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DOI:10.2214/AJR.05.0866
AJR 2007; 189:W163-W165
© American Roentgen Ray Society


Case Report

Fat-Fluid Levels in Renal Caliceal Cavities: A CT Sign of Lipolysis Due to Urine Extravasation After Kidney Rupture

Michaël Soussan1, Isabelle Boulay-Coletta1, Vincent Molinié2, Walid Alamé3 and Marc Zins1

1 Department of Radiology, Saint Joseph Hospital Foundation, 185 rue Raymond Losserand, 75014 Paris, France.
2 Department of Pathology, Saint Joseph Hospital Foundation, Paris, France.
3 Department of Urology, Saint Joseph Hospital Foundation, Paris, France.

Received May 23, 2005; accepted after revision July 20, 2005.

 
Address correspondence to I. Boulay-Coletta (iboulay{at}hopital-saint-joseph.org).

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Keywords: CT • genitourinary tract imaging • kidney • lipolysis


Introduction
Top
Introduction
Case Report
Discussion
References
 
Urine extravasation is a rare complication of urinary tract obstruction. Urine leaks out of tears in the caliceal fornix and, more rarely, the renal pelvis or ureter. In exceptional cases, urine leaks through perforations in the renal wall. Lipolysis of perihilar tissues occurs within a few days of urine extravasation [1]. We describe caliceal fat-fluid levels visualized on CT in a patient who had chronic obstructive pyelonephritis complicated by extensive kidney rupture with extravasation of infected urine. We suggest that urine-induced lysis of perirenal fat may have caused this CT finding. To our knowledge, this is the first report of fat-fluid levels in renal calices.


Case Report
Top
Introduction
Case Report
Discussion
References
 
A 57-year-old man was admitted to our emergency department with a 2-week history of left flank pain, malaise, fever (38.1°C), asthenia, and anorexia. He had a history of untreated type 2 diabetes. Cutaneous erythema over the left lumbar area and hemodynamic instability were found at physical examination. Helical CT (Light-Speed Pro 16, GE Healthcare) of the abdomen and pelvis was performed immediately with and without iodinated contrast material and delayed scanning. An 8-mm stone obstructing the distal portion of the left ureter was seen, as were diffuse pelvicaliceal dilatation and extensive perirenal and pararenal fluid collections. The left kidney was diffusely enlarged (length, 15 cm), and an extensive parenchymal tear was seen in the upper pole (Figs. 1A and 1B). Fat-fluid levels were visible in most of the dilated calices and in the pelvis. Density was -100 H for the top component and 10 H for the bottom component (Fig. 1C). A fat-fluid level was also seen in the bladder (Fig. 1D). Enhancement was less marked in the left than the right kidney, and excretion was asymmetric.


Figure 1
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Fig. 1A 57-year-old man with left flank pain, malaise, and fever. Axial contrast-enhanced CT scan through kidneys shows parenchymal rupture of left kidney with perirenal collection and fatlike attenuation (arrowhead) in superior calix.

 

Figure 2
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Fig. 1B 57-year-old man with left flank pain, malaise, and fever. Coronal reformatted CT scan shows extensive tear (arrow) in left renal parenchyma, large heterogeneous perirenal collection, and low fatlike attenuation (arrowhead) in superior calices.

 

Figure 3
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Fig. 1C 57-year-old man with left flank pain, malaise, and fever. Coronal oblique reformatted CT scan shows multiple fat-fluid levels in renal cavities.

 

Figure 4
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Fig. 1D 57-year-old man with left flank pain, malaise, and fever. Axial contrast-enhanced CT scan through renal pelvis shows impacted stone (arrowhead) in left ureter and fat-fluid level (arrows) in bladder.

 
Blood test abnormalities included leukocytosis (WBC count, 22,000/mm3) with predominance of neutrophils (18,000/mm3), C-reactive protein elevation (312 mg/L), hyperglycemia (17.8 mmol/L), and hyponatremia (123 mmol/L). The hemoglobin concentration was 10.3 g/dL, and the hematocrit was 27%. The serum creatinine concentration was normal. Urine and blood culture results were positive for ß-hemolytic streptococci. Although the urine was turbid and orange to the naked eye, test results were negative for cholesterol and triglycerides.

IV antibiotics were given, a ureteral catheter was inserted, and 1 L of pus was drained surgically from the perirenal region. The left kidney showed no evidence of function and was removed surgically 2 weeks later. The renal calices were dilated and filled with pus. Histologic examination of the kidney showed not only chronic tubulointerstitial pyelonephritis with lymphoplasmacytic infiltrates but also foci of acute pyelonephritis with neutrophilic infiltrates. There was no necrosis of the renal fat sinus. Within the perirenal tissue, foci of lipolysis with marked inflammation and granuloma formation were seen. The granuloma was composed of foamy macrophages and of neutrophilic infiltrates containing multinucleate giant cells and lymphocytes (Fig. 1E). Ulcers without perforation were visible in the pelvicaliceal urothelium, and necrotic fatty tissue was found in the caliceal lumens (Fig. 1F). There was no histologic evidence of xanthogranulomatous pyelonephritis (XGP).


