Compression Of Renal Parenchyma Research Articles

Reversed diastolic intrarenal flow in page kidney following renal biopsy.

Page's kidney is a condition that occurs due to external renal compression, usually caused by a subcapsular haematoma, generating a renal compartmental syndrome with parenchymal damage and renal perfusion alteration. Classically associated with renal trauma, Page's kidney can also arise after invasive renal procedures, such as renal biopsies or percutaneous nephrostomies. Clinically, it can trigger hypertension due to activation of the renin-angiotensin system induced by hypoperfusion secondary to renal parenchymal compression and can also present with varying degrees of renal function impairment. Furthermore, severe acute renal failure may be found particularly in patients with solitary kidneys or renal transplants. We present two cases of Page's kidney after renal biopsy and their PoCUS ultrasound findings. We would like to highlight the reversed diastolic flow on Doppler ultrasound in this entity, a pattern we have found in all two cases.

Unexpected presentation of allograft dysfunction triggered by page kidney phenomenon immediately after kidney transplantation: a case report

BackgroundPage kidney phenomenon is caused by strong renal parenchymal compression and leads to renal hypoperfusion and microvascular ischemia, resulting in renal dysfunction and hypertension. Although the development of Page kidney phenomenon in allograft is rare, most of its cases are induced by allograft biopsy or trauma. We observed a case of Page kidney phenomenon that was induced by unusual causes immediately after kidney transplantation.Case presentationA 66-year-old man, whose wife donated a kidney, underwent ABO-compatible living kidney transplantation. The allograft had three renal arteries that were trimmed and formed into one piece on the back table, and subsequently, it was anastomosed to the internal iliac artery. Intraoperative Doppler ultrasonography (US) revealed adequate blood flow of each renal artery. Urine output was also observed as soon as allograft blood flow was reperfused. After the surgery, the urine output decreased, and serum creatinine level increased to 6.0 mg/dL. Doppler US did not show evidence of acute rejection, ureteral obstruction, or anastomotic stenosis of the renal arteries. On postoperative day 7, surgical exploration was performed and revealed that the blood flow of each renal artery was adequate but subcapsular hematoma was detected at the upper pole of the allograft. Capsulotomy and hematoma evacuation were performed. Subsequently, urine output increased and serum creatinine level decreased up to 1.7 mg/dL. Allograft sample was obtained 1 h after the transplantation from the lower pole of the allograft. Although the cause of subcapsular bleeding was unclear in this case, a small cyst of the allograft, which might have ruptured during donor nephrectomy, was located in the middle of the hematoma, and oozing around the cyst was observed.ConclusionsOur case indicated that the small ruptured cyst of the allograft could be the cause of subcapsular hematoma and Page kidney phenomenon. Subcapsular hematoma caused by oozing over time could be difficult to diagnose using Doppler US, and thus, other imaging modalities, such as computed tomography, should be considered. Knowledge of the Page kidney phenomenon in the allograft can lead to early diagnosis and intervention, resulting in better outcomes for recipients with allograft dysfunction.

Nefrectomía parcial robótica con compresión selectiva del parénquima (pinza de Simon)

ObjectiveTo present our initial experience using selective renal parenchymal ischemia, without hilar clamping, in robotic-assisted partial nephrectomy. Material and methodsIn four patients with T1a renal tumor we performed robotic-assisted partial nephrectomy, using the Simon's clamp (Aesculap®). It provides selective parenchymal compression without the need of vascular clamping. All patients had exofitic renal tumors in polar location. Renal parenchymal reconstruction was done as the standard technique. ResultsThe median age was 49.6 years (42-59), 3 male and 1 female patient. Median operative time was 71,6minutes (40-120). Mean stimated bleeding was 250ml (50-400). Average tumor size was 3,25cm (1,5-5,3). There were no complications and the average hospital stay was 3,5 days (1-7). The pathology was informed as renal cell carcinoma in three patients and one hemorrhagic cyst. The surgical margins were negative. ConclusionOur preliminary results shows that selective renal parenchymal compression, with the Simon's clamp, provides an alternative to vascular control in selected patients with polar renal tumors.

