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Temperature and sea level are predicted to rise with climate change, bringing an urgency to evaluating future viability of native fish. Lamprey are confronted with widespread habitat degradation, migratory barriers, and episodes of environmental change projected to be commonplace in the future. In California, range contraction likely shifted lamprey rearing downstream, but the extent and physiological constraints that restrict estuarine rearing are unclear. We used a single-season occupancy model to describe juvenile lamprey estuarine distribution and found occupancy was regionally variable and constrained by temperature. Habitat and hydrology providing thermal refugia may be critical for future persistence.

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This multicentre study analysed 12 alumina ceramic-on-ceramic components retrieved from squeaking total hip replacements after a mean of 23 months in situ (11 to 61). The rates and patterns of wear seen in these squeaking hips were compared with those seen in matched controls using retrieval data from 33 'silent' hip replacements with similar ceramic bearings. All 12 bearings showed evidence characteristic of edge-loading wear. The median rate of volumetric wear was 3.4 mm(3)/year for the acetabular component, 2.9 mm(3)/year on the femoral heads and 6.3 mm(3)/year for head and insert combined. This was up to 45 times greater than that of previously reported silent ceramic-on-ceramic retrievals. The rate of wear seen in ceramic components revised for squeaking hips appears to be much greater than in that seen in retrievals from 'silent' hips.

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OBJECTIVE: The induction of transplantation tolerance across xenogeneic barriers by bone marrow transplantation holds great promise, but engraftment of xenogeneic stem cells has been difficult to achieve. Part of this difficulty is due to species-specific differences in regulatory cytokines and elements of the stromal microenvironment, which we studied here. MATERIALS AND METHODS: We developed a system where fresh bone marrow cells from swine and human are cultured on human bone marrow stroma in order to study these limiting factors in a clinically relevant species combination. RESULTS: We report here the ability of recombinant swine interleukin (IL)-3 and c-kit ligand (KL) to specifically enhance swine hematopoietic chimerism in this system. In the absence of exogenous swine cytokines, there were about half as many swine progenitors as human progenitors at 1, 2, and 4 weeks of culture. When used alone, swine IL-3 led to a notable but transient increase in the relative ratio of swine progenitors, while addition of swine KL increased the ratio of swine progenitors only modestly and only at later time points. In contrast, when swine IL-3 and KL were added together, there was a two- to fourfold increase in the ratio of swine to human progenitors at all times tested. CONCLUSION: These data demonstrate that both swine IL-3 and KL are needed for prolonged enhancement of swine progenitor chimerism under these conditions, and suggest that the species specificity of either one or both of these cytokines may represent an important barrier to prolonged engraftment of swine bone marrow in humans.

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We performed a comprehensive analysis of the molecular, serological, and clinical features of 16 consecutive cases of invasive streptococcal disease (ISD). The majority of cases were linked to two group A streptococcus (GAS) clones closely related by pulsed-field gel electrophoresis (PFGE) and designated as PFGE-1 and PFGE-1.1. These clones, serotyped as M-3, T-3/B3264, carried an allelic variant of the gene that encodes pyrogenic exotoxin A (speA3) and the gene that encodes streptococcal superantigen (SSA) but different emm alleles that encode M-protein. The characteristics and clinical features of patients were similar to those described in previous reports, regardless of the responsible GAS clone. However, worse clinical outcomes (shock and death) were more frequent when patients infected with PFGE1/1.1 clones were considered as a group and compared with all other patients as a group. One striking feature in some patients with deep tissue infection was a lack of inflammatory cells despite the presence of numerous streptococci. An evaluation of PFGE profiles of GAS isolated elsewhere demonstrated that the PFGE-1 clone has caused invasive disease in other locations in the United States and in Japan.

