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NDT Advance Access published online on November 23, 2006

Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfl685
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© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Looking beyond the obvious—a young woman with septic abortion and acute renal failure

Zulfikar Jabbar1, Vivekanand Jha1, Harinder Kumar Bali2, Harbir Singh Kohli1, Krishan Lal Gupta1 and Vinay Sakhuja1

1Department of Nephrology and 2Department of Cardiology, Postgraduate Institute of Medical Education and Research, Chandigarh, India

Correspondence and offprint requests to: Correspondence and offprint requests to: Dr Vivekanand Jha, Postgraduate Institute of Medical Education and Research, Chandigarh, India 160 012. Email: vjha{at}pginephro.org

Keywords: acute renal failure; fibromuscular dysplasia; percutaneous angioplasty; renovascular hypertension



   Introduction
 Top
 Introduction
 Case report
 Discussion
 References
 
Renal artery stenosis (RAS) is a well-recognized cause of secondary hypertension. Acute renal failure and recurrent flash pulmonary oedema are some of its less frequent presenting features. A high index of suspicion is necessary to make this diagnosis, as the treatment is distinct from other causes. We report a young female who presented with severe hypertension and renal failure following abortion, that was diagnosed as being due to RAS. Successful revascularization led to resolution of all features. The case highlights the need to consider RAS, a reversible cause of severe hypertension and renal dysfunction in an appropriate clinical setting.



   Case report
 Top
 Introduction
 Case report
 Discussion
 References
 
A 30-year-old woman was admitted to our hospital for management of post-abortal acute renal failure. She had been well until 6 years previously, when she started having recurrent headaches and was detected to have hypertension. She was not investigated further, and details on treatment and control were not available. The other remarkable feature was a bad obstetric history: out of five pregnancies over a 12-year-period (all unsupervised), she had had two live births, whereas three had ended in stillbirths at 32, 28 and 32 weeks of gestation.

In her current (sixth) pregnancy, she developed spontaneous bleeding at 16 weeks gestation, was diagnosed as having a spontaneous abortion and underwent an evacuation procedure at a local rural health facility 3 weeks before presentation. This was followed by the appearance of fever with chills, decrease in urine output to the point of anuria and development of respiratory distress. She was given haemodialysis, but as renal failure did not improve, she was referred to our hospital with a diagnosis of post-abortal acute renal failure. There was no history of use of angiotensin converting enzyme inhibitors, angiotensin receptor blockers or non-steroidal anti-inflammatory drugs.

On examination, she was febrile, and had pallor and pitting oedema of lower extremities. The respiratory rate was 32/min, pulse 124 beats/min and blood pressure 170/120 mmHg. All peripheral pulses were well felt. Examination of the cardiovascular and respiratory systems revealed a left ventricular third heart sound and bibasal rales. Abdominal and neurological systems were unremarkable, there was no renal bruit or renal angle tenderness. Fundus examination showed grade II hypertensive changes. Vaginal examination showed contracted uterus, mild purulent discharge from the os and tenderness in the fornices. Investigations revealed haemoglobin of 110 g/l, total leucocyte count 23 x 109/l with polymorphonuclear preponderance, serum creatinine was 707 µmol/l, urea 67 mmol/l, calcium 2.3 mmol/l, and phosphates 1.23 mmol/l. Urinalysis showed 2+ proteinuria, and occasional RBCs and 3–5 pus cells/hpf along with dirty brown casts. The urine culture was sterile, and blood culture grew Escherichia coli. The patient was immediately placed on haemodialysis with aggressive ultrafiltration and anti-microbials were administered according to sensitivity. The sepsis abated, but she continued to have recurrent episodes of pulmonary oedema despite regular dialysis and control of hypertension. Echocardiography was normal. Abdominal ultrasound showed discrepancy in the sizes of the kidneys, the right kidney was 10.6 cm, whereas the left one was only 7 cm. Doppler examination showed no detectable flow in the left renal artery, and evidence of tight stenosis on the right side. CT angiogram showed non-visualization of the left renal artery and a 7 mm-long, smooth attenuation of right renal artery just after the origin with sluggish distal flow and irregularity and poor filling of smaller branches. The aorta and its other branches were normal. A diagnosis of RAS due to fibromuscular dysplasia was made, and baloon angioplasty with stenting (Genesis stent: 5 x 15 mm) of right renal artery was performed. Normal flow to the right kidney was restored post-angioplasty and stenting. Post-procedure angiogram showed normal appearance of smaller branches (Figure 1). Diuresis set in almost immediately after the procedure, she passed 4 l of urine in the first 24 h, and was taken off anti-hypertensive drugs within 48 h. The serum creatinine dropped to 265 µmol/l at 7 days. She is asymptomatic and normotensive at 8 weeks, and the serum creatinine is 155 µmol/l.


