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Extracorporeal CO2 removal.

The extracorporeal carbon dioxide removal (ECCO(2)R) concept, used as an integrated tool with conventional ventilation, plays a role in adjusting respiratory acidosis consequent to tidal volume (Vt) reduction in a protective ventilation setting. This concept arises from the extracorporeal membrane oxygenation (ECMO) experience. Kolobow and Gattinoni were the first to introduce extracorporeal support, with the intent to separate carbon dioxide removal from oxygen uptake; they hypothesized that to allow the lung to 'rest' oxygenation via mechanical ventilation could be dissociated from decarboxy

Blood purification in fulminant hepatic failure.

Fulminant hepatic failure (FHF) can be described as a potentially fatal condition presenting with hepatic encephalopathy (HE) and coagulopathy associated with acute hepatic dysfunction, regardless of its etiology. Blood purification (BP) is expected to be effective against HE and coagulopathy in FHF. In this paper, we outline the objectives and methods of BP in the treatments of cases with FHF and indicate a concrete method for and outcomes of BP at our facility. In high-flow dialysate continuous hemodiafiltration (HFCHDF), the conventional CHDF bedside console is connected to a personal dialy

Renal acidification responses to respiratory acid-base disorders.

Respiratory acid-base disorders are those abnormalities in acid-base equilibrium that are expressed as primary changes in the arterial carbon dioxide tension (PaCO2). An increase in PaCO2 (hypercapnia) acidifies body fluids and initiates the acid-base disturbance known as respiratory acidosis. By contrast, a decrease in PaCO2 (hypocapnia) alkalinizes body fluids and initiates the acid-base disturbance known as respiratory alkalosis. The impact on systemic acidity of these primary changes in PaCO2 is ameliorated by secondary, directional changes in plasma [HCO3¯] that occur in 2 stages. Acutely

How to manage cardiorenal syndromes in the emergency room.

In the emergency department (ED) a prompt diagnosis and appropriate treatment for all diseases improve a patient's outcome. Acute kidney injury (AKI) is defined as an abrupt deficiency of renal function over a period of hours to days resulting in a failure of the kidney to excrete nitrogenous waste products and to maintain fluid and electrolyte homeostasis. AKI diagnosis could be very challenging for ED physicians because it is often very difficult to obtain some anamnestic data such as daily urine output or a preexisting value of BUN and serum creatinine. The incidence of AKI is progressively

Familial renal tubular acidosis.

The kidney maintains systemic acid-base homeostasis through proximal tubular reclamation of filtered bicarbonate, and excretion of the daily mineral acid load by collecting duct type A intercalated cells. Impairment of either process produces renal tubular acidosis (RTA). This article will provide an overview of familial forms of proximal and distal renal tubular acidosis (pRTA and dRTA). Recessive pRTA with ocular and central nervous system abnormalities is caused by loss-of-function mutations in basolateral membrane Na-HCO3- cotransporter NBCe1/ SLC4A4. Recessive dRTA with deafness is caused

Fracture Risk Assessment in Chronic Kidney Disease, Prospective Testing Under Real World Environments (FRACTURE): a prospective study.

BACKGROUND: Chronic kidney disease (CKD) is associated with an increased risk of fracture. Decreased bone mass and disruption of microarchitecture occur early in the course of CKD and worsens with the progressive decline in renal function so that at the time of initiation of dialysis at least 50% of patients have had a fracture. Despite the excess fracture risk, and the associated increases in morbidity and mortality, little is known about the factors that are associated with an increase in fracture risk. Our study aims to identify prognostic factors for bone loss and fractures in patients wit

Bilateral renal vein thrombosis and subsequent acute renal failure due to IVC filter migration and thrombosis.

A 53-year-old man developed a deep venous thrombus (DVT) and pulmonary embolism (PE) shortly after an open Roux-en-Y gastric bypass was performed. He later suffered a life-threatening gastrointestinal bleed while on anticoagulation for the DVT. Thus, anticoagulation was held and an inferior vena cava (IVC) filter (G2, Bard Inc., Tempe, AZ, USA) was placed for PE prophylaxis. About 10 days after filter placement, he presented with severe low back pain and syncope. He also presented with hypotension and anuria unresponsive to intravenous fluids. A STAT non-contrast CT scan of the abdomen reveale

Genetics and genetic testing in hemolytic uremic syndrome/thrombotic thrombocytopenic purpura.