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BACKGROUND: IgA Nephropathy (IgA N) is one of the most common glomerulopathies and may lead to renal failure in 10-20% of cases. After renal transplantation, IgA N has a strong tendency to recur in the graft. Initially considered a benign condition, graft losses from recurrent IgA N have been reported over the last 20 yr, casting doubt on the initial premise. Since large single-center studies of the fate of renal allografts in IgA N are rare and the Mayo Clinic transplant experience for IgA N is extensive (dating back to 1970), a review of these issues appeared worthwhile. METHODS: A retrospective study was done of all renal transplant patients who had had biopsy-proven IgA N as underlying disorder. We extracted data on the underlying disease, history leading to renal transplantation, factors affecting transplant outcome, and on the course after transplantation with special attention to rejection activity and recurrence of the primary disease. Standard statistical methods were employed. RESULTS: 53 renal allografts were transplanted to 51 biopsy-proven IgA N patients: 12 were cadaveric (CAD) grafts, 3 HLA-mismatched living related donor (LRD) kidneys, 29 one haplotype-matched LRD and 9 HLA-identical LRD organs. Five-year actuarial graft survival was 100% in HLA-identical LRD, 88% in one haplotype-matched LRD, and 74% in CAD grafts. All three HLA-mismatched LRD kidneys were functioning up to 1.6 yr (longest follow-up). Only one patient died after acute rejection of the CAD graft. There were 3 early graft losses from acute rejection and 4 late losses. IgA N recurred in 26% of allograft and led to significant loss of graft function in 10 of the 14 patients (71%) over a long period of observation. Three of four late graft losses were in patients with recurrent IgA N. Recurrence was not related to the type of graft, i.e. CAD vs. LRD, nor to the extent of HLA-matching in LRD transplantation. CONCLUSION: Renal transplantation in patients with IgA N has excellent patient and graft survival. There is a high rate of recurrence of the primary glomerulopathy in the renal allograft, and this event is by no means inconsequential. Loss of renal function and even graft loss occur over prolonged periods of time. There is no disadvantage getting a well matched LRD in regard to incidence of recurrent IgA N. Thus, we encourage LRD transplantation in IgA N.

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We describe a 39-year-old bisexual man with clinical category B2 human immunodeficiency virus (HIV) infection who subsequently developed systemic lupus erythematosus (SLE). SLE was diagnosed on the basis of a clinical presentation of malar rash, polyarthritis, membranous glomerulonephritis, and characteristic serology. To our knowledge, this is the fourth reported case of a patient with HIV infection to develop SLE and the second adult patient with HIV and coexistent SLE nephropathy.

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OBJECTIVE: To investigate the frequency of membranous nephropathy associated with nonsteroidal anti-inflammatory drug (NSAID) use and identify associated clinical characteristics. DESIGN: Retrospective chart review. SETTING: A large group practice that staffs 2 large teaching hospitals. PATIENTS: All patients diagnosed as having stage I or early stage II membranous nephropathy by renal biopsy between January 1975 and May 1995. MAIN OUTCOME MEASURES: Nephrotic syndrome was said to be associated with NSAID use if patients developed nephrotic syndrome while taking an NSAID and if other causes of membranous nephropathy were excluded and a rapid remission of the nephrotic syndrome followed withdrawal of the drug. RESULTS: Of 125 patients identified with early membranous nephropathy, 29 were taking NSAIDs at the time symptoms of nephrotic syndrome developed. Thirteen of these patients met the criteria for NSAID-associated membranous nephropathy. None of these patients had any evidence of renal insufficiency or significant proteinuria after follow-up periods ranging from 5 months to 13 years. In addition to diclofenac and fenoprofen, which have previously been implicated, ibuprofen, nabumetone, naproxen, and tolmetin were found to be associated. CONCLUSIONS: Nephrotic syndrome due to membranous nephropathy should be recognized as an idiosyncratic drug reaction to many NSAIDS. Because withdrawal of the drug may result in prompt and complete recovery of normal renal function, a history of NSAID intake should be sought in patients with membranous nephropathy.

