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[Renal involvement in multiple myeloma. Physiopathology and therapy]
F Fiorini1, S Napoli, L Giordano
1Bussana di Sanremo (Imperia), Servizio Dialisi.
Abstract:
Renal failure (RF) is a common accompaniment of multiple myeloma and is identified in over half of patients at presentation. RF is usually related to the presence of Bence-Jones protein (immunoglobulin light chain) which damages all the compartments of the kidney: glomerule, tubulo-interstitium and vasculature. The most common renal lesion is cast nephropathy, named "myeloma kidney": Cast are produced by two mechanisms: proximal tubule damage and intratubular cast formation. The predominant pathophysiologic mechanism of tubule damage appears to be a precipitation of Bence-Jones protein and Tamm-Horsfall glycoprotein produced by cells of ascending limb of Henle's loop in the tubule lumen. The therapeutic maneuvers to reduce renal damage and preserve renal function are reduction of plasma concentration of light chain with chemotherapy, elimination of factors which favour coprecipitation of Tamm-Horsfall protein with light chain (hypercalcemia, acid urine, radiocontrast material, furosemide, oliguria). At last, colchicine (1.2 mg/day) will also be efficacious in the acute management of patients with cast nephropathy.
Insights
Renal failure in multiple myeloma is often caused by Bence-Jones protein damaging kidney structures. Treatment focuses on reducing light chain levels and avoiding factors that worsen cast nephropathy, with colchicine showing efficacy.
Area of Science:
- Nephrology
- Oncology
- Pathology