bluuebunny/crossref_metadata_2025_split huggingface dataset:
Recombinant Human Erythropoietin Resistance in Iron-Replete Hemodialysis Patients: Role of Aluminum Toxicity
Authors: Tarng Der-Cherng , Huang Tung-Po 
Published: April 2003

The present study was designed to investigate the impact of aluminum toxicity on the response to recombinant human erythropoietin (rHuEPO) therapy in hemodialysis patients, when iron deficiency has been corrected or excluded. We studied 39 patients on regular hemodialysis (20 males and 19 females; mean age 58.8 years), who were under maintenance rHuEPO treatment for at least 6 months, and who had stable hematocrit levels for more than 3 months. All patients had adequate iron stores and availability with serum ferritin >100 µg/l and iron saturation >25%. They were classified into two groups: 19 poor responders, who required subcutaneous rHuEPO doses >100 U/kg/week and failed to achieve the target hematocrit level of 30%, and 20 good responders, who needed doses of ≤100 U/kg/week to maintain the target level. Serum aluminum levels including basal (Al<sub>basal</sub>) and 44 h after desferrioxamine (DFO) infusion (Al<sub>post-DFO</sub>), intact parathyroid hormone, and inflammatory and hemolytic indices were examined in both groups. The results showed that the mean weekly rHuEPO doses were significantly lower and the mean hematocrit levels higher in the good responders than in the poor responders. Although the poor responders had markedly higher mean Al<sub>basal</sub> and Al<sub>post-DFO</sub> levels, no differences were observed in the other parameters between the two groups. Furthermore, the poor responders significantly had the greater increment in the serum aluminum levels after DFO infusion (ΔAl =Al<sub>post-DFO</sub> – Al<sub>basal</sub>). The mean corpuscular volume had a strong inverse correlation with ΔAl in the poor response group (r = –0.711, p < 0.001). We concluded that the post-DFO rise of serum aluminum can be used as a means of estimating tissue stores. Subclinical aluminum toxicity may exhibit an inhibitory effect on erythropoietic response to rHuEPO therapy.
Acute Bone Pain following Renal Transplantation: Differentiation between Benign Bone Edema and Avascular Necrosis
Authors: Pilmore Helen , Walker Robert , McMillan Bruce , Paranjpe Dhananjay , Berkeley Barrie 
Published: April 2003

Two patients are reported who presented within the first 3 months posttransplantation with acute bone pain where serial magnetic resonance imaging (MRI) allowed differentiation between bone edema, which resolved spontaneously, and avascular necrosis (AVN) requiring core decompression. Case 1 had ill-defined images consistent with bone edema that resolved, whereas case 2 developed well-demarcated lesions in the femoral condyles and tibial epiphyses which were confirmed as AVN at surgery. Alternative explanations for bone edema were not evident. We would suggest that in any transplant recipient who develops acute bone pain, MRI is the initial diagnostic modality of choice. Evidence of development of well-demarcated lesions on serial MR scans indicate early AVN. However, on current evidence it is difficult to predict which lesions will progress and until greater experience becomes available, we would recommend intraosseous plethysmography and venography so that incipient or early AVN can be treated by core decompression of the affected bone.
Timing of Initiation of Uremia Therapy and Survival in Patients with Progressive Renal Disease
Authors: Ifudu Onyekachi , Dawood Mohammed , Homel Peter , Friedman Eli A. 
Published: April 2003

We conducted a prospective cohort study to detect any relationships between specific clinical features and laboratory indices at initiation of hemodialysis and long-term survival. One hundred and thirty-nine consecutive patients with chronic renal failure hospitalized to start maintenance hemodialysis between January 1990 and December 1994 were enrolled, and follow-up was completed through December 1995. At baseline, subjects were assigned to one of five groups based on their major indication for initiation of hemodialysis. The indications were: (a) nausea and vomiting; (b) severe weakness; (c) no major symptom (dialysis started because of ‘high’ serum creatinine and blood urea nitrogen concentrations); (d) volume overload, and (e) miscellaneous (angina, pericarditis, seizure, pruritus, and hyperkalemia). Blood urea nitrogen, serum creatinine and serum albumin concentrations were measured once before the first dialysis. The main outcome measure was death. The 139 study subjects included 77 women and 62 men comprising 116 Blacks (83%), 15 Hispanics (11%), and 8 Whites (6%) of mean age 54 ± 15 years. Mean length of follow-up was 39 months. At baseline, mean blood urea nitrogen concentration was 121 ± 38 mg/dl, mean serum creatinine concentration was 12.6 ± 5.2 mg/dl, and mean serum albumin concentration was 3.5 ± 0.62 g/dl. Forty-two subjects (30%) died during follow-up. Cox regression analysis showed that there was no significant association between mortality and any of the indicators evaluated (indication for initiation of dialysis (p = 0.2), serum creatinine concentration (<10 vs. ≥10 mg/dl) (p = 0.8), blood ure nitrogen concentration (<100 vs. ≥100 mg/dl) (p = 0.68) and serum albumin concentration (<4 vs. ≥4 g/dl) (p = 0.62). All analyses included adjustment for age and diabetes.We conclude that in patients with chronic renal failure, the clinical features and laboratory indices used as guidelines for initiation of renal replacement therapy do not correlate with survival. Objective parameters that will permit initiation of dialysis at a time that will maximize survival in patients with chronic renal failure are needed.
Acute Oliguric Renal Failure Associated with Unilateral Renal Embolism: A Successful Treatment with Iloprost
Authors: Levin Moshe , Nakhoul Farid , Keidar Zohar , Green Jacob 
Published: April 2003

