Anna Masajtis-Zagajewska

Effect of moxonidine and amlodipine on serum YKL-40, plasma lipids and insulin sensitivity in insulin-resistant hypertensive patients—a randomized, crossover trial

Moxonidine is a selective imidazoline receptor agonist with comparable blood pressure-lowering efficacy to first-line antihypertensives and favorable metabolic effects. YKL-40 (chitinase-3-1-protein) has been proposed as a new marker of inflammation, atherosclerosis and endothelial dysfunction in neoplastic, cardiovascular and metabolic diseases but has not yet been studied in the context of essential hypertension. Fifteen patients (10 M, 5 F; age 48±14 years) with arterial hypertension and insulin resistance (HOMA-IR index >2.77) on at least two antihypertensive drugs were randomized to receive either moxonidine (0.4 mg) or amlodipine (10 mg) for two 8-week periods with a 7-day wash-out. Serum insulin, glucose, C-reactive protein (CRP), lipids, uric acid, YKL-40 and blood pressure were measured and insulin sensitivity was calculated (HOMA) at the beginning and end of each study phase. Mean BP decreased significantly with both moxonidine and amlodipine (−9.8±7.6 and −10.4±7.3 mm Hg, respectively). Serum high-density lipoprotein cholesterol increased with both therapies, but only moxonidine-affected serum triglycerides. No significant changes in serum uric acid, CRP, YKL-40 (2.3 and 3.3 ng ml–1, respectively) or HOMA index (0.70±2.4 and 0.76±2.8) were observed. There was a strong negative correlation between serum uric acid and YKL-40 concentration at baseline (r=−0.77, P=0.01). Serum YKL-40 did not correlate with blood pressure, biochemical parameters or HOMA index. Moxonidine is an effective adjunctive antihypertensive agent for use in patients with hypertension and insulin resistance that induces beneficial effects on serum lipid profile but does not reduce insulin resistance, inflammation or serum YKL-40 concentration.

Similar prevalence but different characteristics of pain in kidney transplant recipients and chronic hemodialysis patients

Masajtis‐Zagajewska A, Pietrasik P, Krawczyk J, Krakowska M, Jarzębski T, Pietrasiewicz B, Zbróg Z, Nowicki M. Similar prevalence but different characteristics of pain in kidney transplant recipients and chronic hemodialysis patients. 
Clin Transplant 2011: 25: E144–E151.

Influence of dual blockade of the renin-angiotensin system on thirst in hemodialysis patients.

Background/Aims: Angiotensin II promotes sodium retention and influences the central regulation of fluid intake. Clinical studies on the effect of an angiotensin-converting enzyme inhibitor (ACEI) on xerostomia and thirst in chronic hemodialysis (HD) patients were scarce and gave contradictory results. We hypothesized that a more effective inhibition of the renin-angiotensin-aldosterone axis with the combined ACEI and angiotensin receptor antagonist administration may reduce thirst and xerostomia,thereby decreasing interdialytic weight gain (IWG) in HD patients. Methods: Twenty-one chronic HD patients (16 men, 5 women, mean age 54 ± 13 years, time on dialysis 50 ± 58 months) who had been on chronic ACEI therapy were studied. In a double-blind, crossover study, all subjects received in a random order either losartan (50 mg/day) or placebo for two 4-week periods with a 7-day wash-out. Basic biochemistry, serum electrolytes, plasma aldosterone, measurements of salivary flow rate after stimulation with paraffin chewing, and subjective xerostomia and thirst questionnaires were collected before dialysis sessions both before and after each treatment period. IWG and blood pressure were assessed at each dialysis. Results: The volume of saliva increased after losartan (from 1.2 ± 0.7 to 1.5 ± 1.0 ml/min, respectively; p = 0.03), but this was reflected neither by the severity of the symptoms of xerostomia assessed by the patients on a visual analog scale (31 ± 9 vs. 31 ± 8 mm, respectively) nor by the intensity of thirst (final score 22 ± 5 vs. 21 ± 5 at baseline). No changes of the mean IWG were observed during the treatment with losartan (2.5 ± 0.6 kg before and 2.4 ± 0.8 kg at the end of the treatment). Plasma aldosterone decreased at the end of the losartan therapy (from 151 ± 86 to 111 ± 51 pg/ml; p = 0.02). Predialysis serum potassium did not change during the study. Conclusions: The addition of an angiotensin receptor blocker to chronic ACEI therapy is not effective in reducing thirst and thereby IWG in chronic HD patients.

