[Bilateral renal infarction: A rare complication of fibromuscular dysplasia]. / Infarto renal bilateral: una rara complicación de la displasia fibromuscular.

Bilateral renal infarction complicating Fibromuscular Dysplasia (FMD) is extremely rare and has so far been reported only in a handful of cases. We report a 44-year-old man who presented with complaints of abdominal pain and severe hypertension. Computed tomography of the abdomen revealed bilateral renal infarction and a renal angiography confirmed the bilateral and irregular stenosis due to FMD, in the absence of systemic vasculitis and other risk factors for thromboembolic events. Therefore, angioplasty with balloon was performed in order to obtain a good vessel patency and to improve patency in the long term follow-up. After the endovascular treatment the blood pressure improved markedly, maintaining this result at 3-months follow-up. Our case highlight the importance of recognizing renal infarction as an initial presentation of FMD.

Severe renal failure and thrombotic microangiopathy induced by malignant hypertension successfully treated with spironolactone.

Malignant hypertension can cause thrombotic microangiopathy (TMA) characterized by hemolytic anemia and thrombocytopenia. On the other hand, severe hypertension is sometimes associated with hemolytic uremic syndrome (HUS) or thrombotic thrombocytopenic purpura (TTP). Distinguishing these entities is important because of therapeutic implications. Plasmapheresis should be initiated as soon as possible if we are dealing with TTP. We describe the case of a 30-year-old man referred to our hospital with malignant hypertension, severe renal failure and TMA: haemoglobin=9g/dL, total bilirubin=0.4mg/dL, haptoglobin≤10mg/dL, platelet count=59,000/µL and schistocytes on peripheral smear. He required initiation of hemodialysis. Additionally, we considered that the possible cause of TMA was malignant hypertension according to the presence of hypertensive retinopathy and thrombocytopenia which remitted only with blood pressure control, hence, plasmapheresis was not given. Renal function did not improve and the patient remained chronic hemodialysis. Intensive therapy for hypertension with a combination of antihypertensive drugs including spironolactone successfully lowered his blood pressure without developing hyperkalemia.

Relation between Kaufman Brief Intelligence Test and WISC-III scores of children with RD.

Concurrent validity of the Kaufman Brief Intelligence Test (K-BIT) with the Wechsler Intelligence Scale for Children-Third Edition (WISC-III) was evaluated, as well as the K-BIT's accuracy as a predictor of WISC-III scores, in a sample of young children with reading disabilities. The two measures were administered to 65 children from Atlanta, Boston, and Toronto who ranged from 6-5 to 7-11 years of age at testing. Correlations between the verbal, nonverbal, and composite scales of the K-BIT and WISC-III were .60, .48, and .63, respectively. Mean K-BIT scores ranged from 1.2 to 5.0 points higher than the corresponding WISC-III scores. Standard errors of estimation ranged from 10.0 to 12.3 points. In individual cases, K-BIT scores can underestimate or overestimate WISC-III scores by as much as 25 points. Results suggest caution against using the K-BIT exclusively for placement and diagnostic purposes with young children with reading disabilities if IQ scores are required.

Unilateral injury of posterior parietal cortex and spatial learning in hooded rats.

The influences of bilateral or unilateral injuries within the posterior parietal cortex (PPC) upon spatial learning in a water maze were examined in three experiments. Place-learning and response-learning were investigated in a four-alley 'Greek-cross' shaped water maze with extra-maze visual cues available. No differences were detected on any of several measures sensitive to learning between the lesion groups on the place-learning task. Microanalysis of behavior within trials revealed that animals with either bilateral or right unilateral PPC injuries committed significantly more total errors, initial alley entrance ('reference memory') errors, and re-entry ('working memory') errors in the response-learning paradigm than did either the control or left PPC-injured rats. No differences were detected between the latter two groups on these measures. Unilateral lesions resulted in asymmetrical placing responses ipsilateral to the injury 10 days after surgery whereas bilateral injuries resulted in asymmetrical placing with mixed directionality. The acquisition of the response-learning problem in the absence of visual cues was studied on animals prepared with unilateral lesions and housed post-operatively either in isolation or in a 'complex environment.' In the absence of visual cues both right and left PPC-injured rats committed more errors than sham controls, and differential post-surgical housing did not attenuate these impairments. These same animals were trained on the landmark navigation task. Although no differences appeared between the lesion groups, a generalized but transient facilitation of learning was observed in animals housed in the 'complex' environment. Unilateral injuries placed in sham controls failed to disturb retention of the landmark navigation strategy. Because none of the PPC-injured animals were deficient in the landmark task, a result which is contrary to observations in other laboratories, the influence of post-surgical recovery interval upon acquisition of the landmark navigation strategy was explored. Animals were prepared with right PPC injuries and trained following either a 5 or 35 day recovery interval. Only those animals limited to the short recovery interval proved to have a spatial deficit in the landmark task. It is concluded that injuries in the PPC of either hemisphere disturb egocentric spatial functions. However, animals with left PPC injuries are able to compensate by using allocentric visual cues if they are available. It is due to the special role played by the right PPC in complex visuospatial functions that animals with this injury are unable to compensate.