Prevalence of hypertension in the neonate
The indication for blood pressure measurement in the youngest age group is limited to sick children. Therefore, the diagnosis of nt generally relates to children with existing other serious pathology, and prevalence data are derived from specific patient groups. Numerous studies show that the incidence of nt in hospitalised newborns is quite low, ranging from 0.2-0.3 %. However, it increases significantly in neonates born prematurely and in selected risk groups. Among neonates hospitalised in neonatal intensive care units, the proportion of patients with nt is much higher, reaching 0.81% and close to 9% when additional risk factors are present (umbilical catheterisation, persistent ductus arteriosus - GCFA, intraventricular bleeding). In chronic bronchopulmonary disease (BGCF), the nt rate reaches 40%, but it should be remembered that this diagnosis generally affects children after the neonatal period. Hypertension, albeit at a low rate, may also affect neonates discharged from the OIRN. Friedman and Hustead found nt at the second month of corrected age in 2.6% of patients discharged from the OIRN.

Causes of neonatal hypertension
Hypertension in neonates is generally secondary in nature and, as in older age groups, the causes of nt in neonates include mainly renal pathologies, with renal vascular disease predominating (Table 4). nt in the nature of renal vascular hypertension can be led to by thrombosis-embolism of the renal artery, most commonly associated with umbilical artery catheterisation. For the risk of renal artery thrombosis, the height of the catheter tip is not relevant. What seems to be relevant is damage to the endothelium of the umbilical artery during catheterisation. Congenital hypercoagulable states, e.g. associated with mutations in the MTHFR gene, are also a risk factor for renal artery thrombosis. Congenital renal artery stenosis(s) can cause heart failure and nt only becomes apparent after haemodynamic stabilisation has been achieved. Congenital fibromuscular dysplasia may involve the main trunk of the renal artery, but may also involve the intrarenal branches of the artery. Renal vein thrombosis, causes nt and may affect neonates born at term and of normal weight but exposed to maternal diabetes and/or at risk of hypercoagulability (Leiden mutation, MTHFR gene mutations). Severe nt can be caused by compression of the renal arteries(s) by abdominal tumours and, in turn, renal and adrenal tumours can cause severe high-renin nt due to local renal ischaemia.

Congenital anomalies of kidney and urinary tract (CAKUT) and cystic kidney disease, both recessive and dominant, also present with nt. The pathogenesis of nt in these cases is related to both renin generation and reduced glomerular filtration rate and sodium and water retention. A rare cause of nt in neonates is haemolytic uremic syndrome, most often an early manifestation of congenital complement defects.

As nt mainly affects neonates in severe general condition and burdened with additional medical conditions, renal failure developing as a complication of the underlying disease and fluid retention is an important cause of nt. This phenomenon is of particular importance in children born with very low birthweight because, in addition to the various factors generating nt, inhibition of nephrogenesis and the phenomenon of 'low nephron mass' are important. A particular form of severe nt is hyponatraemia-hypertensive syndrome, in which hyponatraemic conductance and severe, treatment-resistant nt occur. This syndrome most often affects newborns with congenital kidney disease, often with significantly impaired glomerular filtration rate in whom adequate fluid balance is not applied.

Coarctation of the aorta presents with nt and arterial pressure asymmetry depending on the location of the obstruction. A rare cause of severe nt is idiopathic infantile hypercalcaemia, which causes generalised calcification of large arterial vessels that may also lead to renal artery stenosis.
The cause of nt is also neurological complications that present with seizures and/or cerebral oedema. In the neonatal period, monogenic forms of nt such as pseudo mineralocorticoid excess syndrome running with intrauterine dystrophy and nephrocalcinosis, steroid hydroxylase 11 beta block and hyperaldosteronism may manifest. These forms of nt present a typical intermediate phenotype.

Other factors associated with the occurrence of nt are the use of assisted breathing, and increased pulmonary resistance. Nt is a particularly common complication of BGCF (see above). In addition to a very large group of organic and haemodynamic causes (Table 4), iatrogenic causes are an important aetiology. In addition to the most common and easily manageable problem, which is pain in the neonatal period, the influence of inotropic drugs, corticosteroids, conductivity and, mentioned above, the use of CPAP or ECMO, are also of great importance. The identification of the presence of specific extrinsic factors that can determine blood pressure levels, in most cases, allows causal treatment to be applied and drug therapy to be avoided.

Principles of diagnosis of neonatal hypertension
The principles of diagnosis of nt in the neonate do not differ from those in older age groups. Hypertension is generally found during routine blood pressure measurements performed on children admitted to the NICU. Knowledge of the main causes of elevated BP adequately guides both the physical examination and laboratory and imaging diagnostics. Every infant suspected of having an nt should have blood pressure measured in the four extremities. Attention should also be paid to any symptoms suggestive of cardiovascular pathologies, as well as abnormal abdominal resistances. In addition to basic biochemical investigations, including assessment of renal function, ionogram and blood gas, an abdominal ultrasound with assessment of the kidneys, urinary tract and an ultrasound with Doppler flow assessment of the renal vessels and aorta should be performed in every case. Doppler ultrasound is subject to a high rate of both false-positive and false-negative results and the reliability of the result largely depends on the skill of the examiner . Nevertheless, due to its non-invasiveness and the fact that OIRNs are generally located in highly specialised centres where the examination can be performed by an experienced ultrasonographer, it is a basic imaging study.

Due to the possibility of haemorrhage into the central nervous system (CNS) as a potential cause of nt, it is necessary to extend the diagnosis to include transcranial usg. Selected patients require additional imaging and endocrine diagnostics, including renal scintigraphy, assessment of plasma renin activity, aldosterone, cortisol, urine steroid profile, daily excretion of catecholamines and assessment of thyroid hormones.
Assessment of renin and aldosterone activity/concentration is of additional importance, mainly in cases suspected of hyperaldosteronism or nt monogenic. In interpreting the results, it should be borne in mind that physiologically renin activity/concentrations in the newborn are relatively high and should be analysed together with the assessment of aldosterone concentrations.

Additional imaging studies are directed at the diagnosis or exclusion of renal and renal vascular pathology and aortic pathology. These investigations include renal scintigraphy, renal and/or aortic angiotomography and classical arteriography. Renal angiotomography allows fairly good imaging of the large arterial vessels, including the trunk and main branches of the renal arteries, but does not provide adequate resolution to assess the intrarenal branches of the renal arteries. Due to its invasiveness, arteriography and aortography should be combined with the possibility of a repair procedure. An important limitation of a possible procedure to dilate the renal arteries and their branches is the diameter of the vessels.

In every neonate with nt, organ damage should be assessed. Diagnosis should be targeted to look for hypertensive angiopathy, encephalopathy, left ventricular hypertrophy and proteinuria. These tests are also useful in assessing the efficacy of hypotensive therapy (Table 5). Despite the relative ease of assessing organ damage in older children and adults, in neonates difficulties are related to the lack of standards for microalbuminuria, carotid intima-media complex, left ventricular mass, as well as the technical feasibility of assessing the above parameters (e.g. thickness of the intima-media complex). However, there are reports defining cardiomyopathy and hypertensive aortopathy in neonates. The features of hypertensive cardiomyopathy in neonates were defined by Peterson et al. These include impaired systolic function, decreased left ventricular dimension and increased ventricular mass, as well as indirect features of impaired diastolic function, expressed as left atrial dilatation. In addition, the authors considered aortic dilatation as an indicator of organ damage (Table 5).