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  • 1. Burlaka, Ievgeniia
    et al.
    Liu, Xiao Li
    Rebetz, Johan
    Arvidsson, Ida
    Yang, Liping
    Brismar, Hjalmar
    KTH, School of Engineering Sciences (SCI), Applied Physics, Cell Physics. KTH, Centres, Science for Life Laboratory, SciLifeLab.
    Karpman, Diana
    Aperia, Anita
    Ouabain Protects against Shiga Toxin-Triggered Apoptosis by Reversing the Imbalance between Bax and Bcl-xL2013In: Journal of the American Society of Nephrology, ISSN 1046-6673, E-ISSN 1533-3450, Vol. 24, no 9, p. 1413-1423Article in journal (Refereed)
    Abstract [en]

    Hemolytic uremic syndrome, a life-threatening disease often accompanied by acute renal failure, usually occurs after gastrointestinal infection with Shiga toxin 2 (Stx2)-producing Escherichia coli. Stx2 binds to the glycosphingolipid globotriaosylceramide receptor, expressed by renal epithelial cells, and triggers apoptosis by activating the apoptotic factor Bax. Signaling via the ouabain/Na,K-ATPase/IP3R/NF-B pathway increases expression of Bcl-xL, an inhibitor of Bax, suggesting that ouabain might protect renal cells from Stx2-triggered apoptosis. Here, exposing rat proximal tubular cells to Stx2 in vitro resulted in massive apoptosis, upregulation of the apoptotic factor Bax, increased cleaved caspase-3, and downregulation of the survival factor Bcl-xL; co-incubation with ouabain prevented all of these effects. Ouabain activated the NF-B antiapoptotic subunit p65, and the inhibition of p65 DNA binding abolished the antiapoptotic effect of ouabain in Stx2-exposed tubular cells. Furthermore, in vivo, administration of ouabain reversed the imbalance between Bax and Bcl-xL in Stx2-treated mice. Taken together, these results suggest that ouabain can protect the kidney from the apoptotic effects of Stx2.

  • 2. Burlaka, Ievgeniia
    et al.
    Nilsson, Linnea M.
    KTH, School of Engineering Sciences (SCI), Applied Physics, Cell Physics. KTH, Centres, Science for Life Laboratory, SciLifeLab.
    Scott, Lena
    Holtback, Ulla
    Eklöf, Ann-Christine
    Fogo, Agnes B.
    Brismar, Hjalmar
    KTH, School of Engineering Sciences (SCI), Applied Physics, Cell Physics. KTH, Centres, Science for Life Laboratory, SciLifeLab. Karolinska Institutet, Sweden.
    Aperia, Anita
    Prevention of apoptosis averts glomerular tubular disconnection and podocyte loss in proteinuric kidney disease2016In: Kidney International, ISSN 0085-2538, E-ISSN 1523-1755, Vol. 90, no 1, p. 135-148Article in journal (Refereed)
    Abstract [en]

    There is a great need for treatment that arrests progression of chronic kidney disease. Increased albumin in urine leads to apoptosis and fibrosis of podocytes and tubular cells and is a major cause of functional deterioration. There have been many attempts to target fibrosis, but because of the lack of appropriate agents, few have targeted apoptosis. Our group has described an ouabain-activated Na,K-ATPase/IP3R signalosome, which protects from apoptosis. Here we show that albumin uptake in primary rat renal epithelial cells is accompanied by a time-and dose-dependent mitochondrial accumulation of the apoptotic factor Bax, down-regulation of the antiapoptotic factor Bcl-xL and mitochondrial membrane depolarization. Ouabain opposes these effects and protects from apoptosis in albumin-exposed proximal tubule cells and podocytes. The efficacy of ouabain as an antiapoptotic and kidney-protective therapeutic tool was then tested in rats with passive Heymann nephritis, a model of proteinuric chronic kidney disease. Chronic ouabain treatment preserved renal function, protected from renal cortical apoptosis, up-regulated Bax, down-regulated Bcl-xL, and rescued from glomerular tubular disconnection and podocyte loss. Thus we have identified a novel clinically feasible therapeutic tool, which has the potential to protect from apoptosis and rescue from loss of functional tissue in chronic proteinuric kidney disease.

