Lupus Nephritis With Mild Asymptomatic Hypercalcemia in Children: A Case Report and Literature Review

Abstract

Lupus nephritis (LN) in Children is caused by Kidney involvement in systemic lupus erythematosus (SLE). SLE is a chronic, multi-systemic, paroxysmal autoimmune disease with a wide spectrum of autoantibodies. Hypercalcemia is a common manifestation of primary hyperparathyroidism and other malignant tumors. LN or SLE with hypercalcemia is rare. We report a case of LN with hypercalcemia and review the literature. It suggests that the pathogenesis of SLE complicated with hypercalcemia complicates the response of drug therapy.

Concomitant primary hyperparathyroidism and systemic lupus erythematosus: coincidence or not? A new case report

“…Women are affected two to three times more than men [ 2 ]. Approximately 80% to 85% of patients with PHP have parathyroid adenoma [ 3 ]. Other causes of hypercalcemia are represented mainly by malignancy, multiple myeloma or a lymphoproliferative disease.…”

“…Other causes of hypercalcemia are represented mainly by malignancy, multiple myeloma or a lymphoproliferative disease. Rarely, hypervitaminosis D, sarcoidosis, other granulomatous diseases, some drugs and endocrine diseases with increased bone turnover may be responsible [ 3 ]. The association of systemic lupus erythematosus and hypercalcemia is rare.…”

“…The association of systemic lupus erythematosus and hypercalcemia is rare. To our knowledge, only 18 cases of patients with SLE with hypercalcemia, have been previously reported in a recent literature review [ 3 ]. Mechanisms by which hypercalcemia may occur in patients with SLE have been only partially clarified.…”

“…PTHrP may be produced by non-malignant lymphoid tissue in SLE. Polyclonal overactivation of B-lymphocytes in SLE may produce anti-PTH receptor autoantibodies, which may activate PTH receptors, bind to PTH receptors and activate PTH-mimetic effects, and inhibit the expression of PTH and PTHrP, leading to hypercalcemia [ 3 ]. Moreover, proinflammatory cytokines such as tumor necrosis factor alpha (TNF alpha), transforming growth factor beta (TGF ß), interleukins IL-1, IL-2 and IL-6, prostaglandins E2, and granulocyte-macrophage colony stimulating factors GM-CSF) are elevated during active SLE phases and could have a direct influence on bone turnover and may stimulate osteoclast bone resorption and lead to hypercalcemia [ 1-3,7 ].…”

“…Hypercalcemia may represent a marker of disease activity [ 6 ]. However, hypercalcemia did not occur in all active SLE patients [ 3 , 6 ]. Patients with SLE may have hypercalcemia, due to secondary or tertiary hyperparathyroidism due to chronic renal failure related to lupus nephritis [ 2 ].…”