Acute renal failure, hypertension and skin necrosis in a patient with streptokinase therapy.
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Biomedical subjects
Publications and source records attributed to R J Glassock.
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In a study of renal allografts with acute rejection primarily or exclusively of the cellular type, extratubular Tamm-Horsfall protein was identified in 63.6% of the specimens, representing 76.1% of the patients whose tissues were examined. There was no evidence of extrarenal obstruction in any patient. This high incidence has not been previously reported. A pattern of development of this phenomenon was determined using combined light and electron microscopies and specific anti-Tamm-Horsfall antiserum. Interstitial lymphocytes and monocytes infiltrated into the walls of tubules causing disruptions of basement membranes, thereby creating free communications between lumina and interstitium. In distal tubules with casts, the matrices extended into the interstitium where they were admixed with leukocytes and few erythrocytes. In a small number of specimens, polyps of Tamm-Horsfall protein were identified in veins or interstitial capillaries. Extratubular Tamm-Horsfall protein was not associated with diminished graft survival. These findings delineate, in detail, one of several mechanisms of escape of Tamm-Horsfall protein from tubules into the interstitium; they may be applicable for the genesis of this abnormality in other forms of acute interstitial nephritis.
Herein we report the first case of reconstruction of a long-standing transected proximal urethra, following a pelvic fracture and resultant rectourethral fistula before renal transplantation. This case supports the viewpoint that before creation of a supravesical diversion in potential transplant patients with lower urinary tract dysfunction, reconstruction of the lower urinary tract should be attempted when there is a reasonable chance for successful outcome.
The effects of disturbances of nutrition and renal function (e.g., uremia) on immune function have been compared. The two disturbances share many common effects, and it seems likely that some of the abnormalities in cell-mediated immunity in uremia may be the result of depletion or deprivation of essential nutrients (e.g., protein, zinc, pyridoxine). Ample evidence is also available to incriminate the emergence of a family of immunoregulatory lipoproteins (and perhaps other endogenous uremic toxins) in the pathogenesis of the disordered immune function in uremia. Finally, depletion of other specific dietary constituents (e.g., calories, fatty acids, phosphate) may also have profound effects on the immunologic or mediator systems involved in the pathogenesis of glomerulonephritis. Exploitation of these dietary manipulations may permit modulation of the natural history of these diseases.
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The influence of pindolol, other antihypertensive agents, or placebo upon plasma renin activity (PRA) was examined in five separate studies involving 249 subjects (pindolol), n = 149; propranolol, n = 43; methyldopa, n = 13; chlorthalidone, n = 16; placebo, n = 28). In addition, the subjects were stratified in for studies into low (n = 104), medium (n = 96), or high (n = 15) PRA categories according to baseline PRA and sodium excretion measurements. The response to antihypertensive therapy was analyzed in each PRA category. Pindolol and propranolol lowered PRA comparably at equivalent dosages, although this effect was not consistently observed in all studies or at all dosage levels. Methyldopa therapy was not associated with a decline in PRA and chlorthalidone elevated PRA. Pindolol and propranolol lowered both supine and erect diastolic blood pressure (BP) comparably. This effect was similar in subjects categorized as having low or medium PRA. Too few patients were studied with high PRA to derive statistically meaningful data. Pindolol lowered standing systolic BP to a greater extent than did propranolol, especially in the medium PRA category. It was concluded that pindolol, like other beta-adrenergic blockers, lowers PRA, that the effect of pindolol on diastolic BP is independent of the baseline PRA category, and that pindolol is more effective than propranolol in lowering standing systolic BP, at least in the medium PRA category.
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Administration of iron to rats exacerbated early inflammatory changes of pyelonephritis produced by intravenous inoculation of Escherichia coli. This effect was noted with four of eight strains of E. coli tested and was dependent on bacterial inoculum. Despite this increase in severity of acute pyelonephritis as judged by numbers of bacteria in the kidney and careful gross and microscopic evaluation, there was no enhancement of chronic changes seen 6 months later.
Recurrence of thrombotic microangiopathy (TMA) has rarely been reported following renal transplantation. We describe a 24-year-old man who developed irreversible renal failure due to thrombotic microangiopathy. Following renal transplantation, he developed recurrent episodes of microangiopathic hemolysis; during one of these episodes a biopsy revealed the development of thrombotic microangiopathy in the graft. In each of five recurrences to date, plasma infusion, either alone or combined with other forms of therapy, has produced a prompt remission. This is the first report, to our knowledge, of the successful treatment of recurrent TMA in a renal transplant recipient.
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An immunopathological study of renal biopsies from 38 patients with glomerulonephritis with greater than 30% crescents was performed. All had evidence of immune deposits in glomeruli: 9 were characterized by linear fluorescence staining (antiglomerular basement membrane antibodies) and 29 had granular capillary wall and/or mesangial deposits. In the former group, 3 (33%) had associated pulmonary hemorrhage. In the latter group, the glomerular lesions in 18 (62%) were part of well-defined systemic illnesses, whereas in the remainder, the abnormalities were apparently limited to the kidney. The prognosis was uniformly grave, for all patients with adequate follow-up developed end-stage renal failure or died. In contrast to other reports of crescentic glomerulonephritis, we could not document the existence of an 'immunofluorescence negative' form of crescentic glomerulonephritis.
Despite the relative paucity of well controlled studies, there is reason for cautious optimism with respect to favorably influencing the course of certain primary glomerular diseases with pharmacologic therapy. Particularly promising in this regard is the role of corticosteroids in membranous nephropathy, anticoagulant and antithrombotic agents in membranoproliferative glomerulonephritis and high-dose "pulse" steroids, "quadruple therapy" or plasma exchange with immunosuppression in idiopathic crescentic glomerulonephritis. Further controlled trials are urgently needed in the various forms of mesangial proliferative glomerulonephritis, including Berger's disease, in focal and segmental glomerulosclerosis and membranous nephropathy in which reduced GFR or steroid resistance has been demonstrated. It seems quite clear that even a temporary delay in the onset of ESRD, if such can be obtained with a minimum of lasting side effects, is a reasonable goal of therapy considering the expense of maintenance dialysis and transplantation.
Serial serum samples from 48 patients with systemic lupus erythematosus (SLE) were assayed for C3, anti-DNA antibody, and circulating immune complexes (CIC). CIC were measured by the fluid phase (FClq) and solid phase (SClq) Clq binding assays. Elevations of the SClq results were associated with the presence of manifestations of SLE (P less than 0.001), including active renal disease (P less than 0.005) and arthritis (P less than 0.001), as well as changes in degree of disease activity which prompted physician action. A change in the SClq results correctly predicted a change in disease activity 82% of the time (P less than 0.005). Abnormalities of FClq, anti-DNA antibody, and C3 were neither associated with nor predictive of changes in disease activity of SLE. These data suggest that the SClq method of determining CIC is the most reliable laboratory indicator of clinical activity in SLE.
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