Methotrexate-associated B-cell lymphoma presenting with acute renal failure and bilateral nephromegaly.
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Acute Kidney Injury↗
Biomedical subjects
J M Jacobs
Publications and source records attributed to J M Jacobs.
Integrated molecular signature of disease: analysis of influenza virus-infected macaques through functional genomics and proteomics.
Recent outbreaks of avian influenza in humans have stressed the need for an improved nonhuman primate model of influenza pathogenesis. In order to further develop a macaque model, we expanded our previous in vivo genomics experiments with influenza virus-infected macaques by focusing on the innate immune response at day 2 postinoculation and on gene expression in affected lung tissue with viral genetic material present. Finally, we sought to identify signature genes for early infection in whole blood. For these purposes, we infected six pigtailed macaques (Macaca nemestrina) with reconstructed influenza A/Texas/36/91 virus and three control animals with a sham inoculate. We sacrificed one control and two experimental animals at days 2, 4, and 7 postinfection. Lung tissue was harvested for pathology, gene expression profiling, and proteomics. Blood was collected for genomics every other day from each animal until the experimental endpoint. Gross and microscopic pathology, immunohistochemistry, viral gene expression by arrays, and/or quantitative real-time reverse transcription-PCR confirmed successful yet mild infections in all experimental animals. Genomic experiments were performed using macaque-specific oligonucleotide arrays, and high-throughput proteomics revealed the host response to infection at the mRNA and protein levels. Our data showed dramatic differences in gene expression within regions in influenza virus-induced lesions based on the presence or absence of viral mRNA. We also identified genes tightly coregulated in peripheral white blood cells and in lung tissue at day 2 postinoculation. This latter finding opens the possibility of using gene expression arrays on whole blood to detect infection after exposure but prior to onset of symptoms or shedding.
Animals↗
QSYP peptide sequence is selected from phage display libraries by bovine IgG contaminants in monoclonal antibody preparations.
A consensus peptide sequence, QSYP, appears as an artifact during the mapping of monoclonal antibodies (MAbs) using a random peptide phage display library. Phage bearing this QSYP sequence were independently selected by four different laboratories screening separate MAb preparations with the same phage library. In each case, the QSYP sequence was selected in addition to a consensus sequence specific to the MAb. Phage that displayed the QSYP sequence were not bound by the MAb of interest, but rather bound to bovine IgG derived from the FBS present in the hybridoma growth media. The implications of this finding for the interpretation of phage library screening results and possible methods for the removal of bovine IgG from MAb preparations are discussed.
Amino Acid Sequence↗
Hyperopic laser in situ keratomileusis to treat overcorrected myopic LASIK.
PURPOSE: To evaluate the safety and efficacy of hyperopic laser in situ keratomileusis (LASIK) in treating hyperopia caused by overcorrected myopic LASIK and to evaluate a new technique to place the hyperopic treatment after lifting the initial myopic flap. SETTING: Open-access outpatient excimer laser surgical facility. METHODS: A retrospective analysis was performed of 54 eyes in 47 patients who had spherical hyperopic LASIK by 21 surgeons for the treatment of significant hyperopia after overcorrected LASIK for myopia. In 42 eyes, the initial LASIK flaps were lifted and in 12 eyes, new flaps were cut. The mean age of the 25 men (53%) and 22 women (47%) was 48.2 years +/- 8.4 (SD). Outcome measures included refractive error, uncorrected visual acuity (UCVA), best spectacle-corrected visual acuity (BSCVA), and complications. The mean follow-up was 2.97 months. RESULTS: In eyes in which postoperative emmetropia was attempted (n = 45), the mean spherical equivalent improved from +1.21 +/- 0.49 diopters (D) preoperatively to -0.38 +/- 0.50 D postoperatively (P <.001). The mean UCVA improved from 20/38.6 +/- 16.3 to 20/27.4 +/- 9.4 (P <.001). At the last follow-up, 69% of eyes were within +/-0.5 D and 96% were within +/-1.0 D of emmetropia; 42% had a UCVA of 20/20 and 96% had a UCVA of 20/40 or better. No eyes lost 2 or more lines of BSCVA. No vision-threatening complications occurred. Results in patients who had initial flaps lifted and those who had new flaps cut were statistically indistinguishable. On average, achieved hyperopic corrections were 18% greater than intended. CONCLUSION: Hyperopic LASIK was safe, predictable, and effective in the treatment of hyperopia caused by overcorrected myopic LASIK. Results were similar whether the original flap was lifted or a new one was cut.