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A potential injury mechanism for triangular fibrocartilage tears and ulnar styloid fractures was investigated in cadaver specimens. The distal radioulnar joint was distracted to failure, thus applying a tensile force to the triangular fibrocartilage. During distraction, strains in the triangular fibrocartilage and the anatomic site of disruption were recorded with an image analysis system. Complete avulsion of the triangular fibrocartilage from the ulnar head occurred in 7 of 10 specimens. No ulnar styloid fractures occurred. Although strains were high in the radial portion of the disk (28%), no tears occurred in the substance of the disk or at its attachment to the radius. These findings suggest that distal radioulnar joint distraction can cause avulsion of the triangular fibrocartilage. However, ulnar styloid fractures and tears within the disk are more likely caused by injury mechanisms that include shear or compressive forces. Since complete avulsions of the triangular fibrocartilage occurred without a fracture, the absence of a fracture does not rule out a destabilizing injury to the distal radioulnar joint.

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Over the past 50 years, survival has improved in patients with systemic lupus erythematosus and associated nephritis. Yet, there are few long-term outcome studies in patients with well-defined nephropathy. We examined the outcome of 439 patients with lupus nephritis who were seen at the Mayo Clinic between 1964 and 1986 in whom renal biopsies were assessed using the World Health Organization (WHO) classification. There were 341 women and 98 men (mean +/- s.d., age 33.5 +/- 14 years); 200 (46%) patients were hypertensive and 249 (57%) had impaired renal function at renal biopsy. All WHO morphologic classes were represented and 339 (77%) patients had class III, IV and V (the more severe forms of nephritis). Follow-up averaged 10.2 years per patient. At last contact, 286 (65%) patients were alive and 153 (35%) were dead. Overall patient survival was 80%, 69% and 53% at 5, 10 and 20 years after biopsy that was significantly worse than expected survival (P < 0.001). Ten-year cumulative patient survival improved comparing earlier to more recent time spans: 64% in 231 patients seen during 1964-75; 76% in 2089 patients studied during 1976-86 (P = 0.03). Survival free of renal failure was 83%, 74% and 64% at 5, 10 and 20 years, and survival was unfavorably influenced by progressive WHO class, hypertension, impaired renal function, nephrotic range proteinuria, hypoalbuminemia and anemia. Multivariate analysis found impaired renal function, increased urine protein, anemia and younger age to be independent predictors of renal failure. WHO class was not a significant predictor when adjusted for these four factors. Cardiovascular events accounted for 48% of the known deaths and were equally distributed across all WHO classes, followed by infections, renal failure, malignancy, respiratory failure and gastrointestinal bleeding.(ABSTRACT TRUNCATED AT 250 WORDS)

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Cyst formation in conditions associated with increased renal ammoniagenesis (hypokalemia, distal renal tubular acidosis, renal mass reduction) and experimental links between increased ammoniagenesis and interstitial inflammation have suggested a role for ammonia in the pathogenesis of polycystic kidney disease (PKD). To explore this hypothesis, Han:SPRD rats, a PKD model that affects male more severely than female animals, have been used. Heterozygous cystic (Cy/+) and homozygous normal (+/+) male and female offspring of Cy/+ rats were divided at 3 wk of age into control groups drinking water and experimental groups drinking 300 mM NH4Cl, 300 mM KHCO3, 200 mM KHCO3, 200 mM KCl, 200 mM NaHCO3, or 200 mM NaCl. At 2 months of age, the rats were kept fasting from 8:00 p.m. to 8:00 a.m. in metabolic cages and urine samples were collected under mineral oil. The rats were then weighed and anesthetized for the collection of blood and kidneys. The administration of 300 mM NH4Cl, and to a lesser extent that of 200 mM NaCl, was accompanied by an increase in the urinary excretion of ammonia and aggravation of the renal cystic disease. On the other hand, the administration of 300 mM KHCO3, 200 mM KHCO3, or 200 mM NaHCO3 lowered the urinary excretion of ammonia and markedly reduced the severity of the cystic disease and interstitial inflammation. The administration of 300 mM KHCO3, and to a lesser extent that of 200 mM KHCO3, resulted in the precipitation of calcium phosphate in the medullary collecting ducts.(ABSTRACT TRUNCATED AT 250 WORDS)

