[Investigation of 70-kDa heat shock protein in the serum and urine of patients with chronic glomerulonephritis].

AIM: To determine the levels of 70-kDa heat shock protein (HSP70) in urine and anti-HPS70 antibodies (Abs) in serum and to assess their clinical and prognostic value in patients with different forms of chronic glomerulonephritis (CGN). SUBJECTS AND METHODS: Seventy-nine patients with CGN, including 15 with inactive nephritis (Group 1), 35 with active CGN and preserved renal function (Group 2), 14 with the highest CGN activity and transient creatininemia (Group 3), and 15 with persistent proteinuria and chronic renal failure (Group 4) were examined. ELISA was used to estimate urinary HSP70 levels and serum anti-HSP70 Abs in the examined groups. RESULTS: The patients with active CGN were found to have higher excretions of urinary HSP70 and serum anti-HSP70 Abs. Urinary HSP70 excretion was significantly higher in the patients with transient renal function (Group 3) than in those from the other groups. At the same time, there was a decrease in serum anti-HSP70 Abs, which was a poor factor of persistent nephrotic syndrome despite immunosuppressive therapy (IST). Despite long-term IST, the nephrotic syndrome was persistent in 9 (60%) of the 15 patients with low serum Ab titers. At the same time, 8 (80%) of the 10 patients with higher serum Ab titers responded to IST during 9 months. CONCLUSION: The investigation demonstrates the great value of HSP70 as an index of the severity of lesion and the activation of kidney self-defense mechanisms in patients with CGN. Determination of serum anti-HSP70 Abs may be used to assess the prognosis of CGN.

[Clinical significance of serum and urinary biomarkers for water-salt metabolism in patients with proteinuric forms of chronic glomerulonephritis].

AIM: To determine the nature and magnitude of changes in the detectable serum and urinary biomarkers of water-salt metabolism in patients with proteinuric forms of chronic glomerulonephritis (CGN), their importance for assessing the activity and prognosis of the disease. SUBJECTS AND METHODS: Forty-seven patients with CGN were examined. Group 1 included 10 patients with nephrotic syndrome (NS) and decreased renal function; Group 2 comprised 16 patients with persistent NS and normal renal function; Group 3 consisted of 10 patients with partial remission of NS; Group 4 included 11 patients with active hematuric CGN. A control group consisted of 9 healthy individuals matched for gender and age with the patients with CGN. The serum level of copeptin and the urinary excretion of aquaporine-2 (AQP-2) and kidney injury molecule-1 (KIM-1) were determined by indirect enzyme-linked immunosorbent assay (ELISA). RESULTS: In the NS patients with and without renal dysfunction, the serum copeptin concentration was significantly higher than that in those with partial remission of NS or hematuric CGN and in the controls. In the patients with hematuric CGN, this indicator was virtually different from that in the control group. Urinary AQP-2 excretion was significantly similar in 3 NS groups. In the patients with hematuric CGN, the urinary AQP-2 concentration was higher than that in those with NS, but it was significantly lower than in the control group. The highest urinary excretion of KIM-1 was found in the patients with NS and diminished renal function while its excretion was significantly lower in the patients with NS and stable renal function, as in those with partial remission of NS. The lowest values were seen in the patients with hematuric CGN and in the control group; the differences between these groups were statistically insignificant. Correlation analysis showed that there was an inverse correlation between serum copeptin and urinary AQP-2 levels and between urinary AQP- 2 and KIM-1 levels. CONCLUSION: Serum copeptin levels and urinary AQP-2 secretion may be used to assess the activity of CGN and NS and to evaluate therapeutic effectiveness. The determination of urinary KIM-1 excretion may be of the same practical value in patients with NS. It has been shown that the concentrations of copeptin, APQ-2, and KIM-1 may be used as a differential diagnostic criterion for hematuric CGN.

[Clinical value of the determination of markers for endothelial dysfunction (endothelin-1, microalbuminuria) and tubulointerstitial tissue lesion (ß2-microglobulin, monocyte chemotactic protein-1) in hypertensive patients with uric acid metabolic disorders].

