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Progressive elevations of fibroblastic growth factor 23 [FGF23] in chronic kidney disease may reduce serum 25-hydroxyvitamin D [25(OH)] and 1,25-dihydroxyvitamin D [1,25(OH)2D] levels, via stimulation of 24-hydroxylase (Cyp24A1) mediated catabolism of these vitamin D metabolites. To test this possibility, we measured serum concentrations of 24,25-dihydroxyvitamin D [24,25(OH)2D], a product of Cyp24A1 hydroxylation of 25(OH)D, in the Col4α3 knockout mouse, a model of Alport syndrome-derived chronic kidney disease, and in patients with chronic kidney disease of variable severity. There was an inverse correlation between serum FGF23 and both 25(OH)D and 1,25(OH)2D in the mouse model but no significant relationship was observed in the cross-sectional patient cohort. The FGF23-dependent increase in Cyp24a1 mRNA expression in the mouse kidneys was consistent with the possibility that FGF23 induces vitamin D catabolism. There was, however, a reduction in serum 24,25(OH)2D levels, rather than the expected elevation, in both the mice and patients with chronic kidney disease. Low 25(OH)D and elevated FGF23 and parathyroid hormone levels were correlated with the reduced serum 24,25(OH)2D concentrations of these patients. Thus, we failed to find support for FGF23-mediated catabolism of vitamin D metabolites in chronic kidney disease assessed by 24,25(OH)2D levels.

Modest elevations of serum 25(OH)D levels after cholecalciferol treatment are sufficient to induce compensatory degradative pathways in patients with sufficient renal reserves, suggesting that optimal circulating 25(OH)D levels are approximately 20 ηg/mL. In addition, catabolism of 25(OH)D may also contribute to the low circulating vitamin D levels in CKD, since elevations of FGF-23 in CKD are associated with increased 24,25(OH)2D after cholecalciferol administration.

IntroductionAlthough membranoproliferative glomerulonephritis has been reported to occur in association with non-Hodgkin's lymphoma, information concerning the long term effects of treatment of non-Hodgkin's lymphoma on the associated membranoproliferative glomerulonephritis is limited.Case presentationThe current report describes a patient who presented with the abrupt onset of hypertension, mixed nephritic/nephrotic syndrome and acute renal failure. Kidney biopsy was consistent with membranoproliferative glomerulonephritis, type 1. Bone marrow biopsy performed in the evaluation of periaortic lymphadenopathy, hepatosplenomegaly, and thrombocytopenia confirmed the diagnosis of low grade B-cell non-Hodgkin's lymphoma. The patient's renal function improved and proteinuria resolved after initial treatment of non-Hodgkin's lymphoma with chemotherapy. During eleven years of follow up, membranoproliferative glomerulonephritis has remained in remission, as confirmed by repeatedly negative urinalyses, normal blood pressure and absence of clinical signs and symptoms suggestive of nephritic/nephrotic syndrome.ConclusionMembranoproliferative glomerulonephritis has been known to be associated with both chronic lymphocytic leukemia and non-Hodgkin's lymphoma, particularly with B cell lymphocytic type non-Hodgkin's lymphoma. There is limited information available concerning the effects of treatment of non-Hodgkin's lymphoma on the progression of non-Hodgkin's lymphoma associated membranoproliferative glomerulonephritis. In the few reported cases we found, long term follow up after initial resolution of the membranoproliferative glomerulonephritis was lacking. This report presented a rare case of non-Hodgkin's lymphoma associated membranoproliferative glomerulonephritis, that continued to be in remission during eleven years of follow up after initial chemotherapy treatment of lymphoma.

The presence of CKD and diabetes mellitus is associated with resistance to correction of 25(OH)D deficiency with vitamin D2 therapy. The underlying mechanism needs to be evaluated in prospective studies.

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Study design: A retrospective analysis. Objectives: The objective of this study is to determine whether dipstick protein analysis (DSP) or random urine protein:creatinine ratios (UPC) are accurate in predicting clinical proteinuria in the chronic spinal cord injury (SCI) population. Methods: A retrospective analysis was performed in 219 veterans with SCI, comparing DSP and 24-h urine protein excretion. Sensitivity, specificity, predictive values (PV) and receiver-operator characteristic (ROC) curves of DSP in predicting clinical proteinuria were calculated with and without correction for specific gravity (SG). A prospective study was also performed in 62 SCI patients, comparing the UPC and 24-h urines. Sensitivity, specificity, PV and ROC curves of UPC in predicting clinical proteinuria were calculated. Results: Any level of positive DSP had high specificity, but low sensitivity, for detecting the presence of clinical proteinuria. ROC curves of DSP for identifying clinical proteinuria yielded area under the curve of 0.749 (95% confidence interval 0.699-0.794), and adjustment for SG did not significantly improve accuracy. A UPC of o0.3 was sensitive with a high negative PV for ruling out clinical proteinuria, whereas a ratio 40.8 was specific with a high positive PV. A UPC between 0.3-0.8 had an intermediate sensitivity and specificity. Conclusion: Urine collections of 24-h are still needed in the chronic SCI population for accurate detection of clinically significant proteinuria. DSP may not reliably detect low-grade clinical proteinuria, whereas a UPC below 0.3 may be used to rule out clinical range proteinuria.