The Napa Meeting explored potential relationships between CKD and acutekidney injury (AKI). Both IRIS CKD Stages 1 and IRIS AKI Grade I represent early kidneydisease states which may not be recognized until they proceed to a more advanced classifications. If progressive CKD is associated with active episodic or ongoing injury to the kidney, and if AKI is linked to progressive CKD (see below), could both these disease syndromes be explained by the same pathological process or processes progressing concurrently at different rates to establish both categories? Should early CKD and AKI be viewed as interconnected rather than separate clinical conditions? To this issue, the following questions relative to early CKD and early AKI were proposed by the participants:
For a number of reasons the extent to which critically ill patients, with de novo AKI specifically, are at risk of CKD and ESRD is unknown. First, many studies lack pre-ICU data on CKD and hence, have not excluded patients with CKD. Therefore, it is difficult to differentiate the risks of developing CKD and ESRD in patients with true de novo AKI from those with acute on chronickidneydisease. Second, large studies have lacked ICU cohort comparisons, often studying AKI in heterogeneous populations such as hospital patients and therefore, generalisation of findings to ICU populations is prob- lematic. Third, in those studies with long-term follow up of critically ill AKI survivors, mortality and ESRD but not CKD have been followed. No previous large-magnitude study has investigated CKD outcome in AKI survivors after intensive care treatment. Last, national data for outcome after AKI in Sweden have not previously been described.
The severity of AKI was evaluated according to the sta- ging system devised by the AcuteKidney Injury Network . The increase of creatinine was used as the main marker of the severity of AKI (increase of creatinine to equal or more than 3-fold of the baseline creatinine value). None of the patients had previously known chronickidneydisease. Therefore, basal creatinine values were estimated from normal glomerular filtration rates that are nor- mal for sex and age, standardized on body surface area (1.73 m 2 ) . To calculate normal plasma creatinine levels, creatinine levels were backtraced from the CKD-EPI equation (ChronicKidneyDisease Epidemiology Collabor- ation) by solving the equation for this variable.
All data were prospectively collected. Data variables included demographic data, comorbid diseases, septic AKI developed post-surgery (or not), and the indications for RRT. Biochemistry data such as complete blood cell count, blood urea nitrogen (BUN), serum creatinine (sCr), serum glutamate oxaloacetate transaminase (GOT), serum total bilirubin, serum albumin, and serum potassium (sK + ) were recorded upon ICU admission and RRT initiation [18,20]. Moreover, the clinical parameters and severity score were also recorded at these two time points. The clinical parameters included heart rate, sys- tolic and diastolic blood pressures, central venous pres- sure (CVP) level, partial pressure of arterial blood gas oxygen and fraction of inspired oxygen. Severity scores included Glasgow Coma Scale (GCS) score, Acute Phy- siology and Chronic Health Evaluation II (APACHE II) score , Sequential Organ Failure Assessment (SOFA) score , and Simplified Acute Physiology Score III (SAPS III) . The usage of mechanical ventilation was recorded and the inotropic equivalent dose was calcu- lated . Definitions were made as follows: hyperten- sion was blood pressure above 140/90 mmHg or usage of anti-hypertension agents; diabetes was previous usage of insulin or oral hypoglycemic agents; congestive heart failure was low cardiac output with a CVP above 12 mmHg and dopamine equivalent above 5 μg/kg/min ; and chronickidneydisease (CKD) was sCr of 1.5 mg/dl or greater documented prior to this admission.