  • 3. Butt, Linus
    et al.
    Unnersjö-Jess, David
    Rinschen, Markus
    Höhne, Martin
    Edwards, Aurelie
    Ebert, Lena
    Castrop, Hayo
    Brismar, Hjalmar
    Blom, Hans
    Brinkkötter, Paul
    Schermer, Bernhard
    Benzing, Thomas
    Elucidating the pathogenesis of focal segmental glomerulosclerosis using CRISPR/Cas9 mediated genome editingManuscript (preprint) (Other academic)
  • 4.
    Donker, Dirk W.
    et al.
    Univ Utrecht, Univ Med Ctr Utrecht, Dept Intens Care Med, Utrecht, Netherlands..
    Brodie, Daniel
    Columbia Univ, Coll Phys & Surg, New York Presbyterian Hosp, Div Pulm Allergy & Crit Care Med, New York, NY USA..
    Henriques, Jose P. S.
    Univ Amsterdam, Acad Med Ctr, Dept Cardiol, Amsterdam, Netherlands..
    Broomé, Michael
    KTH, School of Technology and Health (STH), Medical Engineering, Medical Imaging. Karolinska Univ Hosp, ECMO Dept, SE-17176 Stockholm, Sweden.;Karolinska Inst, Dept Physiol & Pharmacol, Anaesthesiol & Intens Care, Stockholm, Sweden.
    Left Ventricular Unloading During Veno-Arterial ECMO: A Simulation Study2019In: ASAIO journal (1992), ISSN 1058-2916, E-ISSN 1538-943X, Vol. 65, no 1, p. 11-20Article in journal (Refereed)
    Abstract [en]

    Veno-arterial extracorporeal membrane oxygenation (VA ECMO) is widely used in cardiogenic shock. It provides systemic perfusion, but left ventricular (LV) unloading is suboptimal. Using a closed-loop, real-time computer model of the human cardiovascular system, cardiogenic shock supported by peripheral VA ECMO was simulated, and effects of various adjunct LV unloading interventions were quantified. After VA ECMO initiation (4 L/min) in cardiogenic shock (baseline), hemodynamics improved (increased to 85 mm Hg), while LV overload occurred (10% increase in end-diastolic volume [EDV], and 5 mm Hg increase in pulmonary capillary wedge pressure [PCWP]). Decreasing afterload (65 mm Hg mean arterial pressure) and circulating volume (-800 mL) reduced LV overload (12% decrease in EDV and 37% decrease in PCWP) compared with baseline. Additional intra-aortic balloon pumping only marginally decreased cardiac loading. Instead, adjunct Impella T enhanced LV unloading (23% decrease in EDV and 41% decrease in PCWP). Alternative interventions, for example, left atrial/ventricular venting, yielded substantial unloading. We conclude that real-time simulations may provide quantitative clinical measures of LV overload, depending on the degree of VA ECMO support and adjunct management. Simulations offer insights into individualized LV unloading interventions in cardiogenic shock supported by VA ECMO as a proof of concept for potential future applications in clinical decision support, which may help to improve individualized patient management in complex cardiovascular disease.

  • 5. Hilderman, Marie
    et al.
    Qureshi, Abdul R
    Al-Abed, Yousef
    Abtahi, Farhad
    KTH, School of Technology and Health (STH), Medical Engineering, Medical sensors, signals and systems.
    Lindecrantz, Kaj
    Anderstam, Björn
    Bruchfeld, Annette
    Cholinergic anti-inflammatory pathway activity in dialysis patients: a role for neuroimmunomodulation?2015In: Clinical Kidney Journal, ISSN 2048-8505, E-ISSN 2048-8513, Vol. 8, no 5Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: The cholinergic anti-inflammatory pathway (CAP) modulates inflammatory responses through the vagus nerve and the α-7-nicotinic acetylcholine receptor (α7nAChR) on macrophages and immune cells. Sympathetic/parasympathetic imbalance and chronic inflammation are both linked to poor outcome in dialysis patients. The aim of this study was to investigate CAP activity in these patients.

    METHODS: Twenty dialysis patients, 12 hemodialysis (HD) and 8 peritoneal dialysis (PD) patients (12 male, 8 female; age range 47-83 years) and 8 controls (5 male, 3 female; age range 31-52 years) were analyzed for C-reactive protein (CRP), tumor necrosis factor (TNF), interleukin-1b (IL-1b), IL-6 and IL-10 at baseline. The cytokines were then assessed after whole blood stimulation ex vivo with lipopolysaccharide (LPS) (10 and 100 ng/mL) and again in the presence of 45 and 90 μmol/L GTS-21, a cholinergic α7nAChR agonist.

