Individualization of dialysate calcium concentration according to baseline pre-dialysis serum calcium.

BACKGROUND: A positive calcium balance may contribute to vascular calcification, while a negative balance increases iPTH. We explored the impact of different dialysate calcium concentrations on bone and mineral metabolism parameters according to pre-dialysis serum calcium levels. RESULTS: Fifty-six hemodialysis patients were dialyzed with 3.0 or 2.5 mEq/l dialysate [calcium] in a crossover study of two weeks. Bone mineral metabolites were measured prior to and following the hemodialysis session. A 3.0 mEq/l dialysate [calcium] increased more post-dialysis total calcium and ionized calcium than 2.5 mEq/l dialysate [calcium]. The mildest dialysis-induced changes in calcium and PTH were observed in patients with pre-dialysis serum calcium <8.75 mg/dl dialyzed with 2.5 mEq/l dialysate [calcium] and in patients with pre-dialysis serum calcium >9.15 mg/dl dialyzed with 3.0 mEq/l calcium dialysate. CONCLUSION: In conclusion, the individualization of dialysate calcium concentration according to baseline pre-dialysis serum calcium may prevent major excursions in post-dialysis serum calcium and iPTH levels. SHORT SUMMARY: High calcium dialysate may increase serum calcium in hemodialysis patients, while low dialysate calcium may increase PTH. Individualization of dialysate calcium according to predialysis serum calcium levels may prevent or decrease unwanted excursions of both serum calcium and PTH.

Rituximab-associated interstitial lung disease in fibrillary glomerulonephritis.

Rituximab (RTX) is a chimeric monoclonal antibody against CD20+ B cells increasingly used to treat kidney disorders. RTX-induced pulmonary disease has been reported in patients treated for haematological disorders, and a few cases have been observed in patients with underlying rheumatological conditions. We report a case of non-infectious interstitial pneumonitis associated with RTX use in a 49-year-old patient with primary (fibrillary) glomerulonephritis. As typically observed, discontinuation of the drug and prompt initiation of glucocorticoids led to resolution of pulmonary manifestations. However, fatalities have been reported and nephrologists treating glomerulonephritis patients with RTX should be aware of the existence of this potentially lethal complication.

Tenofovir nephrotoxicity: 2011 update.

Tenofovir is an acyclic nucleotide analogue reverse-transcriptase inhibitor structurally similar to the nephrotoxic drugs adefovir and cidofovir. Tenofovir is widely used to treat HIV infection and approved for treatment of hepatitis B virus. Despite initial cell culture and clinical trials results supporting the renal safety of tenofovir, its clinical use is associated with a low, albeit significant, risk of kidney injury. Proximal tubular cell secretion of tenofovir explains the accumulation of the drug in these mitochondria-rich cells. Tenofovir nephrotoxicity is characterized by proximal tubular cell dysfunction that may be associated with acute kidney injury or chronic kidney disease. Withdrawal of the drug leads to improvement of analytical parameters that may be partial. Understanding the risk factors for nephrotoxicity and regular monitoring of proximal tubular dysfunction and serum creatinine in high-risk patients is required to minimize nephrotoxicity. Newer, structurally similar molecular derivatives that do not accumulate in proximal tubules are under study.