Figure 1
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Fig. 1. (A) CT angiogram with 3-D reconstruction showing non-visualization of the left renal artery and a long stenotic segment (arrows) in right main renal artery, (B) selective angiogram shows the stenotic segment with poor distal flow, (C) angiogram following balloon angioplasty shows restoration of flow, albeit with residual stenosis (arrows) and (D) complete correction of stenosis following stenting.

 


   Discussion
 Top
 Introduction
 Case report
 Discussion
 References
 
ARF following complications of pregnancy, e.g. septic abortion, ante- and post partum haemorrhage and puerperal sepsis is common in developing world, and other aetiological possibilities are rarely considered in this setting [1]. The history of hypertension at a young age, recurrent fetal losses, persistence of pulmonary oedema despite aggressive ultrafiltration and finding of asymmetric kidneys prompted us to look for secondary causes, and led to the discovery of renovascular disease. The left kidney was atrophic secondary to complete occlusion of the left renal artery. Critical stenosis of artery supplying a solitary functioning kidney was responsible for renal failure, as restoration of flow led to prompt resolution of all clinical features. Insults surrounding the abortion, i.e. blood loss and sepsis, may have played a role in precipitation of renal ischaemia.

The most common aetiology of RAS in the Indian subcontinent is Takayasu arteritis (TA), an inflammatory panarteritis that involves the aorta and its major branches including the renal arteries. However, isolated involvement of renal vessels is not described in this condition [2]. As the abdominal aorta and its other major branches were completely normal, we did not consider TA to be responsible for this patient's renovascular disease. Fibromuscular dysplasia (FMD), a non-atherosclerotic, non-inflammatory disease encountered usually in young females, most commonly affects the renal and internal carotid arteries and accounts for about 10% of all RAS [3]. FMD is subtyped, according to the most affected arterial wall layer, into intimal, medial and adventitial types, with the medial one further subdivided into three categories: hyperplasia, fibroplasia and dissection [4]. Medial fibroplasia is the most common, but has a typical angiographic appearance that was absent in this case. Moreover, it almost never progresses to the point of total occlusion. Intimal fibroplasia, however, can present at a young age and lead to total vascular occlusion. The finding of a long, smooth narrowing of proximal third of the right renal artery and complete occlusion of the left renal artery at the ostium were consistent with this variant of FMD [5]. The irregularities noted in the smaller branches on the reconstructed CT image were probably due to a high-renin state, as confirmed by restoration of normal branching pattern after successful revascularization.

This was a long and tight lesion, and a difficult one to negotiate by percutaneous route. The criteria for revascularization in less severe presentations of RAS remain a matter of debate. The current approach is to wait until there is a demonstrable decline in glomerular filtration rate. However, evidence suggests that pre-emptive revascularization is associated with better outcomes [6–8].

Presentation with unexplained renal failure is usually encountered in a setting of atherosclerotic renovascular disease. Despite extensive searching, we were unable to find a case where ARF was the presenting feature in FMD at a young age, and was successfully treated with percutaneous intervention. A previous report describes a 28-year old woman who presented with chronic renal failure and was on regular dialysis for 9 months. RAS was suspected in that case because of severe hypertension, and surgical revascularization using a saphenous vein graft led to recovery of kidney function [9].

