Lymphocyte to monocyte ratio and blood pressure variability in childhood hypertension-a pilot study.

BACKGROUND AND AIMS: The investigation of inflammatory background of hypertension (HTN) concentrates mainly on patients with primary HTN. The aim of the study was to analyze the role of new parameters of inflammation-lymphocyte to monocyte ratio (LMR), neutrophil to lymphocyte ratio (NLR), and platelet to lymphocyte ratio (PLR), in the population of children with primary (pHTN) and secondary renal hypertension (rHTN). MATERIAL AND METHODS: The study group consisted of 70 children with pHTN, 46 patients with rHTN, and 30 age-matched normotensive controls. The retrospective analysis focused on the evaluation of LMR, NLR, and PLR values in relation to blood pressure (BP) parameters from in-office and ambulatory BP monitoring measurements. Twenty-four hours, daytime, and nighttime periods were evaluated. Blood pressure variability (BPV) was defined by standard deviation and coefficient of variation of analyzed values. RESULTS: LMR and NLR values in HTN patients differed significantly vs. controls. Dippers with pHTN demonstrated significant correlations between LMR, NLR, PLR, and markers of BPV, in 24 h and daytime diastolic BP and mean arterial pressure. In dippers with rHTN such correlations concerned only LMR. CONCLUSIONS: LMR may become a promising marker of BPV, useful in children with primary and secondary hypertension. IMPACT: Lymphocyte to monocyte ratio is a novel marker of blood pressure variability, connected to target-organ damage, in children with primary and secondary renal hypertension. Our study analyzes for the first time the connections between blood cell count-driven inflammatory markers (lymphocyte to monocyte, neutrophil to lymphocyte, and platelet to lymphocyte ratios) and parameters of blood pressure variability, and compares those ratios in children with primary and secondary hypertension. The increasing incidence of hypertension among children urges the search for simple methods of assessment of its complications. LMR may be of added value in the analysis of the inflammatory background of hypertension.

KIM-1, IL-18, and NGAL, in the Machine Learning Prediction of Kidney Injury among Children Undergoing Hematopoietic Stem Cell Transplantation-A Pilot Study.

Children undergoing allogeneic hematopoietic stem cell transplantation (HSCT) are prone to developing acute kidney injury (AKI). Markers of kidney damage: kidney injury molecule (KIM)-1, interleukin (IL)-18, and neutrophil gelatinase-associated lipocalin (NGAL) may ease early diagnosis of AKI. The aim of this study was to assess serum concentrations of KIM-1, IL-18, and NGAL in children undergoing HSCT in relation to classical markers of kidney function (creatinine, cystatin C, estimated glomerular filtration rate (eGFR)) and to analyze their usefulness as predictors of kidney damage with the use of artificial intelligence tools. Serum concentrations of KIM-1, IL-18, NGAL, and cystatin C were assessed by ELISA in 27 children undergoing HSCT before transplantation and up to 4 weeks after the procedure. The data was used to build a Random Forest Classifier (RFC) model of renal injury prediction. The RFC model established on the basis of 3 input variables, KIM-1, IL-18, and NGAL concentrations in the serum of children before HSCT, was able to effectively assess the rate of patients with hyperfiltration, a surrogate marker of kidney injury 4 weeks after the procedure. With the use of the RFC model, serum KIM-1, IL-18, and NGAL may serve as markers of incipient renal dysfunction in children after HSCT.

Update on Innate Immunity in Acute Kidney Injury-Lessons Taken from COVID-19.

The serious clinical course of SARS-CoV-2 infection is usually accompanied by acute kidney injury (AKI), worsening prognosis and increasing mortality. AKI in COVID-19 is above all a consequence of systemic dysregulations leading to inflammation, thrombosis, vascular endothelial damage and necrosis. All these processes rely on the interactions between innate immunity elements, including circulating blood cells, resident renal cells, their cytokine products, complement systems, coagulation cascades and contact systems. Numerous simultaneous pathways of innate immunity should secure an effective host defense. Since they all form a network of cross-linked auto-amplification loops, uncontrolled activation is possible. When the actions of selected pathways amplify, cascade activation evades control and the propagation of inflammation and necrosis worsens, accompanied by complement overactivity and immunothrombosis. The systemic activation of innate immunity reaches the kidney, where the damage affecting single tubular cells spreads through tissue collateral damage and triggers AKI. This review is an attempt to synthetize the connections between innate immunity components engaged in COVID-19-related AKI and to summarize the knowledge on the pathophysiological background of processes responsible for renal damage.

