbonate 8 mmol/L, chloride 113 mmol/L, glucose 4.6 mmol/L, total serum calcium 1.8 mmol/L, phosphorus 3.1 mmol/L, alkaline phosphatase 264 IU/L, albumin 27 gm/L, aspartate aminotransferase 20 IU/L, alanine aminotransferase 20 IU/L, total bilirubin 23 痠ol/L and antinuclear antibody 1/160 IU/ml, speckled pattern. Both C and P antineutrophil cytoplasmic antibody were negative, anti-DNA, antibodies against hepatitis C virus (anti HCV), Human Immuno苓eficiency Virus (HIV) and Hepatitis B Surface Antigen (HbsAg) were all negative. Serum complement levels (C3 and C4) were normal. Serum anti-GBM antibodies were negative. Chest X-ray revealed evidence of congested lungs and a normal cardiac size. Ultrasound of kidneys showed right kidney 12.3 cm, left kidney 12.9 cm with no evidence of obstruction; there was a single viable fetus.

Urine culture revealed E. coli sensitive to a wide range of antibiotics. She was managed as acute renal failure and the possible causes entertained were acute pyelonephritis, acute interstitial nephritis (cefuroxime induced) and rapidly progressive glomerulonephritis. The patient was admitted to the intensive care unit, underwent HD and was started on antibiotics, pulsed with intravenous methylprednisolone 1 gm daily for three days followed by oral prednisolone 1 mg/kg/day and received blood transfusions as well as plasmapharesis. Her intensive management was carried out in collaboration with an obstetrician. The fetus was monitored regularly by ultrasound and cardiotocography (CTG) and the patient was maintained on HD 5-6 times per week aiming at a blood urea level of less than 16 mmol/L. At 34 weeks of gestation, she developed labor pains and was delivered by Cesarean Section. The baby was normal but small for gestational age weighing 1.6 kg and was observed in neonatal intensive care unit for 48 hours. A left percutaneous renal biopsy was performed one week after delivery.

   Renal Biopsy Top

Light Microscopy

Ten glomeruli were present in the biopsy all of which showed prominent cellular crescents, compressing the glomerular tufts [Figure - 1]. Areas of fibrinoid change within the cellular crescents were noted. Occasional glomeruli showed fibrosed crescents, and a few areas of hyalinization were present. Moderate tubular loss with replacement by fibrosis and mild lymphocytic and plasmacytic infiltration was seen. Arteries were normal.

Immunofluorescence Microscopy

Two glomeruli present in the sections were stained for IgG, IgM, IgA, C3, C1q and fibrinogen. Both showed prominent 3+ linear staining for IgG and 2+ segmental staining for IgM and C3. Other stains were negative.

Electron Microscopy

One glomerulus taken for study showed collapse of the glomerular tuft with wrinkling of the basement membrane. No electron-dense deposits were noted.

A repeat test for anti-GBM antibodies on a serum sample taken post-delivery was positive and continued to be detected up to 10 months while on dialysis. The baby's serum checked for anti-GBM was negative. Hemoptysis did not develop at any stage. The patient is on maintenance HD three times per week waiting for kidney transplantation.

   Discussion Top

Anti-GBM antibody glomerulonephritis com計licating pregnancy is rare and the present case in particular has many distinctive features. They inlude presentation as acute renal failure in the last trimester of pregnancy, no response to immunosuppressive therapy and plasma計heresis, continuing to be dialysis-dependent and, demonstration of serum anti-GBM anti-bodies post-delivery and not during pregnancy. The patient did not show evidence of pulmo要ary hemorrhage at any stage of the disease. [Table 1] depicts the characteristics of patients reported with anti-GBM disease in pregnancy.

