N2-(4-Amino-cyclohexyl)-9-cyclopentyl-N6-(6-furan-2-yl-pyridine-3-ylmethyl)-9H-purine-2,6-diamine (BP-14) and 2-(5-{[2-(4-amino-cyclohexylamino)-9-cyclopentyl-9H-purine-6-ylamino]-methyl}-pyridine-2-yl)-phenol (BP-20) are novel cyclin-dependent kinase inhibitors, structurally related to roscovitine, with significant biological activity. A simple, selective and sensitive liquid chromatography - tandem mass spectrometry method for determining them in rat plasma, using roscovitine as an internal standard, was developed and validated. Chromatographic separation was performed in reversed phase mode on Acquity BEH C18 column (100 × 2.1 mm, 1.7 μm) by gradient elution with mobile phases composed of 15 mM ammonium formate pH 4.0 and methanol at flow rate 0.25 mL/min at 40 °C. The analytes were detected based on their characteristic multiple reaction monitoring transitions in positive electrospray ionization mode m/z 473.07 > 157.93 for BP-14, m/z 499.62 > 184.2 for BP-20 and m/z 355.5 > 90.86 for internal standard. In plasma the method provided good linearity within the entire concentration range: 1-10,000 nmol/L (r2 = 0.9989) for BP-14 and 10-25,000 nmol/L (r2 = 0.9994) for BP-20; the limit of detection was 0.6 nmol/L for BP-14 and 6.1 nmol/L for BP-20. Validation was also performed in bile and urine. The results of validation fit within the acceptance limits following European Medicines Agency guidelines. The method was applied in a pharmacokinetic study of BP-14 and BP-20 in vivo in rats following intravenous and intraduodenal administration including plasma pharmacokinetics, tissue distribution and excretion (renal and biliary). Both compounds showed low bioavailability after intraduodenal administration (0.630 and 1.58% for BP-14 and BP-20, respectively). Distribution into all the analyzed tissues (brain, lungs, liver, kidney, spleen, muscle, adipose tissue) was observed 3 h after single dose administration, the highest and lowest concentrations being reached in the adipose tissue and brain, respectively. The biliary excretion of the parent BP-14 and BP-20 compounds accounted for 4.81% and 10.6% of the doses, respectively, and renal excretion for <0.5% in both cases. The obtained results represent pilot knowledge for further development of a new generation of compounds with strong anticancer activities.

• Klíčová slova
• BP-14, BP-20, Cyclin-dependent kinase inhibitor, Pharmacokinetics, Tissue distribution,
• MeSH
• 2-aminopurin analogy a deriváty   analýza   farmakokinetika   MeSH
• biologická dostupnost MeSH
• cykliny chemie   MeSH
• hepatobiliární exkrece účinky léků   MeSH
• inhibitory proteinkinas aplikace a dávkování   analýza   chemie   farmakokinetika   MeSH
• intravenózní podání metody   MeSH
• kalibrace MeSH
• krysa rodu Rattus MeSH
• lidé MeSH
• limita detekce MeSH
• molekulární struktura MeSH
• potkani Wistar MeSH
• protinádorové látky aplikace a dávkování   analýza   chemie   farmakokinetika   MeSH
• reprodukovatelnost výsledků MeSH
• tandemová hmotnostní spektrometrie metody   MeSH
• tkáňová distribuce účinky léků   MeSH
• vysokoúčinná kapalinová chromatografie metody   MeSH
• vztahy mezi strukturou a aktivitou MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• lidé MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• 2-aminopurin MeSH
• cykliny MeSH
• inhibitory proteinkinas MeSH
• N2-(4-aminocyclohexyl)-9-cyclopentyl-N6-((6-(2-furyl)-3-pyridyl)methyl)purine-2,6-diamine MeSH Prohlížeč
• protinádorové látky MeSH

