Cryoglobulinemia due to Hepatitis C with Pulmonary Renal Syndrome.

Cryoglobulinemia is an uncommon condition typically due to hepatitis C infection. Its clinical presentation is varied and often reflects deposition of immune complex and complement deposition. Renal compromise is observed in approximately one third of patients with mixed cryoglobulinemia and reports of concomitant pulmonary involvement are quite rare. We report a case of a patient who presented with pulmonary and renal manifestations of cryoglobulinemia with a serum rheumatoid factor over one hundred times the upper limit of normal and benefited from high-dose steroids and plasmapheresis in the acute setting.

Effect of month-long treatment with oral N-acetylcysteine on the oxidative stress and proteinuria in patients with diabetic nephropathy: a pilot study.

INTRODUCTION: Oxidative stress plays an important role in the pathogenesis of diabetic nephropathy (DN). This study examined if use of N-acetylcysteine for a month in moderate doses would reduce the oxidative stress in patients with DN and reduce the proteinuria. METHODS: Fifteen volunteers with DN participated in the study. Participants took capsule form of N-acetylcysteine 1 gm twice a day for a month. Spot urines were collected and tested for protein/creatinine on days 1 and 30. Sera were collected on days 1, 15, 30, and 60 and tested for several oxidative stress biomarkers. RESULTS: There was no significant change in proteinuria or any of the oxidant stress markers at any point: protein-creatinine ratio (day 1, 1.6 +/- 1.8; day 30, 1.3 +/- 1.3), 8-isoprostane (day 1, 5.9 +/- 4.2 pg/mL; day 15, 4.67 +/- 2.4 pg/mL; day 30, 5.1 +/- 2.8 pg/mL; and day 60, 4.7 +/- 1.9 pg/mL), total antioxidant status (day 1, 1.5 +/- 0.1 mM; day 15, 1.6 +/- 0.2 mM; day 30, 1.5 +/- 0.1 mM; and day 60, 1.5 +/- 0.2 mM), aconitase (day 1, 7.9 +/- 5.9 mU/mL; day 15, 10.1 +/- 5.9 mU/mL; day 30, 8.9 +/- 6.2 mU/mL; and day 60, 7.8 +/- 5.5 mU/mL), glutathione peroxidase (day 1, 261.4 +/- 56.4 mU/mL; day 15, 263.9 +/- 57.2 mU/mL; day 30, 269.2 +/- 66.0 mU/mL; and day 60, 257.5 +/- 48.2 mU/mL), and superoxide dismutase (day 1, 242.6 +/- 79.3 mU/mL; day 15, 252.1 +/- 68.1 mU/mL; day 30, 262.0 +/- 73.3 mU/mL; and day 60, 255.7 +/- 61.5).However, 4 patients with initial high isoprostane levels showed nonsignificant decline at each subsequent time point. CONCLUSIONS: N-acetylcysteine in moderate doses given over a month did not have significant effect on the overall oxidative stress in patients with DN and did not reduce proteinuria.

Effects of additive therapy with spironolactone on proteinuria in diabetic patients already on ACE inhibitor or ARB therapy: results of a randomized, placebo-controlled, double-blind, crossover trial.

INTRODUCTION: Aldosterone seems to have deleterious effects on the kidneys. Many animal studies and a few clinical trials have shown that suppression of aldosteroneby aldosterone receptor blockers ameliorates these effects. METHOD: In a double-blind crossover study, patients with diabetic nephropathy who were already receiving either angiotensin converting enzyme inhibitor (ACEI) or angiotensin receptor blocker (ARB) were given spironolactone or matching placebo with 1 month of washout in between. Blood pressure (BP), serum creatinine, serum potassium, and spot urine protein/creatinine were measured at the beginning and end of each study period. RESULTS: Mean systolic BP on spironolactone went down from 153.64 (+/-25.95) at the beginning to 141.60 (+/-16.54) at the end of study (P = 0.01). Diastolic BP during spironolactone therapy did not change significantly. The urine protein/creatinine increased from 1.24 (+/-1.13) to 1.57 (+/-2.13) on placebo (P = 0.35) and decreased from 1.80 (+/-1.78) to 0.79 (+/-0.99) during spironolactone therapy (P = 0.004). In other words proteinuria increased by 24% during the placebo treatment period but decreased by half (57%) during the active treatment. Serum potassium increased from 4.29 (+/-0.47) to 4.64 (+/-0.55) during spironolactone therapy (P = 0.002), no significant change with placebo. Whereas serum creatinine did not change on placebo, it increased from 1.35 (+/-0.54) to 1.56 (+/-0.62) on spironolactone (P = 0.006). Glomerular filtration rate decreased from 61.91 (+/-23.4) to 53.94 (+/-23.58) on spironolactone (P = 0.0001) but not on placebo. CONCLUSIONS: Addition of a modest dose of spironolactone to a regimen of ACEI or ARB in patients with diabetic proteinuria causes further reduction in proteinuria and also lowers the systolic BP. As with ACEI or ARB, spironolactone modestly reduces the glomerular filtration rate and raises serum potassium.