Renal Failure and Renal Replacement therapy in Intensive Care Unit

Abstract

SUMMARY A cute kidney injury (AKI) is currently the most commonly used term to define sudden worsening of kidney function in hospitalized patients. It implies the concept that renal damage is a continuum with a broad range from mild to severe forms. Acute kidney injury is a clinical syndrome with several different etiologies, pathophysiologic mechanisms and prognostic features: It is likely, even if currently not described, that different AKIs will require different treatments. Definition and early diagnosis of AKI is the focus of intense research. As a matter of fact, the AKI syndrome is a consequence of multiple (cumulative) insults in susceptible patients as well as single hit of highly nephrotoxic entity: Currently, the amount of time over these insults occurs is unknown and their clinical expression is almost silent. The identification of the risk factors of AKI is probably more important than the definition and diagnosis of AKI itself. The hope relies on novel biomarkers and the possibility of being informed on silent hits occurring to the kidneys allowing the specialists to act before frank AKI developed. The presentation of (AKI) is dependent on the cause as the patient is often asymptomatic and the AKI is discovered on subsequent investigations. In the diagnosis of AKI, The aim of testing renal function is to approximate the glomerular filtration rate (GFR) which can be viewed as the best global measure of kidney excretory function reflecting the sum of the filtration rates for all functioning nephrons. The baseline GFR is affected by many factors including age, sex, race, diet and muscle mass and also demonstrates significant variation within individuals. The basis of use of creatinine for assessment of renal function relies on its rate of excretion being approximately proportional to GFR. Creatinine levels will, initially, significantly underestimate the severity of renal dysfunction following a significant fall in GFR until steady-state is achieved. Changes in creatinine production can alter measured plasma creatinine concentration as much as changes in excretion and this is of particular relevance in the critically ill. Cystatin C, a low molecular weight cysteine proteinase inhibitor, is synthesized at a relatively constant rate by all nucleated cells and almost exclusively filtered at the glomerulus. Although confounders of Cystatin measurement are probably less than creatinine, there is a lack of a standardized Cystatin C method of measurement at present. Simple urinary dipstick analysis should be undertaken in all patients where possible, as proteinuria may complicate AKI particularly in the presence of sepsis. So, the presence of premorbid proteinuria has significant prognostic implications. Hematuria, particularly in the presence of proteinuria, should alert the clinician to the possibility of parenchymal renal disease.