A 66-year-old woman presented with acute-onset rapid atrial fibrillation and right upper quadrant pain which had appeared 24 h prior to admission. The patient also manifested acute oliguric renal failure (serum creatinine 6.9 mg/dl). Selective renal angiography revealed total occlusion of the right renal artery with normal visualization of the left kidney vasculature. The patient was treated with intra-arterial urokinase and intravenous heparin, with no response. Intravenous administration of the prostacyclin analogue, iloprost, resulted in rapid resolution (within hours) of the oliguric acute renal failure, in spite of the continuing presence of a nonfunctioning right kidney. We conclude that the etiology of the acute renal insult in this patient is probably related to unilateral renal arterial embolization accompanied by arterial spasm of the unaffected kidney. The contralateral vasospasm can be reversed by iloprost, which then leads to a rapid recovery from acute renal failure. We are unaware of prior reports documenting the beneficial effect of iloprost in a clinical setting as described here.
Nephrotic Mice (ICGN Strain): A Model of Diffuse Mesangial Sclerosis in Infantile Nephrotic Syndrome
Authors: Mizuno Shinya , Mizuno-Horikawa Yoko , Yue Bing-Fei , Okamoto Munehiro , Kurosawa Tsutomu 
Published: April 2003

The ICGN mouse strain is a unique model for naturally occurring nephrotic syndrome. In the present study, we examined the onset of the clinical manifestation of nephrotic syndrome and determined the sequence of intraglomerular events associated with progression of nephrotic conditions. Laboratory analysis revealed that homozygous (nep/nep) mice showed urinary albumin excretion during the suckling stage, rapidly leading to hypoalbuminemia accompanied by body growth failure. Renal pathology demonstrated that an initial intraglomerular event in the nephrotic mice was observed 3 weeks after birth in the form of mesangiolytic lesions, characterized by microaneurysm, platelet accumulation and capillary ballooning. In 6-week-old homozygous mice, mesangial sclerosis, characterized by mesangial expansion and glomerular hypertrophy, was observed in a diffuse fashion. Immunohistochemistry revealed that the glomerular cells in the 3-week-old homozygous suckling mice were positive for α-smooth muscle actin, suggesting a phenotypic change in the mesangial cells. Mesangial expansion, confirmed by the over-deposition of type I collagen, was evident until 6 weeks after weaning, while it was of interest that fibrogenic cytokines such as platelet-derived growth factor and transforming growth factor-β were not detected in the sclerotic glomeruli throughout the observations. Furthermore, the nephrotic features were shown to be resistant to steroid therapy with a high dose of prednisolone. Our results suggest that diffuse mesangial sclerosis, a hereditary glomerular disease, may be genetically generated through early myofibroblast formation, which occurs and develops probably independently of up-regulation of these fibrogenic cytokines. In conclusion, the homozygous nephrotic mouse (ICGN strain) is believed to be a good model for investigating not only nephrotic conditions but also cellular and molecular pathogenesis of diffuse mesangial sclerosis in steroid-resistant infantile nephrotic syndrome.
Diagnosis of Renal Disease at the Beginning of the 20th Century
Authors: Cioffi M. , Esposito L. , De Santo D. , Giannattasio P. , Cappabianca F. , Mangiacapra S. , Materiale T. , Conte G. 
Published: April 2003