Mild X-linked Alport syndrome due to the COL4A5 G624D variant originating in the Middle Ages is predominant in Central/East Europe and causes kidney failure in midlife.

A study of 269 children enrolled into a National Registry for children with persistent glomerular hematuria identified 131 individuals with genetically confirmed X-linked Alport Syndrome. A single variant c.1871G>A p.Gly624Asp (G624D) in COL4A5 was predominant and accounted for 39% of X-linked Alport Syndrome in unrelated Polish families (44 of 113). To evaluate its origins, the genetic variation in a 2.79 Mb segment encompassing the COL4A5 locus on chromosome X was assessed. All G624D alleles were found on the same rare haplotype background, indicating a founder effect dating back to the 12-13th century. The phenotypic data of 131 children with X-linked Alport Syndrome and their 195 affected adult relatives revealed that the G624D variant was associated with a significantly milder clinical course in comparison to other pathogenic COL4A5 variants. Furthermore the clinical course of this genetically uniform cohort was milder than that observed in individuals with other COL4A5 missense mutations. In spite of the benign clinical manifestation throughout childhood and early adulthood, the G624D variant confers significant risk for both kidney failure and deafness in males, albeit 20-30 years later than that observed in individuals with other COL4A5 pathogenic variants (50% cumulative risk of starting dialysis at 54 years (95% confidence interval: 50-62) v. 26 years (95% confidence interval: 22-30)). Thus, males with G624D are candidates for existing and emerging therapies for Alport Syndrome.

Clinical profile of a Polish cohort of children and young adults with cystinuria.

BACKGROUND: Cystinuria is an inherited disorder that results in increased excretion of cystine in the urine. It accounts for about 1-2% of pediatric kidney stones. In this study, we sought to identify the clinical characteristics of patients with cystinuria in a national cohort. METHODS: This was a retrospective study involving 30 patients from the Polish Registry of Inherited Tubulopathies. Initial data and that from a 6-month follow-up were analyzed. Mutational analysis was performed by targeted Sanger sequencing and, if applicable, MLPA analysis was used to detect large rearrangements. RESULTS: SLC7A9 mutations were detected in 15 children (50%; 10 males, 5 females), SLC3A1 mutations in 14 children (47%; 5 males, 9 females), and bigenic mutations in one male patient. The first clinical symptoms of the disease were detected at a median of 48 months of age (range 3-233 months). When individuals with different mutations were compared, there were no differences identified in gender, age of diagnosis, presence of UTI or urolithiasis, eGFR, calcium, or cystine excretion. The most common initial symptoms were urolithiasis in 26 patients (88%) and urinary tract infections in 4 patients (13%). Urological procedures were performed in 18 out of 30 (60%). CONCLUSIONS: The clinical course of cystinuria is similar among patients, regardless of the type of genetic mutation. Most patients require surgery before diagnosis or soon after it. Patients require combined urological and pharmacological treatment for prevention of stone recurrence and renal function preservation.

New markers of cell migration and inflammation in children with chronic kidney disease.

Context: Chronic kidney disease (CKD) is characterized by immunocompetent cell migration and inflammation. Monocyte chemoattractant protein (MCP)-1 and macrophage colony-stimulating factor (MCSF) stimulate monocyte migration and transition into macrophages with subsequent release of neopterin. Objective: The aim of the study was to analyze these parameters in children with various stages of CKD. Material and methods: The study group consisted of 41 CKD children, 19 patients on haemodialysis (HD), 22 children on automated peritoneal dialysis (APD) and 23 controls. Serum concentrations of MCP-1, MCSF and neopterin were assessed by ELISA. Correlations to matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs) were analyzed. Results: MCP-1, MCSF and neopterin were significantly elevated in all patients versus controls and the highest values concerned HD children. A single HD session lessened the concentrations of all parameters, yet they rose back before the next HD session. All markers correlated with MMPs and TIMPs in different combinations. Conclusions: Systemic inflammation and cell migration are triggered by CKD and additionally aggravated by chronic dialysis, with the more evident negative impact of HD than APD. Discrepancies in MCP1, MCSF and neopterin serum concentrations suggest they may serve as new markers of cellular and inflammatory responses in children with CKD.

[Chronic kidney disease in children up to 2 years of age - a single center data analysis]. / Przewlekla choroba nerek u dzieci do 2. roku zycia ­ analiza danych z jednego osrodka.