Anaplastic thyroid carcinoma (ATC) is an extremely aggressive human malignancy characterized by a marked degree of invasiveness, absense of features of thyroid differentiation and resistance to current medical treatment. It is well known that ATCs are characterized by deregulation of genes related to cell cycle regulation, i.e., cyclin-dependent kinases (CDKs) and endogenous cyclin-dependent kinase inhibitors (CDKIs). Therefore, in the present study, the effect of a novel exogenous cyclin-dependent kinase inhibitor, BP-14, was investigated in three human ATC cell lines. The ATC-derived cell lines FRO, SW1736 and 8505C were treated with BP-14 alone or in combination with the mTOR inhibitor everolimus. In all ATC cell lines, treatment with BP-14 decreased cell viability and, in two of them, BP-14 modified expression of genes involved in epithelial-mesenchymal transition. Thus, our data indicate that BP-14 is a potential new compound effective against ATC. Combined treatment with BP-14 and the mTOR inhibitor everolimus had a strong synergistic effect on cell viability in all three cell lines, suggesting that the combined used of CDK and mTOR inhibitors may be a useful strategy for ATC treatment.

• MeSH
• 2-aminopurin analogy a deriváty   farmakologie   MeSH
• anaplastický karcinom štítné žlázy farmakoterapie   genetika   MeSH
• epitelo-mezenchymální tranzice účinky léků   MeSH
• everolimus farmakologie   MeSH
• inhibitory proteinkinas farmakologie   MeSH
• lidé MeSH
• nádorové buněčné linie MeSH
• nádory štítné žlázy farmakoterapie   genetika   MeSH
• protokoly protinádorové kombinované chemoterapie farmakologie   MeSH
• regulace genové exprese u nádorů účinky léků   MeSH
• synergismus léků MeSH
• viabilita buněk účinky léků   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• 2-aminopurin MeSH
• everolimus MeSH
• inhibitory proteinkinas MeSH
• N2-(4-aminocyclohexyl)-9-cyclopentyl-N6-((6-(2-furyl)-3-pyridyl)methyl)purine-2,6-diamine MeSH Prohlížeč

The 14-3-3 proteins, a family of conserved regulatory molecules, participate in a wide range of cellular processes through binding interactions with hundreds of structurally and functionally diverse proteins. Several distinct mechanisms of the 14-3-3 protein function were described, including conformational modulation of the bound protein, masking of its sequence-specific or structural features, and scaffolding that facilitates interaction between two simultaneously bound proteins. Details of these functional modes, especially from the structural point of view, still remain mostly elusive. This review gives an overview of the current knowledge concerning the structure of 14-3-3 proteins and their complexes as well as the insights it provides into the mechanisms of their functions. We discuss structural basis of target recognition by 14-3-3 proteins, common structural features of their complexes and known mechanisms of 14-3-3 protein-dependent regulations.

• MeSH
• DNA vazebné proteiny MeSH
• Eukaryota metabolismus   MeSH
• fosforylace MeSH
• genetická variace MeSH
• interakční proteinové domény a motivy * MeSH
• konformace proteinů MeSH
• lidé MeSH
• molekulární modely MeSH
• protein - isoformy chemie   metabolismus   MeSH
• proteiny 14-3-3 chemie   genetika   metabolismus   MeSH
• terciární struktura proteinů MeSH
• vazba proteinů MeSH
• vazebná místa MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH
• Názvy látek
• DNA vazebné proteiny MeSH
• protein - isoformy MeSH
• proteiny 14-3-3 MeSH

Beside of the protein crystallography or NMR, another attractive option in protein structure analysis has recently appeared: computer modeling of the protein structure based on homology and similarity with proteins of already known structures. We have used the combination of computer modeling with spectroscopic techniques, such as steady-state or time-resolved fluorescence spectroscopy, and with molecular biology techniques. This method could provide useful structural information in the cases where crystal or NMR structure is not available. Molecular modeling of the ATP site within the H4-H5-loop revealed eight amino acids residues, namely besides the previously reported amino acids Asp443, Lys480, Lys501, Gly502 and Arg544, also Glu446, Phe475 and Gln482, which form the complete ATP recognition site. Moreover, we have proved that a hydrogen bond between Arg423 and Glu472 supports the connection of two opposite halves of the ATP-binding pocket. Similarly, the conserved residue Pro489 is important for the proper interaction of the third and fourth beta-strands, which both contain residues that take part in the ATP-binding. Alternatively, molecular dynamics simulation combined with dynamic fluorescence spectroscopy revealed that 14-3-3 zeta C-terminal stretch is directly involved in the interaction of 14-3-3 protein with the ligand. Phosphorylation at Thr232 induces a conformational change of the C-terminus, which is presumably responsible for observed inhibition of binding abilities. Phosphorylation at Thr232 induces more extended conformation of 14-3-3zeta C-terminal stretch and changes its interaction with the rest of the 14-3-3 molecule. This could explain negative regulatory effect of phosphorylation at Thr232 on 14-3-3 binding properties.