Traumatic page kidney induced hypertension in critical care: immediately resolved or long-term resistant problem.

Page kidney is a well-known phenomenon causing hypertension, due to compression of renal parenchyma by a subcapsular hematoma, of either traumatic or non-traumatic origin. The main therapeutic approach is based on surgical approach (nephrectomy or hematoma evacuation) and antihypertensive treatment. In this paper we present a post-traumatic case of Page Kidney in a Critical Care unit. We discuss different therapeutical opportunities to extremely elevated systemic blood pressure resistant to traditional drug therapy.

Hypertension and Hydronephrosis: Rapid Resolution of High Blood Pressure Following Relief of Bilateral Ureteric Obstruction

Hypertension secondary to hydronephrosis is not commonly reported in the medical literature. Tubuloglomerular feedback and the renin-angiotensin-aldosterone axis are thought to mediate this process. We describe a patient presenting with acute kidney injury and bilateral hydronephrosis secondary to pelvic malignancy in which peripheral venous renin and aldosterone were elevated. Her blood pressure improved rapidly following insertion of bilateral nephrostomies. The speed of resolution of hypertension following relief of obstruction suggests that humorally mediated vasoconstriction can play an important role in the mechanism by which hydronephrosis causes hypertension. We also discuss other causes of renal parenchymal compression that may lead to the development of hypertension.

Robotic partial nephrectomy: An initial experience in 25 consecutive cases

ObjectiveTo report our initial experience with robotic partial nephrectomy (RPN) in a series of 25 consecutively operated patients. Material and methodsA series of 25 consecutive patients who underwent RPN from April 2010 to February 2011 were studied. We used the da Vinci S HD robotic system with transperitoneal approach. Total renal hilum control was used for 22 cases and 3 patients underwent selective renal parenchymal compression with an ad hoc device. ResultsMean age was 55.8 years (26–77) with a male/female ratio of 2:1. Mean operative time was 117.6min (54–205) and the warm ischemia time was 20.2min (9–34). Mean estimated blood loss was 440ml (20–2000) and the mean tumor size was 3.25cm (1–5.3). Five patients (20%) had complications, the most frequent being intraoperative bleeding (Clavien II). There was no conversion to open or laparoscopic surgery. Mean hospital stay was 3.5 days (1–7). The pathological study revealed renal cell carcinoma in 19 cases and benign lesions in 6 patients. There were no positive surgical margins and no mortality. ConclusionsOur preliminary results show that RPN is a feasible surgical approach in small-sized renal tumors.

Nefrectomía parcial robótica: experiencia inicial en 25 casos consecutivos

Objective To report our initial experience with robotic partial nephrectomy (RPN) in a series of 25 consecutively-operated patients. Material and methods A series of 25 consecutive patients who underwent RPN from April 2010 to February 2011 were studied. We used the da Vinci S HD robotic system with transperitoneal approach. Total renal hilum control was used 22 cases and 3 patients underwent selective renal parenchymal compression with an ad-hoc device. Results Mean age was 55.8 years (26-77) with a male/female ratio of 2:1. Mean operative time was 117.6 minutes (54-205) and the warm ischemia time was 20.2 minutes (9-34). Mean estimated blood loss was 440 ml (20-2000) and the mean tumor size was 3.25 cm (1-5.3). Five patients (20%) had complications, the most frequent being intraoperative bleeding (Clavien II). There was no conversion to open or laparoscopic surgery. Mean hospital stay was 3.5 days (1-7). The pathological study revealed renal cell carcinoma in 19 cases and benign lesions in 6 patients. There were no positive surgical margins and no mortality. Conclusions Our preliminary results show that RPN is a feasible surgical approach in small-sized renal tumors.