This study has limitations; it was affected by underre- porting, a problem common to most register studies of this magnitude. AKI diagnosis, interventions and in par- ticular renal replacement therapy, were not always re- corded, meaning that we were not exhaustively able to identify all patients with AKI and AoC disease. However, cases where these diagnoses were recorded should repre- sent those with the most severe disease. As a result, some patients with mild acutedisease may have been misclassified to no renal disease or CKD only groups. Table 5 Secondary outcome; multivariable Poisson regression for risk of developing ESRD according to renal disease status
We performed a retrospective analysis on all in- and outpatient diagnostic and procedural data of CLI patients classified in the Rutherford grades 5 (Rutherford grade 5; ICD-10 I70.23; n = 6916) and 6 (Rutherford grade 6; ICD- 10 I70.24; n = 8416) (Additional file 1: Table S1). Patients with ischemic rest pain (Rutherford grade 4), that are also commonly recognized as CLI, were not included in the analysis, since particularly in diabetic patients rest pain may not be dependably ascertainable due to diabetic poly- neuropathy. In contrast, tissue loss (Rutherford grades 5 and 6) is a much better objectifiable parameter. Within these Rutherford grades, we identified the patient sub- group with the co-diagnosis of diabetes mellitus (IDC-10 E10*, E11*) to be compared with the subgroup without encoded diabetes mellitus. We analyzed these in-hospital cases with respect to baseline characteristics such as age, sex, and the further co-diagnoses hypertension (ICD- 10 I10-15*), obesity (ICD-10 E66), dyslipidemia (ICD-10 E78*), smoking (ICD-10 F17*), chronickidneydisease (ICD-10 N18*; CKD), coronary artery disease (ICD-10 I25*; CAD), chronic heart failure (ICD-10 I50*; CHF), and malignancies (ICD-10 C*). Further, we analyzed the encoded procedures during the index hospitaliza- tion: angiography (OPS 3-605, 3-607), any revasculariza- tion (OPS 5-380*, 5-381*, 5-383*, 5-386*, 5-388*, 5-393*, 5-395*, 8-836*, 8-84*), endovascular revascularization (EVR; OPS 8-836*, 8-84*), surgical revascularization (OPS 5-380*, 5-381*, 5-383*, 5-386*, 5-388*, 5-393*, 5-395*), thrombendartherectomy (TEA; OPS 5-381*), peripheral bypass surgery (OPS 5-393*). We evaluated the in-hospi- tal complications acute renal failure (ICD-10 N17*), acute myocardial infarction (ICD-10 I21*), ischemic stroke (ICD-10 I63*), infection (ICD-10 A30-49*), and sepsis (ICD-10 B95-99*) as well as the in-hospital amputation (OPS 5-864*, 5-865*, 5-866*) and in-hospital mortality. A detailed listing on the diagnosis and procedural defining codes is presented in Additional file 1: Table S1.
PubMed, EMBASE, and Cochrane Central Register of Controlled Trials databases were searched for observational studies, up through November 4, 2016, using the terms “proton pump inhibitor” or “proton pumps” or “anti- ulcer agent” or “antacid” or “esomeprazole” or “omeprazole” or “ilaprazole” or “dexlansopra- zole” or “rabeprazole” or “lansoprazole” or “pantoprazole” and “chronickidneydisease” or “chronickidney failure” or “chronickidney insuf- ficiency” or “chronickidney dysfunction” or “chronic renal failure” or “chronic renal insuffi- ciency” or “chronic renal dysfunction” or “end stage kidneydisease” or “end-stage renal dis- ease” or “acute renal insufficiency” or “acutekidney injury” or “kidney injury” or “acute kid- ney failure” or “acute interstitial nephritis” or “interstitial nephritis” or “acute tubulointersti- tial nephritis” or “kidney failure” or “renal dis- ease” or “kidneydisease” or “renal insufficien- cy” or “renal failure” or “kidney failure” or “risk”
Physical appearance of humans is regarded as important for physical attractiveness. More emphasis is given to as well as the skin care as it has enormous cosmetic value and prefers many physi logical facts. Oedema is defined as abnormal and excessive accumulation of free fluid in interstitial tissue spaces and serous cavities. Oedema is a clinical condition which may manifest either by local cause with minimal tissue involvement or as a consequence of multi system tissue injury. A major attention to oedema is given when it is a clinical manifestation of cardiac, renal, hepatic disease. Word oedema and inflammation takes shelter under , swelling where patient seeks medical attention frequently. Renal oedema is an outcome of kidneydisease which may be acute category like acutekidney injury or chronic category like chronickidneydisease. Incidence of kidneydisease especially chronic category has doubled in 15 years, having prev lence approximately 14% which needs extreme alertness. Shotha is treated as separate dis
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 acutekidney 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 chronickidneydisease. 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 chronickidneydisease in the growing subgroup of critically ill post-AKI survivors.
Abstract: Diseases of the kidney are difficult to diagnose and treat. This review summarises the definition, cause, epidemiology and treatment of some of these diseases including chronickidneydisease, diabetic nephropathy, acutekidney injury, kidney cancer, kidney transplantation and polycystic kidney diseases. Numerous studies have adopted a metabolomics approach to uncover new small molecule biomarkers of kidney diseases to improve specificity and sensitivity of diagnosis and to uncover biochemical mechanisms that may elucidate the cause and progression of these diseases. This work includes a description of mass spectrometry-based metabolomics approaches, including some of the currently available tools, and emphasises findings from metabolomics studies of kidney diseases. We have included a varied selection of studies (disease, model, sample number, analytical platform) and focused on metabolites which were commonly reported as discriminating features between kidneydisease and a control. These metabolites are likely to be robust indicators of kidneydisease processes, and therefore potential biomarkers, warranting further investigation.