• MeSH
• adenosintrifosfát chemie   metabolismus   MeSH
• alkoholoxidoreduktasy MeSH
• DNA vazebné proteiny fyziologie   MeSH
• fluorescenční spektrometrie metody   MeSH
• fosfoproteiny fyziologie   MeSH
• fosforylace MeSH
• konformace proteinů * MeSH
• konzervovaná sekvence MeSH
• molekulární modely * MeSH
• počítačová simulace * MeSH
• proteiny 14-3-3 chemie   metabolismus   MeSH
• sekvence aminokyselin MeSH
• sekvenční homologie aminokyselin MeSH
• sodíko-draslíková ATPasa chemie   fyziologie   MeSH
• threonin fyziologie   MeSH
• vazebná místa MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• adenosintrifosfát MeSH
• alkoholoxidoreduktasy MeSH
• C-terminal binding protein MeSH Prohlížeč
• DNA vazebné proteiny MeSH
• fosfoproteiny MeSH
• proteiny 14-3-3 MeSH
• sodíko-draslíková ATPasa MeSH
• threonin MeSH

Various proteins play a decisive role in the pathology of different neurodegenerative diseases. Nonetheless, most of these proteins can only be detected during a neuropathological assessment, although some non-specific biomarkers are routinely tested for in the cerebrospinal fluid (CSF) as a part of the differential diagnosis of dementia. In antemortem CSF samples from 117 patients with different types of neuropathologically confirmed neurodegenerative disease with dementia, we assessed total-tau (t-tau), phosphorylated-tau (181P) (p-tau), amyloid-beta (1-42) (Aβ42), TAR DNA binding protein (TDP)-43, progranulin (PGRN), and neurofilament light (NfL) chain levels, and positivity of protein 14-3-3. We found t-tau levels and the t-tau/p-tau ratios were significantly higher in prion diseases compared to the other neurodegenerative diseases. Statistically significant differences in the t-tau/Aβ42 ratio predominantly corresponded to t-tau levels in prion diseases and Aβ42 levels in AD. TDP-43 levels were significantly lower in prion diseases. Additionally, the TDP-43/Aβ42 ratio was better able to distinguish Alzheimer's disease from other neurodegenerative diseases compared to using Aβ42 alone. In frontotemporal lobar degeneration, PRGN levels were significantly higher in comparison to other neurodegenerative diseases. There is an increasing need for biomarkers suitable for diagnostic workups for neurodegenerative diseases. It appears that adding TDP-43 and PGRN to the testing panel for neurodegenerative diseases could improve the resolution of differential diagnoses.

• MeSH
• amyloidní beta-protein mozkomíšní mok   MeSH
• biologické markery mozkomíšní mok   MeSH
• demence mozkomíšní mok   klasifikace   diagnóza   MeSH
• diferenciální diagnóza MeSH
• DNA vazebné proteiny mozkomíšní mok   MeSH
• lidé středního věku MeSH
• lidé MeSH
• neurofilamentové proteiny mozkomíšní mok   MeSH
• peptidové fragmenty mozkomíšní mok   MeSH
• pitva MeSH
• progranuliny mozkomíšní mok   MeSH
• proteiny 14-3-3 mozkomíšní mok   MeSH
• proteiny tau mozkomíšní mok   MeSH
• proteiny v mozkomíšním moku mozkomíšní mok   MeSH
• regulace genové exprese MeSH
• retrospektivní studie MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• senzitivita a specificita MeSH
• Check Tag
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• amyloid beta-protein (1-42) MeSH Prohlížeč
• amyloidní beta-protein MeSH
• biologické markery MeSH
• DNA vazebné proteiny MeSH
• GRN protein, human MeSH Prohlížeč
• MAPT protein, human MeSH Prohlížeč
• neurofilament protein L MeSH Prohlížeč
• neurofilamentové proteiny MeSH
• peptidové fragmenty MeSH
• progranuliny MeSH
• proteiny 14-3-3 MeSH
• proteiny tau MeSH
• proteiny v mozkomíšním moku MeSH
• TARDBP protein, human MeSH Prohlížeč