Cornea↗
From eyelid bumps to thyroid lumps: report of a MEN type IIb family and review of the literature.
PURPOSE: We present a two-generation family with multiple endocrine neoplasia (MEN) type IIb diagnosed by their ophthalmologists based on characteristic ophthalmic findings. METHODS: A family consisting of a 33-year-old female proband and her 8- and 7-year-old children had prominent corneal nerves; eyelid, lip, and tongue nodules; and a characteristic facies. A polymerase chain reaction-based genetic assay was obtained to detect the genetic mutation most commonly associated with MEN type IIb. Serum calcitonin and urine catecholamine studies were obtained. RESULTS: Molecular genetic studies detected in all 3 patients a mutation at codon 918 of the RET proto-oncogene known to be present in 95% of the cases of MEN type IIb. Serum calcitonin was elevated in the proband and her son. Urine catecholamine levels were elevated in the proband. Surgical treatment and histologic analysis confirmed pheochromocytoma and medullary thyroid carcinoma (MTC) in the proband. Surgical exploration revealed the MTC to be metastatic to the liver. CONCLUSIONS: This family demonstrates the characteristic findings of MEN type IIb: prominent corneal nerves in a clear stroma and multiple submucosal neuromas of the conjunctiva, eyelids, lips, and tongue. Ophthalmologists have a critical role to play in recognizing these signs, because the early diagnosis of medullary thyroid carcinoma and pheochromocytoma may be life saving.
Adrenal Gland Neoplasms↗
Effect of arsenite on the induction of CYP1A4 and CYP1A5 in cultured chick embryo hepatocytes.
We had reported previously that 2.5-5 microM sodium arsenite decreased the phenobarbital-mediated induction of CYP2H activity and protein but not CYP2H1 mRNA in chick-embryo hepatocyte cultures. Induction of a CYP1A activity and protein by 3-methylcholanthrene was also decreased by low arsenite concentrations; however, CYP1A mRNAs were not measured in those studies. We report here that low concentrations of arsenite decreased induction of activities and mRNAs of two chicken cytochromes P450, CYP1A (1A4 and 1A5), by 3-methylcholanthrene in chick-embryo hepatocyte cultures. Arsenite treatment did not affect the turnover of either mRNA, nor did it decrease the superinduction of each mRNA caused by treatment with cycloheximide in addition to 3-methylcholanthrene. Glutathione depletion enhanced the effect of arsenite to decrease induction of CYP1A4. These results indicate the induction of CYP1A4 and 1A5 is inhibited by sodium arsenite at the level of transcription, suggesting that the Ah receptor complex may be involved.
Animals↗
Effect of sodium arsenite on heme metabolism in cultured chick embryo hepatocytes.
We had previously reported that low concentrations of sodium arsenite (1-5 microM) decreased the induction of cytochrome P450 CYP1A and CYP2H in cultured chick embryo hepatocytes in parallel with increases in heme oxygenase. However, in those studies exogenous heme did not prevent the decrease in CYPs. In this study, we investigated the effect of arsenite on the synthesis and degradation of heme. Arsenite had no effect on induction of 5-aminolevulinic acid synthase mRNA or activity. Arsenite, at concentrations from 1 to 25 microM, had no effect on protoporphyrin synthesis from 5-aminolevulinic acid and did not increase the accumulation of other porphyrins, indicating that the enzymes in the pathway between 5-aminolevulinic acid synthase and ferrochelatase were unaffected by arsenite. Synthesis of heme from radioactive 5-aminolevulinic acid was slightly decreased (less than 20%) by 2.5 microM arsenite, a concentration that decreased induction of CYP1A and CYP2H by greater than 50%. Rates of biliverdin formation and degradation of exogenous heme were not different in cultures treated simultaneously with arsenite and heme or with heme alone. However, arsenite treatment increased biliverdin formation from heme synthesized from added 5-aminolevulinic acid by 60% and decreased the endogenous heme content of the cells by 30%. Our results suggest that although 2.5 microM arsenite induced heme oxygenase four- to sixfold, this had no effect on degradation of exogenous heme. Degradation of heme synthesized from 5-aminolevulinic acid was increased but this did not affect the regulatory heme pool.
