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Biomedical subjects

R J Glassock

Publications and source records attributed to R J Glassock.

At least 55 records · Page 3Linked to original sources
PubMed1988

Declining incidence of wound infection in cadaveric renal transplant recipient.

Over a five-year period 100 cadaveric renal transplants were performed. In 91 of these recipients, a prophylactic parenteral antibiotic (cefoperazone) was administered and closed wound drainage was used. Of these 91 patients, 33 received azathioprine/prednisone immunosuppression, whereas cyclosporine/prednisone with or without azathioprine was used in the remaining 58. The incidence of wound infections was significantly reduced from 12 per cent (4/33) in the azathioprine group to 1.7 per cent (1/58) in the cyclosporine group (p less than 0.01). When conventional immunosuppression (azathioprine/prednisone) is employed in renal transplantation, triple antibiotic prophylaxis that includes an aminoglycoside is most effective in preventing wound infections. A single non-nephrotoxic antibiotic, cefoperazone, offers similar protection in the cyclosporine/prednisone-treated renal transplant recipient.

Cadaver↗
PubMed1988

Infection patterns in cyclosporine-treated cadaveric renal transplant patients.

Immunosuppression with Cs regimens has not significantly altered infection patterns relative to earlier modalities. However, reports of increased infection, especially with CMV/PCC, are not borne out in our experience both in numbers and timing of infections. Patients on low-dose Cs immunosuppression do continue to acquire infectious complications but, in general, rarely will lose their grafts or lives.

Cyclosporins↗
PubMed1987

The current role of pre-transplant blood transfusions and tissue typing in cadaveric renal transplantation.

In a retrospective analysis of 74 consecutive cadaveric renal transplants performed at our center during a 38-month period we assessed the influence of random blood transfusions and tissue matching on graft and patient survival. All patients received cyclosporine and low dose prednisone with or without azathioprine as immunosuppressive therapy. Actual patient survival was 100 per cent at 1 year and actuarial 1-year graft survival was 82 per cent. Random blood transfusions and histocompatibility matching at the HLA-DR locus did not influence graft survival. Matching at 2 or more HLA-A and B loci was associated with a significant detrimental influence (p less than 0.05) on graft survival. We conclude that the use of cyclosporine-based immunosuppression overcomes much of the adverse effect of poor tissue matching and may obviate the need for random blood transfusions in cadaveric renal transplantation during the first year of engraftment.

Azathioprine↗
PubMed1987

Clinical aspects of glomerular diseases.

This article discusses the current concepts of the pathophysiology of disturbed glomerular structure and/or function that lead to the cardinal clinical manifestations of glomerular disease, ie, alterations in glomerular filtration rate, disturbances in sodium homeostasis, proteinuria, and hematuria. The functional and anatomic bases of these alterations include changes in filtering surface area, filtration pressure and/or nephron mass, primary and secondary renal sodium and water retention, defects in size and/or charge-selective barriers to filtration of plasma proteins, and defects in capillary wall integrity. Longitudinal evaluation of albuminuria/gamma globulinuria and the investigation of dysmorphic hematuria may be helpful approaches to the study of glomerular disease.

Glomerular Filtration Rate↗
PubMed1987

The effect of verapamil in reducing the severity of acute tubular necrosis in canine renal autotransplants.

Calcium channel blockade has been shown to prevent warm renal ischemic damage. The ability of verapamil to decrease the severity of acute tubular necrosis (ATN) after 24-hr cold storage and autotransplantation was studied in a randomized paired study of 12 dogs. Experimental animals pretreated with intraarterial verapamil and flushing of the harvested kidney with cold intracellular solution containing verapamil demonstrated significantly (P less than .05) greater renal function preservation over their matched controls. A subsequent nonpaired study of 6 dogs treated only with flushing of the harvested kidney with perfusate containing verapamil demonstrated no significant preservation advantage over controls. We conclude that verapamil, administered prior to the ischemic event, can enhance the protective effect of hypothermia and decrease the severity of ATN in ischemically injured kidneys.

Acute Kidney Injury↗
PubMed1986

Glomerular filtration rate fails to increase following protein ingestion in hypothalamo-hypophyseal-deficient adults. Preliminary observations.

Oral protein loads are known to induce an increase in glomerular filtration rate (GFR) in man and animals. The mechanism underlying this phenomenon is currently unknown. In order to study the possible role of growth hormone (GH) or other hypothalamo-hypophyseal (HH) factors in the response of GFR to a protein meal, we studied 4 chronically GH- or HH-deficient adults and age-matched controls, free of renal disease, before and after ingestion of a large protein meal (red cooked meat). GFR, measured by inulin clearance and corrected for body surface area, was 18.5% lower during basal conditions (89.1 +/- 6.0 ml/min) in the GH- or HH-deficient population when compared to controls (109.7 +/- 9.1 ml/min), but this difference did not achieve statistical significance for this small patient population (p greater than 0.1, less than 0.2). For a 3-hour postprandial period, mean GFR increased by 25.3% in the control population (136.8 +/- 10.7 ml/min; p less than 0.01), while mean GFR failed to increase in the GH- or HH-deficient patients (86.8 +/- 10.9 ml/min; p greater than 0.10). Male control subjects, not pretreated with diethylstilbestrol, had no change in GH levels (p greater than 0.2). However, 1 female control was found to increase GH levels 10 times preprandial levels. These studies suggest that HH factors other than GH are mediators of the augmentation of GFR following a large protein load in human adults.

