Endogenous testosterone, muscle strength, and fat-free mass in men with chronic kidney disease.

OBJECTIVE: Testosterone deficiency is a common finding in men with chronic kidney disease (CKD). Testosterone is thought to play an important anabolic role in muscle synthesis, and muscle wasting is an important and deleterious characteristic of protein-energy wasting (PEW) in CKD. It is presently unknown if reduced endogenous testosterone associates with features of muscle wasting in men with CKD. METHODS: This was a cross-sectional observational study of 267 men with CKD stages 2-4 (mean ± standard deviation age 67 ± 13 years, estimated glomerular filtration rate 42.9 [interquartile range 30.2-56.7] mL/min/1.73 m²) with measurements of endogenous testosterone and surrogates of PEW such as albumin, prealbumin, high-sensitivity C-reactive protein (CRP) and normalized protein nitrogen appearance (nPNA). Fat-free mass was estimated by bioelectrical impedance vector analysis (BIVA) and muscle strength by handgrip dynamometry. RESULTS: Across decreasing thirds of testosterone distribution, patients were incrementally older and CRP levels rose significantly. Prealbumin, hemoglobin, nPNA, handgrip strength, and BIVA estimated surrogates of muscle mass and nutritional status (fat-free mass, body cell mass, and phase angle) were progressively reduced (P < .05 for all). In multivariate regression analyses including age, renal function, and other important confounders, testosterone significantly and independently contributed to explain the variances of handgrip strength and fat-free mass (P < .05 for all). CONCLUSIONS: Endogenous testosterone independently associates with muscle strength and fat-free mass in men with moderate CKD. It is plausible that the reduction in testosterone levels that accompanies CKD may further contribute to the procatabolic environment leading to muscle wasting.

Plasmapheresis in diffuse alveolar hemorrhage as perinuclear antineutrophil cytoplasmic antibody-associated vasculitis relapse on hemodialysis.

Unlike Goodpasture's syndrome with diffuse alveolar hemorrhage (DAH), there are scarce reports on the use of plasmapheresis for patients with a recurrence of DAH associated with antineutrophil cytoplasmic antibody (ANCA)-associated small vessel vasculitis (AAV) on hemodialysis. We report a case of a relapse of perinuclear-AAV with DAH, five months after starting hemodialysis. The patient received apheresis and induction immunosuppressive therapy, added to a short course of daily hemodialysis treatments. The DAH resolved with seven apheresis procedures and there were no adverse effects. We suggest that patients on hemodialysis with a relapse of AAV and DAH would benefit from the prompt initiation of apheresis in combination with aggressive immunosuppressive therapy. Pulmonary hemorrhage is not included in the current guidelines for therapeutic apheresis; therefore, we report this case and, if warranted, propose this condition to be included in the guidelines.