Sally Fitzgibbons Foundation

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RENAL MANIFESTATIONS OF PLASMA CELL DYSCRASIAS
INTRODUCTION:
Plasma cell dyscrasias are usually confronted malignancies which are mainly associated with kidney disease through the production of monoclonal immunoglobulin (Ig). Over production of monoclonal (M) protein is the result of this clonal expansion it can be either the whole immunoglobulin or its fragment (heavy or light chain alone). These disorders are unitedly called Monoclonal Gammopathy. Lytic bone disease, anemia, and immunodeficiency are some other symptoms. But renal failure is the frequent obstacles in patient with plasma cell dyscrasias that cause serious misery.
Renal failure due to this complication is identified in 20-40% of newly examined patients. Here renal failure is defined by examining serum creatinine 41.5 mg per 100 ml, and the frequency kidney impairment increases up to 30% or even 50% in some series. Although the degree of renal failure is usually moderate and serum creatinine levels are lower than 4 mg per 100 ml, in series from tertiary hospitals up to 10% of patients with newly diagnosed plasma cell dyscrasias have renal failure severe enough to require renal replacement with dialysis at the time of diagnosis.
Mechanisms of kidney failure plasma cell degeneration are grouped in to Ig dependent and Ig independent categories. Most prevalent forms of Ig-dependent kidney injury include: (1) Cast nephropathy; here casts and crystals that composed of filtered monoclonal Ig and other urinary proteins and obstruct distal renal tubules which cause tubulointerstitial nephritis. (2) AL amyloidosis; here primarily monoclonal light chains and other proteins together form ?-pleated sheets in the glomeruli and (3) MIDD (Monoclonal Immunoglobulin Deposition Disease); here intact or fragmented light chains, heavy chains, or both deposit along glomerular and in tubular basement membranes. Glomerulonephritis can occur, of either a membranoproliferative or diffuse proliferative. Patients with circulating monoclonal IgM can flourish kidney failure due to hyper viscosity or when deposits composed of monoclonal IgM obstruct glomerular capillaries. Crystalline inclusions in the proximal convoluted tubule which consist of monoclonal Ig can cause mild tubulointerstitial nephritis.
For a patient with intense kidney damage and serum or the urine detected with monoclonal Ig presents, kidney biopsy data is uncertain, since here the most common underlying pathologic pattern is tubular injury. Alkalization of the urine can increase the hazard of metastatic calcium-phosphate deposition in the kidney. And if hypercalcemia or hyper-phosphatemia is present, hypercalcemia should be handled with intravenous saline and bisphosphonate therapy (dosed for impaired renal function). Allopurinol is effective for hyperuricemia. Non-steroidal anti-inflammatory drugs and renin-angiotensin inhibitors should be avoided.5
This research focus on the different treatments used to cure the patients and choosing the best treatment.
METHODOLOGY
The research is developed using search engines such as Google and Google scholars and also make useful of library resources. The main objectives of this research is to find the different kinds of treatments because Kidney transplant has not been considered beneficial in the presence of plasma dyscrasias because the immunosuppressive therapy may increase the risk of neoplasia progression, and paraprotein may affect the graft So it is essential to find other effective treatments. And to find which treatment is better the research mainly focuses on the treatment with fewer demerits and Side effects on patients. It finds the patients with more lifetimes after the treatment.
Inclusion criteria: The research used articles and reports if they fulfilled the following criteria; Mechanism of kidney injuries, Diagnostic method and which include different kinds of treatments.
DISCUSSION
Vital medical management will correct modest degrees of renal impairment in a substantial fraction of incident patients.
Systemic therapy: Strong suspicion of renal deposition of monoclonal Ig requires prompt antiplasma cell therapy when renal function is impaired. Chemotherapeutic agents that act rapidly are preferred. Even dialysis-dependent patients benefit from systemic therapy, and a substantial minority of patients may experience long-term survival with reasonable quality of life. Bortezomib has emerged along with high-dose dexamethasone as among the most effective approaches for treating myeloma when associated kidney injury is present. It is characterized by a median time to best response of approximately 30 days in previously treated patients. As malignant plasma cells synthesize and assemble large quantities of Ig, they are particularly susceptible to proteasome inhibitors, which induce myeloma cell apoptosis in part by interfering with protein handling. Also be useful for a range of other nephrologic conditions mediated by long-lived plasma cells, including antibody-mediated kidney allograft rejection, with studies ongoing in this regard.
Stem cell transplantation: Patients with myeloma and renal failure can successfully receive SCT with an appropriately dose-reduced conditioning regimen, but toxicity is increased. 90% of myeloma patients who undergo autologous SCT will eventually relapse, allogeneic SCT offers a potential cure because of the graft-versus-myeloma effect, with acceptable treatment related mortality when reduced intensity conditioning is used.
Plasmapheresis: The high volume of distribution of light chains and IgG results in low clearance relative to body stores, and rapid plasma refill occurs after each pheresis session. Initial clinical studies provided conflicting results and the largest randomized controlled trial of more than 90 patients showed no benefit of plasmapheresis compared with usual care. An uncontrolled, retrospective analysis claimed a benefit to pheresis in the subset of patients with cast nephropathy whose light chain burden was reduced by more than 50%. Pheresis remains the standard of care in cases of hyper viscosity syndrome (seen with IgA or IgG3 subtypes) or IgM immunoglobulin.
Kidney transplantation: Kidney transplantation is occasionally contemplated as an alternative therapy to dialysis and yet multiple factors including the risk of myeloma recurrence and infection conspire against the success of transplantations in patients with plasma cell malignancies. The risk of monoclonal Ig-mediated allograft dysfunction among patients undergoing transplantation is low among patients who remain in remission if the original kidney lesion was cast nephropathy, but high among patients who had MIDD. To be considered for kidney transplantation, most centers require that patients with myeloma achieve and maintain a durable remission, typically for 3 to 5 years. For all forms of plasma cell malignancy, including MGUS, monoclonal Ig levels must be low and stable before transplantation, Pretransplantation informed consent must address the risk of early graft loss from recurrent disease and the risk that transplant immunosuppression will accelerate the underlying malignancy or premalignant condition. Kidney transplantation is feasible in highly selected patients with MIDD and amyloid who achieve complete hematologic remission from SCT.

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