Although anomalies in the urinary tract are the leading cause of chronic kidney disease (CKD) in the pediatric population, there are few studies focusing on etiological discrepancies between younger and older children. AIM: The aim of the study was to perform a comparative analysis of etiology of CKD in children hospitalized in the Department of Pediatric Nephrology at the Wroclaw Medical University, with reference to the patients' age and gender. MATERIALS AND METHODS: The retrospective analysis considered medical records of 174 patients aged 0-18 years, diagnosed with CKD, hospitalized in our Department in the years 2011-2017. The analyzed population was divided regarding the patients' age. Group A contained children up to 2 years of age (45 patients), group B - children aged 2-18 years (129 patients). RESULTS: In younger children, boys prevailed, in older children gender distribution was equal. The most common causative factors of CKD in group A were: urinary tract anomalies (66,7%), perinatal acute kidney injury (17,8%) and hereditary renal disorders (8,9%). In children over 2 years of age, urinary tract anomalies were also the leading cause of CKD (48,8%), followed by glomerulopathies (16,3%) and hereditary renal disorders (15,5%). CONCLUSIONS: Anomalies within the urinary tract are the predominant cause of CKD in children, irrespective of age. Male predominance concerned only children up to 2 years of age. The second causative factor for CKD in the youngest children is acute kidney injury, mainly in the perinatal period. Glomerulopathies and hereditary renal disorders are significant etiological factors for CKD in older children.

Epidermal growth factor, growth differentiation factor-15, and survivin as novel biocompatibility markers in children on chronic dialysis.

CONTEXT: Chronic dialysis results in aggravation of apoptosis and cell damage, triggered by bioincompatibility of dialysis membranes and peritoneal fluids. OBJECTIVE: The aim of study was to assess the usefulness of epidermal growth factor (EGF), growth differentiation factor (GDF)-15, and survivin as novel markers of biocompatibility in dialyzed children. MATERIALS AND METHODS: Parameters were assessed by ELISA in 19 patients on hemodialysis and 22 children on peritoneal dialysis. RESULTS: Serum concentrations of analyzed parameters in children on chronic dialysis differed significantly from controls and depended strongly on the dialysis technique. CONCLUSIONS: EGF, GDF-15, and survivin may serve as new biocompatibility markers in children on chronic dialysis.

Urine survivin, E-cadherin and matrix metalloproteinases as novel biomarkers in children with chronic kidney disease.

CONTEXT: Epithelial-mesenchymal transition (EMT) leads to renal fibrosis and chronic kidney disease (CKD). OBJECTIVE: The aim of this study was to assess the usefulness of survivin, E-cadherin and metalloproteinases (MMPs) as biomarkers of CKD-related complications. MATERIAL AND METHODS: Survivin, E-cadherin, MMP-2, MMP-9 and TGFbeta1 were assessed by ELISA in 41 children with CKD stages 3 to 5 and in 23 controls. RESULTS: The serum and urine values of analyzed parameters were significantly elevated in CKD patients versus controls and correlated with each other. CONCLUSIONS: The observed parameter changes indicate apoptosis, tissue remodeling and fibrosis in CKD children. Urine survivin may become a new biomarker of kidney-specific EMT.

Urine matrix metalloproteinases and their extracellular inducer EMMPRIN in children with chronic kidney disease.

BACKGROUND: Transforming growth factor (TGF)beta1 and matrix metalloproteinases (MMPs) play an essential role in CKD-related tissue remodeling. However, there are no data on urine MMPs and their extracellular inducer EMMPRIN in CKD patients. The aim of study was to assess the concentrations of MMP-2, MMP-7, MMP-9, EMMPRIN and TGFbeta1 in serum and urine of CKD children and to analyze the potential relations between those parameters. METHODS: Forty-one pre-dialysis CKD children and 23 age-matched controls were enrolled in the study. The concentrations of analyzed parameters were assessed by ELISA. RESULTS: Serum and urine values of MMP-2, MMP-7, MMP-9, EMMPRIN and TGFbeta1 were significantly elevated in CKD patients versus controls. The MMP-2 and MMP-9 levels in urine correlated significantly with the corresponding values in serum, whereas MMP-7, EMMPRIN and TGFbeta1 urine concentrations did not. There were also significant correlations between urine values of all parameters. CONCLUSIONS: The increased urine levels of MMPs, EMMPRIN and TGFbeta1 indicate enhanced proteolysis and renal tissue remodeling. In the case of MMP-7, EMMPRIN and TGFbeta1 those disturbances seem independent of enhanced serum activity of the corresponding enzymes. The urine MMP-7 and EMMPRIN concentrations may serve as new independent indices of tissue remodeling and renal interstitial fibrosis in children with CKD.

