Effect of Increased Renal Venous Pressure on Renal Function

Doty, James M.; Saggi, Bob H.; Sugerman, Harvey J.; Blocher, Charles R.; Pin, Richard Jong A; Fakhry, Itaf; Gehr, Todd W.B.; Sica, Domenic A.

doi:10.1097/00005373-199912000-00002

Cited by 228 publications

(96 citation statements)

References 13 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packed with cotton until an intra-abdominal pressure (IAP) of 15 mm Hg was reached; 2) hypovolemia (HYPO): blood was withdrawn until a mean arterial pressure ~60 mm Hg was reached; 3) IAH + HYPO (to resemble clinical ACS); and 4) sham surgery.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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“…Increased intra-abdominal pressure from visceral fat, a common occurrence in morbidly obese individuals (140 -142), may cause renal vein compression and may therefore raise renal venous pressure and diminish renal perfusion (143). In addition, raised intra-abdominal pressure may cause increased inferior vena cava pressure, and this may impair venous outflow from the renal veins (144).…”

Section: Other Potential Hemodynamic Factorsmentioning

confidence: 99%

Obesity and Obesity-Initiated Metabolic Syndrome

Wahba

Mak

2007

Clinical Journal of the American Society of Nephrology

460

343

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There is an epidemic of obesity and the metabolic syndrome in the United States and across the world. Both entities are associated with high mortality, mainly as a result of cardiovascular disease. The epidemic of obesity has been paralleled by an increase in the incidence of chronic kidney disease (CKD). Several recent epidemiologic studies have shown that obesity and the metabolic syndrome are independent predictors of CKD. In addition to diabetes and hypertension, several other mechanisms have been postulated to initiate and maintain kidney injury in patients with obesity and the metabolic syndrome. This article reviews the recent epidemiologic data linking obesity and the metabolic syndrome to CKD and summarizes the potential mechanisms of renal injury in this setting, with a focus on the role of inflammation, lipotoxicity, and hemodynamic factors. Potential preventive and therapeutic modalities based on the limited evidence available are discussed.Clin , and the increase occurred for both men and women and for all age groups (2). Since then, the trend for increased prevalence has continued, particularly for adolescents and men (1). Obesity is also on the rise in other industrialized countries (3-5). The metabolic syndrome, previously known as syndrome X and a major consequence of obesity, is also on the rise (6). According to the Third National Health and Nutrition Examination Survey (NHANES III), the prevalence of the metabolic syndrome in the United States is 23% in those who are 20 yr or older and Ͼ40% in those who are 60 yr or older (7). According to the Third Adult Treatment Panel of the National Cholesterol Education Program, the metabolic syndrome is defined as the presence of at least three of the following criteria, with or without diabetes: Central obesity (waist circumference in men Ͼ102 cm and in women Ͼ88 cm), hypertriglyceridemia (Ն150 mg/dl), low HDL cholesterol (men Ͻ40 mg/dl, women Ͻ50 mg/dl), elevated fasting glucose (Ͼ110 mg/dl), and hypertension (Ն130/85 mmHg) (8). A central feature of the metabolic syndrome is insulin resistance, which results in hyperglycemia and hyperinsulinemia, and eventually leads to the development of diabetes (9). Central obesity is the most important predisposing factor for insulin resistance (9). Chronic inflammation is another feature of the metabolic syndrome, which, together with insulin resistance, results in complex metabolic derangements that contribute to the pathogenesis of hypertension, lipoprotein abnormalities, atherosclerosis, coronary artery disease, and other organ dysfunction (10,11). Both obesity and the metabolic syndrome are associated with high mortality, mainly related to cardiovascular disease (12,13). Overweight, obesity, and the metabolic syndrome have recently emerged as strong independent risk factors for chronic kidney disease (CKD) and ESRD. This article reviews the epidemiology of CKD in relationship to obesity and the metabolic syndrome and the possible mechanisms of renal injury that is caused by obesity and obesity-initiated metab...

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“…It indicated that the high renin activity was corrected with NCP. Some investigators have suggested that elevated renal pressures (venous and interstitial) reduce glomerular filtration, affect intrarenal blood flow, and stimulate release of renin [11]. With reduced glomerular filtration, there is reduction of sodium delivery to the macula densa, which triggers renin secretion from the juxtaglomerular cells.…”

Section: Discussionmentioning

confidence: 99%

An Incidental Detection of Nutcracker Phenomenon in an Adolescent with Transient High Blood Pressure: A Case Report

Min¹,

Chen²,

Wang³

et al. 2016

CRCM

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Nutcracker phenomenon (NCP) is caused by a compression of left renal vein between aorta and superior mesenteric artery. The traditional clinical manifestations of nutcracker syndrome is usually accompanied with abdominal pain, hematuria, orthostatic proteinuria, and varicocele formation, however, hypertension is rarely reported as main clinical feature. We describe a male adolescent with manifestation of hypertension who was identified as NCP. Renal ultrasound and computed tomography angiography have provided evidences of left renal vein dilatation, probably due to the compression through the decreased angle between aorta and superior mesenteric artery. There were no other signs for secondary hypertension for the blood levels of renin and aldosterone being between normal limits and urinalysis being negative of hematuria and proteinuria. This patient was conservatively observed without any anti-hypertensive drugs and was asked for appropriately putting on weight. Three months later, the hypertension symptom was alleviated. In conclusion, although there were no established direct pathogenetic links between hypertension and NCP, no other definite etiology was shown to be the cause of this main manifestation. Thus we speculate that the NCP might be the main cause of hypertension in this patient.

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Effect of Increased Renal Venous Pressure on Renal Function

Cited by 228 publications

References 13 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

Obesity and Obesity-Initiated Metabolic Syndrome

An Incidental Detection of Nutcracker Phenomenon in an Adolescent with Transient High Blood Pressure: A Case Report

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