traceable Schwartz GFR Calculator for Children was used to stage patients and ESRD was established accord- ing to KidneyDisease Improving Global Outcomes guide- lines. The diagnoses were based on established clinical criteria . AKI was defined as an acute deterioration in renal excretory function, with a serum urea >10 mmol/l and/or a rise in serum creatinine (Scr) by ≥0.3 mg/dl, or a percentage increase in Scr of ≥50% from baseline using the AcuteKidney Injury Network(AKIN) criteria . AKI patients who required dialysis presented with an acute deterioration in renal excretory function and had in- dications for dialysis (anuria, electrolyte imbalance, fluid overload and uremia). ESRD had progressive chronic kid- ney disease with eGFR ≤15 mL/min/1.73 m2 with/without other indications for haemodialysis. ESRD was diagnosed in patients who had a progressive chronickidneydisease with eGFR ≤15 mL/min/1.73 m2, patients who had nor- mochromic normocytic anaemia and findings on ultra- sound that had features suggestive of chronickidneydisease. Outcome measures in those patients who absconded/lost to follow up and those patients who died after starting haemodialysis were not included. Patients gave informed consent and ethical approval was obtained before starting haemodialysis.
From February 1999 to August 2001, the PICARD study personnel evaluated for potential study participation all patients from five academic medical centers who under- went a nephrology consultation for AKI in the ICU. The study protocol was approved by the institutional review boards of the participating institutions and informed consent was obtained from all patients or their legal rep- resentatives. AKI was defined as an increase in sCr of 0.5 mg/dL or more for baseline sCr of less than 1.5 mg/dL or an increase in sCr of 1.0 mg/dL or more for baseline sCr of 1.5 mg/dL or more and less than 5.0 mg/dL. Chronickidneydisease (CKD) status was determined at enroll- ment for each patient by evaluating available clinical and laboratory data and history. At time of enrollment, patients were identified as having CKD if they had evi- dence of elevated sCr, proteinuria, or an abnormal renal ultrasound within a year prior to the index hospitaliza- tion. Patients were classified as 'CKD with AKI' if they met criteria for CKD as defined above. All remaining patients were considered as 'new-onset AKI'. A complete description of generation of the PICARD cohort, data elements, data collection, and management strategies have been previously described . Of the 618 patients included in the database, 398 required dialysis, some as early as at the first day of consultation. We identified 253 AKI patients with three to seven days of consecutive increase, with no fluctuations in sCr before dialysis initia- tion. We excluded patients with one day of missing data for sCr during that phase. sCr was measured at least once every 24 hours. In this analysis, we compared the first sCr value available each day with the first sCr value in the observational period (reference value).
However, using a crude marker of renal function such as serum creatinine outside steady-state conditions has significant limitations. Serum creatinine is used as a sur- rogate for the glomerular filtration rate (GFR) during AKI in critically ill unstable patients. The GFR is rarely measured in clinical practice but equations, such as the modification of diet in renal disease (MDRD) and the chronickidneydisease epidemiology collabor- ation (CKD-EPI) equations, estimate the GFR (eGFR) from the serum creatinine where differences in age, sex, and race are considered [6–8]. However, as noted, creatinine is a biomarker for the GFR only under clinically stable conditions . In the critically ill there is a significant overestimation of the eGFR due to, for example, reduced creatinine levels due to reduced muscle bulk and creatinine generation. Sev- eral studies have compared formal measurement of the GFR and eGFR with considerable disparity ob- served . Most importantly, of course, is that there is a delay between renal injury and any ob- served rise in creatinine, which may be masked for up to 48 h.
Practice Guidelines for the Evaluation and Management of ChronicKidneyDisease . The uKIM-1 level at the time of AKI occurrence was 2.37 (1.10, 6.22) ng/mg, and the peak level of creatinine was 2.43 (1.41, 3.74) mg/dl. There were 123 patients in AKI stage I, 26 patients in stage II and 35 patients in stage III. Patients with renal AKI accounted for 53.26 %. The clinical etiology of AKI included insufficient renal blood perfusion or ischemia (22 %) (insufficient volume, gastrointestinal loss, cardiac failure, or renal vascular factors), nephrotoxicity (20 %) (nephrotoxic agents and contrast medium injury, etc.), in- fection factor (23 %) (sepsis, severe pneumonia and any kind of infection that caused renal injury), aggravation or activation of glomerular disease (19 %), and obstruction (11 %). The proportion of patients with renal function progression was 39.67 % at the one-year follow up (Table 1).