AIM: To identify the risk factors of kidney injuries in hypertensive patients with uric acid (UA) metabolic disorders in order to choose the optimal management tactics, by analyzing the changes in markers for endothelial dysfunction (endothelin-1 (ET-1), microalbuminuria (MAU), intima-media thickness (IMT)) and tubulointerstitial tissue lesion (beta2-microglobulin (beta2-MG, monocyte chemotactic protein-1 (MCP-1)). SUBJECTS AND METHODS: Eighty-one patients with grade 1 hypertension without associated diseases, diabetes mellitus, or metabolic syndrome were examined. There were 3 study groups: 1) hyperuricosuria (n = 7); 2) hyperuricemia (n = 53); 3) hyperuricemia and renal failure (n = 6); and a control group of 15 hypertensive patients without UA metabolic disorders who were matched for age and gender with the patients of the study groups. RESULTS: The hypertensive patients with hyperuricemia, as compared with those without UA metabolic disorders, showed higher plasma concentrations of ET-1 (p = 0.003) and MAU (p = 0.009) and more marked increases in common carotid IMT (p = 0.044), urinary excretion of beta2-MG (p = 0.010), and MCP-1 (p = 0.030). There were direct correlations between all the examined biomarkers and the degree of uricemia (Rs = 0.453; p < 0.001; Rs = 0.411; p < 0.001; Rs = 0.322; p = 0.067; Rs = 0.537; p < 0.001; and Rs = 0.318; p = 0.004, respectively) and between the markers of endothelial dysfunction and those of tubulointerstitial tissue lesion (Rs = 0.295 for ET-1 and MCP-1; p = 0.008; Rs = 0.399 for ET-1 and beta2-MG; p < 0.001; Rs = 0.462 for MAU and beta2-MG; p < 0.001; and Rs = 0.188 for MAU and MCP-1; p = 0.094). Multivariate analysis of the clinical and laboratory parameters under study confirmed the role of serum MCP-1, beta2-MG, MAU, creatinine levels as independent predictors for decreased relative urinary gravity, the clinical sign of tubulointerstitial tissue lesion/fibrosis, and that of a wider range of the indicators, such as MAU, ventricular septal thickness, glomerular filtration rate, relative urinary gravity, systolic blood pressure, MPC-1, low-density lipoproteins, as risk factors for renal filtrating dysfunction.

[Significance of the morphogenetic proteins FGF-23 and Klotho as predictors of prognosis of chronic kidney disease].

AIM: To study the role of the morphogenetic proteins FGF-23 and Klotho in the progression of chronic kidney disease (CKD) and in the development of cardiovascular events, inflammation, protein-energy deficiency, and other complications. SUBJECTS AND METHODS: Examinations were made in 70 patients with Stages I-VD CKD: 41 with chronic glomerulonephritis (including 10 with nephritis in the presence of diffuse connective tissue diseases), 22 with tubulointerstitial nephritis, and 7 with hypertensive nephrosclerosis. There were a total of 30 men and 40 women whose age was 20 to 84 years; the mean age at the study inclusion was 41 +/- 6.7 years. The serum levels of FGF-23 (Human FGF-23 ELISA kit using monoclonal antibodies to complete molecule of FGF-23) and Klotho (Human alpha-K1 ELISA using anti-Klotho antibodies) were investigated in all the 70 patients with CKD. RESULTS: The sera of all the examinees with CKD showed elevated FGF-23 and decreased Klotho levels, the magnitude of a change in which increased from Stage I to VD. In patients with different stages of CKD, the increase in FGF-23 levels, as glomerular filtration rate reduced, outstripped that in the serum levels of phosphorus and intact parathyroid hormone. There was a strong correlation of the serum level of the morphogenetic proteins, Klotho in particular, with proteinuria, C-reactive protein level, protein-energy deficiency, indicating the pleiotropic effects of these proteins. There was also a strong correlation between serum Klotho and ferritin levels and transferrin saturation percentage, which suggests that Klotho may be involved in iron regulation. CONCLUSION: The results of the investigation lend credence to the experimental and clinical findings that the serum levels of the morphogenetic proteins FGF-23 (an increase) and Klotho (a decrease) are early markers for progressive CKD and that their changes begin just in Stage III CKD and progress as renal failure worsens.

[New markers of cardio-renal links in chronic kidney disease].

