Elevated Intra-abdominal Pressure Increases Plasma Renin Activity and Aldosterone Levels

Bloomfield, Geoffrey L.; Blocher, Charles R.; Fakhry, Itaf; Sica, Domenic A.; Sugerman, Harvey J.

doi:10.1097/00005373-199706000-00002

Cited by 186 publications

(105 citation statements)

References 40 publications

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“…Our results are in line with the previous literature reporting renal [19][20][21][22] and hepatic [21] dysfunction (Tables 1, 2, Figs 1, 2). Toens et al [23] used a porcine model with IAP ~30 mm Hg for 24 h, induced by CO 2 insufflation, and observed necrosis in the central vein of the liver, as well as tubular and glomerular necrosis.…”

Section: Impact Of Intra-abdominal Hypertension On the Liver Kidneyssupporting

confidence: 93%

Early impact of abdominal compartment syndrome on liver, kidney and lung damage in a rodent model

Lima¹,

Silva²,

Capelozzi³

et al. 2017

Anaesthesiol Intensive Ther

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Background: Abdominal compartment syndrome (ACS) sometimes occurs in critically ill patients following damage control surgery. The purpose of the present study was to develop a model of ACS and to evaluate its pathologic impact on liver, kidney, and lung morphology. Methods: Twenty Wistar rats (mass 300-350 g) were randomly divided into four groups: 1) intra-abdominal hypertension (IAH): a laparotomy was performed and the abdomen packed with cotton until an intra-abdominal pressure (IAP) of 15 mm Hg was reached; 2) hypovolemia (HYPO): blood was withdrawn until a mean arterial pressure ~60 mm Hg was reached; 3) IAH + HYPO (to resemble clinical ACS); and 4) sham surgery. After 3 hours of protective mechanical ventilation, the animals were euthanized and the liver, kidney and lungs removed to examine the degree of tissue damage. Results: IAH resulted in the following: oedema and neutrophil infiltration in the kidney; necrosis, congestion, and microsteatosis in the liver; and alveolar collapse, haemorrhage, interstitial oedema, and neutrophil infiltration in the lungs. Furthermore, IAH was associated with greater cell apoptosis in the kidney, liver and lungs compared to sham surgery. HYPO led to oedema and neutrophil infiltration in the kidney. The combination of IAH and HYPO resulted in all the aforementioned changes in lung, kidney and liver tissue, as well as exacerbation of the inflammatory process in the kidney and liver and kidney cell necrosis and apoptosis. Conclusions: Intra-abdominal hypertension by itself is associated with kidney, liver and lung damage; when combined with hypovolemia, it leads to further impairment and organ damage.

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Section: Impact Of Intra-abdominal Hypertension On the Liver Kidneyssupporting

confidence: 93%

Early impact of abdominal compartment syndrome on liver, kidney and lung damage in a rodent model

Lima¹,

Silva²,

Capelozzi³

et al. 2017

Anaesthesiol Intensive Ther

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“…9 To summarize, it is presumed that an increase in renal venous pressure and/or renal capsular pressure and/or a decrease in cardiac output, secondary to decreased venous return from an increased pleural pressure, individually or together lead to activation of the renin-angiotensin-aldosterone system with increased sodium and water reabsorption and vasoconstriction. 39,40 Despite the compensated state with¯uid retention and an increased cardiac output, patients with central obesity and hypertension have a decreased effective renal blood and plasma¯ow, 41 a phenomenon which is probably due to increased renal venous pressure and decreased renal perfusion. The increased pleural pressure impedes venous return from the brain, leading to an increased intracranial pressure.…”

