Purpose The potential nephrotoxicity of intravenous iodinated contrast media is a major concern for acute ischaemic stroke imaging evaluation. This study aimed to assess the incidence of acute kidney injury after intravenous iodinated contrast media exposure in acute ischaemic stroke patients. Methods We conducted a retrospective cohort analysis between January 2012 and July 2018 to select adult patients admitted to the emergency department with acute ischaemic stroke. The exposed patients received a uniform intravenous dose of low osmolar non-ionic iodinated contrast media, as part of the imaging protocol for acute ischaemic stroke. The unexposed patients underwent a non-enhanced cranial computed tomography scan. Acute kidney injury was defined according to the Kidney Disease Improving Global Outcomes criteria, limited to the first 72 hours. Results A total of 161 and 105 patients were included in the exposed and unexposed groups, respectively. The median age was 72.8 years (interquartile range 20), 53% were men and 97% were white. Demographic and baseline characteristics were similar between the groups. The incidence of acute kidney injury between exposed ( n = 10, 6.2%) and unexposed ( n = 1, 1%) groups ( P = 0.073) was similar and contrast exposure was not a significant predictor of acute kidney injury. Conclusion Intravenous iodinated contrast media exposure during acute ischaemic stroke imaging protocols is not an independent predictor of acute kidney injury in patients with normal or near-normal renal function. Studies with larger sample sizes would help to clarify if patients with both cardiovascular risk factors and impaired renal function could benefit from prophylactic measures.

One of the most common causes of rapidly progressive glomerulonephritis (RPGN) is pauci-immune crescentic glomerulonephritis (CrGN). In the majority of cases, this condition has a positive serologic marker, the anti-neutrophil cytoplasmic antibodies (ANCAs), but in approximately 10% there are no circulating ANCAs, and this subgroup has been known as the ANCA-negative pauci-immune CrGN. RPGN can be associated with systemic diseases, but there are only few case reports describing the association with mixed connective tissue disease (MCTD). The authors report a case of ANCA-negative CrGN associated with a MCTD.

Introduction: Therapeutic plasmapheresis is a therapeutic procedure in which the patient’s blood is passed through a medical device which separates out plasma from other components of blood. The plasma is removed and replaced with a replacement solution. Studies on the use of plasmapheresis in critically ill patients are scarce. The aim of this study was to review all therapeutic plasmapheresis sessions carried out in the Hospital Beatriz Ângelo intensive care unit.Material and Methods: An observational retrospective study was conducted between April 2012 and March 2019. All patients who underwent therapeutic plasmapheresis in the intensive care unit were included, and plasmapheresis sessions held outside the intensive care unit were excluded.Results: Of 46 patients, 63% were men (n = 29), with a median age of 53 years. The most frequent diagnoses were hypertriglyceridemia-induced pancreatitis, vasculitis, autoimmune haemolytic anaemia, and atypical haemolytic-uremic syndrome. A total of 198 plasmapheresis sessions were carried out in the intensive care unit. Most of the used replacement solutions were fresh frozen plasma (34.4%), albumin/crystalloid (24.2%), and albumin/fresh frozen plasma (19.2%). The most common complications were hydroelectrolytic changes (84; 42.4%) and coagulation disorders/thrombocytopenia (65; 32.8%). There was no need to interrupt any plasmapheresis session due to complications related to the patient.Discussion: Therapeutic plasmapheresis is an urgent procedure that can reduce morbidity and mortality in critically ill patients. This justifies that 37% of patients started the technique before the diagnostic confirmation. The indications for plasmapheresis and the choice of replacement solution were in agreement with the guidelines. Despite the risk of bleeding, no haemorrhagic complications were recorded.Conclusion: Therapeutic plasmapheresis is a complex technique that requires specific training. The indications are diverse, and some are not consensual. Complications were frequent, but they did not increase morbidity.

Metabolic acidosis is a common clinical disturbance due to increased plasma acidity caused by a primary decrease in serum HCO3- concentration. It is classified as normal or high anion gap metabolic acidosis. High anion gap metabolic acidosis can result from either a decrease in unmeasured cations (K+, Ca2+, Mg2+) or an increase in unmeasured anions (PO43−, albumin). However, other anions such as lactic acid or keto acids may cause this acid-base disorder. It can also result from renal failure and intoxication (salicylate, methanol, ethylene glycol), or more rarely, from massive rhabdomyolysis and pyroglutamic (5-oxoproline) acidemia. Acidemia due to pyroglutamic acid should be considered when no other aetiology is found. High anion gap metabolic acidosis is diagnosed in children with inherited defects in enzymes of the γ-glutamyl cycle. In adults, this disorder from pyroglutamic acid has been described in association with chronic acetaminophen misuse. We report a case of pyroglutamic acidosis in a woman with acute misuse of acetaminophen concurrent with chronic use.LEARNING POINTParacetamol is an easily available drug with potentially harmful consequences.Accumulation of pyroglutamic acid (5-oxoproline) may be a cause of high anion gap metabolic acidosis.Reporting cases of 5-oxoprolinemia acidosis contributes to better understanding of the condition.

