The global burden of chronic kidney disease (CKD) is rapidly increasing with a projection of becoming the 5th most common cause of years of life lost globally by 2040. Aggravatingly, CKD is a major cause of catastrophic health expenditure. The costs of dialysis and transplantation consume up to 3% of the annual healthcare budget in high-income countries. Crucially, however, the onset and progression of CKD is often preventable. In 2020, the World Kidney Day campaign highlights the importance of preventive interventions – be it primary, secondary or tertiary. This complementing article focuses on outlining and analyzing measures that can beimplemented in every country to promote and advance CKD prevention. Primary prevention of kidney disease should focus on the modification of risk factors and addressing structural abnormalities of the kidney and urinary tracts, as well as exposure to environmental risk factors and nephrotoxins. In persons with pre-existing kidney disease, secondary prevention, including blood pressure optimization and glycemic control, should be the main goal of education and clinical interventions. In patients with advanced CKD, management of co-morbidities such as uremia and cardiovascular disease is a highly recommended preventative intervention to avoid or delay dialysis or kidney transplantation. Political efforts are needed to proliferate the preventive approach. While national policies and strategies for non-communicable diseases might be present in a country, specific policies directed toward education and awareness about CKD screening, management and treatment are often lacking. Hence, there is an urgent need to increase the awareness of the importance of preventive measures throughout populations, professionals and policy makers.

The Kidney Disease: Improving Global Outcomes (KDIGO) initiative organized a Controversies Conference on glomerular diseases in November 2017. The conference focused on the 2012 KDIGO guideline with the aim of identifying new insights into nomenclature, pathogenesis, diagnostic work-up, and, in particular, therapy of glomerular diseases since the guideline’s publication. It was the consensus of the group that most guideline recommendations, in particular those dealing with therapy, will need to be revisited by the guideline-updating Work Group. This report covers general management of glomerular disease, IgA nephropathy, and membranous nephropathy.

Hypercalcemia is a result of a wide range of hereditary and acquired conditions encountered by general physicians and pediatricians. Calcium participates in several key physiological functions, control of blood coagulation, bone calcification. Calcium homeostasis is tightly regulated by the interplay between absorption from the small intestine and renal tubular reabsorption, bone remodeling, and disposal through the gut and the kidney. These processes are regulated by local and circulating factors. The two main hormones influencing the homeostasis of calcium are PTH and calcitriol. Cancer-associated hypercalcemia and primary hyperparathyroidism are the most frequent causes of hypercalcemia in adults. In neonates and infants, one should look first at genetic and iatrogenic etiologies. The clinical manifestations of hypercalcemia in children are nonspecific due to damage to various organs and systems and depend on the degree of blood calcium level. Mild hypercalcemia is asymptomatic and often discovered during routine blood work. Moderate and severe hypercalcemia may cause cardiac arrhythmias, affect the nervous system. The differential diagnosis of the possible etiologies of hypercalcemia should start with the assessment of serum parathyroid hormone (PTH) concentration. The causes of hypercalcemia can be divided between PTH-mediated and non-PTH-mediated. Identification of the main causes of hypercalcemia contributes to the timely elimination of trigger factors, beginning of treatment, correction of nutrition and lifestyle. The article highlights physiological mechanisms of calcium homeostasis, clinical manifestations, diagnostic algorithms and treatment of hypercalcemia in children.

Steroid-resistant focal-segmental glomerulosclerosis (FSGS) with nephrotic syndrome (NS) is a progressive kidney disease with the rapid development of end-stage renal failure (ESRD). In recent years, attempts have been made to treat steroidresistant FSHS with anti-CD20 monoclonal antibodies, rituximab. Currently, only a few clinical case reports and series with contradictory results have been published. THE AIM of our study was to evaluate the effect of rituximab in patients with resistant to the therapy focal segmental glomerulosclerosis. MATERIALS AND METHODS: The study included 6 patients with confirmed diagnosis of FSGS. The inclusion criteria were the presence of steroid-resistant NS or to the other treatment regimens, including cyclosporin A, tacrolimus, mycophenolate mofetil, cyclophosphamide, and exclusion criteria were the secondary form of the disease. Patients were treated with one course of rituximab – 2 to 4 infusions (the total dose was 1.0–2.0 g). Laboratory parameters (daily proteinuria, albumin and eGFR CKD-EPI) were analyzed before rituximab, as well as 6 and 12 months after treatment. RESULTS: A partial remission of FSGS was achieved in one patient, stable renal function was maintained for 12 months follow-up. In 4 out of 6 patients, progression of the disease was observed with the development of ESRD in the period from 1 to 3 years, despite a decrease in the severity of NS. In one patient, the NS of the same severity persisted for 6 months after the treatment; no positive dynamics in proteinuria or serum proteins were observed. CONCLUSION: Thus, we did not show a significant effect of rituximab in patients with steroid-resistant FSGS. However, according to the literature the effect of rituximab has been achieved in approximately half of steroid-resistant FSGS cases, therefore further prospective clinical trials are needed.