The impact of dialysis modality on novel markers of stress reaction, matrix remodeling and endothelial damage in children on chronic dialysis.

BACKGROUND/AIMS: Dialysis triggers stress reaction, matrix remodeling and endothelial damage, but little is known about the changes it induces on selected heat shock proteins (Hsp90α), adhesion molecules (E-cadherin, sE-selectin), metalloproteinases (MMP-8) and their extracellular inducer (EMMPRIN). The aim of this study was to assess serum concentrations of the above-mentioned parameters in children on chronic dialysis. METHODS: 19 patients on hemodialysis (HD), 22 children on peritoneal dialysis (PD) and 30 age-matched controls were examined. Serum concentrations of parameters were assessed by ELISA. RESULTS: Hsp90α, MMP-8, EMMPRIN and E-cadherin concentrations were significantly increased in children on dialysis vs. controls and higher levels were in HD than PD patients. There was no difference in the level of sE-selectin between HD and PD modalities. A single HD session diminished Hsp90α, MMP-8, EMMPRIN and E-cadherin values, but had no impact on sE-selectin levels. CONCLUSIONS: Hemodialysis evokes stress reaction, matrix and endothelium destruction, to a greater extent than peritoneal dialysis. Single hemodialysis influences circulating cells rather than endothelial cells.

Assessment of Risk Factors for Acute Kidney Injury with Machine Learning Tools in Children Undergoing Hematopoietic Stem Cell Transplantation.

Background: Although acute kidney injury (AKI) is a common complication in patients undergoing hematopoietic stem cell transplantation (HSCT), its prophylaxis remains a clinical challenge. Attempts at prevention or early diagnosis focus on various methods for the identification of factors influencing the incidence of AKI. Our aim was to test the artificial intelligence (AI) potential in the construction of a model defining parameters predicting AKI development. Methods: The analysis covered the clinical data of children followed up for 6 months after HSCT. Kidney function was assessed before conditioning therapy, 24 h after HSCT, 1, 2, 3, 4, and 8 weeks after transplantation, and, finally, 3 and 6 months post-transplant. The type of donor, conditioning protocol, and complications were incorporated into the model. Results: A random forest classifier (RFC) labeled the 93 patients according to presence or absence of AKI. The RFC model revealed that the values of the estimated glomerular filtration rate (eGFR) before and just after HSCT, as well as methotrexate use, acute graft versus host disease (GvHD), and viral infection occurrence, were the major determinants of AKI incidence within the 6-month post-transplant observation period. Conclusions: Artificial intelligence seems a promising tool in predicting the potential risk of developing AKI, even before HSCT or just after the procedure.

Changes of Dissociative Properties of Hemoglobin in Patients with Chronic Kidney Disease.

Background: The ability of hemoglobin to bind and dissociate oxygen is crucial in delivering oxygen to tissues and is influenced by a range of physiological states, compensatory mechanisms, and pathological conditions. This may be illustrated by the oxyhemoglobin dissociation curve (ODC). The key parameter for evaluating the oxygen affinity to hemoglobin is p50. The aim of this study was to evaluate the impact of hemodialysis on p50 in a group of patients with chronic kidney disease (CKD). An additional goal was to assess the correlation between p50 and the parameters of erythropoiesis, point-of-care testing (POCT), and other laboratory parameters. Methods: One hundred and eighty patients (106 male, 74 female), mean age 62.5 ± 17 years, with CKD stage G4 and G5 were enrolled in this cross-sectional study. Patients were divided into two groups, including 65 hemodialysis (HD) patients and 115 patients not receiving dialysis (non-HD). During the standard procedure of arteriovenous fistula creation, blood samples from the artery (A) and the vein (V) were taken for POCT. The causes of CKD, as well as demographic and comorbidity data, were obtained from medical records and direct interviews. Results: The weekly dose of erythropoietin was higher in HD patients than in non-HD patients (4914 ± 2253 UI vs. 403 ± 798 UI, p < 0.01), but hemoglobin levels did not differ between these groups. In the group of non-HD patients, more advanced metabolic acidosis (MA) was found, compared to the group with HD. In arterial and venosus blood samples, the non-HD group had significantly lower pH, pCO2 and HCO3-. This group had a higher proportion of individuals with MA with HCO3- < 22 mmol/L (42% vs. 24%, p < 0.01). The absolute difference of p50 in arterial and venous blood was determined using the formula Δp50 = (p50-A) - (p50-V). Δp50 was significantly higher in the HD group in comparison to non-HD (0.08 ± 2.05 mmHg vs. -0.66 ± 1.93 mmHg, p = 0,02). There was a negative correlation between pH and the p50 value in arterial (pH-A vs. p50-A, r = -0.56, p < 0.01) and venous blood (pH-V vs. p50-V, r = -0.45, p < 0.01). In non-HD patients, hemoglobin levels correlated negatively with p50 (r = -0.29, p < 0.01), whereas no significant relation was found in HD patients. Conclusions: The ODC in pre-dialysis CKD (non-HD) patients is shifted to the right due to MA, and this is an additional factor influencing erythropoiesis. Hemodialysis restores the natural differences in hemoglobin's dissociation characteristics in the arterial and venous circulation.

