Quiz Page August 2008:
Acute Kidney Injury Post–Cesarean Delivery: Is GFR Reduced?
Article Outline
Clinical Presentation
A 24-year-old African American woman presented 2 weeks after cesarean delivery with epigastric pain, nausea, and vomiting that began the previous day. Her pregnancy was complicated by gestational diabetes and postoperative urinary tract infection treated with nitrofurantoin. She had normal kidney function throughout the pregnancy. Physical examination was significant for blood pressure of 132/86 mm Hg, pulse of 130 beats/min, and abdominal distension with shifting dullness. Laboratory tests showed hematocrit of 31%, platelet count of 489 × 103/μL (489 × 109/L), blood urea nitrogen level of 54 mg/dL (19.3 mmol/L), serum creatinine level of 7.0 mg/dL (619 μmol/L), negative hepatitis panel, and normal liver function, except for a serum albumin level of 2 g/dL (20 g/L) and total bilirubin level of 1.6 mg/dL (27.36 μmol/L). Urinalysis was remarkable for large blood, 30 mg/dL (0.3 g/L) of protein, and 10 red blood cells and 69 white blood cells/high-power field. Spot urine sodium and creatinine levels were 35 mEq/L (35 mmol/L) and 343 mg/dL (30,321 μmol/L), respectively. An abdominal ultrasound showed moderate to large abdominal ascites and normal-sized kidneys without hydronephrosis. A Foley catheter was placed, and normal saline was administered. Serum creatinine levels decreased from 7 mg/dL (619 μmol/L) to 1.9 mg/dL (168 μmol/L) in less than 24 hours.
■ What is the most likely cause of acute kidney injury (AKI) in this patient?
■ Which tests are needed to confirm the diagnosis?
Discussion
■ What is the most likely cause of acute kidney injury (AKI) in this patient?
Our patient had the triad of ascites, abdominal pain, and AKI, which prompted therapy based on 2 erroneous assumptions: the ascites was hepatic in origin and AKI was caused by underperfusion of the kidney. Because of concerns for Budd-Chiari syndrome, paracentesis was performed. Analysis of the ascitic fluid showed a creatinine concentration of 2.1 mg/dL (185.6 μmol/L), much less than the urinary creatinine analyzed simultaneously. However, because of high clinical suspicion, a computed tomographic cystogram was obtained (Fig 1), which showed a large fluid collection in the pelvis (C) and extravasation of the intravesicular contrast from the anterior dome of the bladder (B) into the large intraperitoneal fluid collection, consistent with a bladder rupture. In retrospect, the dramatic improvement in serum creatinine levels and low creatinine concentration in ascitic fluid relative to urinary creatinine concentration were caused by decompression of the bladder leak with a Foley catheter. Despite the patient's initial improvement, continued bladder leak prompted exploratory laparotomy with successful repair of the bladder dome.
Figure 1.
Computed cystogram showing bladder leak (B) along with urinary ascites (C). Urinary bladder is denoted by (A).
Bladder perforation occurs in the setting of cesarean delivery with a frequency of 0.1% to 5%.1 Patients with urinary ascites usually present with severe abdominal pain and oliguric AKI.2, 3 AKI associated with urinary ascites is actually a “pseudo renal failure” because serum creatinine and blood urea nitrogen levels increase because of the systemic reabsorption of urea and creatinine from the intraperitoneal urine collection,4 not because of an actual decrease in glomerular filtration rate or kidney damage.
■ Which tests are needed to confirm the diagnosis?
In a patient with clinical suspicion for urinary leak, a ratio between ascitic fluid creatinine concentration and serum creatinine level greater than 1.0 is suggestive, but not diagnostic, of an intraperitoneal urinary leak.3 The increase in ascitic fluid creatinine concentration relative to serum creatinine level is caused by a slower rate of removal of intraperitoneal fluid and macromolecules by subdiaphragmatic lymph flow relative to their rate of entry.3 Although the ratio usually is greater than 2,1 the ratio of 0.3 in our patient likely reflects analysis of ascitic fluid long after decompression of the bladder leak and serum equilibration had occurred. The diagnosis was confirmed with a computed tomographic cystogram, which is highly sensitive for diagnosing bladder rupture.5
Final Diagnosis
Pseudo renal failure secondary to intraperitoneal bladder perforation during cesarean delivery.
References
- . Post-partum ‘acute renal failure.'. Nephrol Dial Transplant. 2002;17:1703–1705
- . Urinary ascites due to retroperitoneal fibrosis: A case report. Acta Radiol. 2007;48:119–121
- . Urinary ascites: Spontaneous bladder rupture presenting as acute oliguric renal failure. Am J Med. 1998;105:347–349
- . Acute abdomen—Remember spontaneous perforation of urinary bladder. J R Coll Surg Edinb. 2001;46:316–317
- . CT cystography with multiplanar reformation for suspected bladder rupture: Experience in 234 cases. AJR Am J Roentgenol. 2006;187:1296–1302
Case provided and authored by Chika N. Okafor, MD, and Monika Gupta, MD, Medical University of South Carolina, Charleston, SC.
Financial Disclosure: None.
Support: None.
PII: S0272-6386(08)00761-0
doi:10.1053/j.ajkd.2008.03.032
© 2008 National Kidney Foundation, Inc. Published by Elsevier Inc All rights reserved.