    RESULTS: CRP, TNF, IL-1 and IL-6 were significantly higher, whereas IL-10 was significantly lower at baseline in patients compared with controls. After LPS stimulation, TNF increased significantly more in patients than in controls but decreased to similar levels in both groups after addition of GTS-21. IL-6 attenuation was comparable with TNF and the IL-1b pattern was similar but remained significantly higher in patients. Interestingly, IL-10 increased after GTS-21 in a dose-dependent manner, but only in patients. Results in HD and PD patients did not differ.

    CONCLUSIONS: The response of immune cells after LPS exposure and cholinergic stimulation suggests a functional CAP in dialysis patients. It may thus be possible to target the α7nAChR control of cytokine release as an anti-inflammatory strategy and thereby improve outcome in these patients.

  • 6.
    Jess, David Unnersjö
    KTH, School of Engineering Sciences (SCI), Applied Physics, Biophysics.
    High-resolution Imaging of Cleared and Expanded Kidney Tissue Samples2019Doctoral thesis, comprehensive summary (Other academic)
    Abstract [en]

    The kidney is one of the most important and complex organs in the humanbody with the task of filtering hundreds of litres of blood daily. It is responsiblefor the salt and acid/base balance in the body, as well as secretinghormones important for red blood cell production and blood pressure regulation. Kidney disease is one of the fastest growing causes of death in the modern world, and this motivates extensive research for better understandingthe function of the kidney in both health and disease. Kidney failure or end stage renal disease (ESRD) is irreversible and requires treatment with dialysisor transplantation. Some of the most important cellular structures for blood filtration in the kidney are of very small dimensions (below 200 nanometers), and thus electron microscopy has previously been the only method with high enough resolution to study the morphology and topology of these minute structures. In three studies included in this thesis, we show that the finest elements of the kidney can now be resolved using different light microscopy techniques. In study 1, we show that by combining optical clearing with STED microscopy, protein localizations in the slit diaphragm of the kidney can be resolved, with widths around 75 nanometers. In study 3, a novel sample preparation method, expansion microscopy, is utilized to isotropically expand kidney tissue samples in space. Expansion improves the effective resolution by a factor of 5, making it possible to resolve podocyte foot processes and the slit diaphragmusing diffraction-limited confocal microscopy. We also show that by combining expansion microscopy and STED microscopy, the effective resolution can be improved even further (<20 nm). In our most recent work, study 5, we apply a simplified, moderate tissue swelling protocol which together with optimization of the confocal imaging provides sufficient resolution to resolve foot processes and parts of the filtration barrier. This new protocol is fast and technically simple, making it ideal for routine use, such as for future clinical pathology. In collaboration with kidney researchers, we have applied both STED microscopy and expansion microscopy to various disease models, showing that these tools can be used to both visualize and quantify pathologies occurring in different parts of the glomerular filtration barrier (GFB). In study 2, STED microscopy in combination with optical clearing is used to study the localization of Coro2b in secondary foot processes in both mouse and human tissue. In two ongoing studies with preliminary results presented in the thesis, we use STED microscopy and optical clearing to study the pathogenesis of focal segmental glomerulosclerosis (FSGS) by the use of genetic mouse models. Based on STED images, we extract different morphological parameters from foot processes and the glomerular filtration barrier (GFB) at different stages of the disease. In study 4, we apply a tissue expansion protocol to answer questions about the phenotype seen in podocytes where the mediator complex subunit 22 (Med22) is inactivated. By inactivating Med22 in a transgenic mouse line with cytosolic expression of tdTomato in podocytes, we saw strong indications that the vesicle-like structures seen in EM micrographs were indeed intracellular vesicles and not dilated sub-podocyte space. In summary, the work presented in this thesis has contributed to the development of a new toolbox for imaging renal ultra-structure using light microscopy, a field previously reserved for electron microscopy.

