Nephrotic syndrome after treatment with pamidronate

Markowitz, Glen S.; Fine, Paul L.; D’Agati, Vivette D.

doi:10.1053/ajkd.2002.32797

Cited by 57 publications

(32 citation statements)

References 19 publications

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“…Patients with pamidronate-associated renal toxicity may present with nephrotic syndrome which apparently is not reversible [11,24,43]. Histologically, these cases show collapsing focal segmental glomerulosclerosis, acute tubular injury, or minimal change disease without glomerular pathology [43].…”

Section: Side Effects Of Osteoclast Inhibitorsmentioning

confidence: 99%

Side Effects of Bone-Targeted Therapies in Advanced Breast Cancer

Domschke

Schuetz²

2014

Breast Care

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In up to 75% of cases, advanced breast cancer patients eventually develop bone metastases with often debilitating skeletal-related events (SREs). Osteoclast inhibitors are commonly used as therapeutic mainstay with clinical studies showing superiority of denosumab over bisphosphonates (e.g., zoledronate) for the prevention of SREs. The present review discusses the adverse event profile of these agents, and addresses the prevention and management of untoward side effects. Adverse events associated with osteoclast inhibitors comprise osteonecrosis of the jaw and hypocalcemia. Hypocalcemia is more common with denosumab, particularly in severe renal dysfunction. During therapy, the appropriate prevention of these adverse events includes close attention to dental health, avoidance of invasive dental procedures, supplementation with calcium and vitamin D unless patients are hypercalcemic, and regular monitoring of relevant serum values. Relating to the risk of nephrotoxicity, bisphosphonates but not denosumab have been incriminated. Therefore, serum creatinine levels should be checked prior to each dose of zoledronate, and in severe renal dysfunction (creatinine clearance < 30 ml/min) zoledronate is contraindicated anyway. Acute-phase reactions are particularly linked to bisphosphonates. Consequently, if these adverse events predominate, switching to denosumab is recommended.

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Section: Side Effects Of Osteoclast Inhibitorsmentioning

confidence: 99%

Side Effects of Bone-Targeted Therapies in Advanced Breast Cancer

Domschke

Schuetz²

2014

Breast Care

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“…Patients with pamidronate-associated C-FSGS present with florid NS and renal insufficiency, often have received doses of pamidronate that exceed recommended levels, and in most cases, have poor outcomes, with approximately one half showing improvement in renal function after drug discontinuation but none returning to baseline. In one patient, a partial remission was seen after discontinuation of pamidronate, the drug was later reintroduced, and proteinuria immediately worsened (9). There are rare reports of MCD and FSGS-NOS with pamidronate; not surprisingly, the best outcomes are seen in patients with MCD (10).…”

Section: Bisphosphonatesmentioning

confidence: 98%

Drug-Induced Glomerular Disease

Markowitz¹,

Bomback

Perazella

2015

Clinical Journal of the American Society of Nephrology

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100

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The potential of medications to cause kidney injury is well known. Although nephrotoxicity is most commonly associated with injury in the tubulointerstitial compartment as either acute tubular necrosis or acute interstitial nephritis, a growing body of literature has also highlighted the potential for drug-induced glomerular lesions. This review surveys the three primary patterns of drug-induced glomerular diseases stratified by the cell type at which the glomerular lesion is focused: visceral epithelial cell (or podoctye) injury, endothelial cell injury, and mesangial cell injury. A number of commonly prescribed medications, including IFNs, bisphosphonates, nonsteroidal antiinflammatory drugs, antiplatelet agents, and antiangiogenesis drugs, that are both prescribed and available over the counter, have been implicated in these iatrogenic forms of glomerular disease. Recognition of these druginduced etiologies of glomerular disease and rapid discontinuation of the offending agent are critical to maximizing the likelihood of renal function recovery.

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“…However, bisphosphonate-associated nephrotoxicity affecting both glomerular and tubular structures has been described in both case series and randomized clinical trials (35). In terms of glomerular toxicity, bisphosphonates (most commonly, pamidronate and, only rarely, zoledronate) have been associated with collapsing focal segmental glomerulosclerosis (FSGS), noncollapsing FSGS, and minimal-change disease in several case series (52)(53)(54)(55)(56). The most common lesion is collapsing FSGS, which is seen with high-dose IV pamidronate often in patients with underlying multiple myeloma and usually after repeated doses (35).…”

Section: Bisphosphonatesmentioning

confidence: 99%

Onco-Nephrology

Rosner

Dalkin

2012

Clinical Journal of the American Society of Nephrology

134

108

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SummaryHypercalcemia complicates the course of 10%-30% of all patients with malignancies and can be a sign of very poor prognosis and advanced malignancy. Prompt recognition of the nonspecific signs and symptoms of hypercalcemia and institution of therapy can be lifesaving, affording the opportunity to address the underlying etiology. The mechanisms of malignancy-associated hypercalcemia generally fall into three categories: humoral hypercalcemia due to secreted factors (such as parathyroid-related hormone), local osteolysis due to tumor invasion of bone, and absorptive hypercalcemia due to excess vitamin D produced by malignancies. The mainstays of therapy for hypercalcemia are aggressive intravenous volume expansion with saline, bisphosphonate therapy, and perhaps loop diuretics. Adjunctive therapy may include calcitonin and corticosteroids. In refractory cases, gallium nitrate and perhaps denosumab are alternatives. In patients presenting with severe AKI, hemodialysis with a low-calcium bath can be effective. In most cases, therapy normalizes calcium levels and allows for palliation or curative therapy of the malignancy.

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Nephrotic syndrome after treatment with pamidronate

Cited by 57 publications

References 19 publications

Side Effects of Bone-Targeted Therapies in Advanced Breast Cancer

Side Effects of Bone-Targeted Therapies in Advanced Breast Cancer

Drug-Induced Glomerular Disease

Onco-Nephrology

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