5-Aminolevulinate Synthetase↗
Genetic engineering of crops as potential source of genetic hazard in the human diet.
The benefits of genetic engineering of crop plants to improve the reliability and quality of the world food supply have been contrasted with public concerns raised about the food safety of the resulting products. Debates have concentrated on the possible unforeseen risks associated with the accumulation of new metabolites in crop plants that may contribute to toxins, allergens and genetic hazards in the human diet. This review examines the various molecular and biochemical mechanisms by which new hazards may appear in foods as a direct consequence of genetic engineering in crop plants. Such hazards may arise from the expression products of the inserted genes, secondary or pleiotropic effects of transgene expression, and random insertional mutagenic effects resulting from transgene integration into plant genomes. However, when traditional plant breeding is evaluated in the same context, these mechanisms are no different from those that have been widely accepted from the past use of new cultivars in agriculture. The risks associated with the introduction of new genes via genetic engineering must be considered alongside the common breeding practice of introgressing large fragments of chromatin from related wild species into crop cultivars. The large proportion of such introgressed DNA involves genes of unknown function linked to the trait of interest such as pest or disease resistance. In this context, the potential risks of introducing new food hazards from the applications of genetic engineering are no different from the risks that might be anticipated from genetic manipulation of crops via traditional breeding. In many respects, the precise manner in which genetic engineering can control the nature and expression of the transferred DNA offers greater confidence for producing the desired outcome compared with traditional breeding.
Crops, Agricultural↗
Effect of arsenite on induction of CYP1A, CYP2B, and CYP3A in primary cultures of rat hepatocytes.
In earlier studies, sodium arsenite treatment was shown to decrease induction of enzymatic activities associated with hepatic CYPs in rats. Here we investigated the effect of sodium arsenite on induction of CYP2B, CYP1A, and CYP3A in primary cultures of rat hepatocytes. Arsenite decreased the induction of all three families of CYP, as measured enzymatically and immunochemically. These decreases in CYPs occurred at concentrations of arsenite (2.5-10 microM) at which no toxicity was observed; however, toxicity was observed at 25 microM arsenite. With 3-methylcholanthrene as inducer, 5 microM arsenite caused a 55% decrease in CYP1A1 immunoreactive protein and enzyme activity, but only a 25% decrease in CYP1A1 mRNA. With phenobarbital (PB) as the inducer, 2.5 microM arsenite decreased CYP2B enzyme activity and immunoreactive protein 50%, with only a 25% decrease in CYP2B1 mRNA. 5 microM Arsenite decreased CYP2B enzyme activity and immunoreactive protein 80%, but decreased CYP2B1 mRNA only 50%, while CYP3A protein was decreased greater than 75% with no decrease in CYP3A23 mRNA. With dexamethasone (DEX) as inducer, 5 microM sodium arsenite caused a 50% decrease in immunoreactive CYP3A and a 30% decrease in CYP3A23 mRNA. Although arsenite-mediated increases in heme oxygenase (HO) inversely correlated with decreases in CYP2B or CYP1A activity, inclusion of heme in cultures treated with inducers of CYP1A or CYP2B did not prevent the arsenite-mediated decreases in these CYPs. Even though added heme induced HO to similar levels with and without arsenite, decreases in CYPs were only observed in the presence of arsenite. These results suggest that, in rat hepatocytes, elevated levels of HO alone are not responsible for arsenite-mediated decreases in CYP.
Animals↗
Effect of NGF and anti-NGF on neuropathic pain in rats following chronic constriction injury of the sciatic nerve.