The hemolytic uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP) are rare diseases that manifest with thrombocytopenia and microangiopathic hemolytic anemia accompanied by renal and neurologic dysfunction. Most childhood cases of HUS are caused by Shiga-toxin-producing bacteria and have a good prognosis. The other form, atypical HUS (aHUS), accounts for 10% of cases. Prognosis of aHUS and TTP has changed over time from fatal disorders to 60% to 80% survival in the plasma therapy era. In the past 10 years the molecular bases of aHUS and TTP have been discovered that mostly lead

SGK, renal function and hypertension.

Serum- and glucocorticoid-inducible kinase 1 (SGK1) is expressed following cell stress and exposure to a variety of hormones including glucocorticoids and mineralocorticoids. It is activated by insulin and growth factors via phosphatidylinositol-3-kinase and the 3-phosphoinositide-dependent kinase PDK1. SGK1 enhances the activity of a variety of ion channels such as ENaC, TRPV5, ROMK, KCNE1/KCNQ1 and ClCKb; carriers such as NHE3, NKCC2, NCC and SGLT1; as well as the Na+/K+-ATPase. SGK1 contributes to Na+ retention and K+ elimination of the kidney as well as mineralocorticoid stimulation of sal

Cardiorenal syndrome - a new classification and current evidence on its management.

Patients with chronic kidney disease (CKD) are at high risk for major cardiovascular (CV) morbidity and mortality, especially when they range among the elderly. The co-existence of renal dysfunction is common in patients with chronic heart failure (CHF), and renal failure is among the strongest predictors of mortality in patients with heart failure. Approximately one-third of dialysis patients also suffer from heart failure. The term "cardiorenal syndrome" has been increasingly described in recent literature, as there is growing recognition of the frequent association of combined renal and car

Different cardiovascular responses to hemodialysis-induced fluid depletion and blood pressure compliance.

BACKGROUND: On the basis of cardiovascular compliance, hemodialysis (HD) patients can be classified as hypotension prone (HP) or hypotension resistant (HR). METHODS: We compare the hemodynamic behavior and myocardial performances in 6 HP and 6 HR patients before and after an isolated ultrafiltration (IU) session removing 3% of total body water. RESULTS: HP show higher basal plasma angiotensin II levels during IU (p<0.01), whereas angiotensin II remained unchanged in HR patients (p<0.001 between groups). The percentage changes of plasma volume (PV) was similar in the 2 groups. A significant r

Use of loop diuretics in the critically ill.

Diuretics are commonly used in the intensive care unit, especially for patients with oliguric acute kidney injury. This practice is controversial since there is a lack of evidence regarding any beneficial effects of diuretics either on prevention or treatment of acute kidney injury. Some data even suggest harm when diuretics are used with the goal to influence renal function. However, diuretics can minimize fluid overload, making patient management easier and potentially avoiding many cardiopulmonary and non-cardiopulmonary complications. We will briefly review the available evidence for and a

Diuretic therapy in fluid-overloaded and heart failure patients.

Diuretics are the most commonly used drugs to treat clinically diagnosed fluid overload in patients with heart failure. There is no conclusive evidence that they alter major outcomes such as survival to hospital discharge or time in hospital compared to other therapies. However, they demonstrably achieve fluid removal in the majority of patients, restore dry body weight, improve the breathlessness of pulmonary edema and are unlikely to be subjected to a large double-blind randomized controlled trial in this setting because of lack of equipoise. The effective and safe use of diuretics requires

Extracorporeal fluid removal in heart failure patients.

More than one million hospitalizations occur annually in the US because of heart failure (HF) decompensation caused by fluid overload. Congestion contributes to HF progression and mortality. Apart from intrinsic renal insufficiency, venous congestion, rather than a reduced cardiac output, may be the primary hemodynamic factor driving worsening renal function in patients with acutely decompensated HF. According to data from large national registries, approximately 40% of hospitalized HF patients are discharged with unresolved congestion, which may contribute to unacceptably high rehospitalizati

Biopsy proven acute interstitial nephritis after treatment with moxifloxacin.

