A prospective controlled trial on effect of percutaneous transluminal angioplast on functioning arteriovenous fistulae survival

Balloon angioplasty (PTA) is an established treatment modality for stenosis in dysfunctional arteriovenous fistulae (AVF), although most studies showing efficacy have been retrospective, uncontrolled, and nonrandomized. In addition, it is unknown whether correction of stenosis not associated with significant hemodynamic, functional, and clinical abnormality may improve survival in AVF. This study was a prospective controlled open trial to evaluate whether prophylactic PTA of stenosis not associated with access dysfunction improves survival in native, virgin, radiocephalic forearm AVF. Sixty-two stenotic, functioning AVF, i.e., able to provide adequate dialysis, were enrolled in the study: 30 were allocated to control and 32 to PTA. End points of the study were either AVF thrombosis or surgical revision due to reduction in delivered dialysis dose. Kaplan-Meier analysis showed that PTA improved AVF functional failure-free survival rates (P = 0.012) with a fourfold increase in median survival and a 2.87-fold decrease in risk of failure. Cox proportional hazard model identified PTA as the only variable associated with outcome (P = 0.012). PTA induced an increase in access blood flow rate (Qa) by 323 (236 to 445) ml/min (P < 0.001), suggesting that improved AVF survival is the result of increased Qa. PTA was also associated with a significant decrease in access-related morbidity by approximately halving the risk of hospitalization, central venous catheterization, and thrombectomy (P < 0.05). This study shows that prophylactic PTA of stenosis in functioning forearm AVF improves access survival and decreases access-related morbidity, supporting the usefulness of preventive correction of stenosis before the development of access dysfunction. It also strongly supports surveillance program for early detection of stenosis

Proteinuria, hypertension and renal failure in a patient with unilateral renal agenesis [clinical conference]

Proteinuria, hypertension and renal failure in a patient with unilateral renal agenesis [clinical conference

Evaluation of a patient with hypertension and mild renal failure in whom facial and digital abnormalities are noted

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Un caso di insufficienza renale acuta secondaria a malattia di MC-Ardle ad esordio tardivo. [A case of acute renal failure secondary to late-onset McArdle's disease].

INTRODUZIONE: La malattia di McArdle, o glicogenosi tipo V, è una malattia autosomica recessiva dovuta alla carenza della fosforilasi muscolare, un enzima che gioca un ruolo chiave nella demolizione del glicogeno durante un esercizio fisico, ed è caratterizzata da affaticamento, mialgia, crampi e debolezza muscolare con un importante aumento nei livelli ematici di creatinchinasi e rabdomiolisi con mioglobinuria, che può portare ad insufficienza renale acuta. La malattia di McArdle generalmente si manifesta tra i 15 ed i 30 anni; una comparsa tardiva è davvero inusuale. CASO CLINICO: riportiamo il caso di un paziente, maschio, di 68 anni, giunto in pronto soccorso per astenia, vertigini, diarrea ed oligoanuria. Il paziente è stato sottoposto a cinque sedute emodialitiche consecutive, con successiva ripresa della diuresi e ripristino della funzione renale. Il nostro paziente soffriva di astenia e dolore muscolare sin dalla giovane età: questi dati anamnestici, insieme ai persistenti livelli elevati di CPK ed in assenza di cause tossiche od infettive, ci hanno portato al sospetto di un disordine metabolico non comune, poi confermato dalla biopsia muscolare. CONCLUSIONI: sino ad oggi non esistono specifiche terapie per la glicogenosi tipo V. Una dieta ricca in proteine e saccarosio, la supplementazione di vitamina B6 e di creatina non hanno portato risultati brillanti. La terapia piu’ adatta sembra essere una moderazione dell’esercizio fisico, che migliora la tolleranza all’attività muscolare e l’afflusso di sangue ai muscoli, provvedendo all’aumento di glucosio ed acidi grassi alle fibre muscolari. INTRODUCTION: Mc Ardles disease, also known as Type V glycogen storage disease, is a rare deficiency of the enzyme glycogen phosphorylase in muscle cells, inherited as an autosomal recessive trait. In the absence of this enzyme, muscles cannot break down glycogen during exercise, so in patients affected by McArdles disease even moderate physical activity produces cramps, pain and fatigue. Anaerobic activity leads to severe fixed contractures and rhabdomyolisis with myoglobinuria and raised serum creatine-kinase, which, in turn, can lead to acute renal failure. Disease onset is usually in early childhood, although diagnosis is often not made until the second or third decade. CASE REPORT: We present the case of a 68-year-old man who presented to the Emergency Room with fatigue, vertigo, diarrhea and oliguria. The patient underwent five daily hemodialysis sessions, diuresis reappeared and there was progressive recovery of renal function. The patient described episodes of fatigue and muscular pain occurring since childhood: the positive personal history, together with persistently raised CPK levels in the absence of any infective or toxic cause of myositis, led us to suspect the presence of this rare metabolic disease, which was subsequently confirmed by muscle biopsy. CONCLUSION: To date, there is no specific treatment for type V glycogenosis, although a diet rich in protein and saccarose, vitamin B6 supplementation and creatine administration are generally recommended. Moderate physical activity can help manage symptoms by improving exercise tolerance and blood supply to the muscles, ensuring provision of glucose and free fatty acids for the muscle fibers

Body fluid spaces in patients on CAPD.

Total body water (TBW) and extracellular water (ECW) were determined in 9 CAPD patients on treatment from 5 to 14 months (mean 8.6 months). The mean value of TBW was normal and directly correlated to body weight, but TBW was abnormally distributed between extracellular and intracellular space. ECW volume was significantly lower than the predicted value (12.1 +/- 1.4 l versus 16.8 +/- 1.9 l) and out of proportion to TBW (34.8 +/- 3.9% versus 47.8 +/- 1.5%). The calculated ICW, therefore, appeared clearly hyperexpanded. The data suggest that cell overhydration was the distinctive feature in our CAPD patients