The systemic administration of anti-nerve growth factor (NGF) antibodies can prevent local sensory hypersensitivity and block nociceptive fibers from sprouting into denervated adult rat skin. However, in the case of chronic constriction injury (CCI) in a rat, there is evidence that NGF reverses some effects of axotomy and alleviates thermal hyperalgesia. It is with this in mind that we investigated the influence of local anti-NGF and NGF on neuropathic pain and collateral sprouting caused by CCI. In our study, we looked at the effects to the ligated nerves after 30 consecutive days of local injections of anti-NGF and NGF. A high-dose of anti-NGF (1800 ng) was found to eradicate heat and cold hyperalgesia during postoperative days 16-28 and from days 8 to 34 after CCI, respectively. Our results show that a low-dose anti-NGF (18 ng) only mildly alleviates heat hyperalgesia but not cold hyperalgesia. There is evidence that a rebound phenomenon occurs for a short period of time after the anti-NGF injections cease. Results show that anti-NGF injections, whether in a high or low dose, significantly reduces the severity of autotomy or prevents the spread of collateral sprouting from the saphenous nerve into the sciatic innervation territory. In contrast, when a NGF (0.75 ng/g body weight) was applied to the ligated nerve immediately after the ligation, heat and cold hyperalgesia were eradicated during postoperative days 4-68 and from days 4 to 28, respectively. The results show that the effect of anti-NGF is delayed at the onset, is short in duration, and is dependent on the dosage. However, anti-NGF but not NGF blocked collateral sprouting and decreased the severity of autotomy, suggesting that anti-NGF may be a better potential alternative analgesic for the treatment of neuropathic pain in humans. The different initiation times to abolish thermal hyperalgesia by anti-NGF (delayed onset) and NGF (early onset) suggests that alterations in neurotrophic factors contribute to the development of behavioral hyperalgesia via a complex mechanism in CCI rats.
Animals↗
Facial nerve pathology in leprosy: searching for the proximal extent of the lesion in facial nerve biopsies.
A light and electron microscope study was made of resin embedded facial nerves in three cases of leprosy involving the facial nerve. The patients had irreversible facial nerve palsies and had requested facial reconstruction. No consistent pattern of nerve fibre damage was found. In one case the temporozygomatic was affected, but the cervical branch was normal, suggesting the damage begins distally. In two cases the loss of nerve fibres in the trunk and all branches was similar, and is likely to emanate from damage at a more proximal site. The presence of increased numbers of unmyelinated axons, often in clusters, is evidence of regeneration. These axons probably have the potential to develop into functional myelinated fibres provided that they can innervate a viable distal target such as a muscle graft. These regenerating axons are distal to the stylomastoid foramen suggesting that the most proximal level of involvement of the facial nerve could be intracranial. The finding of a more proximal level of nerve involvement, implies that the mis-reinnervation seen in partially recovered facial nerve palsies in leprosy, could be due to some regenerating axons being mis-directed at the level of the main trunk bifurcation.
Aged↗
Horseradish peroxidase-dependent oxidation of deuteroporphyrin IX into chlorins.
Chlorins are cyclic tetrapyrrole derivatives of great interest for use in photodynamic therapy. We have found that horseradish peroxidase (EC 1.11.1.7) (HRP) can convert deuteroporphyrin IX (Deutero) into chlorins. Some characteristics of this enzymatic transformation were investigated. The formation of chlorins was determined spectrophotometrically by monitoring the change in absorbance in the Q-band region (638 nm). The reaction occurred without addition of H2O2 and had a pH optimum of 7.5. The presence of thiol-containing reductants, with a great preference for reduced glutathione, was required and could not be substituted by adding H2O2. Ascorbic acid acted as a potent inhibitor of the reaction, while other organic acids (citric and benzoic) had little to no inhibitory effect. The requirement for O2 was suggested by the inhibitory effect of sodium hydrosulfite and was confirmed by carrying the assay in nitrogen-saturated solutions. Though the reaction occurred without adding H2O2, low amounts of H2O2 (3-30 microM) were stimulatory to the assay. However, concentrations of 300 microM H2O2 or higher were inhibitory. Similarly, light was not required, but was stimulatory at low levels and inhibitory at high levels. Catalase and deferoxamine were inhibitory, but superoxide dismutase and mannitol had no effects. Kinetic analysis and respiratory studies suggest that HRP may initially react with reduced glutathione in a reaction that does not consume much oxygen. The ensuing steps, probably involving an oxygen free radical and porphyrin radical intermediates, consume a large amount of O2 to oxidize Deutero into chlorin.
Ascorbic Acid↗
Formation of zinc protoporphyrin in cultured hepatocytes: effects of ferrochelatase inhibition, iron chelation or lead.