AIM: To study the clinical significance of determining the serum concentration of phosphorus and calcium metabolism regulators--the morphogenetic proteins FGF-23 and Klotho in patients with different stages of chronic kidney disease (CKD). SUBJECTS AND METHODS: The serum levels of FGF-23 (a human FGF-23 ELISA kit with full-length anti-FCF-23 monoclonal antibodies) and Klotho (a human alpha-K1 ELISA with anti-Klotno antibodies) were investigated in 70 patients with Stages I--VD CKD (41 patients with chronic glomerulonephritis, including 10 with nephritis in systemic diseases, 22 with tubulointerstitial nephritis, and 7 with hypertensive nephroslerosis). The morphogenetic proteins were studied by the specialists of the LiTECH diagnostic laboratory according to the standard protocol. RESULTS: As CKD progressed from Stage I to VD, there were increased FGF-23 concentrations and decreased Klotho levels in the examinees' serum. The highest FGF-23 level and low Klotho concentration were noted in the group of patients on regular hemodialysis treatment (Stage VD). There was a strong inverse correlation between Klotho levels and proteinuria, C-reactive protein, and protein-energy insufficiency, which suggests that these factors influence the serum level of Klotho. The serum levels of FGF-23 and intact parathyroid hormone correlated with these values to a lesser degree. Analysis of the content of the morphogenetic proteins in patients with anemia versus those with CKD of the same stages and target hemoglobin values revealed low Klotho concentrations and high FGF-23 levels (r = 0.602; p < 0.01 and r = -0.450; p < 0.01, respectively). Forty-nine hypertensive patients showed a direct strong relationship between elevated serum FGF-23 levels and an inverse strong one between the reduced serum Klotho levels and the increased posterior left ventricular wall (r = 0.552; p < 0.01 and r = -0,587; p < 0.01, respectively). The same strong association was found between the higher serum level of FCF-23 (r = 0.492; p < 0.01) and the concentration of Klotho (r = -0.537; p < 0.01) and peripheral vascular resistance index (as evidenced by Doppler ultrasound study). CONCLUSION: Along with the active participation of the morphogenetic proteins (FGF-23 and Klotho) in mineral metabolism and its disturbances in CKD, their role is apparent in the development of cardiovascular events (in particular, through the involvement in the processes of vascular calcification and cardiac remodeling), anemia (through the possible effect on iron metabolism, enhanced ischemia of renal interstitial tissue with impaired Klotho production), and protein-energy insufficiency (through the participation in the processes of inflammation, oxidative stress, and protein synthesis).

[Cardiorenal links in systemic amyloidosis].

The paper gives current general data on the structure of amyloid fibril and the principles in the classification of amyloidosis, information on the clinical course of cardiac and renal involvements in systemic AL and AA amyloidosis, and that on diagnostic and prognostic criteria and the specific features of cardiorenal links. The authors draw the conclusion that the identification of acute and chronic cardiorenal links is of practical value for systemic amyloidosis. Cardiorenal and renocardiac syndromes are not always differentiated clearly in the systemacy of involvement.

[General molecular and cellular mechanisms for renal and cardiac remodeling in chronic kidney disease: a target for nephrocardioprotection].

The lecture considers a number of molecular and cellular mechanisms underlying the structural and functional rearrangement and development of renal and cardiac fibrosis in chronic kidney disease (CKD). It details the key component of disadaptative organ remodeling (the formation of myofibroblasts via epithelial-mesenchymal and endothelial-mesenchymal transdifferentiation) and the role of leading angiofibrogenic mediators (angiotensin II, transforming growth factor-beta type 1, a plasminogen activator inhibitor type 1, etc.) in the regulation of these processes. Investigation of the molecular and cellular bases of organ fibrosis, including the factors of dysregulated activation, differentiation and survival of microfibroblasts, makes it possible to specify the mechanisms of action of traditional nephro- and cardioprotective agents, to offer a possibility for a goal-oriented (target) effect on individual fibrogenic components, and to expand the arsenal of medications suppressing renal and cardiac remodeling.

[Hepatitis C virus-related cryoglobulinemic vasculitis with renal involvement: current possibilities of treatment].

The paper considers the specific features of renal involvement developing in chronic infection caused by hepatitis C virus (HCV) and the current possibilities of treatment. It details the clinical and morphological manifestations of HCV-related cryoglobulinemic glomerulonephritis, and criteria for its diagnosis and prognosis. The author discuss new approaches to treating (severe cryoglobulinemic vasculitis with renal involvement in particular)--antiviral therapy (pegylated interferon-alpha/ribavirin) in combination with biological agents (anti-CD monoclonal antibodies, such as rituximab) to achieve clinical, virological, immunological remissions and a response at a molecular level--to eliminate oligo- and monoclonal B lymphocyte proliferation.

[Hyperuricemia and the problem of chronic kidney disease].