We identified a de novo deletion of 14q11.2 in a Czech patient with developmental delay, mild autistic features, macrosomy, macrocephaly, orthognathic deformities, and dysmorphic facial features. The clinical follow-up of the patient lasting 14 years documented changes in the facial dysmorphism from infancy to adolescence. The deletion affects approximately 200 kb of DNA with five protein-coding genes and two snoRNA genes. Two of the protein-coding genes, SUPT16H and CHD8, have been proposed as candidate genes for a new microdeletion syndrome. Our patient further supports the existence of this syndrome and extends its phenotypic spectrum, especially points to the possibility that orthognathic deformities may be associated with microdeletions of 14q11.2. CHD8 mutations have been found in patients with neurodevelopmental disorders and macrocephaly. The HNRNPC gene, repeatedly deleted in patients with developmental delay, is another candidate as its 5́ end is adjacent to the deletion, and the expression of this gene may be affected by position effect.

• Klíčová slova
• CHD8, Microdeletion 14q11.2, SUPT16H, intellectual disability, macrocephaly, orthognathic deformities,
• MeSH
• chromozomální delece * MeSH
• DNA vazebné proteiny genetika   MeSH
• lidé MeSH
• lidské chromozomy, pár 14 genetika   MeSH
• megalencefalie diagnóza   genetika   MeSH
• mentální retardace diagnóza   genetika   MeSH
• mladiství MeSH
• mnohočetné abnormality diagnóza   genetika   MeSH
• následné studie MeSH
• transkripční faktory genetika   MeSH
• vývojové poruchy u dětí diagnóza   genetika   MeSH
• Check Tag
• lidé MeSH
• mladiství MeSH
• mužské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• kazuistiky MeSH
• práce podpořená grantem MeSH
• Názvy látek
• CHD8 protein, human MeSH Prohlížeč
• DNA vazebné proteiny MeSH
• transkripční faktory MeSH

Translocase of outer mitochondrial membrane 34 (TOMM34) orchestrates heat shock protein 70 (HSP70)/HSP90-mediated transport of mitochondrial precursor proteins. Here, using in vitro phosphorylation and refolding assays, analytical size-exclusion chromatography, and hydrogen/deuterium exchange MS, we found that TOMM34 associates with 14-3-3 proteins after its phosphorylation by protein kinase A (PKA). PKA preferentially targeted two serine residues in TOMM34: Ser93 and Ser160, located in the tetratricopeptide repeat 1 (TPR1) domain and the interdomain linker, respectively. Both of these residues were necessary for efficient 14-3-3 protein binding. We determined that phosphorylation-induced structural changes in TOMM34 are further augmented by binding to 14-3-3, leading to destabilization of TOMM34's secondary structure. We also observed that this interaction with 14-3-3 occludes the TOMM34 interaction interface with ATP-bound HSP70 dimers, which leaves them intact and thereby eliminates an inhibitory effect of TOMM34 on HSP70-mediated refolding in vitro In contrast, we noted that TOMM34 in complex with 14-3-3 could bind HSP90. Both TOMM34 and 14-3-3 participated in cytosolic precursor protein transport mediated by the coordinated activities of HSP70 and HSP90. Our results provide important insights into how PKA-mediated phosphorylation and 14-3-3 binding regulate the availability of TOMM34 for its interaction with HSP70.