  • 7. Li, Yanhong
    et al.
    Zelenina, Marina
    KTH, School of Engineering Sciences (SCI), Applied Physics, Cell Physics. Karolinska Institutet, Sweden.
    Plat-Willson, Genevieve
    Marcoux, Marie-Odile
    Aperia, Anita
    Casper, Charlotte
    Urinary aquaporin-2 excretion during ibuprofen or indomethacin treatment in preterm infants with patent ductus arteriosus2011In: Acta Paediatrica, ISSN 0803-5253, E-ISSN 1651-2227, Vol. 100, no 1, p. 59-66Article in journal (Refereed)
    Abstract [en]

    Aim: Water channel AQP2 is the target for vasopressin (AVP) and a major determinant of urinary concentrating capacity. In mature kidneys, prostaglandins counteract the effect of AVP on AQP2 expression at functional sites. We investigated whether disturbances in water homeostasis in infants with patent ductus arteriosus (PDA) treated with prostaglandin inhibitors can be attributed to activation of AQP2. Methods: In 53 infants with symptomatic PDA (gestational age 24-33 weeks), 30 receiving ibuprofen and 23 indomethacin starting at 2-15 days of life, clinical and biochemical data were collected before treatment and after each dose of the drugs. Urinary AQP2 was determined by dot immunoblotting. Results: Urinary AQP2 level and osmolality were decreased in both groups. Urinary osmolality was overall low and correlated inversely with fluid uptake. In ibuprofen group, there was no correlation of AQP2 level with urinary osmolality. Conclusion: There was no AQP2 upregulation in the infants. The low urinary osmolality and dissociation between urinary osmolality and urinary AQP2 level indicate that the fluid retention sometimes observed in PDA infants treated with prostaglandin inhibitors is not caused by increased levels of functional AQP2. Thus, knowledge about the renal physiology of the adult cannot always be transferred to the infant kidney.

  • 8. Nishibori, Yukino
    et al.
    Katayama, Kan
    Parikka, Mataleena
    Oddsson, Asmundur
    Nukui, Masatoshi
    Hultenby, Kjell
    Wernerson, Annika
    He, Bing
    Ebarasi, Lwaki
    Raschperger, Elisabeth
    Norlin, Jenny
    Uhlen, Mathias
    KTH, School of Biotechnology (BIO), Proteomics.
    Patrakka, Jaakko
    Betsholtz, Christer
    Tryggvason, Karl
    Glcci1 Deficiency Leads to Proteinuria2011In: Journal of the American Society of Nephrology, ISSN 1046-6673, E-ISSN 1533-3450, Vol. 22, no 11, p. 2037-2046Article in journal (Refereed)
    Abstract [en]

    Unbiased transcriptome profiling and functional genomics approaches identified glucocorticoid-induced transcript 1 (GLCCI1) as being a transcript highly specific for the glomerulus, but its role in glomerular development and disease is unknown. Here, we report that mouse glomeruli express far greater amounts of Glcci1 protein compared with the rest of the kidney. RT-PCR and Western blotting demonstrated that mouse glomerular Glcci1 is approximately 60 kD and localizes to the cytoplasm of podocytes in mature glomeruli. In the fetal kidney, intense Glcci1 expression occurs at the capillary-loop stage of glomerular development. Using gene knockdown in zebrafish with morpholinos, morphants lacking Glcci1 function had collapsed glomeruli with foot-process effacement. Permeability studies of the glomerular filtration barrier in these zebrafish morphants demonstrated a disruption of the selective glomerular permeability filter. Taken together, these data suggest that Glcci1 promotes the normal development and maintenance of podocyte structure and function.

  • 9. Rodriguez, Patricia Q.
    et al.
    Chen, Ping
    Jess, David Unnersjö
    KTH, School of Engineering Sciences (SCI), Applied Physics, Biophysics. KTH, Centres, Science for Life Laboratory, SciLifeLab.
    Zambrano, Sonia S.
    Guo, Jing
    Schwarz, Angelina
    Möller-Hackbarth, Katja
    Axelsson, Jonas
    Blom, Hans
    Sandberg, Rickard
    Jahnukainen, Timo
    Ebarasi, Lwaki
    Patrakka, Jaakko
    Mediator complex subunit 22 is necessary for glomerular homeostasis by regulation of podocyte vesicular traffickingManuscript (preprint) (Other academic)
  • 10. Schwarz, Angelina
    et al.
    Katja, Möller-Hackbarth
    Ebarasi, Lwaki
    Unnersjö-Jess, David
    Zambrano, Sonia
    Blom, Hans
    Wernerson, Annika
    Lal, Mark
    Patrakka, Jaakko
    Coro2b, a podocyte protein downregulated in human diabetic nephropathy, is involved in the development of protamine sulphate-induced foot process effacementManuscript (preprint) (Other academic)
  • 11.
    Seoane, Fernando
    et al.
    KTH, School of Technology and Health (STH), Medical Engineering, Medical sensors, signals and systems. Univ Boras, Fac Care Sci Work Life & Social Welfare, Sweden.
    Abtahi, Shirin
    Abtahi, Farhad
    KTH, School of Technology and Health (STH), Medical Engineering, Medical sensors, signals and systems. Karolinska Inst, Dept Clin Sci Intervent & Technol, Sweden.
    Ellegård, Lars
    Johannsson, Gudmundur
    Bosaeus, Ingvar
    Ward, Leigh C
    Mean Expected Error in Prediction of Total Body Water: A True Accuracy Comparison between Bioimpedance Spectroscopy and Single Frequency Regression Equations2015In: BioMed Research International, ISSN 2314-6133, E-ISSN 2314-6141, article id 656323Article in journal (Refereed)
    Abstract [en]