Atheroembolic renal disease (AERD) is a kidney manifestation of atherosclerosis as a systemic disease. AERD is defined as a renal impairment secondary to embolization of cholesterol crystals with consequent occlusion of renal vascularization. The current case report describes one patient with multiple risk factors but without any inciting event history who presents a very atypical clinical course of a severe and massive atheroembolic disease that developed spontaneously and silently.

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Background and Aims Hyperkalemia (HK) is a common and dangerous complication of CKD because of impaired kidneýs ability for potassium elimination. On the other hand, HK is a common complication of extremely beneficial therapeutic agents acting on the renin–angiotensin–aldosterone system (RAAS). Its initiation at early CKD stages is even more benefic but HK could lead to stop it. We wonder if there is a possible relation between HK, therapeutic changes in RAAS inhibition (not initiating or stopping it) and mortality. Our goal was to investigate incidence, prevalence and clinical outcomes of at least one episode of HK in a CKD population outpatient setting. Additionally, we investigated the association of HK with changes in RAAS inhibition and mortality risk. Method We conducted a patient-level, retrospective, cohort analysis of all adult patients referred to a nephrology clinic over a 6 years period. We included CKD stage 3 patients with at least 24 months of follow up and three or more serum potassium determinations. The prevalence of HK (blood potassium level ≥ 5,5mmol/L) at first consultation and incidence during follow up were accessed. Patients were spited in two groups prior to analysis: A) Patients without any HK episode and B) Patients with at least one HK episode. Baseline and follow up covariates included demographics, comorbid conditions, laboratory values, HK-associated drugs [ACEis, ARBs, potassium-sparing diuretics and diuretics]. The impact of HK and therapeutic changes on mortality was evaluated through a logistic regression. Results Out of the 3008 patients referred to the nephrology clinic, 575 (19.1%) met the inclusion criteria (mean age: 70.4 years; 63.7% male and 94.0% caucasians). Mean follow-up was 4.1±1.8 years. Important cardiovascular comorbidities included hypertension (HTN) (90.3%); overweigh (67.4%), DM (49.0%) and Heart Failure (31.4%). CKD stage progression was present in 122 (21.2%). The prevalence of HK at first consultation was 8.7% and follow up incidence 21.7%. From this cohort, 164 (28.5%) had at least on episode of HK (Group B) and 101 (17.6%) died. During the follow up, RAAS inhibition drugs was removed or not started in 200 (34.8%) patients and diuretic was initiated in 165 (28.7%). In univariate analysis, at least one HK episode was associated with Diabetes (65.9 vs 42.3%, p<0.001), Heart failure (36.6 vs 28.0%, p=0.007), Macroalbuminuria (34.1 vs 21.2%, p=0.001), CKD progression (33.5 vs 16.3. p<0.001) higher frequency of diuretic initiation (38.4 vs 24.8%, p<0.001) and higher mortality (27.6 vs 13.7%, p<0.001). In multivariate logistic regression analysis, the independent predictors of mortality were: At least one HK episode (OR 1.82, 95% CI 1.08-3.04, p=0.02); Heart Failure (OR 1.97, 95% CI 1.16-3.35, p=0.01); Older age (OR per 1 year increase 1.04, 95% CI 1.02-1.07, p=0.001); CKD progression (OR 4.18, 95% CI 2.43-7.19, p<0.001). Predictors of lower mortality risk were: Patients who maintained RAAS inhibition during follow up (OR 0.50, 95% CI 0.26-0.96, p=0.03); Patients who started RAAS inhibition during follow up (OR 0.38, 95% CI 0.16-0.88, p=0.02). Conclusion Our study confirms that RAAS inhibition had a protector and independent impact in mortality when prescribed in CKD early stages. On the other hand, patients with at least one episode of HK have a higher risk of mortality. All efforts should be made to maintain these therapeutic agents, looking for other ways to control hyperkalemia rather than stop it.

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