• Klíčová slova
• 14-3-3 protein, 70-kDa heat shock protein (Hsp70), HSP70, Hsp70, Tomm34, dimerization, hydrogen-deuterium exchange, molecular chaperone, phosphorylation, protein folding, protein import, protein kinase A (PKA), protein-nucleic acid interaction, protein–protein interaction, translocase of outer mitochondrial membrane 34 (TOMM34),
• MeSH
• DNA vazebné proteiny genetika   metabolismus   MeSH
• fosforylace fyziologie   MeSH
• lidé MeSH
• MFC-7 buňky MeSH
• mitochondriální importní komplex MeSH
• mitochondriální membrány metabolismus   MeSH
• mitochondriální proteiny metabolismus   MeSH
• molekulární chaperony metabolismus   MeSH
• proteinkinasy závislé na cyklickém AMP metabolismus   MeSH
• proteiny 14-3-3 metabolismus   MeSH
• proteiny tepelného šoku HSP70 metabolismus   MeSH
• proteiny tepelného šoku HSP72 metabolismus   MeSH
• proteiny tepelného šoku HSP90 metabolismus   MeSH
• signální transdukce MeSH
• transkripční faktory genetika   metabolismus   MeSH
• transportní proteiny mitochondriální membrány genetika   metabolismus   MeSH
• vazba proteinů MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• BCL2-associated athanogene 1 protein MeSH Prohlížeč
• DNA vazebné proteiny MeSH
• mitochondriální importní komplex MeSH
• mitochondriální proteiny MeSH
• molekulární chaperony MeSH
• proteinkinasy závislé na cyklickém AMP MeSH
• proteiny 14-3-3 MeSH
• proteiny tepelného šoku HSP70 MeSH
• proteiny tepelného šoku HSP72 MeSH
• proteiny tepelného šoku HSP90 MeSH
• TOMM34 protein, human MeSH Prohlížeč
• transkripční faktory MeSH
• transportní proteiny mitochondriální membrány MeSH

Kabuki syndrome is mainly caused by dominant de-novo pathogenic variants in the KMT2D and KDM6A genes. The clinical features of this syndrome are highly variable, making the diagnosis of Kabuki-like phenotypes difficult, even for experienced clinical geneticists. Herein we present molecular genetic findings of causal genetic variation using array comparative genome hybridization and a Mendeliome analysis, utilizing targeted exome analysis focusing on regions harboring rare disease-causing variants in Kabuki-like patients which remained KMT2D/KDM6A-negative. The aCGH analysis revealed a pathogenic CNV in the 14q11.2 region, while targeted exome sequencing revealed pathogenic variants in genes associated with intellectual disability (HUWE1, GRIN1), including a gene coding for mandibulofacial dysostosis with microcephaly (EFTUD2). Lower values of the MLL2-Kabuki phenotypic score are indicative of Kabuki-like phenotype (rather than true Kabuki syndrome), where aCGH and Mendeliome analyses have high diagnostic yield. Based on our findings we conclude that for new patients with Kabuki-like phenotypes it is possible to choose a specific molecular testing approach that has the highest detection rate for a given MLL2-Kabuki score, thus fostering more precise patient diagnosis and improved management in these genetically- and phenotypically heterogeneous clinical entities.

• Klíčová slova
• EFTUD2, GRIN1, HUWE1, Intellectual disability, KMT2D, Kabuki syndrome,
• MeSH
• dítě MeSH
• DNA vazebné proteiny genetika   MeSH
• elongační faktory genetika   MeSH
• exom MeSH
• fenotyp * MeSH
• genetická heterogenita * MeSH
• genotyp * MeSH
• histondemethylasy genetika   MeSH
• jaderné proteiny genetika   MeSH
• krevní nemoci diagnóza   genetika   patofyziologie   MeSH
• lidé MeSH
• lidské chromozomy, pár 14 MeSH
• malý jaderný ribonukleoprotein U5 genetika   MeSH
• mandibulofaciální dysostóza genetika   MeSH
• mentální retardace genetika   MeSH
• mikrocefalie genetika   MeSH
• mnohočetné abnormality diagnóza   genetika   patofyziologie   MeSH
• nádorové proteiny genetika   MeSH
• nádorové supresorové proteiny genetika   MeSH
• obličej abnormality   patofyziologie   MeSH
• předškolní dítě MeSH
• proteiny nervové tkáně genetika   MeSH
• receptory N-methyl-D-aspartátu genetika   MeSH
• srovnávací genomová hybridizace MeSH
• ubikvitinligasy genetika   MeSH
• vestibulární nemoci diagnóza   genetika   patofyziologie   MeSH
• vysoce účinné nukleotidové sekvenování MeSH
• Check Tag
• dítě MeSH
• lidé MeSH
• mužské pohlaví MeSH
• předškolní dítě MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• kazuistiky MeSH
• Názvy látek
• DNA vazebné proteiny MeSH
• EFTUD2 protein, human MeSH Prohlížeč
• elongační faktory MeSH
• GRIN1 protein, human MeSH Prohlížeč
• histondemethylasy MeSH
• HUWE1 protein, human MeSH Prohlížeč
• jaderné proteiny MeSH
• KDM6A protein, human MeSH Prohlížeč
• KMT2D protein, human MeSH Prohlížeč
• malý jaderný ribonukleoprotein U5 MeSH
• nádorové proteiny MeSH
• nádorové supresorové proteiny MeSH
• proteiny nervové tkáně MeSH
• receptory N-methyl-D-aspartátu MeSH
• ubikvitinligasy MeSH

