Saudi Journal of Kidney Diseases and Transplantation

: 2020  |  Volume : 31  |  Issue : 5  |  Page : 1140--1143

Intra-abdominal Hypertension as a Cause of Oliguric Acute Kidney Injury in a Patient with Chronic Lymphocytic Leukemia

Dimitris Xydakis1, Ergini Antonaki1, Anna Boula2, Emilia Stavroulaki2, Aristea Hatzivasili2, Dimitra Liapi2,  
1 Department of Nephrology, Venizeleio Hospital, Crete, Greece
2 Department of Hematology, Venizeleio Hospital, Crete, Greece

Correspondence Address:
Dimitris Xydakis
Department of Nephrology, Venizeleio Hospital, Crete


Acute kidney injury (AKI) is a well-known complication in patients with chronic lymphocytic leukemia (CLL). It could occur via diverse mechanisms such as leukemic infiltration, extrarenal obstruction, tumor lysis syndrome, glomerular diseases, and medication side effects. The incidence of kidney disease at the diagnosis of CLL is about 10%. We report a case of AKI, in a patient with a known history of CLL, due to abdominal compartment syndrome, caused by extremely enlarged intra-abdominal lymph masses. To the best of our knowledge, no case of AKI due to such cause has been reported so far.

How to cite this article:
Xydakis D, Antonaki E, Boula A, Stavroulaki E, Hatzivasili A, Liapi D. Intra-abdominal Hypertension as a Cause of Oliguric Acute Kidney Injury in a Patient with Chronic Lymphocytic Leukemia.Saudi J Kidney Dis Transpl 2020;31:1140-1143

How to cite this URL:
Xydakis D, Antonaki E, Boula A, Stavroulaki E, Hatzivasili A, Liapi D. Intra-abdominal Hypertension as a Cause of Oliguric Acute Kidney Injury in a Patient with Chronic Lymphocytic Leukemia. Saudi J Kidney Dis Transpl [serial online] 2020 [cited 2023 Feb 2 ];31:1140-1143
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Full Text


Chronic lymphocytic leukemia (CLL) is a B-cell lymphocytic neoplasm usually with an indolent clinical course, and it has a wide spectrum of clinical symptoms and presentation. Acute kidney injury (AKI) is common, but oliguric AKI is rare.

The effect of increased abdominal pressure in urine output is known for a little <150 years, now. In 1876, Wendt[1] was the first to describe the reduction of urinary output with intra-abdominal hypertension (IAH).

IAH is defined as a sustained or repeated pathologic elevation of intra-abdominal pressure (IAP) ≥12 mm Hg, and a sustained elevation of IAP of ≥20 mm Hg associated with new organ dysfunction defines abdominal compartment syndrome (ACS).

Increased IAP can affect various intra-abdominal organs and may lead to ACS. ACS is described more frequently in surgical patients, but in the last decade, there is a growing interest in the presence of such conditions in patients with medical problems without any abdominal surgical conditions.

The most important clinical presentation of ACS is respiratory distress due to lung compliance reduction, circulatory failure, and oliguria.

We report a case of AKI as a result of ACS due to lymph node enlargement in a patient with B-cell CLL relapse. In our knowledge, this is the first case reported with oliguric AKI due to ACS, related to lymph node enlargement.

 Case Report

Informed consent was obtained from the patient's relatives before publishing the case.

A 64-year-old man, known case of B-cell CLL, presented to our hospital with oliguria for three days. He also reported a three-week history of malaise, progressive abdominal distension, and pain. There was no history of diarrhea or vomit. He was diagnosed with oliguric AKI and was admitted to the hospital for further investigation.

He denied taking any nephrotoxic medicine (nonsteroidal anti-inflammatory drug, iodine contrast) or any other medicine except those prescribed as a chronic treatment.

The patient was diagnosed with 17p-deleted CLL in 2007. He was treated first line with cyclophosphamide plus rituximab. He had a stable disease ever since and did not receive subsequent systemic treatment for CLL. At presentation, the patient was afebrile, blood pressure was 118/85 mm Hg, heart rate was 87 beats/min, respiratory rate was 19 breaths/min, and blood oxygen saturation was 98% on room air. Skin turgor was normal, mucous membranes were moist, and his orthostatic vital signs were normal. There was no clinically evidence of dehydration. There was severe distension of the abdomen.

Laboratory test revealed the following: creatinine 3.73 mg/dL (his baseline creatinine according to the last reading, 28 days before admission, was 1.2 mg/dL), urea – 89 mg/dL, Na – 141 mmol/L, K – 4.8 mmol/L, Ca – 9.1 mg/dL, P – 4.2 mg/dL, white blood cell – 14,300/μL, Lymphocytes – 7450/μL, platelet – 2,03,000, uric acid – 7.1 mg/dL, hemoglobin – 11.3 g/dL, and C-reactive protein – 0.7 mg/dL. Urinalysis and urine sediment examination were unremarkable. His serologic workup included anti-dsDNA antibody and antinuclear antibody, and serum complement levels were normal.