Plasma Desphospho-Uncarboxylated Matrix Gla Protein as a Marker of Kidney Damage and Cardiovascular Risk in Advanced Stage of Chronic Kidney Disease

Background/Aims: Desphospho-uncarboxylated matrix Gla protein (dp-ucMGP) is formed as a result of vitamin K insufficiency. The aim of this study was to investigate the association between plasma dp-ucMGP, kidney function and cardiovascular risk factors before and after 9-months substitution of vitamin K2 in non-dialysis patients with chronic kidney disease (CKD) stage 4 and 5. Methods: 38 CKD patients were supplemented for 270±12 days with 90 µg vitamin K2 and 10 µg cholecalciferol or 10 µg cholecalciferol alone. At baseline and at follow-up circulating calcium, phosphate, lipids, hemoglobin, albumin and total protein, dp-ucMGP, osteoprotegerin, fetuin A, osteocalcin and fibroblast grown factor 23 (FGF-23) were assessed. Proteinuria was assessed in the first morning void. Results: Baseline plasma dp-ucMGP was 1018.6±498.3 pmol/l and was significantly higher in patients at stage 5 CKD (1388.3 ±505.4 pmol/l) than at stage 4 (885.1±419.7 pmol/l), p=0.04. Vitamin K2 supplementation resulted in a decrease of dp-ucMGP level by 10.7%. Plasma dp-ucMGP was positively associated with proteinuria, serum creatinine, PTH and FGF-23; and inversely associated with glomerular filtration rate, serum hemoglobin and albumin. Conclusions: High dp-ucMGP level, reflecting a poor vitamin K status seems to be associated with kidney damage and may be also a marker of cardiovascular risk in CKD patients. Supplementation with vitamin K2 may improve the carboxylation status of MGP.

Guillain-Barré syndrome in the course of EBV infection after kidney transplantation--a case report.

BACKGROUND Neurological complications are quite frequent in patients after solid organ transplantation, mostly affecting the central nervous system, and less frequently the peripheral nerves. Guillain-Barré syndrome (GBS), a reactive autoimmune disease of the nervous tissue, is the most common cause of acute polyneuropathy in adults following a viral or bacterial infection. GBS has been also linked to neurotoxic adverse effects of calcineurin inhibitors. This syndrome occurs relatively frequently in patients after bone marrow transplantation, but has been a rare complication in solid organ transplant recipients. Epstein-Barr virus (EBV) infection is relatively common in transplant recipients and in some cases may lead to neurological complications. CASE REPORT In this report we present an interesting case of a patient who developed GBS in the course of EBV infection 1 year after kidney transplantation. CONCLUSIONS In patients with rapid development of polyneuropathy after transplantation, Guillain-Barré syndrome should be excluded.

Diabetes Modifies Effect of High-Phosphate Diet on Fibroblast Growth Factor-23 in Chronic Kidney Disease

