246 research outputs found
Cholesterol crystal embolism (atheroembolism)
Cholesterol crystal embolism, known as atheroembolic disease, is caused by showers of cholesterol crystals from an atherosclerotic plaque that occludes small arteries. Embolization can occur spontaneously or as an iatrogenic complication from an invasive vascular procedure (angiography or vascular surgery) and after anticoagulant therapy. The atheroembolism can give rise to different degrees of renal impairment. Some patients show a moderate loss of renal function, others severe renal failure requiring dialysis. Renal outcome can be variable: some patients deteriorate or remain on dialysis, some improve and some remain with chronic renal impairment. Clinically, three types of atheroembolic renal disease have been described: acute, subacute or chronic. More frequently a progressive loss of renal function occurs over weeks. Atheroembolization can involve the skin, gastrointestinal system and central nervous system. The diagnosis is difficult and controversial for the protean extrarenal manifestations. In the past, the diagnosis was often made post-mortem. In the last 10 yrs, awareness of atheroembolic renal disease has improved. The correct diagnosis requires the clinician to be alert. The typical patient is a white male aged >60 yrs with a history of hypertension, smoking and arterial disease. The presence of a classic triad (precipitating event, renal failure and peripheral cholesterol crystal embolization) suggests the diagnosis. This can be confirmed by a biopsy of the target organs. A specific treatment is lacking; however, it is an important diagnosis to make because an aggressive therapeutic approach can be associated with a more favorable clinical outcome
Manifestazioni renali in corso di rene policistico autosomico dominante (ADPKD)
Abstract non disponibil
Low cerebrovascular event rate in subjects with patent foramen ovale and different clinical presentations: results from a prospective non randomized study on a population including patients with and without patent foramen ovale closure.
PREDICTORS OF RENAL AND PATIENT OUTCOMES IN ATHEROEMBOLIC RENAL DISEASE: A PROSPECTIVE STUDY.
A model to predict disease progression in patients with autosomal dominant polycystic kidney disease (ADPKD): the ADPKD Outcomes Model.
Background: Autosomal dominant polycystic kidney disease (ADPKD) is the leading inheritable cause of end-stage
renal disease (ESRD); however, the natural course of disease progression is heterogeneous between patients. This study
aimed to develop a natural history model of ADPKD that predicted progression rates and long-term outcomes in patients
with differing baseline characteristics.
Methods: The ADPKD Outcomes Model (ADPKD-OM) was developed using available patient-level data from the placebo
arm of the Tolvaptan Efficacy and Safety in Management of ADPKD and its Outcomes Study (TEMPO 3:4; ClinicalTrials.gov
identifier NCT00428948). Multivariable regression equations estimating annual rates of ADPKD progression, in terms of
total kidney volume (TKV) and estimated glomerular filtration rate, formed the basis of the lifetime patient-level simulation
model. Outputs of the ADPKD-OM were compared against external data sources to validate model accuracy and
generalisability to other ADPKD patient populations, then used to predict long-term outcomes in a cohort matched to
the overall TEMPO 3:4 study population.
Results: A cohort with baseline patient characteristics consistent with TEMPO 3:4 was predicted to reach ESRD at a mean
age of 52 years. Most patients (85%) were predicted to reach ESRD by the age of 65 years, with many progressing to
ESRD earlier in life (18, 36 and 56% by the age of 45, 50 and 55 years, respectively). Consistent with previous research and
clinical opinion, analyses supported the selection of baseline TKV as a prognostic factor for ADPKD progression, and
demonstrated its value as a strong predictor of future ESRD risk. Validation exercises and illustrative analyses confirmed
the ability of the ADPKD-OM to accurately predict disease progression towards ESRD across a range of clinically-relevant
patient profiles.
Conclusions: The ADPKD-OM represents a robust tool to predict natural disease progression and long-term outcomes in
ADPKD patients, based on readily available and/or measurable clinical characteristics. In conjunction with clinical
judgement, it has the potential to support decision-making in research and clinical practice
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