New markers of apoptosis in children on chronic dialysis.

Enhanced apoptosis is characteristic for chronic kidney disease (CKD). A specific type of apoptosis, anoikis, is connected with the extracellular matrix turnover and cell detachment. Although E-cadherin, extracellular matrix metalloproteinase inducer (EMMPRIN) and matrix metalloproteinase (MMP)-8 may play an important role in this process, they have not been analyzed in any nephrological aspect, either in CKD. The aim of study was to evaluate the serum concentrations of E-cadherin, EMMPRIN and their potential regulators (MMP-8, MMP-7, TIMP-1, TIMP-2), with relevance to apoptosis/cell damage markers (sFas, sFasL, Hsp27), in children with CKD. 39 CKD children stages 3-4, 26 CKD children stage 5 still on conservative treatment, 19 patients on hemodialysis (HD), 22 children on automated peritoneal dialysis (APD) and 30 controls were examined. Serum concentrations of those parameters were assessed by ELISA. Median E-cadherin, EMMPRIN and MMP-8 values were significantly increased in patients on dialysis versus those in pre-dialysis period and versus controls. The highest values were noticed in the HD subjects. Regression analysis revealed that EMMPRIN and MMP-8 predicted various apoptosis markers, whereas E-cadherin turned out the best predictor of both apoptosis (Hsp27, sFas, sFasL) and matrix turnover (MMP-7, TIMP-1, TIMP-2) indexes in dialyzed patients. Children with CKD are prone to E-cadherin, EMMPRIN and MMP-8 elevation, aggravated by the dialysis commencement and most evident on hemodialysis. Correlations between parameters suggest their role as indexes of apoptosis in children on dialysis. E-cadherin seems the most accurate marker of anoikis in this population.

Systemic Immune Inflammation Index as a Key Predictor of Dialysis in Pediatric Chronic Kidney Disease with the Use of Random Forest Classifier.

BACKGROUND: Low-grade inflammation is a significant component of chronic kidney disease (CKD). Systemic immune inflammation index (SII), a newly defined ratio combining neutrophil, lymphocyte, and platelet counts, has not yet been evaluated in the pediatric CKD population nor in the context of CKD progression or dialysis. Thus, this study aimed to analyze the complete blood cell count (CBC)-driven parameters, including SII, in children with CKD and to assess their potential usefulness in the prediction of the need for chronic dialysis. METHODS: A single-center, retrospective study was conducted on 27 predialysis children with CKD stages 4-5 and 39 children on chronic dialysis. The data were analyzed with the artificial intelligence tools. RESULTS: The Random Forest Classifier (RFC) model with the input variables of neutrophil count, mean platelet volume (MPV), and SII turned out to be the best predictor of the progression of pediatric CKD into end-stage kidney disease (ESKD) requiring dialysis. Out of these variables, SII showed the largest share in the prediction of the need for renal replacement therapy. CONCLUSIONS: Chronic inflammation plays a pivotal role in the progression of CKD into ESKD. Among CBC-driven ratios, SII seems to be the most useful predictor of the need for chronic dialysis in CKD children.

Crossed renal ectopia: can it be a diagnostic problem?

