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Biomedical subjects

F J Bruns

Publications and source records attributed to F J Bruns.

9 recordsLinked to original sources
PubMed1992

Potentiation of uremic bleeding by hereditary storage pool disease.

This study demonstrates that specific bleeding tests can separate the thrombocytopathy of uremia alone from the bleeding disorders caused by uremia superimposed on preexisting platelet dysfunction. The case history of a uremic patient with exaggerated bleeding tendencies is presented. The findings in this patient are compared with the clinical characteristics and platelet function studies of nine other patients with chronic renal failure. The index and other uremic patients were similar except for the clinical bleeding and results of platelet function studies. The patient's nonocclusive bleeding time and measured blood loss during bleeding time tests were increased compared with the other uremic controls. In addition, her platelet aggregation in response to collagen was lower than that of the other uremic subjects. Repeat studies following renal transplantation were consistent with hereditary storage pool disease. An underlying platelet disorder may potentiate the hemostatic defects of uremia. The diagnosis should be suspected in patients with frequent and severe bleeding manifestations. Renal transplantation led to control of clinical bleeding.

Adult↗
PubMed1991

Sustained remission of membranous glomerulonephritis after cyclophosphamide and prednisone.

OBJECTIVE: To determine the effect of cyclophosphamide and prednisone on progressive renal failure and on nephrotic features in patients with membranous glomerulonephritis. DESIGN: Prospective, nonrandomized time series. SETTING: Outpatient clinic at a university medical center. PATIENTS: Eleven consecutive patients with biopsy-proven membranous glomerulonephritis and rising plasma creatinine levels over at least 6 months. INTERVENTION: Cyclophosphamide and prednisone in ten patients and cyclophosphamide alone in one patient. MEASUREMENTS AND MAIN RESULTS: In ten patients treated with both agents, the median plasma creatinine rose 53 mumol/L (0.6 mg/dL) over the months before treatment from 141 to 194 mumol/L (1.6 to 2.2 mg/dL) (95% CI, 27 to 141 mumol/L; P = 0.002). After combined therapy for 6 months, the median plasma creatinine fell to 133 mumol/L (1.5 mg/dL) for a median decline of 62 mumol/L (0.7 mg/dL) (CI, 44 to 150 mumol/L; P = 0.006). Pretreatment plasma creatinine levels, which ranged from 159 to 371 mumol/L (1.8 to 4.2 mg/dL), decreased in the ten patients by 6 months and remained stable in seven of the eight patients followed 24 to 54 months after therapy was completed. The median urine protein excretion decreased by 9.6 g/d with 12 months of therapy in the ten patients from 11.9 to 2.3 g/d (CI, 6.0 to 15.1 g/d; P less than 0.001). The median plasma albumin rose by 14 g/L from 24 to 38 g/L (CI, 11 to 19 g/L; P less than 0.001). The median plasma cholesterol fell by 3.26 mumol/L (140 mg/dL) from 10.45 to 6.52 mumol/L (405 to 252 mg/dL) (CI, 1.42 to 7.16 mumol/L; P = 0.01). One patient who had a relapse 30 months after completing therapy responded to re-treatment with renal function and nephrotic variables returning toward normal. The eleventh patient received cyclophosphamide alone and had a course similar to that of the combined therapy group. CONCLUSION: Cyclophosphamide plus prednisone can promote prolonged remissions in membranous glomerulonephritis even when renal function is already declining.

Adult↗
PubMed1989

Long-term follow-up of aggressively treated idiopathic rapidly progressive glomerulonephritis.