Nielssen et al described a 19 year-old woman who presented with hematuria and proteinuria in the second trimester, had a stillbirth at 28 weeks of gestation and developed oliguric acute renal failure post-parturm, requiring dialysis. Renal biopsy post-delivery showed crescentic glomerulonephritis with linear deposits of immunoglobulin G (IgG) on immunofluorescence. However, she developed pulmonary changes suggestive of intra苔lveolar hemorrhage. In spite of therapy with plasma exchange, intravenous methylpred要isolone and cylosphosphamide she remained dialysis dependent. The patients with crescentic glomerulonephritis having more than 50% crescents presenting with renal failure and who are dialysis dependent, rarely recover renal function which has led to the recommendation that such patients should be spared immunosuppression. [7] The present case also did not recover renal function despite plasmapheresis and pulse steroid therapy and remained dialysis dependent. Another case of Goodpasture's syndrome has been reported in a 28-year-old woman who had a successful pregnancy and delivery. [4] This patient differs from the present case in that the diagnosis was established before conception and the immunosuppressive therapy was given before and during pregnancy and renal failure was not significant at any time during her course. The anti-GBM antibody became negative during pregnancy. [4] In the present case also, anti-GBM antibody was negative during pregnancy and immediately after delivery, but became positive subsequently till beco衫ing negative again after 10 months on dialysis. Deubner et al described a case of anti-GBM antibody glomerulonephritis during pregnancy in which serum anti-GBM anti苑ody was detected post-delivery and also the patient's renal failure worsened after delivery. The authors postulated that during pregnancy, the anti-GBM antibodies are bound to the placenta but for which these antibodies would have been attached to the renal basement membranes. [6] The absence of anti-GBM antibodies in the neonate in their case and ours could be explained by the ameliorating effect by the placenta.

Peritoneal dialysis and HD are both useful in pregnancy although there are theoretical advantages of peritoneal dialysis in that the metabolic changes are not rapid and fluid removal is gradual. [8] Hemodialysis of at least 20 hours per week has been recommended to achieve a satisfactory fetal outcome. [9] Hemodialysis in the present case was per苯ormed daily to keep the blood urea below 16 mmol/L and supplements of erythropoietin, iron, dihydroxyvitamin D, calcium and vitamins were given as recommended. [8] The delivery occurred at 34 weeks and the baby was normal, but small for gestational age. Eighty five percent of infants born to women on dialysis were born prematurely (mean gestational age 32.4 weeks) and 36% weighed less than 1500 grams at birth. [8]

In conclusion, we report on a 30-year-old seventh gravida who presented as acute renal failure due to anti-GBM antibody glomerulo要ephritis. She was maintained on regular HD for six weeks before delivering a healthy but low birth weight baby by Cesarean section at 34 weeks of gestation.

   References Top

1.Hou SH. The kidney in Pregnancy. In Primer on Kidney Diseases. Greenberg A (Ed.) National Kidney Foundation - Academic Press, 1998; pp 388-94.  Back to cited text no. 1    
2.Thompson C, Verani R, Evanoff G, Weinman E. Suppurative bacterial pyelo要ephritis as a cause of acute renal failure. Am J Kidney Dis 1986;8:271-3.  Back to cited text no. 2  [PUBMED]  
3.Grunfeld JP, Pertuiset N. Acute renal failure in pregnancy. Am J Kidney Dis 1987; 9:359-62.  Back to cited text no. 3    
4.Yankowitz J, Kuller JA, Thomas RL. Pregnancy complicated by Goodpasture syndrome. Obstet Gynecol 1992;79:806-8.  Back to cited text no. 4  [PUBMED]  
5.Nilssen DE, Talseth T, Brodwall EK. The many faces of Goodpasture's syndrome. Acta Med Scand 1986;220:489-91.  Back to cited text no. 5  [PUBMED]  
6.Deubner H, Wagnild JP, Wener MH, Alpers CE. Glomerulonephritis with anti-glome訃ular basement membrane antibody during pregnancy: potential role of the placenta in amelioration of disease. Am J Kidney Dis 1995;25:330-5.  Back to cited text no. 6  [PUBMED]  
7.Savage C OS. Goodpasture's syndrome and anti-GBM Disease. In Primer on Kidney Diseases. Greenberg A (ed). National Kidney Foundation-Academic Press, New York,1998; p 178.  Back to cited text no. 7    
8.Hou S. Pregnancy in chronic renal insufficiency and end-stage renal disease. Am J Kidney Dis 1999;33:235-52.  Back to cited text no. 8  [PUBMED]  
9.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. 9  [PUBMED]  

Correspondence Address:
Ali Al-Harbi
Department of Internal Medicine, Security Forces Hospital Program, P.O. Box 3643, Riyadh 11481
Saudi Arabia
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PMID: 17657125

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