Background: Frailty is an aging-associated state of increased vulnerability, which raises the risk of adverse outcomes. Chronic kidney disease is associated with higher prevalence of frailty. Our aim was to estimate frailty prevalence in a hemodialysis population and its influence on shortterm outcomes. Design: Observational prospective longitudinal study of 277 prevalent hemodialysis patients. Frailty was estimated through the Edmonton Frail Scale (EFS). Demographic and clinical data, comorbidity index, and laboratory parameters were recorded. A 29-month follow-up was conducted on mortality, including hospitalization, and visits to hospital emergency services in the first 12 months of this period. Results: According to the EFS, 82 patients (29.6%) were frail, 53 (19.1%) were vulnerable, and 142 (51.3%) were non-frail. During follow-up, 58.5% frail patients, 30.2% vulnerable, and 16.2% non-frail ones died (p < .005). In the analysis of survival using an adjusted Cox model, a higher hazard of mortality was observed in frail than in non-frail patients (HR 2.34; 95% CI 1.39-3.95; p ¼ .001). During follow-up the hospitalization rate was 852 episodes/1000 patient-years for frail patients, 784 episodes/1000 patient-years for vulnerable patients, and 417 episodes/1000 patientyears for non-frail patients (p ¼ .0005). The incidence ratio of visits to emergency services was 3216, 1735, and 1545 visits/1000 patient-years for each group (p < .001). Conclusions: Hemodialysis patients present high frailty prevalence. Frailty is associated with poor short-term outcomes and higher rates of mortality, visits to hospital emergency services, and hospitalization.
Background Diabetic patients with kidney disease have a high prevalence of non-diabetic renal disease (NDRD). Renal and patient survival regarding the diagnosis of diabetic nephropathy (DN) or NDRD have not been widely studied. The aim of our study is to evaluate the prevalence of NDRD in patients with diabetes and to determine the capacity of clinical and analytical data in the prediction of NDRD. In addition, we will study renal and patient prognosis according to the renal biopsy findings in patients with diabetes. Methods Retrospective multicentre observational study of renal biopsies performed in patients with diabetes from 2002 to 2014. Results In total, 832 patients were included: 621 men (74.6%), mean age of 61.7 ± 12.8 years, creatinine was 2.8 ± 2.2 mg/dL and proteinuria 2.7 (interquartile range: 1.2–5.4) g/24 h. About 39.5% (n = 329) of patients had DN, 49.6% (n = 413) NDRD and 10.8% (n = 90) mixed forms. The most frequent NDRD was nephroangiosclerosis (NAS) (n = 87, 9.3%). In the multivariate logistic regression analysis, older age [odds ratio (OR) = 1.03, 95% CI: 1.02–1.05, P < 0.001], microhaematuria (OR = 1.51, 95% CI: 1.03–2.21, P = 0.033) and absence of diabetic retinopathy (DR) (OR = 0.28, 95% CI: 0.19–0.42, P < 0.001) were independently associated with NDRD. Kaplan–Meier analysis showed that patients with DN or mixed forms presented worse renal prognosis than NDRD (P < 0.001) and higher mortality (P = 0.029). In multivariate Cox analyses, older age (P < 0.001), higher serum creatinine (P < 0.001), higher proteinuria (P < 0.001), DR (P = 0.007) and DN (P < 0.001) were independent risk factors for renal replacement therapy. In addition, older age (P < 0.001), peripheral vascular disease (P = 0.002), higher creatinine (P = 0.01) and DN (P = 0.015) were independent risk factors for mortality. Conclusions The most frequent cause of NDRD is NAS. Elderly patients with microhaematuria and the absence of DR are the ones at risk for NDRD. Patients with DN presented worse renal prognosis and higher mortality than those with NDRD. These results suggest that in some patients with diabetes, kidney biopsy may be useful for an accurate renal diagnosis and subsequently treatment and prognosis.
Recurrence of IgA nephropathy following renal transplantation has been described in 40–50% of patients, and it usually has a good outcome. We present the case of a 54-year-old man wiht IgA nephropathy who developed terminal renal failure in 1985,3 years after the onset of the disease. In March 1986 he received a cadaveric renal allograft following treatment with ciclosporin and steroids. Eight months later he developed microhaematuria and proteinuria and 10 months later he developed acute nephritic syndrome and rapidly progressive renal failure. Renal biopsy disclosed an IgA nephropathy with epithelial crescents in 60% of glomeruli. Treatment with plasma exchange and cyclophosphamide was unsuccessful and the patient lost his graft and returned to regular haemodialysis 15 months after renal transplantation.
We have studied the clinical and morphological implications of renal siderosis, reviewing the autopsy protocols of 33 patients with valve prostheses in the heart. Seventeen patients had variable amounts of iron in the proximal tubules of the kidney. Renal siderosis was more frequent in women, in patients with longest time of evolution from the surgical procedure, and in patients with two valve prostheses. Histologically three degrees of renal siderosis may be defined: mild and moderate degrees of iron overload do not alter the kidney architecture, but kidneys, with severe siderosis show tubular atrophy and interstitial fibrosis. Episodes of acute renal failure (ARF) were more frequent in patients with more pronounced iron deposits, especially in the premortem stages. We conclude that renal siderosis may damage the proximal tubular epithelium of patients with valve prostheses in the heart; patients with renal overload of iron are more susceptible to episodes of ARF.
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