Acute kidney injury (AKI) is a complex disorder for which currently there is no accepted definition. Having a uniform standard for diagnosing and classifying AKI would enhance our ability to manage these patients. Future clinical and translational research in AKI will require collaborative networks of investigators drawn from various disciplines, dissemination of information via multidisciplinary joint conferences and publications, and improved translation of knowledge from pre-clinical research. We describe an initiative to develop uniform standards for defining and classifying AKI and to establish a forum for multidisciplinary interaction to improve care for patients with or at risk for AKI. Members representing key societies in critical care and nephrology along with additional experts in adult and pediatric AKI participated in a two day conference in Amsterdam, The Netherlands, in September 2005 and were assigned to one of three workgroups. Each group's discussions formed the basis for draft recommendations that were later refined and improved during discussion with the larger group. Dissenting opinions were also noted. The final draft recommendations were circulated to all participants and subsequently agreed upon as the consensus recommendations for this report. Participating societies endorsed the recommendations and agreed to help disseminate the results. The term AKI is proposed to represent the entire spectrum of acute renal failure. Diagnostic criteria for AKI are proposed based on acute alterations in serum creatinine or urine output. A staging system for AKI which reflects quantitative changes in serum creatinine and urine output has been developed. We describe the formation of a multidisciplinary collaborative network focused on AKI. We have proposed uniform standards for diagnosing and classifying AKI which will need to be validated in future studies. The Acute Kidney Injury Network offers a mechanism for proceeding with efforts to improve patient outcomes.

Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury

Systemic lupus erythematosus (SLE) is an autoimmune inflammatory disease characterized by the presence of a plethora of autoantibodies and immune complex formation. Virtually every system and organ can be affected by SLE. Gastrointestinal symptoms are common in SLE patients, and more than half of them are caused by adverse reactions to medications and viral or bacterial infections. Though not as common as lupus nephritis, SLE-related gastrointestinal involvement is clinically important because most cases can be life-threatening if not treated promptly. Lupus mesenteric vasculitis is the most common cause, followed by protein-losing enteropathy, intestinal pseudo-obstruction, acute pancreatitis and other rare complications such as celiac disease, inflammatory bowel diseases, etc. No specific autoantibody is identified as being associated with SLE-related gastroenteropathy. Imaging studies, particularly abdominal computed tomography scans, are helpful in diagnosing some SLE-related gastroenteropathies. Most of these complications have good therapeutic responses to corticosteroids and immunosuppressive agents. Supportive measures such as bowel rest, nutritional support, antibiotics and prokinetic medications are helpful in facilitating functional recovery and improving the outcome.

Gastrointestinal involvement in systemic lupus erythematosus: Insight into pathogenesis, diagnosis and treatment

Background—Among the many adipocyte-derived endocrine factors, we recently found an adipocyte-specific secretory protein, adiponectin, which was decreased in obesity. Although obesity is associated with increased cardiovascular mortality and morbidity, the molecular basis for the link between obesity and vascular disease has not been fully clarified. The present study investigated whether adiponectin could modulate endothelial function and relate to coronary disease. Methods and Results—For the in vitro study, human aortic endothelial cells (HAECs) were preincubated for 18 hours with the indicated amount of adiponectin, then exposed to tumor necrosis factor-α (TNF-α) (10 U/mL) or vehicle for the times indicated. The adhesion of human monocytic cell line THP-1 cells to HAECs was determined by adhesion assay. The surface expression of vascular cell adhesion molecule-1 (VCAM-1), endothelial-leukocyte adhesion molecule-1 (E-selectin), and intracellular adhesion molecule-1 (ICAM-1) was measured by cell ELISA. ...

Novel Modulator for Endothelial Adhesion Molecules

Adverse Effects of the Metabolic Acidosis of Chronic Kidney Disease

Patients with cancer represent a growing group among actual ICU admissions (up to 20 %). Due to their increased susceptibility to infectious and noninfectious complications related to the underlying cancer itself or its treatment, these patients frequently develop acute kidney injury (AKI). A wide variety of definitions for AKI are still used in the cancer literature, despite existing guidelines on definitions and staging of AKI. Alternative diagnostic investigations such as Cystatin C and urinary biomarkers are discussed briefly. This review summarizes the literature between 2010 and 2015 on epidemiology and prognosis of AKI in this population. Overall, the causes of AKI in the setting of malignancy are similar to those in other clinical settings, including preexisting chronic kidney disease. In addition, nephrotoxicity induced by the anticancer treatments including the more recently introduced targeted therapies is increasingly observed. However, data are sometimes difficult to interpret because they are often presented from the oncological rather than from the nephrological point of view. Because the development of the acute tumor lysis syndrome is one of the major causes of AKI in patients with a high tumor burden or a high cell turnover, the diagnosis, risk factors, and preventive measures of the syndrome will be discussed. Finally, we will briefly discuss renal replacement therapy modalities and the emergence of chronic kidney disease in the growing subgroup of critically ill post-AKI survivors.

https://biblio.ugent.be/publication/8086011/file/8086013.pdf

Acute kidney injury in critically ill cancer patients: an update.