The article discusses the current possibilities of postinfectious AA-amyloidosis treatment with dimexide on the example of clinical observation, discribes in detail the problem of functional amyloid and debates the prospects of the principle of amyloid resorption in the treatment of systemic amyloidosis. The history of the use of dimexide in medical practice is given, thenecessary dataon the pharmacology of dimexide are presented.

Parvovirus B19 (PV B19) infection can cause pure red cell aplasia (PRCA) and severe normochromic anemia resistant to treatment with erythropoietin in renal transplant recipients. Active parvovirus infection usually develops in the first months after kidney transplantation (KT), but is not always accompanied by clinical symptoms. The incidence of PV B19-associated anemia is low - not more than 1–1.5 %. A confirmation of the etiology of the disease, in addition to the characteristic histological picture of the bone marrow (a decrease in the number of erythrokaryocytes of less than 5% with preserved myelopoiesis and megakaryopoiesis, the appearance of single giant pronormoblasts), is the detection of PV B19 DNA in the blood and / or bone marrow. The detection of specific IgM antibodies to parvovirus plays a less significant role in the diagnosis of active PV B19 infection in patients after KT receiving immunosuppressive therapy and should not be used as the only diagnostic method. There is no specific antiviral treatment for PV B19 infection, therefore other approaches to therapy are used: reduction of immunosuppression, transfusion of red blood cells, administration of intravenous immunoglobulin (IVIG). The article describes the clinical observation of a 33-year-old patient with stage 5 CKD who developed severe normochromic anemia resistant to treatment with erythropoietin 4 weeks after a successful KT. A cytological examination of the bone marrow revealed PRCA, and a large number of copies of PV B19 DNA were detected in the patient’s blood, while antibodies to parvovirus IgG and IgM were not revealed. A decrease of immunosuppression (withdrawal of mycophenolic acid), repeated administration of IVIG in a total dose of 147 g resulted to lasting normalization of red blood cells number and hemoglobin level after five months of treatment. The function of the renal transplant remained normal throughout the observation period.

According to modern concepts, for the development of atypical hemolytic uremic syndrome (aHUS) in predisposed individuals, additional factors are necessary, which today are considered as complement-activating states. The most common of them are infections, pregnancy and childbirth, autoimmune diseases, transplantation of bone marrow and solid organs, some medications. Less commonly, aHUS is preceded by malignant arterial hypertension and glomerular kidney disease. Clinical observation of a patient suffering from a steroid-sensitive relapsing nephrotic syndrome (NS) for 10 years, in which after a viral infection first increased blood pressure, developed impaired renal function and hematological manifestations of thrombotic microangiopathy (ТМА), is given. In the presented observation, aHUS developed as a “second disease” in a patient with previously diagnosed glomerular kidney disease, which led to the rapid progression of chronic kidney disease with the development of terminal renal failure. This is evidenced by the nature of the course of the disease – NS recurring after acute respiratory viral infections, not accompanied by changes in urine sediment, arterial hypertension, impaired renal function and easily stopped by corticosteroids with rapid disappearance of proteinuria and normalization of protein blood counts. The change in the clinical picture of nephritis after a herpes zoster infection made us think about the development of a second renal disease of a different nature, other than glomerulonephritis. Undoubted AKI, combined with severe anemia and thrombocytopenia, was the basis for the exclusion of primarily TMA. The exclusion of TTP, STEC-HUS and the most common causes of secondary TMA made it possible to diagnose atypical HUS. The role of NS in the development of TMA is discussed. Blood coagulation disorders and VEGF-dependent mechanisms are considered as possible mechanisms.

The ability to realize the reproductive function for both patients with systemic lupus erythematosus and patients with a different cause of chronic kidney disease is rightfully considered as one of the most important achievements of modern medicine. The work describes the pregnancy case of the patient with systemic lupus erythematosus and secondary antiphospholipid syndrome. Renal damage with the development of renal thrombotic microangiopathy came to the fore in the clinical picture, which was regarded as nephritis and complicated the diagnosis of systemic lupus erythematosus. A positive pregnancy outcome was achieved with the development of neonatal lupus erythematosus in one twin child. The options for the prevention and treatment of thrombotic complications as well as methods for minimizing gestational complications (including preeclampsia, which the patient had in history) are discussed, inter alia, with the purposed of low-molecular-weight heparins and acetylsalicylic acid preparations. Treatment options are also described to improve the outcome of such pregnancies and to decrease the symptoms of neonatal lupus erythematosus using hydroxychloroquine. The article summarizes current management approaches for these patients with special attention to the interdisciplinary approach.