Acute kidney injury (AKI) is a frequent clinical problem in critically ill patients and the associated mortality is high. Standard serum and urine biomarkers are insensitive and nonspecific for the detection of kidney injury in its early stages which limits the therapeutic options and may compromise the outcome. The study presents new candidates for biochemical markers of AKI, with potentially high sensitivity and specificity, causally related to its pathogenesis and development. Some of these biomarkers measured in serum or urine are well known in laboratory practice but have been used in other tests, while some novel biomarkers have been proposed as a result of experimental and clinical studies. In current clinical practice, identification and classification of AKI is based on elevations in serial serum creatinine concentrations, which are delayed and therefore unreliable in the acute setting. The most promising of the new serum AKI markers are cystatin C, neutrophil gelatinase-associated lipocalin and uric acid. Urinary AKI markers may be classified as enzymes released from damaged tubular cells (alkaline phosphatase, γ-glutamyl transpeptidase, alanine aminopeptidase, isoenzymes of glutathione transferase, N-acetyl-β-D-glucosaminidase), low-molecular-weight proteins (α₁-microglobulin, β₂-microglobulin, retinol-binding protein, cystatin C) and proteins specifically produced in the kidney and associated with the development of AKI [cysteine-rich protein 61, neutrophil gelatinase-associated lipocalin, kidney injury molecule 1, cytokines and chemokines (Gro-α, IL-18), and structural and functional proteins of renal tubules (F-actin, Na⁺/H⁺ exchange isoform 3)]. Based on the different expression of these markers, using a panel of serum and urine markers may potentially help to distinguish between various types of insults, establish the duration and severity of injury, predict the clinical outcome and help to monitor response to treatment in AKI.

Nearly all body organs and systems are affected by the toxicity of uremic compounds retained in the course of renal dysfunction. Knowledge about the origin, chemical structure and composition of the retained endogenous substances responsible for these symptoms is far from complete. Organic retention solutes present a great variety of properties which makes their accurate classification extremely difficult. Their potential toxicity remains to be elucidated with meticulous observation of clearly formulated rules guiding the process. Toxicity assessment is a complex process because not just one but several retained compounds may be simultaneously involved in the same biological and metabolic processes. The search for new uremic compounds and combining them into panels of substances involved in the same pathophysiological processes seems to offer a novel approach to identifying and explaining any so far unexplored specific effects of endogenous compounds on the body organs and systems.

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Diversified intrauterine microbiome may modify the environment of the developing fetus with possible short- and long-term impact on the individual's health and disease. Meconium which provides the individual-specific information about the intrauterine microbiome composition is a biological material with potential uses in routine clinical diagnostic practice.

The aim of the study was the assessment of the concentrations and establishment of mutual relationships between three main protease inhibitors: alpha-1-antitrypsin (AAT), alpha-2-macroglobulin (alpha-2-M) and antithrombin-III (AT-III), and of the total trypsin inhibitory capacity (TIC) in the serum of diabetic and non-diabetic children during adolescence. Forty-nine children (24 girls and 25 boys) with type 1 diabetes mellitus and 24 non-diabetic children (13 girls and 11 boys) were divided according to the Tanner scale into three groups: pre-, peri- and post-pubertal. The concentrations of AAT, alpha-2-M and AT-III were determined by the radial immunodiffusion method on NOR-Partigen plates (Dade-Behring), while TIC was determined by the method using BAPNA as substrate. Means and medians of serum AAT [1.55 g/l, 1.40 (95% confidence interval, 1.42-1.68), respectively] and TIC [10.6 mg trypsin/100 ml, 10.3 (95% CI, 9.5-11.7)] in diabetic children were lower than means and medians of AAT [1.81 g/l, 1.60 (95% CI 1.55-2.07), respectively] and TIC [12.5 mg trypsin/100 ml, 13.2 (95% CI, 10.9-14.1)] in non-diabetic children. A comparison of variables between Tanner groups shows an increasing trend of AAT concentration in diabetic children and a decreasing trend of TIC in non-diabetic subjects. In contrast to pre- and peri-puberty, no correlations were found in the postpubertal period between the studied parameters, either in diabetic or non-diabetic patients. Hyperglycaemia and the duration of diabetes were found to have a significant association with alpha-2-M and AT-III concentrations, but not with AAT serum concentrations. The concentrations and correlations between serum protease inhibitors in diabetic children during adolescence are disrupted compared with non-diabetic children. Taking into account the unfavourable consequences of vascular complications resulting from serum trypsin inhibitor changes and protease- antiprotease imbalance, diabetic children are at greater risk of this occurring during adolescence.