Post-biopsy renal allograft compartment syndrome: Addressing the problem, illustrated with a case report

IntroductionRenal allograft compartment syndrome (RACS) has recently been coined to describe early allograft dysfunction secondary to raised pressure in the retroperitoneal space. This may be caused by direct compression of the renal vessels or by a diffuse renal parenchymal compression. Herein, we report a renal allograft compartment syndrome secondary to a needle core transplant biopsy and discuss the management strategies in line with an updated literature review. Presentation of CaseA retrospective case-note review was carried out where a 45-year-old male had a transplant renal biopsy at 4-weeks after transplant for raising creatinine. Following biopsy patient developed abdominal discomfort and had haematuria. DiscussionDoppler ultrasound scanning of graft demonstrated good perfusion but a small haematoma (2×2×2 cm) in the upper pole of the kidney at the site of the biopsy. Patient was thereafter assessed conservatively with serial ultrasound monitoring. After 24h, significant deterioration of graft function was observed. The third scan, demonstrated reversed flow in diastole in the upper pole of the kidney with a resistive index of 1.0 in the main renal vessel. With the above findings the kidney transplant was explored immediately and the transplant released from a 300ml of liquefied haematoma, which was under considerable pressure. In the next 24-h, the patient showed an immediate return of graft function. ConclusionWe recommend sequential ultrasound Doppler scanning as an invaluable tool to help identify early RACS. The surgical exploration and adequate heamostasis with surgical glue should be sought out in all RACS.

Infarction of middle third posterior cortex of kidney: a complication of extended pyelolithotomy, intra-operative electrohydraulic lithotripsy and extraction of calyceal stones under vision using stone basket and flexible cystoscope in a spinal cord injury patient – a case report

BackgroundSpinal cord injury produces multiple systemic and metabolic alterations. A decrease in micro vascular blood flow to liver, spleen and muscle has been described following spinal cord injury.Case presentationWe present a 46-year-old male patient with C-4 complete tetraplegia, who developed a large stag horn calculus with branches in upper, middle and lower calyces of left kidney. This patient underwent Gil-Vernet extended pyelolithotomy and required intra-operative electrohydraulic lithotripsy and retrieval of stones from upper, middle and lower calyces using flexible cystoscope and stone basket. Computed tomography, performed eighteen days after surgery, showed multiple areas of non-enhancing cortex posteriorly and in the upper pole, suggestive of focal infarction. Magnetic resonance imaging of left kidney confirmed the presence of an area of infarction in middle third of posterior cortex, but there was no evidence of trauma to posterior division of renal artery. Therefore, we postulate that compression of renal parenchyma by Gil-Vernet retractors during surgery, and firm pressure that was applied over the middle of kidney for prolonged periods while several attempts were being made to retrieve fragments of calculi from renal calyces, led to ischaemia and subsequently, infarction of mid-third posterior cortex of left kidney.ConclusionThis case illustrates importance of gentle handling of kidney during extended pyelolithotomy in order to prevent subtle renal trauma, which may be detected only by advanced imaging studies. Further, spinal cord physicians should take a pragmatic approach to management of stones located inside renal calyces. Both spinal cord injury patients and their physicians should remember that in our enthusiasm to achieve complete clearance of stones embedded deeply within renal calyces, we could produce irreversible injury to kidney, as indeed happened in this patient. Therefore, emphasis should be placed on prevention of struvite renal calculi by discarding indwelling urinary catheters and eliminating Proteus bacteriuria.