The formation of zinc protoporphyrin in response to lead or iron depletion has previously been investigated in erythroid systems. Because of its possible metabolic role in non-erythroid tissue, we investigated the formation of zinc protoporphyrin in cultured hepatocytes. The effects of lead and inhibitors of ferrochelatase, the iron insertion step of heme synthesis, on the conversion of 5-aminolevulinic acid to zinc protoporphyrin, protoporphyrin and heme were compared in rat and chick embryo hepatocyte cultures. In rat cultures, zinc protoporphyrin was synthesized enzymatically by ferrochelatase, since N-methylmesoporphyrin, an inhibitor of ferrochelatase. caused 40% or greater decreases in both heme and zinc protoporphyrin accumulation and markedly stimulated protoporphyrin accumulation. In addition, chelation of ferrous iron with 2,2'-dipyridyl decreased heme accumulation by 50%, but increased ZPP accumulation by 200%. Zinc protoporphyrin formation in chick embryo hepatocytes required the addition of zinc as well as 5-aminolevulinic acid and apparently was non-enzymatic, since it was not inhibited by N-methylmesoporphyrin nor increased by iron chelation. In the presence of 5-aminolevulinic acid, lead had no effect on zinc protoporphyrin, protoporphyrin or heme accumulation in chick hepatocytes, but decreased all three in rat hepatocytes, with the decrease in protoporphyrin being far greater than that of zinc protoporphyrin or heme. These findings indicate that, in contrast to the effect of lead in erythroid tissue, it did not specifically increase zinc protoporphyrin accumulation or alter iron availability in cultured hepatocytes.
Aminolevulinic Acid↗
Control of action potential-induced Ca2+ signaling in the soma of hippocampal neurons by Ca2+ release from intracellular stores.
Stimulus-induced increases in neuronal Ca2+ concentration are important signaling events for transcriptional regulation and neuronal plasticity. Electrical inputs are thought to mediate Ca2+ responses in the soma by triggering action potentials, which in turn open voltage-gated Ca2+ channels in the somatic plasma membrane. It is not yet known to what extent internal Ca2+ amplification contributes to the somatic Ca2+ responses. Here we used fluorescent Ca2+ measurements in cultured hippocampal neurons and report that the amplitude of the somatic Ca2+ increase triggered by field stimulation is independent of the extracellular Ca2+ concentration as long as the concentration is greater than 50 microM. Furthermore, significantly more La3+ has to be added extracellularly for blocking Ca2+ responses, as predicted from the reported La3+ dependence of voltage-gated Ca2+ channels. These measurements suggest that field stimulation-induced somatic Ca2+ responses in hippocampal neurons are largely attributable to Ca2+ release from intracellular stores. Only a small number of Ca2+ ions have to enter across the plasma membrane for this intracellular Ca2+ amplification process to occur. Rapid fluorescence-imaging measurements showed that the internal Ca2+ amplification occurs over 10-15 msec and linearly increases intracellular Ca2+ concentrations for up to 40 action potentials. At a fixed number of field pulses, frequencies of 40 Hz were optimal for somatic Ca2+ increases. Our studies suggest that the opening of intracellular Ca2+ release channels plays a crucial part in shaping the action potential-induced neuronal Ca2+ response.
Action Potentials↗
Multiple roles of polyhalogenated biphenyls in causing increases in cytochrome P450 and uroporphyrin accumulation in cultured hepatocytes.
Uroporphyrin (URO) accumulation occurs in chick embryo hepatocytes treated with a number of polyhalogenated aromatic hydrocarbons (PHAHs) that are known inducers of cytochrome P4501As (CYP1A). Previous dose response studies had shown that URO accumulation does not begin until CYP1A, as indicated by ethoxyresorufin O-deethylase (EROD) activity, is maximally induced. The reason why the concentrations of PHAHs required for URO accumulation were higher than those required to induce EROD had not been explained. PHAHs, such as 3,3',4,4'-tetrachlorobiphenyl (PCB77, IUPAC nomenclature, TCB) stimulate uroporphyrinogen (UROGEN) oxidation by microsomes from 3-methylcholanthrene (MC)-treated chick embryos. Here we used a new protocol to investigate whether the requirement for more TCB to stimulate in vitro microsomal UROGEN oxidation extended to TCB-induced URO accumulation in intact cultured hepatocytes. Cultures were treated with increasing concentrations of TCB or other PHAHs to induce CYP1As, then with cycloheximide (CX) to prevent further P450 synthesis. The CX treatment was shown to block any further increases in CYP1A as determined by immunoblots. 5-Aminolevulinic acid and a high concentration of TCB ("postinduction TCB") were then added to stimulate intracellular UROGEN oxidation. Using the protocol with postinduction TCB, the inducing concentrations of TCB which caused URO to begin to accumulate were now much lower than in the absence of postinduction TCB. Increases in CYP1A proteins, measured immunochemically, were detected at about the same inducing TCB concentrations that began to increase URO accumulation. The new protocol, with postinduction TCB, using URO accumulation as the end point, greatly increased the sensitivity of the culture system for detection of PHAHs with EC50s (nM) for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), TCB, 3,3',4,4',5,5'-hexachlorobiphenyl, MC, and hexachlorobenzene being about 0.003, 0.11, 0.75, 3.5, and 30, respectively. As little as 2-4 fmol TCDD per culture dish caused detectible increases in URO accumulation. We conclude that URO accumulation in chick hepatocyte cultures is limited not only by the induction of CYP1A, but also by the stimulation of intracellular UROGEN oxidation.
