Ostry zespół sercowo−nerkowy: powrót funkcji nerek po leczeniu nerkozastępczym

Utilisation of invasive treatment in the form of elective dialysis end extracorporeal ultrafiltration as a method of complementaryto pharmacotherapy was presented by the example of the patient with acute decompensated heart failure with diagnosedcardiorenal syndrome type 1. Such procedure reduced symptoms of overhydration, restored sensitivity to oral diureticsand allow to obtain a partial return of renal function, improved prognosis and quality of life of the patient

Peritoneal Ultrafiltration in the Long-Term Treatment of Chronic Heart Failure Refractory to Pharmacological Therapy

IntroductionDespite continuous improvement in the treatment, heart failure (HF) is a growing health problem and a major cause of mortality and morbidity in the world. There is some positive experience with the removal of the fluid excess via peritoneum in those patients, regardless of their renal function. The aim of this single center pilot study was to assess the efficacy of peritoneal ultra filtration (PUF) with a nightly 12-h exchange in the long-term treatment of refractory HF.MethodsThe study included patients with chronic HF resistant to updated HF therapy (pharmacological and devices if applicable), who had experienced at least three hospitalizations due to HF during the preceding year and were disqualified from heart transplantation. All of them were treated with nightly 12-h 7.5% icodextrin exchange.ResultsThere were 15 patients (13 men), aged 72 ± 9 years, with charlson comorbidity index (CCI) 9 ± 1.2, NYHA class IV (11 patients) or III (4 patients), and eGFR 32 ± 11 ml/min/1.73m2. They were followed up for 24 ± 8 months (range 12–43, median 26 months). During the 1st year, all patients improved their NYHA functional class from 3.7 ± 0.5 to 2.6 ± 0.5; P = 0.0005, with stable (34.3 ± 12.4, and 35.6 ± 16.5%, respectively) left ventricular ejection fraction (LVEF), and inferior vena cava (IVC) diameter decreased from 27.8 ± 2.7 to 24.4 ± 3.4 mm; P = 0.09. Daily diuresis increased from 867 ± 413 to 1221 ± 680 ml; P = 0.25, while the dose of furosemide could be reduced from 620 ± 256 to 360 ± 110 mg/d; P = 0.0005, however, the kidney function deteriorated, with eGFR drop from 32 ± 11 to 25.6 ± 13 ml/min/1.73m2; P = 0.01). HF-related hospitalizations decreased from 8.9 ± 2.8 days/month to 1.5 ± 1.2 days/month (P = 0.003). Mechanical peritoneal dialysis complications occurred in five patients and infectious complications in four (peritonitis rate 1 per 72 patient-month). Patient survival was 93% at 1 year and 73% at 2 year. Technique survival was 100%.ConclusionIn patients with refractory HF, PUF with one overnight icodextrin exchange appears to be a promising therapeutic option as an adjunct to pharmacological management of those who are not transplant candidates. It should be emphasized that the treatment can have a great impact on the quality of life and the total costs of treating these patients

Skuteczne leczenie niewydolności serca opornej na diuretyki za pomocą ultrafiltracji otrzewnowej

We present a case of successful peritoneal ultrafiltration (pUF) treatment in a 60 year-old patient diagnosed with diuretic-resistantcongestive heart failure fulfilling the criteria for type 2 cardio-renal syndrome. Six months of pUF treatment with onedaily dialysis exchange with icodextrin as an osmotic agent resulted in better functional status (from IV to II/III NYHA class),quality of life and improvement of haemodynamic parameters measured by impedance cardiography. During the follow-up(six months), pUF was well tolerated by the patient and he did not require hospitalisation for decompensated heart failure

miRNA-16 as a predictive factor for intracranial aneurysms in autosomal dominant polycystic kidney disease