    For several decades electrical bioimpedance (EBI) has been used to assess body fluid distribution and body composition. Despite the development of several different approaches for assessing total body water (TBW), it remains uncertain whether bioimpedance spectroscopic (BIS) approaches are more accurate than single frequency regression equations. The main objective of this study was to answer this question by calculating the expected accuracy of a single measurement for different EBI methods. The results of this study showed that all methods produced similarly high correlation and concordance coefficients, indicating good accuracy as a method. Even the limits of agreement produced from the Bland-Altman analysis indicated that the performance of single frequency, Sun’s prediction equations, at population level was close to the performance of both BIS methods; however, when comparing the Mean Absolute Percentage Error value between the single frequency prediction equations and the BIS methods, a significant difference was obtained, indicating slightly better accuracy for the BIS methods. Despite the higher accuracy of BIS methods over 50 kHz prediction equations at both population and individual level, the magnitude of the improvement was small. Such slight improvement in accuracy of BIS methods is suggested insufficient to warrant their clinical use where the most accurate predictions of TBW are required, for example, when assessing over-fluidic status on dialysis. To reach expected errors below 4-5%, novel and individualized approaches must be developed to improve the accuracy of bioimpedance-based methods for the advent of innovative personalized health monitoring applications.

  • 12. Sistani, Laleh
    et al.
    Dunér, Fredrik
    Udumala, Sunil
    Hultenby, Kjell
    Uhlén, Mathias
    KTH, School of Biotechnology (BIO), Proteomics.
    Betsholtz, Christer
    Tryggvason, Karl
    Wernerson, Annika
    Patrakka, Jaakko
    Pdlim2 is a novel actin-regulating protein of podocyte foot processes2011In: Kidney International, ISSN 0085-2538, E-ISSN 1523-1755, Vol. 80, no 10, p. 1045-1054Article in journal (Refereed)
    Abstract [en]

    The slit diaphragm and the apical and basal membrane domains of podocytes are connected to each other by an actin-based cytoskeleton critical to the maintenance of the glomerular filtration barrier. In an effort to discover novel regulatory proteins of the podocyte foot process, we identified and characterized pdlim2, a member of the actin-associated LIM protein subfamily of cytosolic proteins typified by an N-terminal PDZ domain and a C-terminal LIM domain. In the kidney, the pdlim2 protein is highly specific for the glomerulus and podocyte foot processes as shown by RT-PCR, western blotting, immunofluorescence, and immunoelectron microscopy. In cultured podocytes, pdlim2 was associated with stress fibers and cortical actin. Pdlim2 seems to regulate actin dynamics in podocytes since stress fibers were stabilized in its presence. Mechanistically, pdlim2 interacts with two actin-associated podocyte proteins, alpha-actinin-4 and angiomotin-like-1, as shown by immunoprecipitation and yeast two-hybrid analyses. By semi-quantitative immunoelectron microscopy, there was a reduced expression of pdlim2 in podocytes of patients with minimal change nephrotic syndrome and membranous nephropathy, whereas its expression was unchanged in patients with focal segmental glomerulosclerosis. Hence, pdlim2 is a novel actin-regulating protein of podocyte foot processes that may have a role in the pathogenesis of glomerular diseases.

