Chronic Kidney  Disease affects approximately 10%  of the  world’s  adult  population: it is within the  top  20  causes of death worldwide, and  its impact on patients and  their families  can  be devastating. World Kidney Day and  International Women’s Day in 2018  coincide, thus  offering an  opportunity to reflect on the  importance of women’s health and  specifically their  kidney health, on the community, and  the next generations, as well as to strive to be more curious about the unique aspects of kidney disease in women so that  we may apply  those learnings more broadly. Girls and  women, who make up approximately 50% of the  world’s  population, are important contributors to society and  their  families. Gender differences continue to exist  around the world in access to education, medical care, and participation in clinical studies. Pregnancy is a unique state for women, offering an opportunity for diagnosis of kidney disease, but also a state where acute and  chronic kidney diseases may manifest, and  which may impact future generations with respect to kidney  health. There are various autoimmune and  other conditions that  are more likely to impact women with profound consequences for child bearing, and  on the fetus. Women  have  different complications on dialysis  than  men, and  are more likely to be donors than  recipients of kidney transplants. In this editorial, we focus on what we do and  do not know about women, kidney health, and  kidney disease, and  what we might  learn  in the future to improve outcomes worldwide.

The growing interest of nephrologists in the problem of kidney injury in preeclampsia is due to its high prevalence (2–14% of all pregnancies) and unpredictable outcome. The pathogenesis of kidney injury in PE is poorly known, however, the role of imbalance of pro- and anti-angiogenic factors – VEGF and sFlt-1 – has been established as one of the most important pathogenetic mechanisms underlying the development of PE. The article presents modern data on the pathogenesis and renal manifestations of PE at different times of its development in comparison with markers of placental angiogenesis. The role of the imbalance of the sFlt-1 / VEGF system in the formation of proteinuria, arterial hypertension and renal dysfunction in PE is discussed, as well as the role of “early” PE as a risk factor for the development of chronic kidney disease.

Acute kidney injury (AKI) in obstetrics is a serious complication of pregnancy, delivery and the postpartum period, which can have a negative impact on the outcome of pregnancy for both the mother and the fetus. Currently, in developing countries the incidence of AKI during pregnancy and in the postpartum period is 4-26% of all pregnancies, and in the economically developed regions of the world – not more than 2.8%. The frequency of obstetric AKI requiring dialysis is 1:10,000 pregnancies. The causes of kidney injury in pregnant women can be hypertensive disorders, various types of thrombotic microangiopathy (HELLP syndrome, atypical hemolytic-uremic syndrome, thrombotic thrombocytopenic purpura, catastrophic antiphospholipid syndrome), acute fatty liver of pregnancy, obstetric hemorrhages, sepsis and septic shock. The article discusses the diagnostic criteria, biomarkers and timing of development of AKI in pregnancy, the principles of treatment and prevention of this complication in obstetrics.

In the first part of our article, we discussed the classification and pathogenesis of vascular calcification in chronic kidney disease and its impact on increased cardiovascular morbidity and mortality. In this review are discussed the imaging methods and effects of supplementation on progression of ectopic calcification in chronic kidney disease. 

THE AIM: to study the frequency of CKD in women suffering from chronic sarcoidosis. PATIENTS AND METHODS: 160 female patients with sarcoidosis without signs of primary renal pathology and severe cardiovascular pathology were divided into 3 groups depending on the activity of the disease: 1 – chronic progressive sarcoidosis, 2 – chronic sarcoidosis in remission 6-12 months, 3 – chronic sarcoidosis in remission more than 14 months. RESULTS: The negative effect of the progression of sarcoidosis on GFR was revealed. The lowest rGFR and the highest albuminuria were observed in the group of patients with progressive sarcoidosis, a reliable correlation was obtained between the progression of pulmonary fibrosis and renal markers of CKD. CONCLUSION: Progression of chronic sarcoidosis leads to a decrease in kidney function and the formation of chronic kidney disease.

Dent’s disease is an X-linked proximal tubulopathy characterized by low molecular weight proteinuria, hypercalciuria, nephrocalcinosis, and progression to chronic kidney failure. The disease is caused by mutations in CLCN5 or OCRL genes and affects males, whereas female carriers are generally asymptomatic. THE AIM: to study phenotype and genotype of patients’ mothers with Dent’s disease to exclude asymptomatic carrier of CLCN5 or OCRL gene mutations responsible for X-linked tubulopathy development. PATIENTS AND METHODS. We conducted clinical and molecular-genetic study of 9 mothers of 10 boys with Dent’s disease from 8 unrelated families. Direct Sanger sequencing of CLCN5 and OCRL genes were carried out with genomic DNA of all patients and their mothers. RESULTS. Carrier status of Dent’s disease 1 (n=7) and 2 types (n=2) was confirmed in all patients’ mothers. The most prevalent features of Dent’s disease in probands’ mothers were decrease in phosphate reabsorption, hypophosphatemia, medullary nephrocalcinosis and progression to CKD 2 stage. Low molecular weight proteinuria and hypercalciuria were rare revealed in carrier females. Full phenotype of Dent’s disease discovered in 2 cousins females carrier for Dent’s disease 1 type. CONCLUSION. We found that all carrier females had phenotypic variation of Dent disease’ symptoms. We speculate that revealed phenotype in carrier females for Dent disease might be a consequence of autosome translocation or nonrandom X chromosome inactivation. These data suggest that clinicians should consider a diagnostic evaluation of mothers of boys with Dent’s disease to determine phenotype and early prevention of progression to chronic kidney disease.

Urinary tract infection (UTI) affecting up to 5–10% of pregnant women. Three clinical types of pregnancy are distinguished: asymptomatic bacteriuria (ASB), acute cystitis and pyelonephritis. ASB is microbiological diagnosis which should be based on results of culturing of urine samples. ASB is the risk factor of a symptomatic UTI, severe maternal and fetal complications. Screening and treatment of asymptomatic bacteriuria is recommended in all pregnant women.

Hereditary hypophosphatemic rickets with hypercalciuria  is a very rare autosomal recessive disease, pathogenic base of which is phosphorus reabsorption disorder in proximal nephron with following development of hypophsphatemia, hypercalciuria calcitriol level increase, decrease of parathyroid hormone, osteopenia and bony deformity. This disease refers to hypophosphatemic rickets, due to mutations in the SLC34A3 gene that encodes the sodium-phosphate cotransporter NaPi-IIc, which is responsible for phosphorus reabsorption in the proximal nephron. In this article, we present a clinical observation for a child with atypical manifestations of hereditary hypophosphatemic rickets with hypercalciuria. The clinical examination showed non constant hypophosphatemia, normal values of  maximum tubular phosphate transport, absence of calcitriol serum concentrations increase, rachitic changes and bone mineral disorders during a long period of observation. It didn’t allow clinically to identify one of the variants of hypophosphatemic rickets in a child. The diagnosis was confirmed by the results of complete exome sequencing which revealed previously undescribed compound heterozygous mutation c.1382G> A (p.Trp461Ter) in exon 13 and p.1094-3C> T in  intron 10 of the SLC34A3 gene. A correct diagnosis allowed us to reconsider the approaches of the treatment: in hereditary rickets recommended only phosphorus supplementation and prescription of vitamin D due to its increased endogenous production.