[Circulating bone turnover markers and their relationships in hemodialysis patients with vitamin D deficiency].

OBJECTIVE: Introduction: Mineral homeostasis is achieved through a complex interplay of several feedback processes involving primarily the bone, intestine and kidney, regulated by different proteins acting on endocrine, paracrine or autocrine levels. The dysregulation of these processes in chronic renal failure, called kidney disease (CKD) - mineral and bone disorder (CKD-MBD), although apparent, is still poorly understood. The aim: The aim of the study was an analysis of potential relationships between selected biomarkers of CKD-MBD in maintenance hemodialysis (HD) patients. PATIENTS AND METHODS: Material and Methods: In the first part of this cross-sectional study, the 25(OH)D serum concentrations were measured in 115 HD vitamin D naïve patients from 5 dialysis units located in central Poland. Thereafter in 81 patients (49 men, 32 women, aged 67 ± 13 years) with vitamin deficiency (25(OH)D <20 ng/ml) serum concentrations of 25(OH)D, 1,25(OH)2D, intact parathyroid hormone (iPTH), intact FGF23, sclerostin (SCL), osteocalcin (OC), and C-terminal telopeptide of type I collagen (CTX1) were determined. RESULTS: Results: Serum levels of both 25(OH)D and 1,25(OH)2D were low (mean values 13.4±6.72 ng/ml and 12.9 ± 9.08 pmol/l, respectively). While serum 25(OH)D correlated only with a declared time spent outside (r= 0.411; p=0.000139), serum 1,25(OH)2D was related to diuresis (r= 0.289; p=0.009), and negatively to time on dialysis (r= -0.272; p=0.014) , serum phosphate (r= -0.393; p=0.000289), FGF23(r= -0.295; p=0.008), and SCL (r= -0.260; p=0.019). There was a marked dispersion of FGF-23 serum levels across the group (mean 823±5647, median 379 pg/ml) , and - as expected - they correlated highly with phosphate (r= 0.549, p=0.000), calcium (r= 0,328, p=0,003), OC (r=0.479; p=0.000), and negatively with z 1,25(OH)2D (r= -0.295, p=0.008). Mean serum SCL levels (89.2±46.7, median 81.9 pmol/l) were 3x higher than in general population, and correlated highly positively with dialysis vintage (r=0.402; p<0.001), age (r=0.356; p=0.001), as well as negatively with 1,25(OH)2D (r= -0.260; p=0.019) and CTX1 (r= -0.293; p=0.008). CONCLUSION: Conclusions: In our hemodialysis population, in addition to profoundly impaired 1,25(OH)2D synthesis, there is also a widespread prevalence of 25(OH)D deficiency. The patients have also markedly increased serum bone-secreted proteins, FGF23, and SCL, which regulate mineral and bone metabolism and are associated with the systemic side effects of uremia. All these hormones interact one with the other, creating a sophisticated cross-talk between the bone, intestine, and the kidney.

[Management of diabetic kidney disease: a summary of European Recommendations 2015].

Diabetes mellitus is the leading cause of end-stage renal disease in patients beginning renal replacement therapy. The epidemic of type 2 diabetes contributed to a new approach for diabetic kidney disease, one of the most common complications of diabetes type 1 and 2. The current recommendations of the management in diabetic kidney disease developed by an international group of experts based on analysis of clinical trials and expert opinion have been reviewed in this article. The guidelines concern several issues as renal replacement modality selection, glycaemic control, the choice of glycaemia controlling drugs and cardiovascular risk management aiming to improve the quality of life of the patients, as well as to reduce the costs of the medical care.

[Metaphylaxis of urolithiasis - a neglected field in medicine?]

Urolithiasis is a common condition linked to lifestyle factors and its prevalence is increasing in Europe and United States. Nevertheless, recurrence of urinary stones can be effectively prevented by dietary and life style changes. The review focuses on general dietary recommendations as well as specific medical therapy for kidney stone formers.

[Erythropoietin stimulating agents in chronic kidney disease: indications and contraindications].

Erythropoietin (EPO) deficiency is important complication of chronic kidney disease. It downregulates red cells maturation and production causing renal anemia. It is associated with reduced quality of life, increased risk of blood transfusions and cardiovascular morbidity. It is possible to substitute EPOwith recombinant human EPOor its derivatives - erythropoiesis stimulating agents (ESA). ESA therapy reduces blood transfusions, improves quality of life and can raise hemoglobin to 10-11.5 g/dl. Higher hemoglobin targets bring more harm than benefit - including increased risk for stroke, hypertension and vascular access thrombosis and mortality. Initiation of ESA therapy should be preceded by excluding the other causes of anemia and balancing ESA advantages and disadvantages in every patient. In patients with previous stroke, previous or current malignancy risks of ESA therapy may outweigh the risks of red cell transfusions.

[Renal diseases in malignancies]. / Choroby nerek w przebiegu nowotworów zlosliwych.

Malignancies may be associated with a variety of renal complications. These include: acute kidney injury, chronic tubulointerstitial and vascular pathologies as well as paraneoplastic glomerulonephritis. Membranous nephropathy consists a main paraneoplastic glomerulopathy in solid tumors, and minimal change disease is the most common in haematologic malignancies, especially in Hodgkin lymphoma. Epidemiology, pathogenesis, clinical manifestations and management of these conditions are described in the paper.

[Acute kidney injury after hematopoietic cell transplantation]. / Ostre uszkodzenie nerek po przeszczepieniu komórek hematopoetycznych.