Subcapsular hematoma evacuation as a method of evaluating injured kidneys for transplant

Approximately one-third of organ donors in the United States are trauma victims. In general, kidneys with large subcapsular hematomas are not used for transplant because of the possibility of significant parenchymal injury. A large subcapsular renal hematoma may cause scarring resulting in renal parenchymal compression and development of the Page syndrome. To elucidate a successful method of evaluating kidneys subject to trauma, while also possibly preventing further damage and improving their function. Data were collected from the donor kidney pool of the New York Organ Donor Network from January 2006 through July 2007. Four kidneys during that period were determined to have significant subcapsular hematomas. Surgical intervention was undertaken and outcomes after transplantation were reviewed. Four of the kidneys underwent a surgical procedure to drain the subcapsular hematoma allowing assessment of the underlying renal parenchyma. All 4 of these kidneys were deemed transplantable. After transplantation, 3 of the 4 kidneys had immediate function and did not require dialysis. The remaining kidney was removed as a result of primary nonfunction. The described surgical intervention allows the transplant surgeon to accurately assess the extent of damage to a traumatized kidney while possibly preventing further damage to the kidney.

Subcapsular Hematoma Evacuation as a Method of Evaluating Injured Kidneys for Transplant

Approximately one-third of organ donors in the United States are trauma victims. In general, kidneys with large subcapsular hematomas are not used for transplant because of the possibility of significant parenchymal injury. A large subcapsular renal hematoma may cause scarring resulting in renal parenchymal compression and development of the Page syndrome. To elucidate a successful method of evaluating kidneys subject to trauma, while also possibly preventing further damage and improving their function. Data were collected from the donor kidney pool of the New York Organ Donor Network from January 2006 through July 2007. Four kidneys during that period were determined to have significant subcapsular hematomas. Surgical intervention was undertaken and outcomes after transplantation were reviewed. Four of the kidneys underwent a surgical procedure to drain the subcapsular hematoma allowing assessment of the underlying renal parenchyma. All 4 of these kidneys were deemed transplantable. After transplantation, 3 of the 4 kidneys had immediate function and did not require dialysis. The remaining kidney was removed as a result of primary nonfunction. The described surgical intervention allows the transplant surgeon to accurately assess the extent of damage to a traumatized kidney while possibly preventing further damage to the kidney.

Erdheim-Chester disease: a rare cause of renal failure

A 52-year-old woman was admitted to our department because of renal failure. She had initially presented at the age of 50, with a thyroid mass requiring hemithyroidectomy. The histological diagnosis of the thyroid mass was that of a pseudo-inflammatory histiocitic tumour. For the next 2 years, the patient had no other problems. One week before admission, the patient noted vomiting and decreased urine volume. On admission, she had elevated blood pressure (180/80mmHg) and serum creatinine was 1060mmol/l (1 year previously, serum creatinine levels were normal). The patient had lower haemoglobin levels (9 g/dl) and hyperkalaemia (serum potassium of 7mmol/l). The rest of the serum biochemical analysis was in the normal range. In spite of a bladder catheter being placed, urine volume was minimal and a haemodialysis session was performed via a femoral catheter. A computed tomography scan (with intravenous medium contrast) was performed and showed bilateral compression of renal parenchyma by retroperitoneal mass (Figure 1). Left mass measured 8 9 13 cm and affected the right kidney, suprarenal gland and spleen. Right kidney showed diffuse infiltration and light hydronephrosis. A biopsy of retroperitoneal mass was performed. The left renal parenchyma was thinned and showed chronic hydronephrosis. Therefore, we decided to perform decompression of the right kidney. Left pyelography showed upper hydronephrosis and a nephrostomy was placed. The patient was free of symptoms and did not require dialysis after the procedure and her serum creatinine level stabilized at around 265mmol/l. Histological examination of the biopsy revealed an accumulation of foamy histiocytes in a background of fibrosis admixed with chronic inflammation (Figure 2). The histiocytic cell population was not immunoreactive for S100, CD21, CD23, CD34, ALK1 and LMP1. These histological findings were similar to the thyroid mass. On the basis of these findings, a diagnosis of Erdheim–Chester disease was made. No other lesions in eyes, long bones, lungs and heart were found in this patient.