Animals↗
Oxidation of porphyrinogens by horseradish peroxidase and formation of a green pyrrole pigment.
When humans or plants are exposed to certain chemicals which interfere with heme biosynthetic enzymes, porphyrinogen intermediates accumulate and are oxidized to cytotoxic porphyrins. Here we have investigated the role of peroxidases in porphyrinogen oxidation. Horseradish peroxidase (HRP) rapidly oxidizes uroporphyrinogen to uroporphyrin and this is inhibited by ascorbic acid. HRP also oxidizes deuteroporphyrinogen (a synthetic porphyrin similar to protoporphyrinogen), but the yield of porphyrin is lower than with uroporphyrinogen as substrate. This low yield is in part due to a rapid, HRP-dependent conversion of deuteroporphyrin (but not uroporphyrin) to a green compound with spectral characteristics of a chlorin with a large peak at 638 nm. This reaction requires addition of a sulfhydryl reductant such as glutathione and is inhibited by ascorbic acid. These findings suggest that cellular peroxidases and ascorbic acid levels may play a role in modifying the phototoxic tetrapyrroles which accumulate in plants and humans after certain environmental exposures.
Horseradish Peroxidase↗
Morphological changes at paranodes in IgM paraproteinaemic neuropathy.
The paranode is one of a number of sites of a specific myelin sheath abnormality found in cases of IgM paraproteinaemic neuropathy. The gammopathy may be malignant or, more frequently, benign, and is often associated with a predominantly demyelinating neuropathy. The circulating paraprotein IgM antibody, usually with kappa light chains, was found in many cases to recognise an antigenic determinant in myelin, identified as myelin-associated glycoprotein (MAG). Other glycoconjugates expressed by Schwann cells may also be recognised by the antibody. MAG is localized to regions of the myelin sheath in which the membranes are uncompacted. The paranode is one such region, and there is evidence that IgM is deposited specifically on the membranes of the terminal loops of the myelin sheath in addition to other MAG-associated regions of the sheath. In many cases the presence of the paraprotein appears not to otherwise affect paranodal organization; in a few it is associated with changes to the termination of the loops on the axolemma and to the associated Schwann cell cytoplasm. These findings do not provide unambiguous evidence that binding of anti-MAG IgM antibodies at the paranode is a direct cause of demyelination. Whilst localization of the paraprotein closely matches that of MAG, proof is still lacking that the relevant antigen is MAG itself.
Animals↗
Percutaneous renal artery stent placement for hypertension and azotemia: pilot study.
To evaluate the efficacy of balloon-expandable (Palmaz) stents in the treatment of atheromatous renal artery stenosis, prospective placement of stents in 24 arteries in 20 patients was performed over an 18-month period. Indications were hypertension in 18 patients and renal insufficiency (serum creatinine > 1.5 mg/dL) in 11, and all lesions failed conventional transluminal angioplasty. Technical success was achieved in 96% of cases. Hypertension benefit was noted in 77% of patients followed for 6 months (n = 13) and 67% of patients at 1 year (n = 8). Improvement in serum creatinine was seen in 71% (n = 7) and 100% (n = 3) of azotemic patients evaluated at 6 and 12 months, respectively. Six-month angiographic patency was identified in 13 of 16 treated sites. Renal artery stent placement resulted in one asymptomatic segmental branch occlusion; there were no other procedural complications. In conclusion, renal artery stent placement is a technically and clinically effective treatment for hypertension and azotemia due to renal artery stenosis.
Aged↗