Morpho-functional damage of the tubulo-interstitial compartment is almost always found in the early stages of renal dis ease, even in nephropathies characterized by prevalent glomerular involvement, and its recognition is of great importance in acute diseases such as AKI. Indeed, the high perfusion of the tubulointerstitial compartment makes this district extremely sensitive to ischemia and hypoxia, which are often the first consequence of a pathological process. In conditions of ischemia followed by rapid reperfusion, which are frequent during complex surgery and accompanied by periods of extra corporeal circulation, tubulointerstitial damage is acute and extensive and identifies the onset of AKI. Moreover, in this area, there is a considerable concentration of solutes, including any exogenous and/or endogenous toxic substances (e.g., drugs, bilirubin, etc.) capable of causing parenchymal dam age. Particularly vulnerable to the toxic insult of many drugs are the cells of the proximal tubule, which, as is known, play a fundamental role in the mechanisms of reabsorption and tubular secretion. However, tubular cells have a marked tendency to “repair” the morpho- functional damage and, in the presence of remission of “noxae,” such as hypoxia, ischemia, iatrogenic toxicity, etc., they demonstrate a rapid anatomic functional recovery. In some cases, such as after antibiotic therapy with aminoglycosides, the speed of glomerular filtration does not decrease significantly in the first 5–7 days after the start of drug administration and this is due to the attempt to repair the toxic damage implemented by the tubular cells. Only when necrotic phenomena prevail over regenerative phenomena, the extension of tubular lesions affects the glomerulus and its filtration function. The evaluation of tubulointerstitial damage is mainly carried out through the study of urinary and plasma biomarkers. Historically, laboratory diagnostics have been based on the assessment of the hydroelectrolytic balance through the measurement of urinary volume, urinary density (specific gravity), osmolality, and acid–base balance. The determination of urinary electrolytes and the balance with plasma electrolytes is also part of the routine evaluation of the tubulointerstitial compartment. To date, there is no single organ-specific biomarker of injury, such as troponin I and T for the myocardium. The search for biomarkers of tubular damage has focused mainly on proteins. Since the second half of the 1970s, urinary biomarkers have been proposed, including some enzymes of renal origin and some low-molecular weight proteins. Subsequently, tubular antigens, prostaglandins, renal-derived fibronectin, tubular adenosine deaminase-binding protein, and epidermal growth factor (EGF) have been evaluated. Many low-MW proteins, including myoglobin, immunoglobulin light chains, β2-microglobulin, cystatin C, and α1-microglobulin (heterogeneous in charge -HC- protein), have demonstrated high sensitivity but low specificity because they may increase in urine due to extrarenal physiological (exercise, posture, etc.) or pathological (proliferative diseases, muscle diseases, trauma, etc.) factors. Moreover, the lack of standardization of some methods on the urinary matrix and the instability of proteins in an “open” system such as urine represent very important barriers to the introduction of these methods in routine practice.

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مواضيع ذات صلة

rheumatoid factor (RF)

reticulocyte count (Retic count)

red blood cell indices (RBC indices, Blood indices)

NGAL

Low-Molecular-Weight Plasma Proteins

Immunofluorescence Assay (IFA)

Enzyme-Linked Fluorescent Assay (ELFA)

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red blood cell count (RBC count, Erythrocyte count)

rabies-neutralizing antibody test

prothrombin time (PT, Protime, International normalized ratio [INR])

Estimation of the Glomerular Filtration Rate by Equations