Kidney international
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Kidney international · Sep 2016
Never make assumptions: the complicated role of complement in urinary tract infections.
Complement activation can cause tissue inflammation and injury, and complement-inhibitory drugs are effective treatments for several inflammatory diseases. The complement cascade is part of the body's defense against bacteria and other pathogens, however, and a major concern regarding inhibition of this system is that it may increase the risk for infection. Now, a study by Choudhry et al. demonstrates that blockade of signaling at one of the C5a receptors (C5a receptor 1 [C5aR1]) reduces renal fibrosis in a mouse model of urinary tract infection with Escherichia coli. ⋯ Other recent studies have also shown that C5a impairs the elimination of tumor cells by the immune system. These data indicate that complement inhibition may have some unexpected benefits. These results also demonstrate, however, that the complement cascade probably has physiologic functions that have yet to be discovered.
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Kidney international · Sep 2016
Randomized Controlled TrialTreatment with patiromer decreases aldosterone in patients with chronic kidney disease and hyperkalemia on renin-angiotensin system inhibitors.
Elevated serum aldosterone can be vasculotoxic and facilitate cardiorenal damage. Renin-angiotensin system inhibitors reduce serum aldosterone levels and/or block its effects but can cause hyperkalemia. Patiromer, a nonabsorbed potassium binder, decreases serum potassium in patients with chronic kidney disease on renin-angiotensin system inhibitors. ⋯ Patients on patiromer had significant reductions in mean systolic/diastolic blood pressure (-6.70 ± 1.59/-2.15 ± 1.06 mm Hg), whereas those on placebo did not (-1.21 ± 1.89 mm Hg/+1.72 ± 1.26 mm Hg). Significant changes in plasma renin activity were found only in the placebo group (-3.90 ± 1.41 μg/l/hr). Thus, patiromer reduced serum potassium and aldosterone levels independent of plasma renin activity in patients with chronic kidney disease and hyperkalemia on renin-angiotensin system inhibitors.