Changes in distribution of intrarenal blood flow were studied in anesthetized rats during the acute phase of postischemic renal failure (1 h renal artery occlusion, 1 h reflow). Distribution of capillary plasma flow was determined by injecting fluorescein-isothiocyanate-globulin and lissamine-rhodamine-B200-globulin 1, 3, or 10 min prior to rapid freezing of the kidney. In histological sections it was possible to differentiate among the vessels perfused during the time of labeling because of their respective fluorescence. In these experiments all glomeruli became labeled within 1 min, although in contrast to the controls, the glomerular capillary network itself was not filled completely in the postocclusion organs. Incomplete labeling was far more pronounced, however, in the postglomerular network of the occlusion experiments. Due to this effect in the cortex and in the medulla, 11 and 58% of tissue, respectively, were found lying at a distance of more than 60 microns from the next vessel labeled after 1 min of dye circulation. In the control experiments there was no tissue within this distance. Prolonging the time of labeling up to 10 min caused little change in this pattern of distribution. In the occlusion experiments, the globulins were observed in nearly all Bowman spaces, but in less than half of the tubular lumina. The results strengthen the view that the ischemic insult leads primarily to disturbance of the postglomerular perfusion, which then results in trophic damage of the tubular system mainly within the renal medulla.
Klinikánkon négy éve alkalmazunk perkután PD katéter-beültetést és peritoenális dialízis kezelést a súlyosan csökkent bal kamra szisztolés funkcióval bíró, diuretikum-refrakter szívelégtelen betegek körében. Célul tűztük ki, hogy leírjuk centrumunk ebben a betegcsoportban szerzett tapasztalatát. Betegek, módszerek: 2014 áprilisától követtük betegeinket a követési idő vége 2018. január volt. Eredmények: Hat páciensünk közül háromnál nem iszkémiás etiológiájú csökkent ejekciós frakciójú szívelégtelenség, háromnál iszkémiás etiológiájú csökkent ejekciós frakciójú szívelégtelenség talaján alakult végstádiumú szívelégtelenség. Charlson komorbiditási index alapján 6-10 pont közötti értékeik voltak. A PD katéterbeültetés perkután technikával történt, az ultrafiltrációt azonnal el tudtuk kezdeni. Két betegünk sikeres szívtranszplantáción esett át. Három betegünk hunyt el, halálok nem PD asszociált szövődmény volt, 1 traumás, 1 egyéb infekció, 1 szívelégtelenség. Következtetések: A diuretikum-refrakter szívelégtelenség esetén a peritonealis dialízissel javulhat a jobb és bal kamra funkciója is. Centrumunkban kezeltünk elsőként PD-vel-áthidaló terápiaként-, hazánkban szívelégtelen beteget a szívtranszplantációig. Peritoneal ultrafiltration for refractory heart failure: single-center experience Introduction: In our centre we have been treated patients with therapy refracter congestive heart failure. The aim of this study was to describe a single-center experience in the treatment of refractory HF patients with peritoneal dialysis (PD). Methods: Our study included in a single PD Unit, showing symptoms and signs of severe refractory congestive HF to optimal pharmacological therapy (NYHA class IV). We followed them till January 2018. Results: Patients were followed for 10 months; population mean age was 58 years and Charlson's comorbidity index was 6-10. We could start peritoneal dialysis immediately after catheter implantation. Three patients died but not according to PD associated infection: 1 traumatic, 1 due to HF, another patient due to infection. Conclusion: PD, applied to refractory HF can improve functional class. In Hungary we used peritoneal dialysis first time as a bridge therapy to heart transplantation in diuretic refracter heart failure.
The age-old axiom that one is as old as his or her vessels are, calls for ongoing critical re-examination of modifiable risk factors of accelerated vascular ageing in chronic kidney diseases. Attempts to modulate vascular risk with cholesterol-lowering agents have largely failed in advanced chronic kidney disease (CKD). In addition to nitrogen waste products, many pathological biochemical processes also play a role in vascular calcification in chronic kidney damage. Magnesium, a cation vital for the body, may substantially reduce cardiovascular diseases’ risk and progression. This narrative review aimed to address the relationship between hypomagnesemia and vascular calcification, which promotes further cardiovascular complications in diabetes, aging, and CKD. Articles with predefined keywords were searched for in the PubMed and Google Scholar databases with specific inclusion and exclusion criteria. We hypothesized that a decrease in serum magnesium levels contributes to increased vascular calcification and thereby increases cardiovascular mortality. In summary, based on existing evidence in the literature, it appears that simple and inexpensive oral magnesium supplementation may reduce the cardiovascular mortality of patients who are already severely affected by such diseases; in this context, the concept of ‘normal’ vs. ‘ideal’ serum magnesium levels should be carefully re-examined.
Background Concomitant occurrence of anti-GBM disease and anti-PLA2R positive membranous nephropathy have been previously described. However, to the best of our knowledge, this is the first case report that documents the co-occurrence of the diseases proven by both serologic and histologic methods. Case presentation A 51-year-old woman presented to hospital with nausea, bilateral lower extremity edema, dyspnea, dark urine, and then anuria. Symptoms developed one month after an upper respiratory tract infection. Laboratory results showed acute kidney injury, and hypoalbuminemia. Immunologic examination revealed both anti-GBM and anti-PLA2R positivity. Kidney biopsy demonstrated the histological features of Goodpasture’s disease and anti-PLA2R positive membranous nephropathy. Steroid, cyclophosphamide, and plasmapheresis were commenced. Despite the combined immunosuppressive, the patient remained on renal replacement therapy. Conclusions Microbial kidney injury can trigger multiple autoimmune diseases. The simultaneous occurrence of anti-glomerular basement (anti-GBM) disease and membranous nephropathy is extremely rare. Delayed recognition leads to delayed treatment, causing worse renal and patient outcomes, as well as increased financial costs.
Hemodialysis reactions (HDRs) resemble complement-activation-related pseudoallergy (CARPA) to certain i.v. drugs, for which pigs provide a sensitive model. On this basis, to better understand the mechanism of human HDRs, we subjected pigs to hemodialysis using polysulfone (FX CorDiax 40, Fresenius) or cellulose triacetate (SureFlux-15UX, Nipro) dialyzers, or Dialysis exchange-set without membranes, as control. Experimental endpoints included typical biomarkers of porcine CARPA; pulmonary arterial pressure (PAP), blood cell counts, plasma sC5b-9 and thromboxane-B2 levels. Hemodialysis (60 min) was followed by reinfusion of extracorporeal blood into the circulation, and finally, an intravenous bolus injection of the complement activator zymosan. The data indicated low-extent steady rise of sC5b-9 along with transient leukopenia, secondary leukocytosis and thrombocytopenia in the two dialyzer groups, consistent with moderate complement activation. Surprisingly, small changes in baseline PAP and plasma thromboxane-B2 levels during hemodialysis switched into 30%–70% sharp rises in all three groups resulting in synchronous spikes within minutes after blood reinfusion. These observations suggest limited complement activation by dialyzer membranes, on which a membrane-independent second immune stimulus was superimposed, and caused pathophysiological changes also characteristic of HDRs. Thus, the porcine CARPA model raises the hypothesis that a second “hit” on anaphylatoxin-sensitized immune cells may be a key contributor to HDRs.
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