Severe Hypocalcemia and Hypomagnesemia with Denosumab in Advanced Chronic Kidney Disease: Case Report and Literature Review.

BACKGROUND: Denosumab has become the preferred agent over zolendronic acid to help prevent skeletal-related events in patients with metastatic bone disease and multiple myeloma because it is approved for use in those with kidney dysfunction. However, denosumab has been linked to cases of hypocalcemia, particularly in those with advanced kidney disease. CASE PRESENTATION: We present the case of a patient with metastatic prostate cancer and chronic kidney disease due to obstructive nephropathy who developed severe hypocalcemia and hypomagnesemia after denosumab injection, which required intensive care unit admission, aggressive calcium supplementation, and hemodialysis assistance. We reviewed the evidence behind the safety profile of denosumab in chronic kidney disease, and we also looked at additional factors that may precipitate severe hypocalcemia with denosumab in advanced kidney disease. CONCLUSION: We believe that denosumab should be avoided in advanced chronic kidney disease due to the potential life-threatening, severe hypocalcemia that has been observed.

Thrombotic Microangiopathies with Rheumatologic Involvement.

Thrombotic microangiopathies are heterogeneous disorders characterized by microangiopathic hemolytic anemia with thrombocytopenia and renal injury. There are a variety of causes, including metabolic disorders, infections, medications, complement disorders, pregnancy, malignancy, and autoimmune disorders. This review focuses on renal thrombotic microangiopathy in the setting of rheumatologic diseases. Systemic lupus erythematosus is the most common autoimmune disease associated with thrombotic microangiopathy. Other etiologies include scleroderma renal crisis and antiphospholipid antibody syndrome, which can be primary or secondary to autoimmune diseases including systemic lupus erythematosus. There have also been case reports of thrombotic microangiopathy in the setting of rheumatoid arthritis and dermatomyositis.

Retrospective analysis of inferior vena cava collapsibility with point of care ultrasound and urine sodium and FENa in patients with early stage acute kidney injury.

Early stage acute kidney injury (AKI) is an independent risk factor for an increase in mortality. Accurate assessment of volume status is a major challenge during the early stages of acute renal injury. Determining volume status based on the history and physical exam lacks accuracy. Urine sodium and free excretion of sodium (FENa) provide objective evidence of intravascular volume status when interpreted carefully and is helpful to delineate prerenal from intrinsic renal failure. In recent years point of care ultrasound has been used to assess volume status. Our team conducted a retrospective chart review to assess the association of inferior vena cava collapsibility by point of care ultrasound (POCUS) and urine electrolytes (urine sodium, fractional excretion of sodium) during early stage AKI (Stage 1-2 of KDIGO guidelines). We reviewed 150 cases based on the provisional diagnosis. 36 patients met the criteria for further review. Using bivariate analysis, we found a strong association between >50% IVC collapsibility with FENa < 0.4% with an odds ratio 5.3 (CI 1.1-24.5, p = 0.04), and urine sodium <20 meq/dl with an odds ratio of 6.7 (Cl 1.5-30, p = 0.02). Subsequently, multivariate analysis and Spearman correlation showed an inverse relation between IVC collapsibility and fractional excretion of sodium FENa (ß = -0.4, p = 0.001) and (r = -0.44, p = 0.01). These findings suggest the role of POCUS and urinary markers in determining the intravascular volume status in AKI. POCUS is also valuable to assess volume status in cases of renal failure where urine studies are difficult to interpret.

Hydralazine-induced pauci-immune glomerulonephritis: intriguing case series with misleading diagnoses.

Hydralazine has been used since the 1950s for the management of hypertension. Evidence for hydralazine-associated vasculitis dates to pre-ANCA (antineutrophil cytoplasmic antibodies) era. This abstract describes two cases of ANCA-positive pauci-immune glomerulonephritis (GN) in challenging scenarios where diagnosis was misconstrued. A comprehensive literature review was done to understand the pathogenesis of drug-induced pauci-immune GN. We have described key diagnostic features that are helpful in distinguishing idiopathic ANCA vasculitis from drug-induced vasculitis. Additionally, we have also described different treatments meant to provide therapy options with the least side effects.