Effects of Increased Renal Parenchymal Pressure on Renal Function

Acute renal failure is seen with the acute abdominal compartment syndrome (AACS). The cause of acute renal failure in AACS is thought to be multifactorial, including increased renal venous pressure, renal parenchymal pressure (RPP), and decreased cardiac output. Previous studies have established the role of renal venous pressure as an important mediator of this renal derangement. In this study, we evaluate the role of renal parenchymal compression on renal function. Two groups of swine (20-26 kg) were studied after left nephrectomy and placement of a renal artery flow probe and ureteral cannula. Two hours were allowed for equilibration, and an inulin infusion was begun to calculate inulin clearance as a measurement of glomerular filtration. In group 1 animals (n = 6), RPP was elevated by 30 mm Hg for 2 hours with renal parenchymal compression. RPP then returned to baseline for 1 hour. In group 2 (n = 6), the RPP was not elevated. The cardiac index, preload, and mean arterial pressure remained stable. Blood samples for plasma renin activity and plasma aldosterone were taken at baseline and at hourly intervals. Elevation of RPP in the experimental group showed no significant decrease in renal blood flow index or glomerular filtration when compared with control animals. There were no significant elevations of plasma aldosterone or plasma renin activity in the experimental animals when compared with control. Elevated renal compression alone did not create the pathophysiologic derangements seen in AACS. However, prior data from this laboratory found that renal vein compression alone caused a decreased renal blood flow and glomerular filtration and an increased plasma renin activity, plasma aldosterone, and urinary protein leak. These changes are partially or completely reversed by decreasing renal venous pressure as occurs with abdominal decompression for AACS. These data strengthen the proposal that renal vein compression, and not renal parenchymal compression, is the primary mediator of the renal derangements seen in AACS.

Capsulectomy: A cure for the page kidney

Hypertension is a known complication after renal trauma. The cause of posttraumatic hypertension can be renal scarring, infarction, hydonephrosis, infection, vascular injury, and parenchymal compression. The authors report on the case of a 16-year-old boy who experienced hypertension after blunt renal trauma. He had a dense fibrous pseudocapsule causing renal parenchymal compression, which lead to hypertension, a Page kidney. Evaluation with computed tomographic (CT) scan, radioisotope renal scan, renal Doppler, and angiogram confirmed the diagnosis. Removal of the renal capsule and the constricting fibrous pseudocapsule was curative.

Oliguria during laparoscopic surgery: evidence for direct renal parenchymal compression as an etiologic factor.

Abdominal insufflation during laparoscopy has been associated with transient oliguria, which abates after desufflation. Direct renal compression evoking a Page kidney effect was proposed as a mechanism. In an effort to confirm this theory, the left kidney was subjected to 15 mm Hg compression in six anesthetized mongrel dogs. For this, a pressure cuff was placed around the kidney excluding the renal hilar structures. The contralateral kidney was left untouched to serve as a control. After a steady-state period, the pressure cuff was inflated to 15 mm Hg for 2 hours. Cuff desufflation was followed by a 1-hour recovery period. Urine output, glomerular filtration rate (GFR), and effective renal blood flow (ERBF) were measured for both kidneys during each clearance period. For the treated kidneys, the mean urine output decreased 63% (P < 0.05) during compression and increased 109% (P < 0.05) after cuff desufflation. The GFR decreased 21% (P < 0.01) during compression and increased 25% (P < 0.05) during recovery. The ERBF decreased 26% (P < 0.05) during compression, and during the 1-hour recovery period, ERBF did not recover to baseline values. For the control kidneys, there were no significant changes in urine output or GFR during the experimental and recovery periods. These data support the view that direct renal parenchymal compression is an important factor in the development of insufflation-induced oliguria. The clinical implications of insufflation-induced oliguria during laparoscopy deserve further investigation.

