91 research outputs found

    Initiation of hemodialysis and sudden cardiac death ÔÇö a constant challenge on the threshold of new therapy

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    The risk of death from cardiovascular diseases in patients initiating hemodialysis therapy is 50% higher than in patients with stage 5 chronic kidney disease before starting renal replacement therapy. Sudden cardiac death is the leading cause of death within the first months after initiation of renal replacement therapy. Identification of risk factors for early mortality in patients with end-stage renal disease is important for their future care. Myocardial stunning, intradialytic hypotension, or pulmonary hypertension in patients with arteriovenous fistula have been known for years to cause deterioration in myocardial function. On the other hand, based on observational studies conducted so far, it is not clear whether diabetes promotes early mortality in patients treated with renal replacement therapy. In addition to standard tests performed routinely in dialysis patients, it is recommended to measure high-sensitivity troponin and natriuretic peptide as well as obtain an echocardiography study during both pre-dialysis care and after the initiation of renal replacement therapy for both prognostic and diagnostic purposes. However, the main focus should be on the dynamics of changes in those parameters rather than single measurements

    Rozpocz─Öcie leczenia hemodializ─ů a nag┼éa ┼Ťmier─ç sercowa ÔÇô nieustaj─ůce wyzwanie u progu nowej terapii.

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    Ryzyko zgonu z powodu przyczyn sercowo-naczyniowych u chorych rozpoczynaj─ůcych leczenie hemodializami jest o 50% wy┼╝sze ni┼╝ u chorych w 5 stadium przewlek┼éej choroby nerek przed rozpocz─Öciem leczenia nerkozast─Öpczego. Nag┼éa ┼Ťmier─ç sercowa jest dominuj─ůc─ů przyczyn─ů zgon├│w w pierwszych miesi─ůcach od rozpocz─Öcia terapii nerkozast─Öpczej. Zidentyfikowanie czynnik├│w ryzyka wczesnej ┼Ťmiertelno┼Ťci u pacjent├│w ze schy┼ékow─ů niewydolno┼Ťci nerek ma wa┼╝ne znaczenie dla ich przysz┼éej opieki. Og┼éuszenie mi─Ö┼Ťnia sercowego, hipotensja ┼Ťr├│ddializacyjna, czy wyst─ůpienie nadci┼Ťnienia p┼éucnego u chorych po wytworzeniu przetoki t─Ötniczo-┼╝ylnej to znane od lat stany powoduj─ůce pogorszenie funkcji mi─Ö┼Ťnia sercowego. Z kolei z bada┼ä obserwacyjnych wynika, ┼╝e nie stwierdzono wy┼╝szej wczesnej ┼Ťmiertelno┼Ťci u chorych z cukrzyc─ů w┼é─ůczonych do programu dializ w por├│wnaniu do chorych bez cukrzycy. W celach prognostycznych i rokowniczych, opr├│cz rutynowych bada┼ä wykonywanych w opiece nad chorymi dializowanymi, wskazane jest zar├│wno w okresie przeddializacyjnym jaki i po w┼é─ůczeniu do leczenia nerkozast─Öpczego oznaczenie st─Ö┼╝enia wysokoczu┼éej troponiny, peptydu natriuretycznego oraz wykonanie badania echokardiograficznego. Uwag─Ö nale┼╝y jednak koncentrowa─ç na dynamice zmian wymienionych parametr├│w, a nie na ocenie pojedynczych oznacze┼ä

    Associations between depressive symptoms and disease progression in older patients with chronic kidney disease: results of the EQUAL study

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    Background Depressive symptoms are associated with adverse clinical outcomes in patients with end-stage kidney disease; however, few small studies have examined this association in patients with earlier phases of chronic kidney disease (CKD). We studied associations between baseline depressive symptoms and clinical outcomes in older patients with advanced CKD and examined whether these associations differed depending on sex. Methods CKD patients (>= 65 years; estimated glomerular filtration rate <= 20 mL/min/1.73 m(2)) were included from a European multicentre prospective cohort between 2012 and 2019. Depressive symptoms were measured by the five-item Mental Health Inventory (cut-off <= 70; 0-100 scale). Cox proportional hazard analysis was used to study associations between depressive symptoms and time to dialysis initiation, all-cause mortality and these outcomes combined. A joint model was used to study the association between depressive symptoms and kidney function over time. Analyses were adjusted for potential baseline confounders. Results Overall kidney function decline in 1326 patients was -0.12 mL/min/1.73 m(2)/month. A total of 515 patients showed depressive symptoms. No significant association was found between depressive symptoms and kidney function over time (P = 0.08). Unlike women, men with depressive symptoms had an increased mortality rate compared with those without symptoms [adjusted hazard ratio 1.41 (95% confidence interval 1.03-1.93)]. Depressive symptoms were not significantly associated with a higher hazard of dialysis initiation, or with the combined outcome (i.e. dialysis initiation and all-cause mortality). Conclusions There was no significant association between depressive symptoms at baseline and decline in kidney function over time in older patients with advanced CKD. Depressive symptoms at baseline were associated with a higher mortality rate in men

