Mechanisms of renal failure in plasma cell dyscrasias in Ig-dependent and -independent categories
Ig-dependent mechanisms . | |
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Mechanism . | Details . |
Cast nephropathy (myeloma kidney) | Risk factors include light chain myeloma with > 10 g/day of monoclonal Ig excretion, IgD myeloma, volume depletion, sepsis, medications (see “Medication toxicity” below) |
MIDD | Often associated with kappa light chains. Systemic syndrome may be present. |
AL amyloidosis | Often associated with nephrotic-range albuminuria and lambda light chains. Systemic syndrome may be present. |
Glomerulonephritis | Membranoproliferative, diffuse proliferative, crescentic, cryoglobulinemic all recognized |
Tubulointerstitial nephritis | May also result from non-Ig mechanisms. |
Minimal change or membranous glomerulopathy | Albuminuria is typically present, in addition to light chain proteinuria |
Henoch-Scholein purpura/IgA nephropathy | Associated with IgA myeloma |
Immunotactoid and fibrillary glomerulopathy | Rare conditions |
Intracapillary monoclonal deposits of IgM thrombi | Associated with Waldenström macroglobulinemia |
TMA | Paraprotein causes endothelial injury with resulting TMA |
Hyperviscosity syndrome | Most common with Waldenström macroglobulinemia |
Ig-dependent mechanisms . | |
---|---|
Mechanism . | Details . |
Cast nephropathy (myeloma kidney) | Risk factors include light chain myeloma with > 10 g/day of monoclonal Ig excretion, IgD myeloma, volume depletion, sepsis, medications (see “Medication toxicity” below) |
MIDD | Often associated with kappa light chains. Systemic syndrome may be present. |
AL amyloidosis | Often associated with nephrotic-range albuminuria and lambda light chains. Systemic syndrome may be present. |
Glomerulonephritis | Membranoproliferative, diffuse proliferative, crescentic, cryoglobulinemic all recognized |
Tubulointerstitial nephritis | May also result from non-Ig mechanisms. |
Minimal change or membranous glomerulopathy | Albuminuria is typically present, in addition to light chain proteinuria |
Henoch-Scholein purpura/IgA nephropathy | Associated with IgA myeloma |
Immunotactoid and fibrillary glomerulopathy | Rare conditions |
Intracapillary monoclonal deposits of IgM thrombi | Associated with Waldenström macroglobulinemia |
TMA | Paraprotein causes endothelial injury with resulting TMA |
Hyperviscosity syndrome | Most common with Waldenström macroglobulinemia |
Ig-independent mechanisms . | |
---|---|
Mechanism . | Details . |
Volume depletion or sepsis | Can cause acute tubular necrosis and/or precipitate cast nephropathy |
Hypercalcemia | Can precipitate cast nephropathy |
Tumor lysis syndrome | Uric acid or phosphate nephropathy |
Medication toxicity | Zoledronate: acute renal failure |
Pamidronate: collapsing focal segmental glomerulosclerosis | |
Nonsteroidal anti-inflammatory drugs, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, loop diuretics, or IV contrast can precipitate cast nephropathy | |
Direct parenchymal invasion by plasma cells | Associated with advanced or aggressive myeloma |
Pyelonephritis | Immunodeficiency from myeloma, deficient Ig, and chemotherapy all contribute |
Ig-independent mechanisms . | |
---|---|
Mechanism . | Details . |
Volume depletion or sepsis | Can cause acute tubular necrosis and/or precipitate cast nephropathy |
Hypercalcemia | Can precipitate cast nephropathy |
Tumor lysis syndrome | Uric acid or phosphate nephropathy |
Medication toxicity | Zoledronate: acute renal failure |
Pamidronate: collapsing focal segmental glomerulosclerosis | |
Nonsteroidal anti-inflammatory drugs, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, loop diuretics, or IV contrast can precipitate cast nephropathy | |
Direct parenchymal invasion by plasma cells | Associated with advanced or aggressive myeloma |
Pyelonephritis | Immunodeficiency from myeloma, deficient Ig, and chemotherapy all contribute |
Ig indicates immunoglobulin; MIDD, monoclonal Ig deposition disease; TMA, thrombotic microangiopathy; and IV, intravenous.