Post-partum ‘acute renal failure’

(Section Editor: M. G. Zeier) Supported by an educational grant from

K.-U. Eckardt1, R. Bittner2, J.W. Dudenhausen3 and U. Frei1

1 Department of Nephrology and Medical Intensive Care 2 Department of Radiology 3 Department of Obstetrics, Charité, Campus Virchow Klinikum, Berlin, Germany

Case

A 34-year-old pregnant woman was admitted to hospital 10 days after term. The course of her pregnancy had so far been uneventful and her past medical history was unremarkable. Her blood pressure was 110/60 mmHg and her body weight was 64.3 kg. Fetal ultrasound showed normal vital signs, but an oligohydramnios. An attempt was made to induce vaginal delivery under peridural anaesthesia. Due to a failure to progress, together with signs of fetal distress and suspected chorioamnionitis, a secondary Caesarean section had to be performed a few hours later, which was uncomplicated. The newborn received antibiotic treatment and was temporarily treated on a neonatology unit. However, infection was not confirmed. The mother also received antibiotic treatment with cefuroxim, with the first dose given before the section. During the section she received 1 litre of 6% hydroxyethylstarch together with the infusion of crystalloids.

Overnight she passed 1.8 litre urine through a bladder catheter, which was removed the next morning. During the following day she started to complain of tenderness and pain in her lower abdomen. Due to her inability to pass urine spontaneously she was catheterized once, which resulted in approximately 100 ml of bloody urine. Abdominal discomfort and pain of varying intensity persisted over the following days. The abdominal wall appeared somewhat indurated, but the laparotomy wound was unremarkable. An X-ray film of the abdomen suggested a subileus, but bowel sounds were present and, following stimulation with metoclopramide and physostigmine, she purged. Abdominal ultrasound showed a regularly involuting uterus, normal sized kidneys without evidence of urinary tract obstruction and moderate intra-abdominal fluid accumulation, which was attributed to the recent section. Another laparotomy was considered, but was not immediately performed after consideration of the patient's overall condition with only moderate impairment of well being, and because a surgical problem could not be identified. On the third day after the Caesarean section it was noticed that the patient's serum creatinine had increased from 0.6 to 4.5 mg/dl and serum urea from 18 to 63 mg/dl. C-reactive protein was elevated to 16.8 mg/dl. Uric acid was 8.4 mg/dl, and liver enzymes were normal. The patient had a leucocytosis of 20.9 per nl, her platelet count was 291 per nl and her haemoglobin level was 12.9 g/dl. When asked, it transpired that she had probably passed only very small amounts of urine during the previous few days, but the exact amount was unclear. A culture of a urine specimen obtained on the day after delivery had not shown bacterial growth. The patient's body temperature was now 37.5°C and her body weight was 64.2 kg. Upon physical examination she appeared well-hydrated overall. Blood pressure was 130/70 mmHg. The chest was clear on auscultation. Her abdominal wall was oedematous, although not acutely inflamed. The swelling was predominantly on her left side and extended to the left flank and thigh. The legs, however, showed no signs of venous obstruction and foot pulses were palpable. No skin rash was detected. Doppler ultrasound showed regular kidney perfusion; there was no evidence for thrombosis of the renal veins or the vena cava inferior. Figure 1Go depicts a native abdominal CT scan that was subsequently performed.



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Fig. 1.  Abdominal CT scan showing marked swelling of abdominal wall and presence of ascites.

 

Question

What is the cause of the acute uraemia?

Answer to the quiz on preceding page

Acute renal failure has become a rare complication with pregnancy in industrialized countries. The differential diagnoses include pre-renal, vascular and post-renal causes, as well as deterioration of pre-existing renal failure [1].

In the present case the temporary coincidence of oliguria and a rise in serum creatinine with the caesarean section made any genuine renal disease, manifesting with acute renal failure, highly unlikely. Furthermore, a normal serum creatinine on admission and normal kidney morphology shown by ultrasound and the CT scan gave no indication of pre-existing chronic renal disease. The patient did not show any signs or symptoms of pre-eclampsia. She had not experienced any episodes of haemodynamic compromise, nor was there any major blood loss, so ischaemic renal failure due to systemic hypoperfusion could be ruled out. In addition, the possibility of renal hypoperfusion due to a renal vascular occlusion was excluded by doppler ultrasound, as was the unliklely possibility of a bilateral renal vein thrombosis. The normal platelet count and haemoglobin levels excluded a pregnancy-associated microangiopathy, such as haemolytic uraemic syndrome. Acute uric acid nephropathy has been described as a rare cause of acute renal failure in a pregnant women [2], but there was no severe hyperuricaemia in the present case. Acute interstitial nephritis due to antibiotic treatment was considered, but appeared unlikely in view of the rapidly developing oliguria and the lack of skin manifestations. Hydroxyethylstarch, which was given during the Caesarean section, may increase the risk of renal failure [3] and has been suggested to be a cause of temporary non-oliguric renal failure after section in a previous report of two cases [4]. An infection of the abdominal wall and/or subacute bacterial peritonitis would have been compatible with some of the clinical and laboratory findings and could also have contributed to renal functional impairment. However, since the patient was not septic, it seemed doubtful that infection could provide a sufficient explanation for the severe and rapid deterioration of renal function. Acute renal failure from an obstruction by the gravid uterus is a rare complication with pregnancy [5,6], but ureteric obstruction appears highly unlikely to be a complication of Caesarean section, and the ultrasound and CT scan showed no distension of the urinary tract.

The most remarkable finding in the CT scan (Figure 1Go) was a significant swelling of the abdominal wall, which corresponded to physical findings, and the presence of ascites in the lower and upper abdomen. The suspected diagnosis of intra-abdominal urinary leakage was confirmed by puncture of the ascites, which revealed a creatinine concentration of 15.8 mg/dl, more than twice as high as the serum creatinine level. To document the site of urinary leakage a cystogram was subsequently performed, which showed extravasation of contrast medium into the abdominal cavity (Figure 2Go). Subsequent laparotomy revealed a 3 cm lesion in the bladder wall. Following bladder suture the patient passed 4 l of urine and normalized her serum creatinine within the following 24 h.



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Fig. 2. Cystography showing extravasation of radiocontrast medium into the abdominal cavity after radiocontrast medium administration.

 
Major injuries to the urinary system tract in association with childbirth have been reported at an incidence of 0.04% [7] and bladder injury after Caesarean section has been documented in 0.1–5% of cases [8,9]. Extravasation of urine into the abdominal cavity, leading to peritonitis and abnormal renal chemistry, has also been reported as a consequence of spontaneous bladder rupture [1012] or as a late, potentially fatal complication of augmentation enterocystoplasty in patients with spinal cord lesions [13,14]. In addition, ureteroperitoneostomy has been used as an experimental model for reduced renal waste excretion [15,16]. Urine constituents are rapidly reabsorbed through the peritoneum, as they are excreted into the peritoneal cavity during peritoneal dialysis. ‘Urine peritonitis’ is believed to be inducible by chemical irritation in the absence of bacterial contamination of the urine [16], but urine colonization may lead to more severe disease [13].

References

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  16. Gittes GK, Gittes RF. The effect of ureteroperitoneostomy on renal mass in fasted rats. J Urol1984; 131: 1206–1207[ISI][Medline]




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