    Symptom Burden before and after Dialysis Initiation in Older Patients

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    For older patients with kidney failure, lowering symptom burden may be more important than prolonging life. Dialysis initiation may affect individual kidney failure-related symptoms differently, but the change in symptoms before and after start of dialysis has not been studied. Therefore, we investigated the course of total and individual symptom number and burden before and after starting dialysis in older patients

    The association between TMAO, CMPF and clinical outcomes in advanced CKD; results from the EQUAL study

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    Background Trimethylamine N-oxide (TMAO), a metabolite from red meat and fish consumption, plays a role in promoting cardiovascular events. However, data regarding TMAO and its impact on clinical outcomes are inconclusive, possibly due to its undetermined dietary source. Objectives We hypothesized that circulating TMAO derived from fish intake might cause less harm compared with red meat sources by examining the concomitant level of 3-carboxy-4-methyl-5-propyl-2-furanpropionate (CMPF), a known biomarker of fish intake, and investigated the association between TMAO, CMPF, and outcomes. Methods Patients were recruited from the European QUALity (EQUAL) Study on treatment in advanced chronic kidney disease among individuals aged >= 65 y whose estimated glomerular filtration rate (eGFR) had dropped for the first time to <= 20 mL/min per 1.73 m(2) during the last 6 mo. The association between TMAO, CMPF, and outcomes including all-cause mortality and kidney replacement therapy (KRT) was assessed among 737 patients. Patients were further stratified by median cutoffs of TMAO and CMPF, suggesting high/low red meat and fish intake. Results During a median of 39 mo of follow-up, 232 patients died. Higher TMAO was independently associated with an increased risk of all-cause mortality (multivariable HR: 1.46; 95% CI: 1.17, 1.83). Higher CMPF was associated with a reduced risk of both all-cause mortality (HR: 0.79; 95% CI: 0.71, 0.89) and KRT (HR: 0.80; 95% CI: 0.71, 0.90), independently of TMAO and other clinically relevant confounders. In comparison to patients with low TMAO and CMPF, patients with low TMAO and high CMPF had reduced risk of all-cause mortality (adjusted HR: 0.49; 95% CI: 0.31, 0.73), whereas those with high TMAO and high CMPF showed no association across adjusted models. Conclusions High CMPF conferred an independent role in health benefits and might even counteract the unfavorable association between TMAO and outcomes. Whether higher circulating CMPF concentrations are due to fish consumption, and/or if CMPF is a protective factor, remains to be verified

    Kontrowersje wok├│┼é leczenia lekami blokuj─ůcymi uk┼éad reninaÔÇôangiotensynaÔÇôaldosteron (RAA) w nefrologii oraz chorobach uk┼éadu sercowo-naczyniowego

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    Leki hamuj─ůce uk┼éad reninaÔÇôangiotensynaÔÇôaldosteron (RAA), takie jak inhibitory konwertazy angiotensyny (ACE-Is) oraz antagoni┼Ťci receptora AT1 dla angiotensyny II (ARBs), s─ů uznanym od lat, podstawowym kanonem nefroprotekcji. Powszechnie stosuje si─Ö je w monoterapii k┼é─Öbuszkowych chor├│b nerek przebiegaj─ůcych z bia┼ékomoczem. Obecnie rzadziej zaleca si─Ö je w leczeniu skojarzonym w formie tak zwanej podw├│jnej blokady uk┼éadu RAA w obawie o ewentualne dzia┼éania niepo┼╝─ůdane. Jednocze┼Ťnie zar├│wno ACE-Is, jak i ARBs s─ů tak┼╝e nies┼éusznie okre┼Ťlane jako leki nefrotoksyczne. Upatruje si─Ö znaczenia terapii tymi lekami w wywo┼éywaniu ostrego uszkodzenia nerek (AKI) czy te┼╝ zaostrzenia przewlek┼éej choroby nerek (PChN). Celem tej pracy jest pr├│ba zweryfikowania pogl─ůd├│w dotycz─ůcych zwi─ůzk├│w pomi─Ödzy prowadzeniem leczenia ACE-Is lub ARBs a rozwojem AKI oraz pr├│ba ponownego spojrzenia na rol─Ö podw├│jnej blokady uk┼éadu RAA w terapii chor├│b nerek. Om├│wiono r├│wnie┼╝ zasady terapii niewydolno┼Ťci serca (HF) z zastosowaniem ACE-Is lub ARBs oraz aktualne dane dotycz─ůce znaczenia podw├│jnej blokady uk┼éadu RAA w nadci┼Ťnieniu t─Ötniczym