  • 13.
    Unnersjö-Jess, David
    et al.
    KTH, School of Engineering Sciences (SCI), Applied Physics, Biophysics.
    Butt, Linus
    Höhne, Martin
    Patrakka, Jaakko
    Schermer, Bernhard
    Benzing, Thomas
    Scott, Lena
    Blom, Hans
    Brismar, Hjalmar
    Renal diagnostics using a simplified optical clearing and swelling protocolManuscript (preprint) (Other academic)
  • 14. Vieux, Rachel
    et al.
    Zelenina, Marina
    Nordic Center of Excellence for Research in Water Imbalance Related Disorders (WIRED), Karolinska Institutet, Stockholm, Sweden. Department of Women's and Children's Health, Karolinska Institutet.
    Aperia, Anita
    Nordic Center of Excellence for Research in Water Imbalance Related Disorders (WIRED), Karolinska Institutet, Stockholm, Sweden. Department of Women's and Children's Health, Karolinska Institutet.
    Hascoët, Jean-Michel
    The renal adverse effects of ibuprofen are not mediated by AQP2 water channels2010In: Pediatric nephrology (Berlin, West), ISSN 0931-041X, E-ISSN 1432-198X, Vol. 25, no 7, p. 1277-1284Article in journal (Refereed)
    Abstract [en]

    The aim of this study was to determine (1) whether ibuprofen treatment in very preterm infants causes an increase in the renal water channel aquaporin-2 (AQP2) activity in the collecting duct via prostaglandin synthesis inhibition and (2) whether AQP2 activity remains disturbed long after ibuprofen treatment has ended. This was a prospective study involving premature infants with a gestation age of 27-31 weeks who received treatment between December 2005 and August 2006 in a tertiary Neonatal Intensive Care Unit. Each ibuprofen-treated infant was matched to two controls. Renal glomerular and tubular function were evaluated weekly for 1 month, and urinary AQP2 was measured by immuno-dotting. In total, 166 longitudinal samples were analyzed in 36 infants. Median [interquartile range] gestational age and birthweight were 28 [27.0-29.5] weeks and 1160 [1041-1242] g, respectively. Perinatal factors were similar in both groups. Urine output was significantly decreased in the ibuprofen-treated infants during the treatment. The urinary AQP2 level decreased significantly from day 2 to day 7 in both groups and was similar thereafter for the first month of life in ibuprofen-treated and control groups. Based on our results, we conclude that ibuprofen-induced oligo-anuria is not associated with a change in AQP2 activity and that ibuprofen does not affect AQP2 activity during the first month of life in very preterm neonates.

  • 15.
    Zelenina, Marina
    et al.
    Nordic Centre of Excellence for Research in Water Imbalance Related Disorders (WIRED), Department of Woman and Child Health, Karolinska Institute.
    Li, Yanhong
    Glorieux, Isabelle
    Arnaud, Catherine
    Cristini, Christelle
    Decramer, Stéphane
    Aperia, Anita
    Casper, Charlotte
    Urinary aquaporin-2 excretion during early human development2006In: Pediatric nephrology (Berlin, West), ISSN 0931-041X, E-ISSN 1432-198X, Vol. 21, no 7, p. 947-952Article in journal (Refereed)
    Abstract [en]

    This study was undertaken to assess one of the determinants of kidney concentrating capacity, aquaporin-2 (AQP2), in order to understand the physiopathology of water balance in newborn babies. Urinary AQP2 excretion has been shown to be proportional to AQP2 level in the apical plasma membrane of the kidney collecting ducts and has been suggested as a marker of vasopressin (AVP) action. Urinary AQP2 excretion in the early postnatal period and at 3 weeks of age was measured in 123 neonates admitted during a 6-month period to the neonatal intensive care unit of the Children's Hospital of Toulouse, France. Clinical and biochemical data were collected for each child. During the first days after birth, higher urinary AQP2 was observed in boys than in girls (P=0.01) and positively correlated with urinary sodium/potassium (Na/K) ratio (r=0.33, P=0.01). When the babies had reached 3 weeks of age, urinary AQP2 was proportional to the gestational age at birth (r=0.33, P=0.0068) and daily weight gain (r=0.36, P=0.003). It did not correlate with urinary osmolality, which was overall very low in all babies. Urinary AQP2 was decreased in conditions of impaired renal function (r=-0.42, P=0.0005) and acidosis (P=0.03). Prenatal corticosteroid treatment had no significant impact on urinary AQP2 level. Our data show that urinary AQP2 correlates with the overall maturity of tubular function in human neonates. In babies at this early age, urinary AQP2 cannot serve as a direct marker of the renal action of AVP but reflects AQP2 expression level associated with different physiopathological conditions.

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