At the beginning of this century, the diagnosis of various renal diseases was made with relative accuracy although neither plasma markers of glomerular filtration nor renal biopsy nor imaging were available. Renal edema was identified by high albuminuria, hyalin cylinders, high urine density and oliguria. Renal hematuria was detected by cylinders of erythrocytes. Hallmarks of chronic renal insufficiency, recognized at autopsy by atrophic kidneys, were hyposthenuria, polyuria and slight albuminuria without edema associated with arterial hypertension, anemia, retinopathy and left ventricular hypertrophy. The detection of increased plasma volume in experimental toxic nephritis by St. Moscati proposed the underlying mechanism of arterial hypertension. Experimental and clinical research in the preinsulin era indicated the central role of the kidney in the functional alterations induced by diabetes. Indeed, glucosuria was known to appear only when glycemia was relatively high. The kidney appeared enlarged and hyperemic, i.e. the so-called glomerular hyperfiltration. Glucosuria was directly correlated with diuresis but it markedly decreased in renal insufficiency. In diabetes complicated by nephropathy, tolerance to carbohydrates improved. Correction of glucosuria by dietary treatment was followed by a prompt rise in body weight, due to retention that counterbalanced the previous losses. Diabetic ketoacidosis, determined by the measurement of urinary ketonic body excretion, was treated with sodium bicarbonate (30–50 g/day in severe acidosis) up to achieving an alkaline urine pH. It was known that high doses of sodium bicarbonate might induce edema which gradually disappeared with a reduction in the alkaline administration. Clinical significance of sodium balance was, in fact, recognized: the external NaCl balance between alimentary ingestion and urinary excretion was neutral in normal conditions and became positive at high body temperature or negative during reabsorption of exudates.
Trimethoprim-Sulfamethoxazole Therapy in Outpatients: Is Hyperkalemia a Significant Problem?
Authors: Alappan Rajendran , Buller Gregory K. , Perazella Mark A. 
Published: April 2003

A prospective, randomized clinical study was undertaken to determine the effect of standard-dose trimethoprim-sulfamethoxazole combination treatment on serum potassium concentrations in outpatients treated in an ambulatory clinic. Ninety-seven patients were treated with oral antibiotics for a variety of infections. Fifty-one patients treated with trimethoprim-sulfamethoxazole (trimethoprim, 320 mg/day; sulfamethoxazole, 1,600 mg/day) constituted the treatment group, while 46 patients treated with other antibiotics served as controls. Serum potassium, sodium, and chloride concentrations, serum carbon dioxide content, blood urea nitrogen level, serum creatinine level, and serum glucose concentration were measured. The baseline serum potassium concentration in the treatment group was 4.30 ± (SD) 0.36 mmol/l, and it increased significantly (p < 0.001) to 4.66 ± 0.45 mmol/l on day 5 of therapy. Subgroup analysis of mean serum potassium concentration on day 5 of therapy failed to detect clinically relevant hyperkalemia. In patients with a serum creatinine level equal to or greater than 1.1 mg/dl (K<sup>+</sup>, 4.83 ± 0.48 mmol/l), a nonsignificant difference (p = 0.3) in the potassium concentration was noted on day 5 as comapred with patients with a serum creatinine level <1.1 mg/dl (K<sup>+</sup>, 4.63 ± 0.44 mmol/l). Although diabetics had a higher serum potassium concentration (K<sup>+</sup>, 4.91 ± 0.44 mmol/l) than nondiabetics (K<sup>+</sup>, 4.61 ± 0.44 mmol/l), the difference was not statistically significant (p = 0.055). Patients aged ≥50 years (K<sup>+</sup>, 4.82 ± 0.59 mmol/l) had a significantly different (p = 0.046) serum potassium concentration on day 5 than patients aged <50 years (K<sup>+</sup>, 4.55 ± 0.28 mmol/l). In contrast, the baseline serum potassium concentration in the control group was 4.37 ± 0.45 mmol/l, and it decreased (p = 0.1) to 4.22 ± 0.4 mmol/l on 5 days of drug therapy. Trimethoprim-sulfamethoxazole therapy, when used to treat a variety of infections, leads to an increase in serum potassium concentration in most patients. After 5 days of therapy with this drug, the treatment group developed a statistically significant rise in the serum potassium concentration as compared with the control group. However, severe hyperkalemia (K<sup>+</sup> ≥5.5 mmol/l) occurred in only 3 patiens (6%) treated with trimethoprim-sulfamethoxazole. In addition, none of the subgroups of treated patients developed clinically important hyperkalemia. This suggests that outpatients, in contrast to acquired immunodeficiency syndrome patients and hospitalized patients with mild renal insufficiency, develop severe or life-threatening hyperkalemia less commonly when treated with this antimicrobial regimen. However, outpatients having risk factors which may predispose to the development of hyperkalemia should be carefully monitored when treated with trimethoprim-sulfamethoxazole.
Serum Hepatocyte Growth Factor Levels in Patients with Renal Diseases
Authors: Nishida Masashi , Kawakatsu Hidekazu , Ishiwari Kohhei , Tamai Megumi , Sawada Tadashi , Nishimura Masato , Yoshimura Manabu 
Published: April 2003