Ultrasonography demonstrated hepatomegaly and massive lymphadenopathy but no evidence of hydronephrosis or increased kidney dimensions from his baseline dimension. Electrocardiogram upon admission showed normal sinus rhythm.

A computerized tomography scan [Figure 1] and [Figure 2] was performed and revealed multiple enlarged superior mesenteric artery lymph nodes fusing into lobular masses with diameters of 7.62–19.68 cm, clear margins, and uniform density. Enlarged lymph nodes were attributed to relapse of B-cell CLL. A bolus dose of furosemide did not affect diuresis.{Figure 1}{Figure 2}

Due to the concomitant presence of oliguric AKI, the abdomen distension, and the absence of findings of active kidney disease, IAP was measured using the trans-bladder method as per the World Society of the Abdominal Compartment Syndrome (WSACS) guidelines[2] and was found a persistent increase in IAP (46 mm Hg – Grade 4). Hence, ACS was diagnosed.

The same day, the patient was treated with venetoclax, a selective inhibitor of the B-cell lymphoma 2 regulator protein, which caused a reduction in tumor burden – mass on the 4th hospital day as a new ultrasound (US) scan revealed. Posttreatment tumor lysis syndrome has not been observed. The patient's IAP decreased to 16 mm Hg, and oliguria gradually resolved. Creatinine levels were reduced from 3.7 (3rd hospital day) to 1.64 mg/dL in a seven-day period. The patient is still in venetoclax, and his kidney function is stabilized to his previous stage.


Strati and Shanafelt found a 7.5% incidence of kidney disease at the diagnosis of CLL,[3] but oliguric renal failure is a rare presenting feature. The most common causes of renal involvement in this particular leukemia are leukemic cell infiltration, acute uric acid nephropathy, use of nephrotoxic drugs, prerenal azotemia, and acute tubular necrosis.[4] Obstructive nephropathy in the setting of CLL can be observed, but it is not a common cause of AKI.[5]

The WSACS, a multidisciplinary comity of critical care specialists, published in 2006 a consensus about IAH and ACS. The IAP is usually below 4 mm Hg. It is affected by obesity, but even in most obese patients, it does not exceed 8 mm Hg.[6] Causes of IAH are divided into primary (i.e., surgical or trauma) or secondary (medical such as ascites, ileus, large-volume fluid replacement, burns, and intra-abdominal sepsis) based on the underlying pathology. When IAP increases slowly in several conditions (ascites, neoplasia, and pregnancy), there is an adaptation process, and the patient has no adverse effects.

If there is an acute increase of IAP or not treated promptly, IAH leads to ACS (IAP >20 mm Hg) causing multiorgan failure.[7]

The pathophysiological mechanisms implicated to AKI in IAH are initially elevated renal vein pressure that leads to intrarenal vascular congestion, but as the IAP evolves to ACS, additional factors are added (reduction in cardiac output, elevated levels of catecholamines, renin, angiotensin, and inflammatory cytokines).

Lymphadenopathy is present in 50%–90% of patients with CLL among various series, and the most commonly affected sites are cervical, supraclavicular, and axillary.

In our case, an extensive workup for AKI that included evaluation for prerenal and intrinsic renal etiologies failed to point to other etiologies. The extremely distended abdomen drove us to take into consideration the post-renal cause of AKI due to urinary tract obstruction by enlarged lymph node external compression. This hypothesis was not supported by the kidney US. The possible diagnosis of ACS was confirmed by the intravesical pressure measurement. AKI and IAP were improved after chemotherapy that reduced the intra-abdominal lymph mass.

Our diagnosis was AKI caused by ACS due to enlarged lymph node mass. This is supported by the presence of unexplained AKI, the concomitant IAH, and the improvement of glomerular filtration rate after chemotherapy, reduction of intra-abdominal lymph nodes, and consequent reduction of IAP.

Venetoclax was chosen first due to the presence of a relapse in a high-risk CLL patient (17p deletion) who had received one prior therapy and second because venetoclax can cause a rapid reduction in tumor size. This may pose a risk of TLS during initial dosing, so prophylaxis and monitoring procedures were implemented to mitigate this risk.

Several previous case reports have demonstrated the relationship between IAP, ACS, and AKI, the majority concerning patients with surgical conditions.[8] However, in our knowledge, this is the first case reported with oliguric AKI due to ACS, related to lymph node enlargement in CLL.


IAH and ACS often complicate the course of critically ill patients. ACS should be in mind in any case of unexplained oliguric AKI and abdominal distension, especially if there is no evidence supporting obstructive uropathy. It should be investigated promptly, and IAP should be measured using the trans-bladder method.

Conflict of interest: None declared.


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