CONTEXT The pathophysiology of calcium-phosphate disturbances in diabetic (DM) kidney disease differs from that in non-DM chronic kidney disease (CKD). OBJECTIVE We compared the effect of a 6-day high-phosphate diet on serum fibroblast growth factor-23 (FGF-23) and other parameters of calcium-phosphate metabolism in DM and non-DM CKD patients. DESIGN AND SETTING This was a prospective interventional study in a research center setting. PARTICIPANTS, INTERVENTION, AND MEASURES: Twenty-six nondialysis patients with stages 3-5 CKD and albuminuria less than 300 mg/g creatinine were recruited from February 2011 to November 2012 (15 DM, 11 non-DM). All patients received a high-phosphate diet (1800 mg/d) for 6 days. At baseline, day 3, and day 7 serum FGF-23, PTH, Ca, P, 25-hydroxyvitamin D, 1,25 dihydroxyvitamin D, monocyte chemoattractant protein-1, and calcium and phosphate urine excretion were measured. RESULTS In DM CKD patients, serum calcium was lower on days 3 and 7 vs baseline (P < .01, respectively), and in non-DM patients, it was unchanged. Serum phosphorus increased significantly only in non-DM patients on days 3 and 7 vs baseline (P < 0.01, respectively). Serum PTH was higher in the DM group on day 7 vs baseline (P = .04). Plasma 25-hydroxyvitamin D, 1,25 dihydroxyvitamin D, and serum monocyte chemoattractant protein-1 were unchanged in both groups. Serum FGF-23 increased in DM patients, from baseline to day 3 (58.1 ± 52.7 and 91.6 ± 71.1 pg/mL, P = .001) but later tended to decrease. In non-DM patients, there was a steady increase of FGF-23 between baseline and day 7 (75 ± 84.3 to 176 ± 197 pg/mL, P = .04). Urine phosphate excretion was significantly higher on day 7 in DM patients only (P < .05). CONCLUSIONS PTH seems to play the major role in the regulation of phosphate excretion in DM CKD. The role of FGF-23 in phosphate disposal in DM CKD remains debatable.

New markers of urinary tract infection

Urinary tract infection (UTI) is the most common bacterial infection independent of age. It is also one of the most common causes of hospitalizations for infections among elderly people and the most common indication for antibiotic prescriptions in primary care. Both diagnostics and management of lower and upper urinary tract infections provide challenges in clinical practice due to their high prevalence and recurrence, and worldwide increase of antibiotic resistance. The clinical symptoms of UTI are often uncharacteristic or asymptomatic. The accurate diagnosis and early treatment are crucial due to risk of septicaemia and long-term consequences. Currently the diagnosis of urinary tract infection is based on the presence of clinical symptoms in combination with the results of nitrite strip test indicating the presence of bacteria in urine and semi-quantitative measurement of white blood cells count in urine. Although urine culture is the gold standard in UTI diagnostics it is both time-consuming and costly. Searching for novel biomarkers of UTI has attracted much attention in recent years. The article reviews several promising serum and urine biomarkers of UTI such as leukocyte esterase, C-reactive protein, procalcitonin, interleukins, elastase alpha (1)-proteinase inhibitor, lactofferin, secretory immunoglobulin A, heparin-binding protein, xanthine oxidase, myeloperoxidase, soluble triggering receptor expressed on myeloid cells-1, α-1 microglobulin (α1Mg) and tetrazolium nitroblue test (TNB).

Diagnosis and Treatment of Metabolic Acidosis in Patients with Chronic Kidney Disease – Position Statement of the Working Group of the Polish Society of Nephrology

Metabolic acidosis is commonly found in patients with chronic kidney disease (CKD), and its causes are: impaired ammonia excretion, reduced tubular bicarbonate reabsorption and insufficient renal bicarbonate production in relation to the amount of acids synthesised by the body and ingested with food. As the consequence, numerous metabolic abnormalities develop, which may lead to dysfunction of several organs. In observational studies, it has been found that CKD patients with metabolic acidosis are characterised by faster progression of kidney disease towards end stage kidney failure, and by increased mortality. Results of interventional studies suggest that alkali therapy in CKD patients slows progression of kidney disease. In view of these facts, the members of “The Working Group of the Polish Society of Nephrology on Metabolic and Endocrine Abnormalities in Kidney Diseases” have prepared the following statement and guidelines for the diagnosis and treatment of metabolic acidosis in CKD patients. Measurement of bicarbonate concentration in venous plasma or venous blood to check for metabolic acidosis should be performed in all CKD patients and metabolic acidosis in these patients should be diagnosed when the venous plasma or venous blood bicarbonate concentration is lower than 22 mmol/l. In patients with metabolic acidosis and CKD, oral sodium bicarbonate administration is recommended. The goal of such a treatment is to achieve a plasma or blood bicarbonate concentration equal to or greater than 22 mmol/l.