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BACKGROUND: The n-3 fatty acids in fish oil affect eicosanoid and cytokine production and therefore have the potential to alter renal hemodynamics and inflammation. The effects of fish oil could prevent immunologic renal injury in patients with IgA nephropathy. METHODS: In a multicenter, placebo-controlled, randomized trial we tested the efficacy of fish oil in patients with IgA nephropathy who had persistent proteinuria. The daily dose of fish oil was 12 g; the placebo was a similar dose of olive oil. Serum creatinine concentrations, elevated in 68 percent of the patients at base line, and creatinine clearance were measured for two years. The primary end point was an increase of 50 percent or more in the serum creatinine concentration at the end of the study. RESULTS: Fifty-five patients were assigned to receive fish oil, and 51 to receive placebo. According to Kaplan-Meier estimation, 3 patients (6 percent) in the fish-oil group and 14 (33 percent) in the placebo group had increases of 50 percent or more in their serum creatinine concentrations during treatment (P = 0.002). The annual median changes in the serum creatinine concentrations were 0.03 mg per deciliter (2.7 mumol per liter) in the fish-oil group and 0.14 mg per deciliter (12.4 mumol per liter) in the placebo group. Proteinuria was slightly reduced and hypertension was controlled to a comparable degree in both groups. The cumulative percentage of patients who died or had end-stage renal disease was 40 percent in the placebo group after four years and 10 percent in the fish-oil group (P = 0.006). No patient discontinued fish-oil treatment because of adverse effects. CONCLUSIONS: In patients with IgA nephropathy, treatment with fish oil for two years retards the rate at which renal function is lost.

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We found that the administration of an angiotensin I-converting enzyme inhibitor and sodium chloride loading lessen the development of renal cystic disease induced by 2-amino-4-5-diphenylthiazole in rats. To determine whether similar effects could be observed in an autosomal dominant model of polycystic kidney disease, heterozygous cystic (Cy/+) and homozygous normal (+/+) Han:SPRD rats were divided into experimental groups at 3 weeks of age. The first study included four groups receiving enalapril (50 mg/L), losartan (400 mg/L), hydralazine (80 mg/L), or no drug in their drinking water. The second study included four groups fed a sodium-deficient diet or the same diet supplemented with 0.25%, 0.6%, or 3.3% sodium chloride. The Cy/+ rats receiving enalapril had lower kidney weights and histologic scores than those in the control group, and lower kidney weights, plasma creatinines, and histologic scores than those in the hydralazine group. The Cy/+ rats receiving losartan had lower plasma creatinines and histologic scores than those in the control and hydralazine treatment groups. A sodium-deficient diet markedly blunted the growth of the animals and the development of cystic disease. Increases in the sodium content of the diet in the other three groups were accompanied by higher relative kidney weights and histology scores, while the levels of plasma creatinine were not significantly different. Regression of the cystic disease was observed between 3 and 4 months of age. These results indicate that the development of autosomal dominant polycystic kidney disease in the rat can be modulated by pharmacologic and nutritional factors.(ABSTRACT TRUNCATED AT 250 WORDS)

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A multicenter, double-blind, placebo-controlled, randomized trial of fish oil in proteinuric patients with IgA nephropathy is being conducted by the Mayo Nephrology Collaborative Group. We completed enrollment of 106 patients into the trial in December 1991. The treatment period is for two years. Hypertension is being managed in all patients with enalapril maleate (Vasotec). We evaluated the associations between a variety of clinical and renal morphologic features and renal function at the entry of all enrolled patients. Among 78 males and 28 females [age(mean +/- SD) 36 +/- 14 years], older age at treatment randomization, hypertension, at disease discovery as well as at study entry, increased fractional excretion of albumin, increased serum triglyceride levels, and more severe tubulointerstitial, vascular, and combined glomerular and tubulointerstitial histologic lesions were all univariately associated (p < or = 0.01) with poorer renal function measured by reciprocal serum creatinine and creatinine clearance levels. In a multiple regression analysis used to predict baseline reciprocal creatinine, the best final model (R2 = 0.48) included male sex (p < .001), hypertension at treatment randomization (p = .001), decreased peripheral blood erythrocytes (p = .001), increased tubulointerstitial score (p = .004), and increased fractional excretion of albumin (p = .025) as independent predictors of decreased kidney function. These associations are similar to those seen in the high-risk subset of patients with IgA nephropathy who develop end-stage renal disease. In the eventual outcome analysis of the clinical trial, we will examine the effects of treatment on the two potentially modifiable risk factors, hypertension and proteinuria, on renal function.

