Is Metabolic Acidosis a Novel Risk Factor for a Long-Term Graft Survival in Patients after Kidney Transplantation?

BACKGROUND: Results of both experimental and clinical studies suggest that metabolic acidosis (MA) contributes to the progression of chronic kidney disease (CKD) and mortality in CKD patients. It is unknown whether the same relationship exists in kidney transplantation (KTx) patients. The aim of this observational study was to examine this relationship between MA and both mortality and renal outcomes in patients after KTx. METHODS: Four hundred eighty-six (290 male; 196 female) patients aged 48 ± 12 years, at least 1 year after KTx, were analyzed. Blood HCO3- was measured, and patients were then observed over 3 years. MA was defined as the blood HCO3- concentration <22 mmol/L. The end points of survival analysis were death and initiation of dialysis therapy. In patients who did not reach the above-mentioned end points, the difference between final (after 3 years of follow-up) and initial estimated glomerular filtration rate (eGFR) was calculated. RESULTS: MA was initially diagnosed in 57 (12%) patients after KTx. Three-year patient survival was 89.5% in the MA group and 97.4% in the non-MA group (p = 0.001). Three-year graft survival was 73.7% for patients with MA and 93.0% for patients without MA (p < 0.001). In patients with MA who did not reach study end points, blood bicarbonate concentration at baseline correlated positively with a change in eGFR (R = 0.48, p = 0.002, n = 36). Such a correlation was not found in patients without MA (n = 388). CONCLUSIONS: (1) MA significantly increases the risk of mortality in patients after KTx. (2) The intensity of MA may be associated with progression of transplanted kidney dysfunction in KTx patients.

Metabolic acidosis in kidney transplant recipients.

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 single­­center case­­control 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 (ß = 0.314, P <0.001 and ß = 0.274, P <0.001, respectively). Similar correlations were observed in CKD patients (ß = 0.273, P <0.001 and ß = 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.

Plasma marinobufagenin immunoreactivity in patients with chronic kidney disease: a case control study.

Experimental data have shown increased plasma levels of marinobufagenin in kidney failure. In this case-controlled retrospective analysis, we evaluated plasma marinobufagenin immunoreactivity in hemodialysis patients compared with subjects with normal kidney function. Sixty-eight adult hemodialysis patients with chronic kidney disease (34 females and 34 males) as well as 68 age-, gender-, and blood pressure-matched subjects without chronic kidney disease were enrolled. Patients on stable hemodialysis regimen for at least 3 mo before the study were included. Exclusion criteria were: age <18 yr, severe liver or heart insufficiency, and overhydration. Subjects without chronic kidney disease must have had an estimated glomerular filtration rate ≥60 ml·min-1·1.72 m-2 according to the Modification of Diet in Renal Disease formula. Plasma marinobufagenin immunoreactivity was significantly ( P < 0.001) higher in hemodialysis patients (1.66 ± 1.13 nmol/l) compared with subjects with normal kidney function (0.46 ± 0.23). In hemodialysis patients, plasma marinobufagenin immunoreactivity was higher in men compared with women. A significant positive correlation has been found between plasma marinobufagenin immunoreactivity and serum NT-proBNP, NT-proANP, or aldosterone concentrations in all analyzed subjects. In hemodialyzed patients with plasma marinobufagenin immunoreactivity above median value 5-yr, all-cause mortality was higher compared with those with plasma marinobufagenin concentration below median. We have shown that plasma marinobufagenin immunoreactivity is increased in patients with end-stage kidney failure treated with hemodialysis parallel to the increase in serum NT-proBNP, NT-proANP, and aldosterone concentrations. Higher marinobufagenin immunoreactivity has been associated with worse survival in hemodialyzed patients.

[Treatment with recombinant parathyroid hormone of advanced osteoporosis--series of cases]. / Leczenie zaawansowanej osteoporozy przy pomocy parathormonu uzyskanego metoda rekombinacji genetycznej--opis przypadków.

Osteoporosis is a systemic skeletal disorder characterized by impaired bone strength, leading to an increased risk of fracture. Patients with severe osteoporosis and multiple vertebral fractures are particularly at risk for subsequent osteoporotic fractures independently of antiresorptive therapy. The effective treatment of osteoporosis should prevent fractures through normalization of bone mass and improving bone microarchitecture. Recombinant human parathyroid hormone (teriparatide) is an anabolic (bone forming) agent. The aim of this study was to describe the results of treatment with teriparatide (Forsteo) of three patients with severe osteoporosis. Teriparatide has proved to be effective in preventing bone loss. New osteoporotic fracture has not occurred in two patients. Treatment with teriparatide was safe and well tolerated.