The paper reviews the literature on the role of hyperuricemia as a risk factor for chronic kidney disease and as one of the factors for the progression of existing kidney disease. It gives epidemiological information on a relationship between hyperuricemia and kidney lesion. The mechanisms for the damaging action of uric acid on kidney tissue, which have experimentally and clinically observed, are considered. The main areas of hyperuricemia correction and its place in the total nephroprotection strategy are defined.

[Muckle-Wells syndrome caused by a new cryopyrin mutation: effective treatment with interleukin-1 antagonist].

A significant progress in the field of molecular-biological investigations resulted in definition of a new group of systemic diseases referred to as autoinflammatory. This group comprises familial periodic fevers: periodic disease (mediterranean fever), Muckle-Wells syndrome, others cryopirinopathy, TRAPS-syndrome. As shown by case reports, Muckle-Wells syndrome is not a rare disease, its sporadic forms are encountered as well as a less severe variant of cryopirinopathy - nonallergic cold urticaria. Awareness of the physicians in respect of this pathology is essential especially because early diagnosis enables control of this disease with use of biological preparations the spectrum of which tends to expansion. Moreover, arrest of inflammation is necessary for prevention of development and progression of such prognostically poor complication as AA-amyloidosis.

[Nephrotic crisis--an urgent condition in patients with nephrotic syndrome].

The lecture considers mechanisms of potassium and water retention underlying nephrotic syndrome, clinical differences between hypo- and hypervolemic variants of nephrotic syndrome, risk factors of nephrotic crisis and its clinical symptoms, current approaches to its treatment.

[Current methods of systemic amyloidosis diagnosis and monitoring of its course].

AIM: To determine clinical significance of measuring blood levels of protein precursors of AA- and AL-amyloidosis - SAA and immunoglobulin free light chains (ILC), respectively. MATERIAL AND METHODS: SAA concentrations were studied with ELISA in 43 rheumatoid arthritis (RA) patients including complicated with reactive AA-amyloidosis (n = 31). Inflammation activity and its severity were studied (indices Li, richi, HAQ, DAS4). A modern quantitative nephelometric method Freelite estimated ILC levels in 31 patients with AL-amyloidosis. RESULTS: Patients with RA complicated with AA-amyloidosis and free of it had a strong correlation between blood serum SAA concentration and activity of joint disease. Elevated SAA concentrations to 160 mg/l (normal 10 mg/l) were detected in many patients with clinical remission of the joint syndrome. Significal inhibition of AA-amyloidosis progression was seen only in SAA concentration drop under 60 mg/l. For AL-amyloidosis patients ILC fall by less than 3 normal value means a 6-time increase in chances of a favourable outcome. CONCLUSION: Monitoring of blood levels of proteins precursors of AA- and AL-amyloidosis is a key factor in prognosis of the disease and treatment efficacy.

[Determination of urinary markers of proteolysis/fibrinolysis and fibroangiogenesis in the kidney in hypertensive patients].

AIM: To determine clinical significance of urinary biomarkers of proteolysis/fibrinolysis and fibroangiogenesis in essential hypertension (EH). MATERIAL AND METHODS: Examination of the kidneys was made in 71 patients with EH degree 1-3. Renal function was assessed by 24-h albuminuria, calculated glomerular filtration rate (GFR) by Cockroft-Golt. Early signs of renal damage were microalbuminuria--MAU (diurnal albuminuria 30-300 mg/day), reduction of GFR (< 90 ml/min/1.73 m2). EH patients with hypercreatininemia and GFR under 60 ml/min/1.73m2 corresponding to stage III of chronic kidney disease were not included in the study. An additional nephropathy marker was an elevated index of resistance of interlobular renal arteries (RI > 0.65) as shown by dopplerometry. ELISA examined urinary biomarkers of intercellular and cell-matrix interactions in the kidney in EHpatients and healthy controls (n = 12). RESULTS: MAU was detected in 54 (76%) of 71 EH patients, elevated RI > 0.65--in 37 (52%) patients. Urinary biomarkers of proteolysis/fibrinolysis and fibroangiogenesis were higher in EH patients then in the controls. Urinary excretion of PAI-1, TGF-beta1, VEGF and collagen of type IV in EH patients with MAU was significantly higher than in patients with normoalbuminuria. A strong direct correlation between MAU and the rest above urinary biomarkers was found as well as between urinary excretion of collagen IV and RI. An inverse negative relationship was seen between RI and GFR. CONCLUSION: Renal impairment in EHpatients is a progressive disorder. Each stage of this process has its own clinicodiagnostic markers. Urinary biomarkers ofproteolysis/fibrinolysis and fibroangiogenesis in the kidney are informative for monitoring of early HNP.