The long-term prognosis of our patient seems excellent, since recurrence of stenosis after percutaneous transluminal renal angioplasty and stenting is uncommon in FMD [10–11], and because her intrarenal vessels were free of radiologically evident dysplastic changes. Intraparenchymal arteries may occasionally be the site of dysplastic alterations causing therapy resistant hypertension [12]. Correlates of successful outcome include an age of less than 50 years, the absence of associated coronary or carotid stenosis, and duration of hypertension of less than 8 years [13].

In conclusion, we present an unusual case where clinical clues led to the discovery of a treatable cause of ARF and prompt therapeutic intervention was rewarding.

Conflict of interest statement. None declared.



   References
 Top
 Introduction
 Case report
 Discussion
 References
 

  1. Chugh KS, Sitprija V, Jha V. (2005) Acute renal failure in the tropical countries. In Davison AM, Cameron JS, Grunfeld J-P (Eds.), et al. Oxford Textbook of Nephrology.(Oxford University Press, Oxford) pp. 1614–1629.
  2. Chugh KS, Jain S, Sakhuja V, et al. (1992) Renovascular hypertension due to Takayasu's arteritis among Indian patients. Q J Med 85:833–843.[Web of Science][Medline]
  3. Safian RD and Textor SC. (2001) Renal-artery stenosis. N Engl J Med 344:431–442.[Free Full Text]
  4. Luscher T, Lie JT, Stanson AW, Houser OW, Hollier LH, Sheps SG. (1987) Arterial fibromuscular dysplasia. Mayo Clin Proc 62:931–952.[Web of Science][Medline]
  5. Begelman SM and Olin JW. (2000) Fibromuscular dysplasia. Current Opin Rheumatology 12:41–47.
  6. Dorros G, Jaff M, Mathiak L, et al. (1998) Four-year follow-up of Palmaz-Schatz stent revascularization as treatment for atherosclerotic renal artery stenosis. Circulation 98:642–647.[Abstract/Free Full Text]
  7. Cambria RP. (1998) Surgery: indications and variables that affect procedural outcome, as well as morbidity and mortality. J Invasive Cardiol 10:55–58.[Web of Science][Medline]
  8. Kennedy DJ, Colyer WR, Brewster PS, et al. (2003) Renal insufficiency as a predictor of adverse events and mortality after renal artery stent placement. Am J Kidney Dis 42:926–935.[Web of Science][Medline]
  9. Nickeleit V, Moll S, Cynke E, Brunner FP, Mihatsch MJ. (1999) A young woman with high blood pressure on haemodialysis: it is never too late to evaluate hypertension. Nephrol Dial Transplant 14:2734–2737.[Free Full Text]
  10. Greminger P, Steiner A, Schneider E, et al. (1989) Cure and improvement of renovascular hypertension after percutaneous transluminal angioplasty of renal artery stenosis. Nephron 51:362–366.[Web of Science][Medline]
  11. Baert AL, Wilms G, Amery A, Vermylen J, Suy R. (1990) Percutaneous transluminal renal angioplasty: initial results and long-term follow-up in 202 patients. Cardiovasc Intervent Radiol 13:22–28.[Web of Science][Medline]
  12. Holm-Bentzen M, Gerstenberg T, Horn T, Larsen S. (1993) Medial fibroplasia: involvement of renal artery and small renal arteries in renal vascular hypertension. Scand J Urol Nephrol 27:263–265.[Web of Science][Medline]
  13. de Fraissinette B, Garcier JM, Dieu V, et al. (2003) Percutaneous transluminal angioplasty of dysplastic stenoses of the renal artery: results on 70 adults. Cardiovasc Intervent Radiol 26:46–51.[CrossRef][Web of Science][Medline]

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