The serum levels of hepatocyte growth factor (HGF) were determined in patients with various renal diseases. In patients with acute-phase acute renal failure (ARF) and chronic tubulointerstitial nephritis (chronic TIN), the serum HGF levels were 0.55 ± 0.24 and 0.44 ± 0.37 ng/ml (mean ± SD), respectively, and were significantly higher than that in the control group (0.12 ± 0.12 ng/ml). The serum HGF level tended to be high also in patients with active-phase steroid-sensitive nephrotic syndrome (SSNS). The serum levels of HGF were not elevated in patients with IgA nephropathy (IgAN), Henoch-Schönlein purpura nephritis (HSPN), membranoproliferative glomerulonephritis (MPGN), poststreptococcal acute glomerulonephritis (PSAGN), unilateral renal atrophy, unilateral nephrectomy, or proximal tubular dysfunction. These observations suggest that glomerular disorders cause no apparent elevation of the serum HGF level, and that elevation of the serum HGF level may be associated with tubulointerstitial damage in renal diseases.
Short- and Long-Term Outcome of Total Parathyroidectomy with Immediate Autografting versus Subtotal Parathyroidectomy in Patients with End-Stage Renal Disease
Authors: Hargrove Gaylene M. , Pasieka Janice L. , Hanley David A. , Murphy M. Brendan 
Published: April 2003

A retrospective study was performed in 36 patients with end-stage renal disease (ESRD) comparing total parathyroidectomy followed by immediate autografting into the forearm (total PTX + IA) with parathyroidectomy (subtotal PTX) over a five-year period. Twenty-eight patients underwent subtotal PTX and 8 had total PTX + IA. The two surgical methods were evaluated with respect to preoperative severity of hyperparathyroidism, perioperative morbidity, and the incidence of recurrent hyperparathyroidism. Eleven patients in total (30.6%) developed recurrent hyperparathyroidism; 2/8 (25%) in the total PTX + IA group compared to 9/28 (32.1%) in the subtotal PTX group (p = 0.699). The median time to recurrence was longer in the total PTX + IA group (39 vs. 16 months), and the median long-term postoperative PTH value was lower (81 vs. 199 ng/l), but these differences did not reach statistical significance. In conclusion, the incidence of recurrent hyperparathyroidism is high regardless of surgical modality. However, total PTX + IA may produce more favorable results with respect to median postoperative PTH level and time to recurrence.
<i>Mycobacterium fortuitum </i>Peritonitis in Two Patients Receiving Continuous Ambulatory Peritoneal Dialysis
Authors: Vera Gilberto , Lew Susie Q. 
Published: April 2003

We present two cases of non-resolving peritonitis treated with a standard peritonitis protocol. The organism identified from the peritoneal effluent was <i>Mycobacterium fortuitum</i>, a group IV (Runyon’s classification) rapidly growing, nontuberculous mycobacterium. <i>M. fortuitum</i> is ubiquitous and can be isolated from a number of natural sources. Risk factors these two patients had for developing <i>M. fortuitum</i> peritonitis included underdialysis, the immunocompromised state associated with end stage renal disease, prior or prolonged broad spectrum antibiotic treatment, and possible exposure to environmental factors, since both were hospitalized at about the same time. The isolates were resistant to the conventional antibiotics recommended for the treatment of this mycobacterium. Both patients, however, responded to catheter removal and antibiotics administered according to the sensitivities of the mycobacterium isolated.
Antioxidant Effect of Zinc on Acute Renal Failure Induced by Ischemia-Reperfusion Injury in Rats
Authors: Ogawa Toshihisa , Mimura Yoshikazu 
Published: April 2003