Low-Renin Hypertension After Extracorporeal Shock Wave Lithotripsy

To the Editor.— The process of stone disintegration by extracorporeal shock wave lithotripsy (ESWL) causes multiple hemorrhages in the adjacent renal parenchyma. These hemorrhages may be reabsorbed completely or may heal by scar tissue formation. 1 Such changes cause reduced blood flow to the traumatized kidney in about 25% of patients, detectable immediately 2 and at 18 months 3 after the procedure. As many as 8% of patients may develop a sustained marked increase in blood pressure within a few days to as long as a year after ESWL. 3 Because renal trauma is a well-recognized cause of renovascular hypertension and there may be a long interval between renal injury and the onset of hypertension, it is likely that there is a causal relationship between renal trauma caused by ESWL and the subsequent onset of hypertension. Both the hypertension following compression of renal parenchyma by subcapsular hematoma (Page kidney) and

“Page Kidney”: Hypertension Caused by Chronic Subcapsular Hematoma

• Conditions analogous to an experimental model of hypertension described by in 1939 are called Page kidney. In chronic subcapsular hematoma, the most common clinical counterpart to Page's model of renal parenchymal compression, a review of the literature reveals that hypertension is usually cured by nephrectomy, but is seldom cured by mere evacuation of the hematoma. To our knowledge, no patient remaining hypertensive after evacuation has undergone nephrectomy. In the patient described herein, a liquified subcapsular hematoma reaccumulated after it was drained percutaneously, and therefore it had to be evacuated surgically. Persistent renin-mediated hypertension, however, prompted curative nephrectomy. The response to more prolonged percutaneous drainage might have guided more effective initial surgery. (Arch Intern Med1985;145:169-171)

'Page Kidney'

• Conditions analogous to an experimental model of hypertension described by Page in 1939 are called "Page kidney." In chronic subcapsular hematoma, the most common clinical counterpart to Page's model of renal parenchymal compression, a review of the literature reveals that hypertension is usually cured by nephrectomy, but is seldom cured by mere evacuation of the hematoma. To our knowledge, no patient remaining hypertensive after evacuation has undergone nephrectomy. In the patient described herein, a liquified subcapsular hematoma reaccumulated after it was drained percutaneously, and therefore it had to be evacuated surgically. Persistent renin-mediated hypertension, however, prompted curative nephrectomy. The response to more prolonged percutaneous drainage might have guided more effective initial surgery. (<i>Arch Intern Med</i>1985;145:169-171)

High renin hypertension associated with renal cortical cyst

A fifty-seven-year-old patient with a five to one elevation of right renal vein plasma renin activity associated with a large, simple cortical cyst of the right lower pole is presented. Marsupialization of the cyst was associated with improvement in the patient's hypertension and the finding of bilaterally equal renal vein renin activity three months postoperatively. Possible mechanisms for hypertension are discussed in context of the experimental models of Goldblatt and Page in such lesions as cortical cysts of large size causing hydronephrosis, vascular stretching, or renal parenchymal compression.

Hydronephrosis and polycythemia: A case of erythrocytosis relieved by decompression of unilateral hydronephrosis and cured by nephrectomy

A case of erythrocytosis relieved by decompression and drainage of unilateral hydronephrosis and cured by nephrectomy is reported. The remission, which was complete within the twenty-five days comprising the drainage and postnephrectomy periods, was chiefly due to depression of erythropoiesis. The characteristics and rate of remission of erythrocytosis during drainage and postnephrectomy periods were similar, suggesting that both caused withdrawal of an excessive stimulus to erythropoiesis. Since erythropoietin or its precursor may originate in the kidney, the compression of renal parenchyma by hydronephrosis and decompression by drainage could have influenced the production of erythropoietin by the affected kidney. The high incidence of congenital anomalies of the urinary tract in cases of non-neoplastic renal disease associated with erythrocytosis suggests that both a congenital anomaly and an intrarenal space-occupying lesion may be necessary for renal erythrocytosis to develop.