    Kidney Failure Prediction Models: A Comprehensive External Validation Study in Patients with Advanced CKD

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    Background: Various prediction models have been developed to predict the risk of kidney failure in patients with CKD. However, guideline-recommended models have yet to be compared head to head, their validation in patients with advanced CKD is lacking, and most do not account for competing risks.Methods: To externally validate 11 existing models of kidney failure, taking the competing risk of death into account, we included patients with advanced CKD from two large cohorts: the European Quality Study (EQUAL), an ongoing European prospective, multicenter cohort study of older patients with advanced CKD, and the Swedish Renal Registry (SRR), an ongoing registry of nephrology-referred patients with CKD in Sweden. The outcome of the models was kidney failure (defined as RRT-treated ESKD). We assessed model performance with discrimination and calibration.Results: The study included 1580 patients from EQUAL and 13,489 patients from SRR. The average c statistic over the 11 validated models was 0.74 in EQUAL and 0.80 in SRR, compared with 0.89 in previous validations. Most models with longer prediction horizons overestimated the risk of kidney failure considerably. The 5-year Kidney Failure Risk Equation (KFRE) overpredicted risk by 10%-18%. The four- and eight-variable 2-year KFRE and the 4-year Grams model showed excellent calibration and good discrimination in both cohorts.Conclusions: Some existing models can accurately predict kidney failure in patients with advanced CKD. KFRE performed well for a shorter time frame (2 years), despite not accounting for competing events. Models predicting over a longer time frame (5 years) overestimated risk because of the competing risk of death. The Grams model, which accounts for the latter, is suitable for longer-term predictions (4 years)

    Fructose-Rich Diet Is a Risk Factor for Metabolic Syndrome, Proximal Tubule Injury and Urolithiasis in Rats

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    Excessive consumption of fructose (FR) leads to obesity, metabolic syndrome (MS) and insulin resistance, which are known risk factors for kidney stones. The epidemiological study has suggested the association between fructose consumption and urolithiasis, but the precise mechanism is still not well understood. Male Wistar rats were assigned for 8 weeks to three groups with different FR content in diet: RD (n = 5)—regular diet with a FR < 3%; F10 (n = 6)—regular diet with an addition of 10% Fr in drinking water; F60 (n = 5)—60% FR as a solid food. Serum concentration of FR, creatinine (Cr), insulin (Ins), triglycerides (Tg), homocysteine (HCS), uric acid (UA), calcium (Ca), phosphate (Pi), magnesium (Mg) and sodium (Na) were measured. Based on 24 h urine collection the following tests were performed: urine pH, proteinuria (PCR), excretion of N-Acetyl-(D)-Glucosaminidase (NAG), monocyte chemoattractant protein (MCP-1), uric acid (uUAEx), phosphate (uPiEx), calcium (uCaEx), magnesium (uMgEx) and sodium (uNaEx). The creatinine clearance (CrCl) was calculated. Calcium deposits in kidney sections were examined using hematoxylin and eosin (HE) and von Kossa stains. The rats on F10 and F60, as compared to the RD diet, showed a tendency for lower CrCl, higher HCS level and some features of MS as higher Ins and TG levels. Interestingly, F10 (fluid) versus F60 (solid) diet led to higher serum Ins levels. F10 and F60 versus RD demonstrated higher urinary excretion of MCP-1 and NAG which were suggestive for inflammatory injury of the proximal tubule. F10 and F60 as compared to RD showed significantly lower uUAEx, although there were no differences in clearance and fractional excretion of UA. F60 versus RD induced severe phosphaturia (>30×) and natriuria (4×) and mild calciuria. F10 versus RD induced calciuria (3×), phosphaturia (2×) and mild natriuria. Calcium phosphate stones within the tubules and interstitium were found only in rats on FR diet, respectively, in two rats from the F10 group and another two in the F60 group. The rats which developed stones were characterized by significantly higher serum insulin concentration and urinary excretion of calcium and magnesium. A fructose-rich diet may promote development of calcium stones due to proximal tubule injury and metabolic syndrome

    The evolutionary development of the renin angiotensin aldosterone system and its importance for the survival of the human species