Section: Discussionmentioning

confidence: 99%

Effects of surgically induced weight loss on urinary bladder pressure, sagittal abdominal diameter and obesity co-morbidity

et al. 1998

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OBJECTIVE: Evaluate the effects of surgically induced weight loss on intra-abdominal pressure at one year, re¯ected in urinary bladder pressure, central obesity, measured by sagittal abdominal diameter and obesity co-morbidity. DESIGN: Prospective, non-randomized trial. SETTING: University Hospital, Operating Room, In-patient, Outpatient Clinics. SUBJECTS: Gastric bypass in 15 severely obese patients. MEASUREMENTS: Patients underwent pre-operative assessment of weight, body mass index (BMI), co-morbid history, urinary bladder pressure and sagittal abdominal diameter. Patients were reassessed one year after gastric bypass with repeat measurement of weight, bladder pressure, and sagittal abdominal diameter and assessment of co-morbidity. RESULTS: There were signi®cant (P`0.001) decreases in weight (140 AE 8±87 AE 6 kg), BMI (52 AE 3±33 AE 2 kg/m 2 ), sagittal abdominal diameter (32 AE 1±20 AE 2 cm), urinary bladder pressure (17 AE 2±10 AE 1 cm H 2 O) and obesity related problems per patient (2.9 AE 0.4±1 AE 0.2) one year after gastric bypass, with 69 AE 4% loss of excess weight. CONCLUSIONS: Increased sagittal abdominal diameter is associated with increased intra-abdominal pressure which contributes to obesity related co-morbidity. Weight loss following gastric bypass decreases abdominal pressure, sagittal abdominal diameter and obesity co-morbidity.

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“…Further, decreased urine output and glomerular filtration are not only altered during SAP with IAH. IAH also affects plasma renin activity (PRA) and aldosterone (ALDO) levels 31 . Direct renal compression and renal venous hypertension increases renal vascular resistance by obstructing renal venous outflow and has been associated with renal dysfunction and significant increase in PRA and ALDO levels 31 .…”

Section: Pathophysiologymentioning

confidence: 99%

“…IAH also affects plasma renin activity (PRA) and aldosterone (ALDO) levels 31 . Direct renal compression and renal venous hypertension increases renal vascular resistance by obstructing renal venous outflow and has been associated with renal dysfunction and significant increase in PRA and ALDO levels 31 . Urinary sodium and chloride concentrations decreased significantly with elevated IAP and returned to normal with abdominal decompression 32 .…”

Section: Pathophysiologymentioning

confidence: 99%

Acute kidney injury following acute pancreatitis: A review

Petejová¹,

Martínek²

2013

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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Backround. Acute kidney injury (AKI) is a common serious complication of severe acute pancreatitis (SAP) and an important marker of morbidity and mortality in critically ill septic patients. AKI due to severe acute pancreatitis can be the result of hypoxemia, release of pancreatic amylase from the injured pancreas with impairment of renal microcirculation, decrease in renal perfusion pressure due to abdominal compartment syndrome, intraabdominal hypertension or hypovolemia. Endotoxins and reactive oxygen species (ROS) also play an important role in the pathophysiology of SAP and AKI. Knowledge of the pathophysiology and diagnosis of AKI following SAP might improve the therapeutic outcome of critically ill patients. Methods and Results. An overview of the pathophysiology, diagnosis and potential treatment options based on a literature search of clinical human and experimental studies from 1987 to 2013. Conclusions. Early recognition of AKI and SAP in order to prevent severe complication like septic shock, intraabdominal hypertension or abdominal compartment syndrome leading to multiple organ dysfunction syndrome is a crucial tool of therapeutic measures in intensive care.

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Elevated Intra-abdominal Pressure Increases Plasma Renin Activity and Aldosterone Levels

Cited by 186 publications

References 40 publications

Early impact of abdominal compartment syndrome on liver, kidney and lung damage in a rodent model

Early impact of abdominal compartment syndrome on liver, kidney and lung damage in a rodent model

Effects of surgically induced weight loss on urinary bladder pressure, sagittal abdominal diameter and obesity co-morbidity

Acute kidney injury following acute pancreatitis: A review

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