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Objective: To assess the therapeutic equivalence of epoetin zeta and epoetin alpha for correction of haemoglobin (Hb) concentration in patients with anaemia and chronic kidney disease (CKD) stage 5 maintained on haemodialysis.Study Design: In total, 609 patients with CKD and anaemia (Hb < 9 g/dL) were randomly assigned to receive either epoetin zeta or epoetin alpha intravenously, one to three times per week for 24 weeks. Dosing was titrated individually to achieve a stable, target Hb concentration of 11-12 g/dL. Primary endpoints were the mean weekly dose of epoetin per kilogram of body weight and mean Hb concentration during the last 4 weeks of treatment. Safety endpoints were the occurrence of anti-erythropoietin antibodies, ratings of tolerability and adverse events (AEs).Results: Mean (+/- standard deviation [SD]) Hb concentration over the last 4 weeks of treatment was 11.61 +/- 1.27 g/dL for patients receiving epoetin zeta, compared with 11.63 +/- 1.37 g/dL for patients receiving epoetin alpha (95% confidence interval [CI]: -0.25 to 0.20 g/dL). Mean (+/- SD) epoetin zeta weekly dose over the last 4 weeks of treatment was 182.20 +/- 118.11 IU/kg/wk, compared with 166.14 +/- 109.85 IU/kg/wk for epoetin alpha (95% CI: -3.21 to 35.34 IU/kg/wk). The most commonly reported AEs (> 5% of patients) were infections and infestations (12.5% and 12.8% of patients treated with epoetin zeta and epoetin alpha, respectively) and vascular disorders (8.5% and 8.9%, respectively). No patients developed neutralizing anti-erythropoietin antibodies.Conclusions: Epoetin zeta, administered intravenously, is therapeutically equivalent to epoetin alpha in the correction of low Hb concentration in patients with CKD undergoing haemodialysis. No unexpected AEs were seen and both epoetin zeta and epoetin alpha were well tolerated. [ABSTRACT FROM AUTHOR]

Thyroid function was evaluated in a group of 36 patients with acute renal failure (ARF) during the oliguric/anuric, polyuric and postpolyuric phase. Serum thyroxine (T) and triiodothyronine (T) concentrations were significantly decreased in the oliguric/anuric phase, as compared with the mean values obtained in the postpolyuric phase and with controls. In contrast to T and T, the concentration of serum reverse triiodothyronine (rT) was elevated in the oliguric/anuric phase and normal in the polyuric phase. The sephadex-T-binding index (TI) was significantly increased in oliguric/anuric patients and in the polyuric phase. The levels of serum thyreotropin were significantly elevated during all phases of ARF as compared with the controls. From the results obtained it is concluded that abnormal peripheral metabolism of T seems to be the primary cause of altered plasma concentrations of thyroid hormones in patients with ARF. [ABSTRACT FROM AUTHOR]

The effects of an intravenous infusion of physiological saline on plasma atrial natriuretic peptide (ANP), guanosine 3′ 5′ monophosphate (cGMP) con centrations, and on urinary CGMP and sodium excre tion were studied in 13 patients with essential hypertension, class I according to WHO criteria, and in 10 healthy subjects. It was found that the groups did not differ as to basal and infusion-induced plasma ANP and cGMP and basal urinary cGMP and sodium excretion, but the sodium chloride infusion resulted in a significantly greater urinary cGMP and sodium excre tion and creatinine clearance in hypertensive than in control subjects. The results of this study demonstrate that patients with essential hypertension respond to an intravenous sodium chloride load not only with exaggerated natri uresis, but also with augmented urinary CGMP excre tion. The latter finding may in part be due to a greater glomerular filtration of cGMP, but increased renal contribution cannot be excluded. Apart from the pos sible stronger intrarenal effect of ANP on cGMP production in patients with hypertension, independent direct effect of volume expansion on cGMP excretion and modified activity of other cGMP generating sys tems may all be responsible for the higher unnary cGMP excretion in essential hypertension. [ABSTRACT FROM PUBLISHER]

The aim of study was to evaluate, during 2-year follow-up, bone mineral density in sites with different cortical/cancellous bone ratios (lumbar spine, total body, distal site of radius) and selected markers of bone turnover (total alkaline phoshatase, osteocalcin, pyridinoline and deoxypirydinoline) in patients with long-standing insulin-dependent diabetes mellitus in comparison with healthy controls. Additionally, the influence of age, sex, smoking, duration of diabetes, the degree of metabolic control, or coexisting chronic complications of diabetes (retinopathy, incipient nephropathy, polyneuropathy) on the studied indices of bone metabolism in patients with insulin-dependent diabetes mellitus were evaluated. It was found that patients with long-standing diabetes mellitus had significantly lower bone mineral density than healthy controls ( p50.003 in lumbar spine and p50.001 in total body). The incidence rate of osteopenia and osteoporosis was significantly higher in this group of patients in comparison with the controls ( p50.005 for lumbar spine and total body and p50.001 for radius). In comparison with healthy subjects, diabetic patients and significantly higher, but within normal reference range, serum alkaline phosphate ( p50.005) and osteocalcin ( p50.05), accompanied by similar pyridinoline and not significantly increased deoxypyridinoline. Duration and metabolic control of diabetes, or the coexistence of its chronic complications, did not correlate with bone mineral density or the studied indices of bone turnover. In conclusion, diabetic osteopenia seems to be a normal bone turnover state, not influenced by the duration or degree of metabolic control of diabetes. [ABSTRACT FROM AUTHOR]