Adult↗
PubMed1985

Role of prostaglandins and angiotensin II in experimental glomerulonephritis.

Moderate autologous nephrotoxic serum nephritis (NSN) in rats causes no reduction in GFR despite a reduction in ultrafiltration coefficient (Kf) to less than one-half of normal. An increase in intraglomerular hydraulic pressure maintains GFR, but the signal and efferent mechanisms for this adaptation remain unknown. Indomethacin and saralasin were used to study the possible roles of prostaglandins and angiotensin II (A-II) in the adaptation to NSN. Indomethacin decreased renal blood flow (RBF) in NSN (-8.6%, P less than 0.001), but not in controls. Renal vascular resistance (RVR) increased in NSN (+ 9.6%, P less than 0.01), but decreased in controls (-5.6%, P less than 0.01). GFR decreased in NSN (-22.3%, P less than 0.01), but increased in controls (+ 10.3%, P less than 0.001). Urinary PGE2 excretion decreased markedly both in NSN and controls. With combined treatment using indomethacin and saralasin, RBF increased in NSN (+ 22.4%, P less than 0.001), but did not change in controls. RVR decreased in NSN (-21.5%, P less than 0.001), but was unchanged in controls. GFR remained unchanged both in NSN and controls. With saralasin alone, RBF increased both in NSN (+ 21.4%, P less than 0.001) and in controls (+ 14.4%, P less than 0.001). RVR decreased both in NSN (-21.8%, P less than 0.001) and controls (-18.7% P less than 0.001). GFR increased (+ 12.3%, P less than 0.05) in NSN, but did not change in controls. Urinary PGE2 excretion was increased in NSN compared to controls, decreased markedly in NSN after either indomethacin or saralasin infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1985

Natural history and treatment of primary proliferative glomerulonephritis: a review.

The immunopathology, clinical characteristics, natural history, and treatment of the lesions that constitute the heterogeneous group of primary proliferative glonerulonephritis have been reviewed. These lesions include pure mesangial proliferative glomerulonephritis, IgA nephropathy, mesangiocapillary glomerulonephritis, focal and segmental proliferative glomerulonephritis, and crescentic glomerulonephritis. A great deal is now known concerning the natural history of these individual entities and some have responded satisfactorily to a variety of therapeutic modalities. Unfortunately, the most common of the proliferative glomerulonephritides, namely, IgA nephropathy, has not yet yielded to therapeutic efforts, except on rare occasions. It is hoped that, through better understanding of the fundamental pathogenetic mechanisms involved and a continued search for etiologic events, better and more effective therapeutic regimens will be devised. Considering the rate of progress that has occurred in the last several decades, there is good reason for optimism that ultimately these proliferative glomerulonephritides that contribute so importantly to the pool of patients with end-stage renal disease will ultimately be controlled or even prevented.

Basement Membrane↗
PubMed1984

Extracellular fluid expansion and autoregulation in nephrotoxic serum nephritis in rats.

Previous studies of the early autologous phase of bilateral nephrotoxic serum nephritis (NSN) in rats showed that whole kidney and single nephron glomerular filtration rate (GFR) were maintained at normal levels despite a 60% reduction in the product of surface area and hydraulic permeability (Kf). Factors responsible for this compensation were an increase of net ultrafiltration pressure, due primarily to an increased glomerular capillary pressure (PGC). This study was designed to investigate some possible causes of the compensation. Rats with bilateral NSN and normal GFR had an increased extracellular fluid volume (ECFV) 2 weeks after induction of NSN; control subjects did not change. To determine whether this ECFV expansion was responsible for triggering the compensation, we developed a unilateral NSN model with one diseased and one normal kidney. Unilaterally diseased rats did not experience an increase of ECFV. Values of Kf were 0.069 +/- 0.012 nl sec-1 mm Hg-1 in control subjects, 0.037 +/- 0.005 in bilateral NSN, and 0.043 +/- 0.006 in unilateral NSN. The elevation in PGC was the same in unilateral NSN as in bilateral NSN subjects and the same was true for the hydrostatic pressure difference across glomerular capillaries (delta P). Furthermore, in paired measurements on both kidneys of rats with unilateral NSN, PGC was significantly higher in the unilaterally diseased kidney than in the nondiseased kidney; sham control subjects had no difference. These results are interpreted to indicate that the signal that causes elevation of net ultrafiltration pressure is not a consequence of a systemic effect of NSN, but arises within the diseased kidney itself. To determine whether that signal involved some change in the mechanisms mediating autoregulation measurements were made of the response of whole kidney GFR and RBF to acute changes in arterial BP. Control rats and rats with NSN autoregulated both GFR and blood flow equally well. Tubuloglomerular feedback was studied by microperfusing loops of Henle and measuring proximal stop-flow pressure and early proximal flow rate. Stop-flow pressure was 4.0 mm Hg higher in rats with NSN at a loop perfusion rate of 10 nl/min, approximately the same difference that was found by direct measurement of PGC, but the sensitivity of response to changes in perfusion rate was the same in NSN as in control subjects. Finally, end proximal tubule flow rate was higher in NSN than in control subjects reflecting decreased proximal reabsorption. Thus, a normal feedback mechanism receives a signal that should cause afferent arteriolar constriction in NSN rats.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