Acute kidney injury (AKI) is associated with extended hospital stays, high risks of in-hospital and long-term mortality, and increased risk of incident and progressive chronic kidney disease. Patients with urological diseases are a high-risk group for AKI owing to the coexistence of obstructive uropathy, older age, and preexistent chronic kidney disease. Nonetheless, precise data on the incidence and outcomes of postoperative AKI in urological procedures are lacking. Benign prostatic hyperplasia and prostate cancer are common diagnoses in older men and are frequently treated with surgical procedures. Whereas severe AKI after prostate surgery in general appears to be unusual, AKI associated with transurethral resection of the prostate (TURP) syndrome and with rhabdomyolysis (RM) after radical prostatectomy have been frequently described. The purpose of this review is to discuss the current knowledge regarding the epidemiology, risk factors, outcomes, prevention, and treatment of AKI associated with prostatic surgery. The mechanisms of TURP syndrome and RM following prostatic surgeries will be emphasized.

Prostatic surgery associated acute kidney injury

/pdf/protein-losing-gastroenteropathy-in-a-patient-with-systemic-1tjo4meavm.pdf

Protein-losing gastroenteropathy in a patient with systemic lupus erythematosus and antiphospholipid antibody syndrome simulating nephrotic syndrome

Background 
Data on renal replacement therapy (RRT) in cancer patients with acute kidney injury (AKI) in the intensive care unit (ICU) is scarce. The aim of this study was to assess the safety and the adequacy of intermittent hemodialysis (IHD) in critically ill cancer patients with AKI.


Methods and Findings 
In this observational prospective cohort study, 149 ICU cancer patients with AKI were treated with 448 single-pass batch IHD procedures and evaluated from June 2010 to June 2012. Primary outcomes were IHD complications (hypotension and clotting) and adequacy. A multiple logistic regression was performed in order to identify factors associated with IHD complications (hypotension and clotting). Patients were 62.2 ± 14.3 years old, 86.6% had a solid cancer, sepsis was the main AKI cause (51%) and in-hospital mortality was 59.7%. RRT session time was 240 (180–300) min, blood/dialysate flow was 250 (200–300) mL/min and UF was 1000 (0–2000) ml. Hypotension occurred in 25% of the sessions. Independent risk factors (RF) for hypotension were dialysate conductivity (each ms/cm, OR 0.81, CI 0.69–0.95), initial mean arterial pressure (each 10 mmHg, OR 0.49, CI 0.40–0.61) and SOFA score (OR 1.16, CI 1.03–1.30). Clotting and malfunctioning catheters (MC) occurred in 23.8% and 29.2% of the procedures, respectively. Independent RF for clotting were heparin use (OR 0.57, CI 0.33–0.99), MC (OR 3.59, CI 2.24–5.77) and RRT system pressure increase over 25% (OR 2.15, CI 1.61–4.17). Post RRT blood tests were urea 71 (49–104) mg/dL, creatinine 2.71 (2.10–3.8) mg/dL, bicarbonate 24.1 (22.5–25.5) mEq/L and K 3.8 (3.5–4.1) mEq/L.


Conclusion 
IHD for critically ill patients with cancer and AKI offered acceptable hemodynamic stability and provided adequate metabolic control.

/pdf/evaluation-of-intermittent-hemodialysis-in-critically-ill-2td24c1l0e.pdf

Evaluation of Intermittent Hemodialysis in Critically Ill Cancer Patients with Acute Kidney Injury Using Single-Pass Batch Equipment.

Hyperleptinemia and metabolic acidosis (MA) are frequently observed in patients on hemodialysis (HD) While the role of leptin in patients on HD is not completely understood, HD only partially corrects MA Both leptin and acidosis have effect on bone disease The goal of the present study was to evaluate the effects of MA correction on chronic kidney disease–mineral and bone disorder laboratory parameters and leptin levels Forty-eight patients on HD, aged 43 ± 19 years, were prospectively studied Individual adjustments in the bicarbonate dialysate concentration were made to maintain pre-dialysis concentration ≥22 mEq/l Blood gas analysis was done monthly for 4 months (M1–M4) From M0 to M4, serum albumin increased (from 35 ± 03 to 40 ± 03 g/l, p < 00001) while β2 microglobulin decreased (from 276 ± 83 to 258 ± 68 µg/ml, p = 0025) Serum leptin decreased in all but three patients, as well as leptin/adiponectin ratio (p < 00001) There was a decrease in ionized serum calcium (from 50 ± 05 to 47 ± 05 mg/dl, p = 0002) and an increase in parathyroid hormone (PTH) [from 191 (85, 459) to 446 pg/ml (212, 983), p < 00001] and in serum phosphate (from 54 ± 14 to 58 ± 11 mg/dl, p = 0048) MA correction in HD patients can decrease leptin, an atherogenic marker The impact of such treatment extends to uremic bone disease, as decrease in serum calcium and increase in PTH However, this could be an undesirable effect because it may aggravate a secondary hyperparathyroidism Whether the reduction in leptin levels has impact on outcomes in patients on hemodialysis deserves further investigation

Correction of metabolic acidosis in hemodialysis: consequences on serum leptin and mineral metabolism

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Papers

Prostatic surgery associated acute kidney injury

Protein-losing gastroenteropathy in a patient with systemic lupus erythematosus and antiphospholipid antibody syndrome simulating nephrotic syndrome

Evaluation of Intermittent Hemodialysis in Critically Ill Cancer Patients with Acute Kidney Injury Using Single-Pass Batch Equipment.

Correction of metabolic acidosis in hemodialysis: consequences on serum leptin and mineral metabolism