Introduction. Autosomal dominant polycystic kidney disease (ADPKD) is the most common genetic renal disorder. It leads to multiple extra-renal complications, with intracranial aneurysms (IA) among the most serious. Biological markers could become tools in identifying patients at risk of an IA. MicroRNAs 16 (miR-16) and 25 (miR-25) have been proposed as being markers of IAs in the general population. In the current study, we attempted to discover if they may also be considered markers of IAs in ADPKD. Material and methods. 64 renal transplant recipients with ADPKD were included. After magnetic resonance angiography of the brain, they were divided into a case group (IA+, n = 13) and a control group (IA-, n = 51). Expression of miRNAs in plasma was analysed by qRT-PCR. Results. The expression of miR-16 was higher in the control (IA-) group. There was no statistically significant difference between the groups in terms of miR-25 expression. Conclusions and clinical implications. MicroRNA-16 is a potential marker of IAs in renal transplant recipients with ADPKD. It may become a tool to identify patients who should undergo screening for an IA

Podłoże genetyczne i diagnostyka nefropatii IgA

Nefropatia IgA należy do najczęściej występujących pierwotnych chorób kłębuszków nerkowych. W Europie stanowi do 30% wszystkich pierwotnych glomerulopatii. Chorobę Bergera cechuje różne tempo rozwoju; w niektórych przypadkach doprowadza ona do skrajnej niewydolności nerek. Nefropatia IgA ma podłoże wieloczynnikowe, pewną rolę w jej powstawaniu przypisuje się różnym genom. Obecnie do ustalenia rozpoznania konieczne jest wykonanie badania histopatologicznego bioptatu nerki. W niniejszym artykule omówiono podłoże genetyczne oraz diagnostykę nefropatii IgA

Czy należy obawiać się niedoborów witaminy B12 w trakcie leczenia metforminą?

Metformin, a biguanide derivative, is the most frequently used antihyperglycaemic agent in the world. Various adverse effects can occur during the drug therapy. One of them is vitamin B12 deficiency, which may be either asymptomatic (biochemical) or may lead to neurological and/or haematological disorders. Causal diagnosis of these disorders is hampered due to the fact that nervous system symptoms are similar to neurological complications developing over the course of diabetes mellitus. It is estimated that 5.8 to 33% of metformin treated patients have a low (below the reference level) serum vitamin B12 concentration. The interrelation between vitamin B12 deficiency and metformin usage has been known for decades and over that time many studies have been carried out to assess the issue. Unfortunately, these studies were mainly observational, retrospective and performed on nonhomogeneous groups of patients. Recently a meta-analysis of studies concerning only diabetic patients was performed and it demonstrated the existence of a relationship between metformin treatment and vitamin B12 deficiency. Nevertheless, further well-designed, large-scale, randomized studies performed on a homogenous group of patients and employing homogenous criteria for diagnosing vitamin B12 deficiency are necessary in order to decide whether serum vitamin B12 concentration should be routinely checked among metformin treated patients.Metformina, pochodna biguanidu, jest najczęściej stosowanym lekiem przeciwhiperglikemicznym na świecie. W trakcie farmakoterapii mogą wystąpić różne działania niepożądane. Jednym z nich jest niedobór witaminy B12, który może być bezobjawowy (biochemiczny) lub prowadzić do zaburzeń neurologicznych i/lub hematologicznych. Diagnostykę przyczynową wymienionych zaburzeń utrudnia fakt, że objawy ze strony układu nerwowego mogą przypominać powikłania neurologiczne rozwijające się w przebiegu cukrzycy. Szacuje się, że od 5,8% do 33% chorych leczonych metforminą charakteryzuje się obniżonym, poniżej wartości referencyjnych, stężeniem witaminy B12 w surowicy krwi. Związek występowania niedoboru witaminy B12 w przebiegu leczenia metforminą znany jest już od kilkudziesięciu lat i w tym czasie przeprowadzono wiele badań, które niestety często miały charakter obserwacyjny, były retrospektywne i obejmowały niejednorodne grupy pacjentów. Dopiero niedawno przeprowadzono metaanalizę badań obejmujących chorych na cukrzycę, w której wykazano obecność związku leczenia metforminą z występowa­niem niedoboru witaminy B12. Niezbędne są jednak dalsze, dobrze zaprojektowane, duże, randomizowane badania, obejmujące jednorodne grupy pacjentów oraz stosujące jednorodne kryteria rozpoznania niedoboru witaminy B12 w celu oceny, czy niezbędne jest rutynowe oznaczanie stężenia witaminy B12 u osób leczonych metforminą