Crossed renal ectopia (C-RE) is a rare congenital anomaly in which both kidneys are located unilaterally. The crossed kidney is situated on the side opposite to its ureteral orifice and usually lies below the normal kidney. The frequency of this malformation is estimated at 0.05% to 0.1%. Most of the patients remain asymptomatic. In other cases C-RE is diagnosed incidentally on routine ultrasonography, due to the presence of unspecific symptoms. The diagnosis of C-RE is possible due to a wide range of imaging techniques: US, IVU, CT, MRI, and TcDMSA scan. Among them IVU, CT, and MRI have the highest degree of confidence. The aim of this retrospective study was to present our own experience with 5 children affected with C-RE, emphasizing the differences in clinical picture and low sensitivity of ultrasound images. In all of them the final diagnosis was established by IVU or MRI.

Biomarkers in Pediatric Nephrology-From Bedside to Bench and Back Again.

The progress in biomarker research is characterized by the perpetual quest for parameters that fulfill the strict criteria of sensitivity, specificity, ease and speed in performance and cost-effectiveness [...].

Matrix metalloproteinases and soluble Fas/FasL system as novel regulators of apoptosis in children and young adults on chronic dialysis.

The system of membrane receptor Fas and its ligand FasL compose one of the main pathways triggering apoptosis. However, the role of their soluble forms has not been clarified yet. Although sFasL can be converted from the membrane-bound form by matrix metalloproteinases (MMPs), there are no data on relations between sFas/sFasL, MMPs and their tissue inhibitors (TIMPs) in patients on chronic dialysis--neither children nor adults. The aim of our study was to evaluate serum concentrations of sFas, sFasL, and their potential regulators (MMP-2, MMP-7, MMP-9, TIMP-1, TIMP-2), in children and young adults chronically dialyzed. Twenty-two children on automated peritoneal dialysis (APD), 19 patients on hemodialysis (HD) and 30 controls were examined. Serum concentrations of sFas, sFasL, MMPs and TIMPs were assessed by ELISA. Median values of sFas, sFasL, sFas/sFasL ratio, MMP-2, MMP-7, MMP-9, TIMP-1 and TIMP-2 were significantly elevated in all dialyzed patients vs. controls, the highest values being observed in subjects on HD. A single HD session caused the decrease in values of all parameters to the levels below those seen in children on APD. Regression analysis revealed that MMP-7 and TIMP-1 were the best predictors of sFas and sFasL concentrations. Children and young adults on chronic dialysis are prone to sFas/sFasL system dysfunction, more pronounced in patients on hemodialysis. The correlations between sFas/sFasL and examined enzymes suggest that MMPs and TIMPs take part in the regulation of cell death in the pediatric population on chronic dialysis, triggering both anti- (sFas) and pro-apoptotic (sFasL) mechanisms.

Heat shock proteins in chronic kidney disease.

Heat shock proteins (HSP) form a heterogenous, evolutionarily conserved group of molecules with high sequence homology. They mainly act as intracellular chaperones, protecting the protein structure and folding under stress conditions. The extracellular HSP, released in the course of damage or necrosis, play a pivotal role in the innate and adaptive immune responses. They also take part in many pathological processes. The aim of this review is to update the recent developments in the field of HSP in chronic kidney disease (CKD), in regard to three different aspects. The first is the assessment of the role of HSP, either positive or deleterious, in the pathogenesis of CKD and the possibilities to influence its progression. The second is the impact of dialysis, being a potentially modifiable stressor, on HSP and the attempt to assess the value of these proteins as the biocompatibility markers. The last area is that of kidney transplantation and the potential role of HSP in the induction of the immune tolerance in kidney recipients.

Current Concepts of Pediatric Acute Kidney Injury-Are We Ready to Translate Them into Everyday Practice?

Pediatric acute kidney injury (AKI) is a major cause of morbidity and mortality in children undergoing interventional procedures. The review summarizes current classifications of AKI and acute kidney disease (AKD), as well as systematizes the knowledge on pathophysiology of kidney injury, with a special focus on renal functional reserve and tubuloglomerular feedback. The aim of this review is also to show the state-of-the-art in methods assessing risk and prognosis by discussing the potential role of risk stratification strategies, taking into account both glomerular function and clinical settings conditioned by fluid overload, urine output, or drug nephrotoxicity. The last task is to suggest careful assessment of eGFR as a surrogate marker of renal functional reserve and implementation of point-of-care testing, available in the case of biomarkers like NGAL and [IGFBP-7] × [TIMP-2] product, into everyday practice in patients at risk of AKI due to planned invasive procedures or treatment.