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The articular disk of the triangular fibrocartilage complex was studied using a video imaging system in a cadaveric laboratory experiment. Changes in disk configuration consistently occurred during pronation and supination and resulted in a nonuniform strain distribution that was dependent upon forearm position. Strains occurred primarily in the radioulnar axis of the disk, with dorsoanterior strains being negligible. Strains were concentrated in the radial portion of the disk and were highest with the forearm pronated. Application of a distraction load to the distal radioulnar joint to simulate the effect of axial wrist loading caused strains to increase the most in the radial portion. These findings suggest that joint distraction loading and forearm pronation are important components of the injury mechanism for the most common type of traumatic tear that occurs near the radial attachment of the disk.

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We prospectively assessed the value of anti-neurtrophil cytoplasmic autoantibodies (ANCA) and nuclear or perinuclear anti-neutrophil autoantibodies measured by indirect immunofluorescence microscopy and antimyeloperoxidase autoantibodies measured by a solid-phase assay in the diagnosis of idiopathic (pauci-immune) necrotizing-crescentic glomerulonephritis (NCGN) and renal vasculitis at our institution. A diagnosis was established on the basis of clinical and renal biopsy findings, and follow-up continued for at least 6 months. ANCA were measured at the conclusion of the study. Of the 111 study patients, 28 had NCGN and renal vasculitis. The immunofluorescence assay had 50% sensitivity and 79% specificity. The combination of the enzyme-linked immunosorbent assay for antimyeloperoxidase autoantibodies and the immunofluorescence assay for cytoplasmic ANCA had 78% sensitivity and 84% specificity. A firm diagnosis was established before the determination of ANCA in 26 of the 28 patients with NCGN and renal vasculitis. The antimyeloperoxidase autoantibody values would have suggested the diagnosis in the other two patients. Of these 28 patients, 5 had negative ANCA results. High antimyeloperoxidase autoantibody values were detected in patients with NCGN and renal vasculitis, whereas lower values were less specific and were detected mainly in patients with anti-glomerular basement membrane antibody disease and lupus glomerulonephritis.

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Histological indices of renal pathology in lupus nephritis have been proposed as prognostic signs and as a method to quantitate therapeutic response. We tested the reproducibility of the activity (AI) and chronicity indices (CI) in the renal biopsies from 83 patients with lupus nephritis, enrolled in a controlled therapeutic trial. The AI/CI were calculated separately by four renal pathologists using published criteria. Pair-wise Spearman's rank correlation coefficient was used to examine the relationship among the scores of the four raters, and their degree of reproducibility was evaluated using the coefficient of reliability. The mean CI scores ranged from 2.84 to 4.61, and the mean AI ranged from 9.64 to 12.89. The correlation among the different pathologist's scores ranged from 0.44 to 0.63 for the AI and 0.60 to 0.76 for the CI. One pathologist (M.M.S.) rated the biopsies twice, and the correlation between the two ratings was 0.58 for the AI and 0.74 for the CI. Thus, the AI and CI calculated by different pathologists and the temporally separate observations of a single observer were only moderately correlated. The reproducibility of a single rating was low, showing a reliability coefficient of 0.48 for the AI and 0.57 for the CI. The low reliability coefficient suggests that the variability among pathologists was the result of interpretative differences. We conclude that the AI/CI are too subjective to be used as therapeutic guides or as prognosticators.

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The cause of hemolytic uremic syndrome after bone marrow transplantation is unknown. Investigators have implicated multiple causes, including cyclosporin A, graft versus host disease, cytomegalovirus infection, and total body irradiation. We report a case of biopsy-supported hemolytic uremic syndrome in a recipient of an autologous bone marrow transplant who did not receive total body irradiation or cyclosporin A and did not have clinical evidence of cytomegalovirus infection. This case casts doubt on the hypothesis that irradiation or any of these factors is the sole and universal cause of hemolytic uremic syndrome in patients receiving bone marrow transplants.

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