Background/Aims: In women with chronic kidney disease (CKD) fertility abnormalities occur frequently. Anti-Müllerian hormone (AMH) inhibits excessive recruitment of primordial follicles. The aim of the study was to evaluate the serum AMH concentration in women on hemodialysis and after kidney transplantation (KTx). Methods: 46 hemodialysed women and 14 with CKD about to undergo kidney transplantation were enrolled into the study. The control group consisted of 40 healthy women. In all subjects serum concentration of AMH was determined (in chronic hemodialysis women and in control group once, and in women after KTx immediately before surgery, and 3 times after the transplantation). Results: Serum AMH concentration in hemodialysed women and in the control group did not differ significantly, while in hemodialysed women with regular menstrual cycles it was significantly lower than in the control group: 2.20 (1.08-3.55ng/ml) and 3.30 (1.80-6.10ng/ml) respectively, (p=0.02). In the KTx group, a significant decrease in serum AMH concentration was found from 3.30ng/ml (2.20-6.50ng/ml) at baseline to 1.90ng/ml (1.30-2.40ng/ml) at 6 months after KTx (p=0.007). Conclusions: 1. Significantly lower serum AMH concentration was found in the regularly menstruating CKD women on hemodialysis in comparison with the healthy controls. 2. Serum AMH decreased significantly after successful KTx.

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Introduction Metabolic acidosis (MA) may accelerate the progression of chronic kidney disease (CKD) and is an important risk factor for increased mortality in CKD patients. The clinical value of MA in kidney transplant (KTx) recipients has not been extensively studied so far. Objectives The aim of this clinical single‑‑center case‑‑control study was to assess the prevalence of MA in KTx recipients in comparison with CKD patients and to identify pathogenic factors for MA in KTx recipients. Patients and methods Venous blood concentrations of bicarbonate (HCO3-) and blood hemoglobin concentrations were measured in 500 KTx recipients and 500 CKD patients matched for sex, age, and estimated glomerular filtration rate (eGFR). None of these patients received alkali treatment before the study. MA was diagnosed in KTx recipients with HCO3- levels lower than 22 mmol/l. Results The prevalence of MA was lower in KTx recipients than in CKD patients (12.0% vs 19.6%; P = 0.001). In both groups, the prevalence increased with progression of CKD stages (P <0.001 for trend) and was higher in patients with anemia. In a multivariable analysis, hemoglobin concentrations correlated independently with eGFR and HCO3- in KTx recipients (β = 0.314, P <0.001 and β = 0.274, P <0.001, respectively). Similar correlations were observed in CKD patients (β = 0.273, P <0.001 and β = 0.123, P = 0.006, respectively). Conclusions Our study revealed that the prevalence of MA is lower in KTx recipients than in CKD patients. Moreover, in KTx recipients, blood bicarbonate concentrations are related to kidney function and blood hemoglobin concentrations.

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Left ventricular hypertrophy (LVH) is frequently observed in chronic dialysis patients and is also highly prevalent in kidney transplant recipients. This study evaluates the impact of long-functioning hemodialysis vascular access on LVH in single center cohort of kidney transplant recipients. 162 patients at 8.7 ± 1.8 years after kidney transplantation were enrolled. Echocardiography, carotid ultrasound, and assessment of pulse wave velocity were performed. LVH was defined based on left ventricular mass (LVM) indexed for body surface area (BSA) and height2.7. There were 67 patients with and 95 without patent vascular access. Both study groups were comparable with respect to gender, age, duration of dialysis therapy, and time after transplantation, kidney graft function, and cardiovascular comorbidities. Patients with patent vascular access were characterized by significantly elevated LVM and significantly greater percentage of LVH, based on LVMI/BSA (66.7 versus 48.4%, P = 0.02). OR for LVH in patients with patent vascular access was 2.39 (1.19–4.76), P = 0.01. Regression analyses confirmed an independent contribution of patent vascular access to higher LVM and increased prevalence of LVH. We concluded that long-lasting patent hemodialysis vascular access after kidney transplantation is associated with the increased prevalence of LVH in kidney transplant recipients.