Figure 5
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Fig. 1E 57-year-old man with left flank pain, malaise, and fever. Photomicrograph of histologic specimen of perirenal tissue shows fat-cell necrosis with severe inflammation and granulomatous lipolysis. (H and E, x200)

 

Figure 6
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Fig. 1F 57-year-old man with left flank pain, malaise, and fever. Photomicrograph of histologic specimen of pyelocaliceal cavity shows necrotic fat in lumen. (H and E, x200)

 

Discussion
Top
Introduction
Case Report
Discussion
References
 
The incidence of spontaneous extravasation of urine related to ureteral stone obstruction has been estimated at 4% in patients undergoing excretory urography [2]. Urine extravasation occurs when elevation of pressure in the renal pelvis causes urine to flow in the retrograde direction through the interstitial lymphatic vessels. This reversal of flow tends to lower renal pelvic pressure. Increased pressure in normal renal parenchyma causes microscopic tears in the fornices of the minor calices, which are the weakest points, and these tears subsequently extend to the renal sinus. Urine leaks into the renal sinus then flows in the retrograde direction into the veins and lymphatic vessels. When the amount of urine exceeds reabsorption, urine can leak around the renal hilus into the perirenal fat tissue and occasionally downward along the ureter or psoas muscle, where a urinoma develops [3]. In rare instances, urine leaks out of a breach in the renal pelvis caused by necrosis at a site of pressure from an impacted pelvic stone.

Rupture of the renal parenchyma is uncommon but has been reported to occur after renal trauma, uroradiologic procedures, and open renal surgery. In patients with ureteral calculus, spontaneous rupture of the renal parenchyma is exceedingly rare. The cases reported to date have occurred in association with renal parenchymal disease such as renal tumor, periarteritis nodosa, chronic pyelonephritis, pyonephrosis, and abscess [4]. Spontaneous rupture of the kidney can cause retroperitoneal hematoma and, when the urine is infected, retroperitoneal abscess and peritonitis [5, 6].

When urine leaks into the perirenal fat, macroscopic edema promptly develops [7]. The first microscopic urine-induced abnormality is lipolysis, which is seen as fat tissue disruption with infiltration by foamy macrophages (xanthoma cells), multinucleate giant cells, and lymphocytes. Later, fibrous tissue is substituted for the perihilar and perirenal fat. The cause of urine-induced lipolysis is unknown. Urine contains no substances capable of inducing lipase activation. Adipocyte membrane disruption may be related to changes in osmotic pressure [1].

Our patient had a 2-week history of ureteral stone obstruction with infection. The extensive tear in the renal parenchyma can be ascribed to pressure elevation and to parenchymal damage produced by the chronic and acute renal infection. Abnormal fragility of the renal parenchyma is a key factor in parenchymal rupture. The massive leakage of pus and urine into the perirenal space in our patient may explain the severe malaise. CT showed a wide communication between the renal cavities and perirenal space. The large amount of urine and pus in the perirenal region caused fat necrosis, as found at histologic examination. No perforation of pelvicaliceal urothelium or lipolysis was found in the renal fat sinus at pathologic examination. For this reason, we hypothesize that the fat-fluid levels in the renal cavities and bladder were more likely due to lipolysis of perirenal fat followed by penetration of fat components into the renal calices than to fat necrosis coming from the renal fat sinus. We are not aware of previous reports describing fat-fluid levels in the renal cavities of a patient with renal colic complicated by urinary tract infection. A plausible explanation is that extensive renal rupture is exceedingly rare in this situation.

Ureteral obstruction with urine extravasation and lipolysis must be differentiated from XGP. Although the clinical manifestations may be similar, at pathologic examination XGP is defined as rounded masses composed of an infiltrative process with accumulation of lipid-laden macrophages intermixed with a variety of inflammatory cells in the renal parenchyma. At CT, however, evidence of XGP is diffuse kidney enlargement with replacement of the parenchyma by multiple low-attenuation (10-15 H) rounded masses corresponding either to dilated calices filled with pus and xanthomatous tissue or to foci of parenchymal destruction [8]. In contrast, in our patient, CT and macroscopic examination showed no mass, and microscopic examination did not reveal accumulation of lipid-laden macrophages in the renal parenchyma. In this case, perirenal fat lipolysis with fat-fluid levels in the renal cavities was clearly a different entity from XGP. This case of CT visualization of fat-fluid levels in the pelvicaliceal cavities of the kidney constitutes, to our knowledge, the first reported evidence of perirenal lipolysis due to urine extravasation through a large renal parenchymal tear.


References
Top
Introduction
Case Report
Discussion
References
 

  1. Carr RA, Newman J, Antonakopulos GN, Parkinson MC. Lesions produced by the extravasation of urine from the upper urinary tract. Histopathology 1997;30 : 335-340[CrossRef][Medline]
  2. Hughes J, De Hart HS, Coppridge AJ, Roberts LC. Ureteral stone: diagnosis in emergency room patients. Urology1977; 10:425 -427[CrossRef][Medline]
  3. Green N, Fingerhut AG, French S. Mechanism of renovascular backflow: a pathophysiologic study. Radiology1969; 92:531 -536[Medline]
  4. Szentgyorgyi E, Kondas J, Varga S, Lorinczy D, Regos I, Kun I. Spontaneous rupture of the kidney: a report on 5 cases. Int Urol Nephrol 1994; 26:133 -140[Medline]
  5. Harrow BR. Spontaneous urinary extravasation associated with renal colic causing a perinephretic abscess. AJR1966; 98:47 -53[Abstract/Free Full Text]
  6. Paraskevaides EC, Cooper-Wilson M. Near fatal urinary peritonitis secondary to ureteric calculus. Br J Urol1989; 63:437 -438[Medline]
  7. Hamperl H, Dallenbach FD. The extravasation and precipitation of urine in the hilus of the kidneys. J Mt Sinai Hosp N Y1957; 24:929 -934[Medline]
  8. Hayes WS, Hartman DS, Sesterbenn IA. Xanthogranulomatous pyelonephritis. RadioGraphics 1991;11 : 485-498[Abstract]

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