[Estimation of podocyte dysfunction by nephrinuria severity in proteinuric forms of chronic glomerulonephritis].

AIM: To evaluate severity of nephrinuria (NU) as a marker of podocyte dysfunction (PD) in patients with proteinuric forms of chronic glomerulonephritis (CGN) and to specify efficacy of this test for assessment of activity and prognosis of CGN. MATERIAL AND METHODS: We examined 74 CGN patients: 18 with inactive nephritis (group 1), 18--with subnephrotic proteinuria (group 2), 38--with nephrotic syndrome--NS (group 3). The control group consisted of 10 healthy subjects. Urinary excretion of nephrin was studied with indirect enzyme immunoassay. A response to immunosuppressive treatment (IST) was studied in 23 NS patients depending on a baseline NU level. RESULTS: An NU level was higher in patients with proteinuric forms of CGN (groups 2 and 3) than in inactive disease and in healthy subjects, in NS patients significantly higher than in less severe proteinuria. NU was significantly higher in arterial hypertension, in persistent NS. Remission of NS was achieved within 6 months of treatment in 9 of 11 (82%) patients with a baseline NU level < 17 ng/ml. Eight from 12 (67%) patients with high NU did not respond to IST conducted for 9 months to 2 years. ROC-curve construction showed that NU assessment in NS patients has high informative value in assessment of prognosis and efficacy of treatment in 6 months to come. CONCLUSION: The NU test in CGN patients is an informative diagnostic test allowing prognosis of a response to IST and assessment of PD severity.

[The role of D2 vitamin metabolite paricalcitol in nephroprotective strategy in chronic disease of the kidneys].

Calcitriol is important in nephroprotective strategy in chronic disease of the kidneys (CDK). However, its long-term use often results in hypercalciemia with metastatic calcification. Compared to calcitriol, paricalcitol (zemplar)--metabolite of vitamin D2--leads to hypercalciemia less frequently, has a more potent nephroprotective effect and more rapidly decreases blood levels of parathyroid hormone. Paricalcitol in combination with lozartan has more pronounced nephroprotective effect. Morphological analysis detected inhibition of development of glomerulosclerosis and tubulointerstitial fibrosis. A cardioprotective effect of paricalcitol manifests with reduction of mortality from cardiovascular complications both at CDKpredialysis stage and in regular hemodialysis.

[An IL-6 level in the serum and urine in estimation of cryoglobulinemic vasculitis activity in patients with chronic hepatitis C associated with renal damage].

AIM: To estimate serum and urine IL-6 levels and to study its role in diagnosis of nephritis activity in patients with cryoglobulinemic glomerulonephritis (CGN) associated with chronic hepatitis C (CHC). MATERIAL AND METHODS: Enzyme immunoassay was used to assay IL-6 in blood serum of 124 patients having different stages of CHC. IL-6 was also estimated in the urine of 57 patients with CHC systemic manifestations including renal damage. RESULTS: Abnormal serum IL-6 level was seen in 36% CHC patients. Patients with elevated level of IL-6 in the serum vs. patients with normal IL-6 level had cryoglobulinemia (CGE) (56% vs. 26%, p < 0.01) and related systemic manifestations including cryoglobulinemic glomerulonephritis (30% vs. 9%, p < 0.01). Most of (90%) patients with CHC-associated CGN had urinary IL-6 excretion correlating with severity of renal damage: the highest urinary level of IL-6 was seen in development of acute nephritic and nephritic syndromes (from 83.5 to 250 pg/ml). It did not correlate with IL-6 in the serum and proteinuria. This is evidence that IL-6 in the urine had a local origin (intrarenal), reflecting activity of immune inflammation in the kidney. CONCLUSION: Control of IL-6 levels in the blood serum and urine of patients suffering from CHC with cryoglobulinemic syndrome and renal damage can be used for monitoring of the disease activity.

[Specific damage to the kidneys in patients with chronic hepatitis C associated with cryoglobulinemia].