Zinc may have an antioxidant effect mediated by induction of metallothionein. Based on the assumption that metallothionein can scavenge oxygen free radicals, we examined whether zinc administration prior to renal ischemia would improve renal dysfunction caused by ischemia-reperfusion injury in rats. Wistar rats weighing 265 g were treated with an intraperitoneal injection of 20 mg/kg zinc 24 h prior to the renal ischemia-reperfusion procedure, which was achieved by a 30-min clamping of the bilateral renal vessels and subsequent 90-min reperfusion. Thirty-minute renal clearance tests were performed before and after renal ischemia in zinc- (n = 11) and saline-treated (n = 8) rats. Thiobarbituric acid reactive substance, conjugated diene, and metallothionein levels in the renal tissues were also determined. Sham-operated rats (n = 5 in each treatment) served as control for the ischemia-reperfusion rats. Ischemia-reperfusion resulted in significantly lower glomerular filtration rate values and marked increases in tissue concentrations of thiobarbituric acid reactive substance and conjugated diene compared with sham-operation. Zinc administration improved the reduced glomerular filtration rate values seen after the ischemia-reperfusion procedure, but not to the extent of pre-ischemic levels. Zinc pretreatment significantly reduced the increased levels of thiobarbituric acid reactive substance and conjugated diene during ischemia-reperfusion and increased metallothionein levels compared with saline injection. These findings suggest that zinc has an antioxidant effect mediated through the induction of metallothionein, but appears only to have a minor protective effect on renal function induced by renal ischemia-reperfusion injury.
High-Resolution Ultrastructural Comparison of Renal Glomerular and Tubular Basement Membranes
Authors: Ogawa Saeko , Ota Zensuke , Shikata Kenichi , Hironaka Kazue , Hayashi Yoshiko , Ota Kosuke , Kushiro Masahiko , Miyatake Nobuyuki , Kishimoto Noboru , Makino Hirofumi 
Published: April 2003

<i>Background/Aims:</i> Glomerular basement membranes (GBM) and tubular basement membranes (TBM) consist of a fine meshwork composed mainly of type IV collagen. Each segment of tubules has specialized physiologic functions, and thus we investigated the ultrastructure of various basement membranes in rat kidneys. <i>Methods:</i> Since purifying basement membranes from different tubule segments is technically challenging, we employed tissue negative staining rather than conventional negative staining to compare the ultrastructures of proximal and distal TBM and GBM in normal rats. We also assessed the distribution of extracellular matrix components including type IV collagen, laminin, heparan sulfate proteoglycan, and fibronectin in the basement membranes by immunohistochemistry. <i>Results:</i> TBM and GBM of normal rats showed a fine meshwork structure consisting of fibrils forming small round to oval pores. Short- and long-pore diameters in proximal tubules were 3.3 ± 0.5 and 3.9 ± 0.6 nm, respectively, and in distal tubules 3.5 ± 0.7 and 4.3 ± 0.8 nm, respectively. For GBM the respective diameters were 2.5 ± 0.5 and 3.0 ± 0.5 nm. Immunohistochemical analysis showed no significant difference in distribution of extracellular matrix components between proximal and distal TBM. However, immunofluorescence scores of α1 chain of type IV collagen, fibronectin, and laminin were higher in the TBM than in the GBM. On the other hand, heparan sulfate proteoglycan was higher in the GBM. <i>Conclusion:</i> Ultrastructural differences in renal basement membranes may be related to differences in physiologic function in each segment.
Granulocyte-Macrophage Colony-Stimulating Factor as an Adjuvant to Hepatitis B Vaccination in Maintenance Hemodialysis Patients
Authors: Anandh Urnila , Bastani Bahar , Ballal Sudarsham 
Published: April 2003

Patients on maintenance hemodialysis (HD) have poor seroconversion rate after hepatitis B vaccination. The present study was designed to test the efficacy of granulocyte-macrophage colony-stimulating factor (GM-CSF) as an adjuvant to hepatitis B vaccination for improving seroconversion rate in maintenance HD patients. Twelve chronic HD patients were randomly assigned to receive either hepatitis B vaccination alone or hepatitis B vaccination 24 h after 1 dose of GM-CSF for primary immunization. A group of 16 chronic HD patients who had not seroconverted after a standard two-dose hepatitis B vaccination were randomly assigned either to a booster dose of hepatitis B vaccine alone or a booster dose given 24 h after one dose of GM-CSF. In the primary immunization group only 2 of 6 patients (33%) who had received vaccination alone, versus 5 of 6 patients (83%) who had received hepatitis B vaccine after one dose of GM-CSF, developed seroprotective antibody titers. Moreover, seroprotective antibody titers (IU/ml) were significantly higher in the latter group (275 ± 286.5 vs. 14 ± 22, p < 0.05). In patients who had not seroconverted with prior hepatitis B vaccination, GM-CSF adjuvant therapy significantly increased the seroconversion rate versus booster dose alone (87.5 vs. 25%, respectively, p < 0.02), with significantly higher seroprotective antibody titers (84 ± 80 vs. 19 ± 33 IU/ml, respectively, p < 0.05). These findings suggest that administration of one dose of GM-CSF, as adjuvant therapy, prior to primary or booster dose hepatitis B vaccination may significantly increase seroconversion rate and seroprotective antibody titers in chronic HD patients.