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    Kidneys produce a number of substances that affect intrarenal blood circulation; however, the key system that regulates blood flow in both general and local circulation (including the renal circulation) is the renin-angiotensinaldosterone system (RAAS). Individual elements of the RAA system are synthesized in separate tissues of the body under the influence of specific local factors. The system functions as a whole due to mutual relations based on feedback and it consists of three basic elements: renin, angiotensin and aldosterone. The history of research on the RAA system dates back to the late 19th century. One of the important stages of exploring the mechanisms related to RAA system functioning was the publication (in 1898) of the results of research on the hypertensive effect on blood pressure of rabbit kidney extracts (containing renin). The observations from 1934 were of similar significance: the correlation between dog kidney ischaemia and the occurrence of hypertension was found. In the following years, the enzymatic properties and structure of renin and angiotensin peptides, resulting from theaction of renin and the enzyme converting angiotensin I (Ang I) to its active form ÔÇö angiotensin II (Ang II), were clarified. The latter belongs to the most important regulators of aldosterone secretion. In 1939, it was proved thatunder the influence of renin blood pressure-rising peptides are formed. Consequently, it was documented that angiotensinwas the cause of hypertension in animals with ischaemic kidney, and in 1954 the sequence of angiotensin I and II was described. In 1960ÔÇô1961 systemic RAA occurrences were identified. However, to provide the insight of evolutionary significance of the RAA system for humans, the phylogenetic development of this enzyme-endocrine system in vertebrates should be investigated. The largest database of information regarding this system in the aforementioned group of animals is the research of Hirofumi Sokabe and Hiroko Nishimura, which, among others, is the basis for this manuscript

    Ewolucyjny rozw├│j uk┼éadu reninaÔÇôangiotensynaÔÇôaldosteron i jego znaczenie dla przetrwania gatunku ludzkiego

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    Nerki wytwarzaj─ů wiele substancji wp┼éywaj─ůcych na wewn─ůtrznerkowe kr─ů┼╝enie krwi, a kluczowym uk┼éadem reguluj─ůcymprzep┼éyw krwi zar├│wno w kr─ů┼╝eniu og├│lnym, jak i lokalnie (w tym w kr─ů┼╝eniu nerkowym), jest uk┼éad reninaÔÇôangiotensynaÔÇôaldosteron (RAAS). Poszczeg├│lne elementy uk┼éadu RAA s─ů syntetyzowane w odr─Öbnych tkankach organizmu pod wp┼éywem specyficznych czynnik├│w lokalnych. Uk┼éad ten funkcjonuje jako ca┼éo┼Ť─ç dzi─Öki wzajemnym zwi─ůzkom opartym na sprz─Ö┼╝eniach zwrotnych, a w jego sk┼éad wchodz─ů trzy zasadnicze elementy: renina, angiotensyna i aldosteron. Historia bada┼ä nad uk┼éadem RAA si─Öga ko┼äca XIX wieku. Jednym z wa┼╝nych etap├│w poznawania mechanizm├│w zwi─ůzanych z jego funkcjonowaniem by┼éo opublikowanie w 1898 r. wynik├│w bada┼ä po┼Ťwi─Öconych hipertensyjnemu wp┼éywowi wyci─ůgu z nerek kr├│lik├│w (zawieraj─ůcego renin─Ö) na ci┼Ťnienie t─Ötnicze krwi. Podobne znaczenie mia┼éy obserwacje z 1934 r., w kt├│rych stwierdzono zwi─ůzek niedokrwienia nerki psa z wyst─ůpieniem nadci┼Ťnienia t─Ötniczego. W nast─Öpnych latach wyja┼Ťniono w┼éa┼Ťciwo┼Ťci enzymatyczne i budow─Ö reniny oraz peptyd├│w angiotensynowych, powstaj─ůcych w wyniku dzia┼éania reniny i enzymu konwertuj─ůcego angiotensyn─Ö I (Ang I) do jej aktywnej postaci ÔÇö angiotensyny II (Ang II). Ta ostatnia nale┼╝y do najwa┼╝niejszych regulator├│w wydzielania aldosteronu (odkrytego przez Simpsona, Tait i Wetsteina w 1953 r.). W 1939 r. udowodniono, ┼╝e pod wp┼éywem reniny powstaj─ů peptydowe zwi─ůzki presyjne. W ten spos├│b udokumentowano, ┼╝e przyczyn─ů nadci┼Ťnienia t─Ötniczego u zwierz─ůt z niedokrwienn─ů nerk─ů jest angiotensyna. Pi─Ötna┼Ťcie lat p├│┼║niej opisano sekwencj─Ö angiotensyny I i II, natomiast latach 1960ÔÇô1961 zidentyfikowano wyst─Öpowanie systemowego uk┼éadu RAA. Aby przybli┼╝y─ç znaczenie ewolucyjne uk┼éadu RAA dla cz┼éowieka, nale┼╝y prze┼Ťledzi─ç filogenetyczny rozw├│j tego uk┼éaduenzymatyczno-hormonalnego u kr─Ögowc├│w. Najwi─Öksz─ů baz─ů informacji dotycz─ůcych tego uk┼éadu w wymienionejgrupie zwierz─ůt s─ů badania Hirofumi Sokabe oraz Hiroko Nishimura, mi─Ödzy innymi na podstawie kt├│rych powsta┼éaniniejsza praca
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