PURPOSE: We wanted to examine the long-term effects of aggressively treating idiopathic rapidly progressive glomerulonephritis (RPGN), with a particular focus on clinically characterizing the patient population, assessing the short- and long-term effects of therapy on renal function, and determining complications of the therapy. PATIENTS AND METHODS: Twenty-three consecutive patients with RPGN were treated and followed from one to 11 years. On renal biopsy, 13 had immune complexes, eight had no immune complexes, and two had antiglomerular basement membrane deposits. All had greater than 25 percent crescents and 19 of 23 had greater than 50 percent crescents. Every patient responded on a short-term basis to either large-dose pulse methylprednisolone or plasma exchange, with reduction of the mean plasma creatinine level from 6.5 +/- 2.0 mg/dl to 2.9 +/- 1.0 mg/dl (p less than 0.001). Each patient received oral prednisone and all but one received cyclophosphamide. RESULTS: Three died of non-renal causes. Fifty percent of the remaining 20 patients maintained stable renal function for at least two years. Four of nine patients followed-up for longer than two years had a relapse, but all responded again to therapy. No characteristic clinical symptoms predicting relapse were found, although nearly all had hematuria and proteinuria. Complications of therapy were frequent and may have contributed to death in two patients. CONCLUSION: Thus, long remissions are seen in most patients with RPGN treated aggressively.

Adult↗
PubMed1989

Hypercalcemia in patients with advanced chronic renal failure not yet requiring dialysis.

Six patients with progressive chronic renal failure not yet requiring dialysis and not consuming supplemental calcium or vitamin D developed hypercalcemia. Three had proven and 1 suspected tertiary hyperparathyroidism, 1 parathyroid carcinoma and 1 aplastic bone. None of the 3 patients who underwent bone biopsy had heavy bone aluminum staining. The patients with proven parathyroid-mediated hypercalcemia had marked elevation of C-terminal parathyroid hormone and alkaline phosphatase values and, when performed, radiographs consistent with osteitis fibrosa. When these findings are absent or the diagnosis is otherwise uncertain, a bone biopsy may provide a definitive diagnosis and guide management.

Adult↗
PubMed1979

Effect of early plasmapheresis and immunosuppressive therapy on natural history of anti-glomerular basement membrane glomerulonephritis: report of a 22-month follow-up.

A patient with anti-glomerular basement membrane (GBM)-mediated necrotizing and proliferative glomerulonephritis with crescents was treated with plasmapheresis, cyclophosphamide, and steroids. Treatment resulted in decreased circulating anti-GBM antibody and prompt improvement of renal function that remained stable for 15 months after all treatment was discontinued. Renal biopsies were performed initially, at seven and 17 months. Immunofluorescent examination showed that anti-GBM antibody continued to be present on GBMs although light and electron microscopic findings demonstrated a transformation to a form of sclerosing glomerulonephritis. To our knowledge, this patient's course is the first demonstration that early treatment with plasmapheresis and immunosuppressions may transform the histologic findings in anti-GBM-induced rapidly progressive glomerulonephritis, thereby altering the natural history of this disease.

Adrenal Cortex Hormones↗
PubMed1975

Effect of hemodilution on the distribution of renal blood flow.

We evaluated the effects of hemodilution, expansion of intravascular volume, and expansion of interstitial volume on the distribution of cortical renal blood flow, utilizing the microsphere technique. Hemodilution without volume expansion (saline exchange) produced an increase in fractional blood flow in zone 1 (outermost zone) of the cortex from 34 plus or minus 1% to 43 plus or minus 2% and a decrease in fractional blood flow in zone 4 (innermost zone) from 16 plus or minus 2% to 13 plus or minus 2%. Hemodilution without volume expansion or a decrease in plasma protein concentration (isoncotic exchange) produced a similar redistribution in blood flow in zone 1 from 34 plus or minus 2% to 41 plus or minus 2% and in zone 4 from 14 plus or minus 2% to 10 plus or minus 1%. Hemodilution with intravascular volume expansion (hyperoncotic albumin infusion) also produced a superficial shift; blood flow in zone 1 increased from 27 plus or minus 1% to 30 plus or minus 1% and that in zone 4 decreased from 19 plus or minus 2% to 15 plus or minus 1%. Previous studies have demonstrated a redistribution to the juxtamedullary area after saline expansion. Our data demonstrate that hemodilution causes flow to redistribute to the superficial rather than the deep cortex. This superficial shift appears to be secondary to decrease hematocrit rather than to dilution of plasma proteins or expansions of intravascular volume. The deep shift in cortical blood flow which occurs during saline loading is presumably a consequence of expansion of interstitial volume.

Animals↗