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Gregory L Braden

Publications and source records attributed to Gregory L Braden.

5 recordsLinked to original sources
PubMed2004

Acute renal failure and hyperkalaemia associated with cyclooxygenase-2 inhibitors.

BACKGROUND: The renal effects of cyclooxygenase-2 (COX-2) inhibitors have been incompletely elucidated, and acute renal failure (ARF) due to COX-2 inhibitors has been reported. METHODS: In order to determine the causes of ARF and hyperkalaemia in five patients during COX-2 inhibitor therapy, we carefully analysed case studies of consecutive in-patients or out-patients referred to our Renal Division over a 6-month period for ARF and hyperkalaemia who had recently received COX-2 inhibitors. RESULTS: ARF developed 2-3 weeks after COX-2 inhibitor therapy in five patients. The ARF was consistent with pre-renal azotaemia from renal hypoperfusion. Four patients were receiving the loop diuretic, furosemide. Four patients developed hyperkalaemia and decreased serum bicarbonate despite diuretic therapy, and one patient had changes in plasma renin activity and aldosterone levels consistent with reversible hyporeninaemic hypoaldosteronism. Renal failure was reversible after discontinuation of diuretics and COX-2 inhibitors. CONCLUSIONS: COX-2 inhibitors may cause reversible ARF and hyperkalaemia in patients with oedematous conditions treated with low sodium diets and loop diuretics.

Acute Kidney Injury↗
PubMed2004

The role of circulating immune complexes and biocompatibility of staphylococcal protein A immunoadsorption in mitomycin C-induced hemolytic uremic syndrome.

Mitomycin-induced hemolytic uremic syndrome (HUS) is a life-threatening complication of this therapy, and increased levels of circulating immune complexes and hypocomplementemia have been found in some patients. We further characterize the role of immune complexes in mitomycin-HUS by showing that removal of these complexes by immunoadsorption with staphylococcal protein A columns correlates with temporal improvement in the microangiopathic hemolytic anemia in this disorder. Two immune complexes bound to the protein A column were identified: an 11S platelet-aggregating protein and a 15S non-platelet-aggregating protein. In addition, the patient had anaphylactoid reactions at the onset of immunoadsorption similar to first-use dialysis reactions that correlated with increases in complement 3a and 5a, interleukin-1 (IL-1), IL-6, and tumor necrosis factor levels. This case suggests that platelet-aggregating and complement-fixing circulating immune complexes are, in part, a proximate cause for mitomycin C-induced HUS. Therapy for mitomycin (HUS) with protein A columns should continue until circulating immune complexes reach undetectable levels and serum complement levels return to the normal range.

Anaphylaxis↗
PubMed2003

Outcome and complications of intraoperative hemodialysis during cardiopulmonary bypass with potassium-rich cardioplegia.

BACKGROUND: Potassium-rich cardioplegia has advantages over other cardioplegic solutions in preserving the myocardium during cardiopulmonary bypass, but it is avoided in patients with renal failure because of hyperkalemia. METHODS: We first determined the ability of intraoperative hemodialysis (IHD) to remove potassium during cardiopulmonary bypass with potassium-rich cardioplegia in 9 patients by measuring potassium levels in all dialysate and urine. We then studied 24 patients with renal failure, grouped with the 9 previous patients, to assess safety, rebound hyperkalemia, and patient outcome with this technique. RESULTS: In the first phase, 9 patients were administered 128 +/- 11 mmol of potassium in potassium-rich cardioplegia, and IHD removed 157 +/- 23 mmol. Urinary potassium excretion was only 10 +/- 3 mmol. Potassium removal occurred at a rate of 1.25 mmol/min with 0-mEq/L (mmol/L) potassium dialysate and a rate of 0.75 mmol/min with 3.0-mEq/L (mmol/L) potassium dialysate. In all 33 patients, successful initiation of cardiac rhythm occurred after cardiopulmonary bypass, and 5 patients had cardiac arrhythmias possibly from hypokalemia. In the next 24 hours, 5 dialysis-dependent patients developed hyperkalemia (potassium > 5.2 mEq/L [mmol/L]) requiring hemodialysis. Postoperative hemodialysis was delayed 2 to 3 days in the other patients. The overall death rate was 24% at 30 days. CONCLUSION: IHD effectively and safely removes potassium administered during potassium-rich cardioplegia during cardiopulmonary bypass in patients with renal failure and prevents postoperative hyperkalemia in the majority of patients. Overall mortality in patients with acute and chronic renal failure undergoing cardiac surgery is high irrespective of control of potassium balance in these patients.

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