BACKGROUND: Acute interstitial nephritis (AIN) is an important cause of reversible acute kidney injury. At least 70% of AIN is caused by various drugs, mainly penicillins and non-steroidal anti-inflammatory drugs. Quinolones are only rarely known to cause AIN and so far cases have been mainly described with older fluoroquinolones. CASE PRESENTATION: Here we describe a case of biopsy proven interstitial nephritis after moxifloxacin treatment. The patient presented with fever, rigors and dialysis dependent acute kidney injury, just a few days after treatment of a respiratory tract infection wit

Gene polymorphisms in renal transplantation.

A vast majority of gene polymorphism studies in renal transplantation focus on short-term outcomes such as acute rejection. The main purpose of this article is to review the literature available and studies that have examined the association between the gene polymorphisms and long-term renal allograft functions. In this review, we focus on commonly reported genes in the renin angiotensin system, transforming growth factor-beta gene, and metalloproteinases on the incidence and progression of chronic renal allograft dysfunction.

The assessment, serial evaluation, and subsequent sequelae of acute kidney injury (ASSESS-AKI) study: design and methods.

BACKGROUND: The incidence of acute kidney injury (AKI) has been increasing over time and is associated with a high risk of short-term death. Previous studies on hospital-acquired AKI have important methodological limitations, especially their retrospective study designs and limited ability to control for potential confounding factors. METHODS: The Assessment, Serial Evaluation, and Subsequent Sequelae of Acute Kidney Injury (ASSESS-AKI) Study was established to examine how a hospitalized episode of AKI independently affects the risk of chronic kidney disease development and progression, cardi

Совпадение в полном тексте источника
… In 2005, the American Society of Nephrology Renal Research Report listed as a "critically important knowledge gap" studies addressing "long-term outcomes" after an episode of AKI [ 1 ]. … Kimmel, MD (Project Officer) Paul Eggers, PhD (Project Officer) References American Society of Nephrology Renal Research Report. J Am Soc Nephrol. 2005;16(7):1886–1903. doi: 10.1681/ASN.2005030285. Waikar SS, Curhan GC, Wald R, McCarthy EP, Chertow GM. …

The changing pattern of acute kidney injury: from one to multiple organ failure.

Acute kidney injury (AKI) is frequently encountered in the intensive care unit, and from its inception, morbidity and mortality increase in these patients compared to those without AKI. Despite numerous clinical trials and newer pharmacological agents, very little progress has been made to reduce the deaths that occur in this population. An important emerging concept is that AKI does not occur in isolation and it frequently involves other organs. Clinical conditions such as shock, trauma, and sepsis lead to an increase in fluid volume, cytokines/chemokines, uremic toxins and other soluble medi

Arterial dissections in autosomal dominant polycystic kidney disease - chance association or part of the disease spectrum?

Autosomal dominant polycystic kidney disease (ADPKD) has been associated with a number of vascular abnormalities of which the most widely known is intracranial aneurysm (Berry aneurysm). Arterial dissections involving both the thoracic and abdominal aorta, coronary, cervical and vertebral arteries have been anecdotally reported usually within the context of a medical emergency. As hypertension is a frequent early accompaniment of ADPKD (50 - 70% of nonazotemic patients) the occurrence of these dissections has commonly been attributed to hypertension. However, the question arises whether ADPKD

Association between routine and standardized blood pressure measurements and left ventricular hypertrophy among patients on hemodialysis.

BACKGROUND: Left ventricular (LV) hypertrophy is common among patients on hemodialysis. While a relationship between blood pressure (BP) and LV hypertrophy has been established, it is unclear which BP measurement method is the strongest correlate of LV hypertrophy. We sought to determine agreement between various blood pressure measurement methods, as well as identify which method was the strongest correlate of LV hypertrophy among patients on hemodialysis. METHODS: This was a post-hoc analysis of data from a randomized controlled trial. We evaluated the agreement between seven BP measurement