OBJECTIVE: To investigate with the use of ambulatory blood pressure (BP) monitoring whether nocturnal BP dip and nighttime BP values are different in children with untreated primary and secondary hypertension. STUDY DESIGN: Ambulatory BP monitoring studies from 145 children with untreated hypertension were retrospectively analyzed. Forty-five children had primary hypertension and 100 children had secondary hypertension. RESULTS: Children with secondary hypertension had lower nocturnal BP dip for systolic and diastolic BP in comparison to children with primary hypertension (8% +/- 5% vs 14% +/- 4% for systolic and 14% +/- 7% vs 22% +/- 5% for diastolic BP, P < .0001 for both). Eleven percent of children with primary hypertension were classified as nondipper (BP dip <10%) for systolic BP and no child for diastolic BP; on the contrary, in children with secondary hypertension, 65% were nondippers for systolic and 21% for diastolic BP. Nocturnal systolic and diastolic BP loads were significantly greater in children with secondary hypertension than in those with primary hypertension. CONCLUSIONS: Reduced nocturnal BP dip and sustained nighttime BP elevation are specific markers of secondary hypertension in children with untreated hypertension. Children with blunted nocturnal BP dip or sustained nighttime hypertension should be thoroughly investigated searching for the underlying cause of hypertension.

• MeSH
• ambulantní monitorování krevního tlaku MeSH
• cirkadiánní rytmus fyziologie   MeSH
• diferenciální diagnóza MeSH
• dítě MeSH
• dospělí MeSH
• hypertenze diagnóza   etiologie   patofyziologie   MeSH
• kohortové studie MeSH
• krevní tlak fyziologie   MeSH
• lidé MeSH
• mladiství MeSH
• retrospektivní studie MeSH
• senzitivita a specificita MeSH
• Check Tag
• dítě MeSH
• dospělí MeSH
• lidé MeSH
• mladiství MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• srovnávací studie MeSH

BACKGROUND/AIM: Unilateral renal agenesis (URA) is a model for a reduced nephron number that is believed to be a risk factor for blood pressure (BP) elevation and reduced renal function. The aim of the study was to investigate BP and renal function in children with URA. METHODS: Data on children with URA from two pediatric nephrology centers were firstly retrospectively reviewed (renal ultrasound and scintigraphy, clinical BP, creatinine clearance, urinalysis). Children with normal renal ultrasound and scintigraphy were thereafter investigated using ambulatory BP monitoring. RESULTS: Twenty-nine children with URA were investigated--14 children with an abnormal kidney (mostly scarring) and 15 children with healthy kidneys. Hypertension was diagnosed on the basis of clinical BP in 57% of the children with abnormal kidneys and on the basis of ambulatory BP monitoring in 1 child (7%) with healthy kidneys. The mean ambulatory BP in children with normal kidneys was not significantly different from that in controls. Forty-three percent of the children with abnormal kidneys had a reduced renal function, but none of children with normal kidneys. CONCLUSIONS: Children with abnormalities of a solitary kidney have often hypertension, proteinuria, or a reduced renal function. In contrast, children with healthy solitary kidneys have BP and renal function similar to those of healthy children.

• MeSH
• albuminurie diagnostické zobrazování   patologie   patofyziologie   MeSH
• ambulantní monitorování krevního tlaku MeSH
• dítě MeSH
• hypertrofie MeSH
• krevní tlak * MeSH
• ledviny abnormality   fyziologie   MeSH
• lidé MeSH
• mladiství MeSH
• předškolní dítě MeSH
• proteinurie diagnostické zobrazování   patologie   patofyziologie   MeSH
• retrospektivní studie MeSH
• ultrasonografie MeSH
• vyšetření funkce ledvin MeSH
• Check Tag
• dítě MeSH
• lidé MeSH
• mladiství MeSH
• mužské pohlaví MeSH
• předškolní dítě MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH