Glycerol-induced acute renal failure in the rat: the protective effect of unilateral nephrectomy

Studies were performed to evaluate the effect of unilateral nephrectomy on glycerol-induced acute renal failure in the rat. Normal rats were subjected to either sham uninephrectomy (n = 43) or right uninephrectomy (n = 53). The functional compensation of the remaining kidney was followed after 1 and 2 weeks. Fourteen days after the operation, acute renal failure was induced by injection of 50% glycerol solution to both groups. Uninephrectomised rats developed a lesser degree of renal failure compared to sham-operated rats. Forty-eight hours after glycerol injection, PCr of uninephrectomised rats was 260 +/- 22 mumol/l compared with 338 +/- 26 in sham-operated rats (P less than 0.0125) and CCr in uninephrectomised rats was greater (0.10 +/- 0.01 ml/min vs 0.07 +/- 0.01; P less than 0.025) in sham rats. Uninephrectomised rats had significantly greater recovery of CCr compared to sham rats at 24 h (20.1% +/- 2.3 vs 13.1% +/- 2.2, P less than 0.025) and at 48 h (32.1% +/- 3.3 vs 19.2% +/- 3.3, P less than 0.005) after glycerol injection. FENa was significantly less in uninephrectomised rats: 0.96 +/- 0.16% vs 2.25 +/- 0.05% (P less than 0.025) in sham rats 24 h post glycerol. Urinary excretion of K+ was greater in rats following uninephrectomy compared to sham rats both after 24 h and 48 h post glycerol (P less than 0.01), accompanied by lower plasma potassium (P less than 0.05). A correlation coefficient (r) of 0.793 was observed between urinary potassium excretion rate and percentage recovery of CCr.(ABSTRACT TRUNCATED AT 250 WORDS)     

Benign intracranial hypertension and recombinant growth hormone therapy in Australia and New Zealand

Benign intracranial hypertension (BIH) is reported in three children from Australia and one from New Zealand, who were being treated with recombinant human growth hormone (rhGH). Three males and one female, aged between 10.5 and 14.2 y, developed intracranial hypertension within 2 weeks to 3 months of starting treatment. A national database, OZGROW, has been prospectively collecting data on all 3332 children treated with rhGH in Australia and New Zealand from January 1986 to 1996. The incidence of BIH in children treated with growth hormone (GH) is small, 1.2 per 1000 cases overall, but appears to be greater with biochemical GHD (<10IUml ^-1), i.e. 6.5/1000 (3 in 465 cases), relative risk 18.4, 95% confidence interval 1.9-176.1, than in all other children on the database. The incidence in patients with Turner's syndrome was 2.3/1000 (1 in 428 cases). No cases in patients with partial GHD (10–20 IUml ^-1) or chronic renal failure were identified. Possible causative mechanisms are discussed. The authors'practice is now to start GH replacement at less than the usual recommended dose of 14IUm-² week^-1 in those children considered to be at high risk of developing BIH. Ophthalmological evaluation is recommended for children before and during the first few months following commencement of rhGH therapy and is mandatory in the event of peripheral or facial oedema, persistent headaches, vomiting or visual symptoms. The absence of papilledema does not exclude the diagnosis.     

Reduced Na-K-ATPase in distal nephron in glycerol-induced acute tubular necrosis

To further characterize changes in tubular Na-K-ATPase in acute tubular necrosis (ATN), segmental analysis was performed in rat nephrons. Na-K-ATPase was assayed in the following segments: proximal convolution (PC), proximal straight (PS), outer medullary thick ascending limb (MTAL), cortical thick ascending limb (CTAL), distal convolution (DC) and cortical collecting duct (CCD) in three groups of rats: 1.) intact; 2.) moderate non-oliguric ATN; and 3.) severe oliguric ATN. GFR and CNa/GFR X 100 were in group 1 0.80 +/- 0.05 ml/min and 0.68 +/- 0.06, in group 2 0.14 +/- 0.02 and 1.46 +/- 0.35, and in group 3 0.04 +/- 0.01 and 0.46 +/- 0.15, respectively. Na-K-ATPase in PC and PS were similar in all three groups. Na-K-ATPase levels were in MTAL: in group 1 37 +/- 2 X 10(-11) mol/mm/min, in group 2 20 +/- 1 X 10(-11), P less than 0.001 versus group 1, and in group 3 24 +/- 2 X 10(-11), P less than 0.001 versus group 1. In CTAL Na-K-ATPase levels were: in group 1 40 +/- 2 X 10(-11), in group 2 33 +/- 1 X 10(-11), P less than 0.001 versus group 1, and in group 3 27 +/- 2 X 10(-11), P less than 0.001 versus groups 1 and 2.(ABSTRACT TRUNCATED AT 250 WORDS)     

Semiconductor manufacturing: an introduction to processes and hazards

Recent studies suggest that semiconductor workers have an increased incidence of work-related illness. Semiconductor manufacturing is a chemically intensive industry involving many potentially hazardous operations. As this industry moves into new geographic areas, health care professionals will be asked to evaluate medical or workplace conditions associated with unfamiliar and complex production processes. This paper provides an overview of semiconductor manufacturing processes for these health practitioners. Each step of device fabrication is detailed with its attendant chemical and physical hazards. Broader concepts of industrial control technology, clean room ventilation, and ergonomics are explained. The hazards are tabulated to allow rapid assessment of the risks inherent to each processing step. References have been chosen to guide the reader to more indepth information.     

The Risk of Sulfasalazine- and Mesalazine-Associated Blood Disorders

Sulfasalazine (SASP) has often been reported to cause serious blood disorders, particularly agranulocytosis; however, little quantitative information is available to estimate the risk or to identify possible modifiers of the risk. We used comprehensive clinical information recorded on office computers by selected general practitioners in Britain to conduct a follow-up study of some 10,000 users of SASP and some 4000 users of mesalazine to estimate the risk of blood disorders associated with these drugs. Overall, the frequency of blood disorders attributable to SASP was 27/10,332 (2.6/1000 users). The risk for SASP users who were treated for arthritic disorders (6.1/1000 users) was some 10 times higher than that for users who were treated for inflammatory bowel disease (0.6/1000 users). There were no cases of blood disorders in users of mesalazine.