Infestations of the human brain with the larval stage of Taenia solium, once an infrequent diagnosis in the United States, is now a more frequently encountered clinical entity especially in population centers with high immigrant flux. During a recent 5-year period 45 cases of intraventricular cysticerosis have been evaluated and treated. Modes of involvement included isolated cyst formation, ependymitis, or combinations of both. Evidence of associated parenchymatous involvement was present in 20% of cases. Sites of infestation included the lateral ventricle (five cases), third ventricle (12 cases), Sylvian aqueduct (four cases), and fourth ventricle (24 cases). Mean post-therapy follow-up periods for this series exceed 36 months. This experience indicates that direct excision is the treatment of choice for ventricular cystic lesions, but that management, operative planning, and expectations should be influenced by considerations of: 1) the potential for acute clinical deterioration (38%); 2) the potential for cyst migration; 3) attendant ependymitis, defined by computerized tomography or verified at surgery; 4) the potential for increase in cyst volume with local mass effect; 5) selection and institution of corridors of surgical access that establish alternative routes of cerebrospinal fluid flow; and 6) the possibility of cyst excision by a stereotaxic endoscopic procedure.

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IgA nephropathy is one of the most common forms of glomerular disease. Nearly 25% of affected patients progress to end-stage renal disease over a 20-25-y follow-up period. IgA-containing immune complexes stimulate oxygen-free radical production by mesangial cells in vitro. The excessive oxidant stress may mediate glomerular injury in this disorder. Therefore, we studied whether dietary supplementation with the antioxidant agent, vitamin E, attenuates renal disease in an experimental model of incipient IgA nephropathy with mild kidney inflammation. IgA nephropathy was induced in male Lewis rats by oral immunization with 0.1% bovine gamma-globulin (BGG)-containing drinking water for 8 wk. At the completion of this period, animals received BGG, 1 mg/dose i.v., on three successive days. Experimental rats (n = 10) received a specially formulated diet containing 100 IU of vitamin E/kg of chow, whereas control animals (n = 10) were fed chow containing 30 IU of vitamin/kg of chow. The BGG immunization regimen induced mesangial IgA deposition in all rats. Vitamin E supplementation resulted in a nearly 5-fold increase in the serum vitamin E concentration. Vitamin E-treated rats gained more weight and had a lower incidence of hematuria, 20% versus 80% (p < 0.03). Moreover, proteinuria was decreased by 50%, and reduced renal plasma flow was restored to normal, compared with untreated rats with IgA nephropathy. Glomerular hypertrophy occurred in animals with IgA nephropathy, but less so in those receiving vitamin E supplementation. Renal cortical malondialdehyde content was reduced from 1.55 +/- 0.10 to 1.22 +/- 0.09 nmol/mg of protein (p < 0.01) in rats fed the vitamin E-enriched diet. Finally, renal transforming growth factor-beta 1 gene expression was reduced by 34% in rats with IgA nephropathy receiving vitamin E treatment (p < 0.05). We conclude that experimental IgA nephropathy is associated with increased renal oxidant injury. Dietary treatment with the antioxidant agent, vitamin E, attenuated renal functional and structural changes in this experimental glomerulopathy. These studies support the importance of clinical trials for the evaluation of the efficacy of antioxidant therapy in patients with IgA nephropathy.

Objectives After completing this article, readers should be able to: 1. Recognize and delineate the causes of acute renal failure. 2. Formulate emergency management of fluid electrolyte disorders in acute renal failure. 3. Characterize the incidence, causes, and costs of chronic renal failure in children. 4. Explain the pathogenesis and treatment of complications of chronic renal failure. 5. Delineate a plan to help the family with the outcome of renal failure. Acute Renal Failure Incidence and Causes ARF is encountered in 3% to 10% of all admissions to neonatal intensive care units. In our experience with a regional pediatric nephrology program serving a catchment area of 1.5 million general population, 6.4% of 3,154 children referred to the program from community physicians suffered from ARF. However, precise figures on the true incidence of ARF in childhood are surprisingly sparse. ARF is a life-threatening, abrupt reduction of urinary output to less than 300 mL/m 2 per day that is precipitated by prolonged renal ischemia in most cases. Occasionally, it may present with a high urinary output but mounting serum urea nitrogen and creatinine levels, the so-called "high output" or "nonoliguric" ARF, more often following severe burns or open heart surgery. The three leading causes of acute renal failure in children (Table 1) in developing countries are: hemolytic-uremic syndrome (31%), glomerulonephritis (23%), and postoperative sepsis/prerenal ischemia (18%). In contrast, for industrialized countries, the three most common causes are: intrinsic renal disease (44%), postoperative septic shock (especially after open heart surgery) (34%), and organ/bone marrow transplantation (13%). Proximal tubular necrosis may follow toxic ingestions (eg, carbon tetrachloride, diethylene glycol, arsenic, mercury, gold, lead, and other heavy metals). Medications, such as

Patients with Bartter syndrome types 1, 2 and 4 present at a younger age than classic Bartter syndrome type 3. They present with symptoms, often quite severe in the neonatal period. Patients with classic Bartter syndrome type 3 present later in life and may be sporadically asymptomatic or mildly symptomatic. The severe, steady-state hypokalemia in Bartter syndrome and Gitelman syndrome may abruptly become life-threatening under certain aggravating conditions. Clinicians need to be cognizant of such renal tubular disorders, and promptly treat at-risk patients.

This study was designed to test the hypothesis that induction of insulin-like growth factor-1 (IGF-1) is reduced in the uremic rat liver, which would help to explain the purported growth hormone resistance noted in uremia. IGF-1 mRNA, in the steady state and after acute induction by two doses of 100 micrograms/100 g body wt recombinant human growth hormone (rhGH), was quantitated by solution hybridization in total liver RNA, extracted by the guanidine thiocyanate/cesium chloride gradient method. Eighteen Sprague-Dawley rats weighing 100 to 102 g were randomly divided into three groups: sham-operated control rats (control group); 5/6 nephrectomized rats (uremic group); and sham-operated controls with dietary intake matching that of the uremic rats (pair-fed group). The results showed that the steady state liver IGF-1 mRNA was 1.7 arbitrary densitometry units (ADU) in the uremic animals, and was lower than the value of 3.2 ADU in the control animals (P < 0.05). After the acute administration of rhGH, the liver IGF-1 mRNA of control, uremic and pair-fed groups showed mean increases of 154% (P < 0.05), 124% (not significant, NS) and 117% (NS), respectively. The lack of IGF-1 induction in the uremic group supported the concept of growth hormone resistance in uremia. In addition, a similar lack of induction was observed in the pair-fed group, whose food intake was 65% that of the control animals. This indicated that the lack of IGF-1 induction was at least partially due to the reduced food intake.(ABSTRACT TRUNCATED AT 250 WORDS)

To test the effect of a therapeutic intervention to ameliorate the rate of progression, this steady and prolonged progression of 0.5 mg/dL per year between serum creatinine concentration of 1.5 to 5 mg/dL would seem the optimal study.