Stem cell transplantation is now a routine and successful therapeutic method in many hematopoietic disorders and cancers. Unfortunately, toxicity of the procedure significantly worsens the outcomes, with acute and chronic kidney injury among the others. Etiology of kidney failure is multifactorial with nephrotoxicity of drugs, septic complications, sinusoidal occlusion syndrome, thrombotic microangiopathy and acute/chronic graft-versus-host disease (GvHD). Understanding these syndromes enables early recognition and proper intervention that can reduce incidence and severity of kidney injury and improve outcomes.

[Anti-cancer agents nephrotoxicity]. / Nefrotoksycznosc leków przeciwnowotworowych.

Nephrotoxicity remains an important complication of chemotherapy. There are many different types of kidney injury that can results from anti-cancer drugs, including: acute and chronic tubular injuries, various podocytopathies, crystal nephropathies, thrombotic microangiopathy, and electrolyte wasting syndromes. All these pathologic changes, their diagnosis and treatment, as well as the preventive measures are shortly summarized in the article.

[Tumor lysis syndrome]. / Zespól lizy guza.

Tumor lysis syndrome (TLS) is a serious adverse event observed in patients treated for hematologic malignancies and solid tumors, particularly those with a high proliferative rate. An abrupt and massive tumor cell lysis with release their contents into the circulation leads to a rapid development of hyperuricemia, hyperkalemia, hyperphosphatemia, followed by hypocalcemia. If not managed appropriately, these metabolic disturbances may result in acute kidney injury and in life-threatening cardiac complications and even death. This short review summarizes current strategies for diagnosis, risk assessment, prophylaxis, and therapy.

Long-term cholecalciferol administration in hemodialysis patients: a single-center randomized pilot study.

BACKGROUND: Data on the potent pleiotropic extraskeletal effects of vitamin D have renewed interest in its use in selected populations, including patients with chronic kidney disease, but the available data are still insufficient to make recommendations. This study assessed the long-term effect of small cholecalciferol doses on serum vitamin D, parathormone (PTH), and bone mineral density (BMD) in hemodialysis patients. MATERIAL/METHODS: Nineteen patients with serum 25(OH)D <20 ng/mL were randomized into cholecalciferol (2000 IU 3×/week) and no-treatment groups, then observed for 1 year. Patients with hypercalcemia, hyperphosphatemia, and receiving vitamin D/calcimimetics were excluded. Serum 25(OH)D, 1,25(OH)2D, PTH, and alkaline phosphatase activity were examined every 2 months and BMD was measured before and after the study. RESULTS: We observed normalization of serum 25(OH)D with an increase in medians from 11.3 to 44.9 ng/mL (P=0.02) in the cholecalciferol group and no change in the controls (P<0.001). Simultaneously, median serum 1,25(OH)2D increased from 18.2 to 43.1 pmol/L (P=0.02) in the cholecalciferol group and from 10.6 to 21.2 pmol/L (P=0.02) in controls (P=0.013). The treatment was associated with a small increase in serum calcium, but serum phosphate, PTH, alkaline phosphatase, and BMD remained unchanged in both groups. CONCLUSIONS: Oral cholecalciferol at a dose of 2000 IU/3×/week is an effective and safe way to treat vitamin D deficiency in hemodialysis patients, leading to a significant increase in serum 1,25(OH)2D. However, it was insufficient to suppress the activity of parathyroid glands or to significantly change BMD.

[Magnesium homeostasis disorders: hypomagnesemia]. / Zaburzenia homeostazy magnezu: hipomagnezemia.

Physiologically, magnesium plays an essential role in bone formation, neuromuscular stability and muscle contraction, and the consequences of its altered homeostasis may be serious. Magnesium deficiency and hypomagnesemia are common and under-recognized problems, which can cause a variety of symptoms and can also affect the other cations metabolism. In this review causes, clinical picture and management of hypomagnesemia and magnesium deficiency are discussed.

[Magnesium homeostasis disorders: hypermagnesemia]. / Zaburzenia homeostazy magnezu: hipermagnezemia mia.

Hypermagnesemia, defined as a plasma total magnesium concentration greater than 1.2 mmol/l, is much less common than hypomagnesemia, however it may be also life-threatening. In this review causes, clinical presentation and treatment of hypermagnesemia is shortly reviewed.

[Alkalosis]. / Zasadowica.

An elevation of arterial blood pH called alkalosis remains an underestimated condition in hospitalized patients. Serious alkalosis can be associated with high risk of death. The disorder can be caused by increased concentration of bicarbonate (metabolic alkalosis) or decreased concentration of carbon dioxide (respiratory alkalosis). In most cases of metabolic alkalosis it is generated by vomiting or diuretic use, whereas respiratory alkalosis is provoked by hyperventilation associated with respiratory or neurological disorder. Maintenance of metabolic alkalosis is possible only in patients with impaired renal base excretion which is most often produced by hypochloremia. In both respiratory and metabolic alkaloses treatment depends on the underlying factor. In hyperventilation syndrome is based on behavioral therapy. In most cases of metabolic alkalosis the administration of sodium and potassium chloride forms a substantial part of therapy.

[Magnesium homeostasis]. / Homeostaza magnezu.

Magnesium is the second most prevalent intracellular cation, which plays a critical role in many cellular processes, essential for life, especially for neuromuscular functioning, cardiovascular health and normal bone formation. Its homeostasis is tightly regulated by a dynamic interplay between intestinal absorption and renal excretion. Additionally, it is controlled through the reservoir in bone tissue. This review summarizes shortly the current knowledge of magnesium homeostasis important for the practitioner to better understand it's disorders.