AIM: To reveal clinical and morphological characteristics of renal damage in patients with cryoglobulinemia (CGE) associated with chronic viral hepatitis C (CVH-C) for upgrading diagnosis, prognosis and optimization of the treatment methods. MATERIAL AND METHODS: Two groups of CVH-C patients were studied: with CGE (group 1, n = 64) and free of CGE (group 2, n = 62) matched for gender, age and duration of the disease. Biopsy of the liver for assessment of the histological activity index and histological sclerosis index by METAVIR scale was conducted in 63 patients. Of patients with CGE-related damage to the kidneys, 48 were examined for clinical picture with morphological investigation of renal tissue in 15 of them including semiquantitative evaluation of fibrosis degree and activity. RESULTS: Patients with CVH-C and CGE had a wider spectrum of systemic lesions than CVH-C patients without CGE. Only CGE patients demonstrated more severe affection of the skin, joints, kidneys and the nervous system. Therefore, CGE can be considered as a marker of poor prognosis. Liver biopsy showed that CGE patients had more pronounced fibrosis (3-6 points) versus 0-2 points in 80% patients from group 2. Duration of CVH-C from probable infection to renal damage in 48 patients with CGE glomerulonephritis (GN) averaged 197.05 +/- 18.5 months. Renal biopsy diagnosed CGE mesangiocapillary GN in 13 patients and membranoproliferative GN in 2 patients. Patients with HCV infection had a more severe proliferative form of nephritis--mesangiocapillary GN. In 48 GN patients with HCV-infection and CGE, GN ran latently with moderate urinary syndrome in 29 (60.4%) patients, with nephrotic syndrome--in 9 (18.6%), with acute nephritic syndrome--in 10 (21.0%) patients. Most of the patients had arterial hypertension, 13 patients had creatinemia (3.02 +/- 0.55 mg/dl), rapidly progressive GN was diagnosed in 4 patients. CONCLUSION: Persistent CGE marks poor prognosis in CHC patients and is an indication for antiviral treatment to prevent severe organ lesions, first of all of the kidneys. Development of CGE vasculitis with severe damage to the kidneys demands immunosuppressive therapy in combination with plasmapheresis or cryapheresis followed by antiviral drugs. As shown by pilot results, a new approach with rituximab is perspective but further evidence is needed for final conclusions.

[New possibilities of the diagnosis and monitoring of the course of AL-amyloidosis].

AIM: to define the clinical value of various concentrations of immunoglobulin light chains (ILCs) in patients with AL amyloidosis. SUBJECTS AND METHODS: The content of free ILCs was studied by a nephelometric technique after their fixation in the blood of 31 patients with AL amyloidosis; monoclonal gammapathy was associated with the hyperproduction of monoclonal ILCs of lambda- and kappa-type in 14 and 17 patients, respectively. The obtained value was compared with the data of physical examination and laboratory and instrumental studies indicating lesions to target organs and with the course of the disease. RESULTS: In patients with the good course of AL amyloidosis, the average level of free ILCs was 1.8 (range 0.77-3) times greater than the normal values (the range of ILCs of lambda and kappa-type was 20.24 to 67.4 and 20.14 to 81.38 mg/l, respectively); in those with the poor course, the excess of ILCs was 5.8 (range 3.7-13) times higher than the normal values (the range of lLCs of lambda and kappa-type was 54.32 to 286.7 and 117.06 to 2606.0 mg/l, respectively). The optimal range of diagnostic sensitivity (75%) and specificity (75%) in the estimation of prognosis was determined at the ILC levels that were three times greater (64.5 mg/l for kappa-ILCs and 80 mg/l for lambda-ILCs). Among the patients with a blood free ILC level of < 3 times more than the normal values, the good and poor courses of AL amyloidosis were noted in 13 and 4 cases, respectively. CONCLUSION: The determination of serum ILC concentration by the Freelite method may be used to diagnose AL amyloidosis and to specify the presence of appropriate organ dysfunction; this study over time makes it possible to monitor the course of the disease and to estimate its response to therapy.

[Mechanisms of phosphorus and calcium homeostatic disorders in the development of cardiovascular events in patients with chronic renal diseases. The role of fibroblast growth factor 23 and Klotho].

The paper deals with the analysis of studies of the role of the bone morphogenetic proteins fibroblast growth factor 23 (FGF-23) and Klothno in the development of vascular wall calcification in chronic renal disease (CRD). FGF-23 is shown to be an important phosphaturic hormone that inhibits hypercalcemic and hyperphosphatemic effects of elevated serum vitamin D concentrations. There is evidence that there is an association between high serum FGF-23 levels and vascular wall calcification irrespective of the content of phosphorus and parathyroid hormone. Most authors regard FGF-23 as a potential uremic toxin in patients with end-stage CRD. There are data that support the renoprotective value of the morphogenetic protein Klotho whose expression in CRD is decreased.