Renal failure in multiple myeloma is frequent; It is present in 20-40% of cases at the time of diagnosis, and is a factor of prognosis. Myeloma kidney and hypercalcemia are the most frequent causes; other factors that can contribute are dehydration, hyperuricemia, iodinated contrast and nephrotoxic drugs. Repeated episodes of hypercalcemia can produce deposits of calcium salts in tissues, especially in those with an alkaline medium such as the kidneys, lungs or the gastric mucosa. We present the case of a 38 year-old man with severe hypercalcemia, acute renal failure, multiple myeloma, metastatic and multiorgan failure calcinocis.
Renal failure as first manifestation of multiple myeloma.
In multiple myeloma, renal failure and hypercalcemia occurs by increase of bone resorption by osteoclast activation due to an overactive receptor RANK/RANK-L. Renal failure occurs due to injury in the renal tubular epithelium that alters the ability to concentrate urine and sometimes cause epithelial cell necrosis and obstruction of the tubules, being able to produce stasis and calcium deposits in the kidney.
The treatment must establish quickly with hydration and therapy antimieloma, including steroids. Calcitonin inhibits bone resorption without the risk of Nephrotoxicity, but its hipocalcemiante effect is modest and transient.
Bisphosphonates are potent inhibitors of osteoclasts, are very effective in severe hypercalcemia, but run the risk of renal toxicity and hypocalcemia; the most commonly used are pamidronate and zoledronic acid, the latter is not recommended when creatinine levels are greater than 3 mg/dl.
There are some studies that advise the use of ibandronate to be the less nephrotoxic in patients with renal failure, even some authors have used the ibandronate in patients with myeloma and renal failure, hypercalcemia or nephrocalcinosis, with recovery of renal function and calcium levels.
Oliguric renal failure must start hemodialysis. In the case we present we began with calcitonin and daily hemodialysis treatment, but the patient presented a rapid evolution with multiorgan failure and respiratory distress by tumoral calcinosis.
We conclude on the need to closely monitor the levels of calcium in patients with multiple myeloma and early start therapeutic measures. Bisphosphonates and more effective therapy in renal failure, are recommended in cases of malignant hypercalcemia used the less nephrotoxic adjusted dose.
Renal failure in multiple myeloma
To measure the population ageing expected an increase in cases of dyscrasia of plasma cells and hence kidney failure associated with the paraproteinemia apneic.
At the time of the diagnosis of multiple myeloma, up to 50% of the patients presented some degree of commitment to renal function. Besides the excretion of light chains, there are other factors responsible for the azotaemia as hypercalcaemia, dehydration and nephrotoxic substance use. The renal compromise is clearly associated with the high tumour mass and is more evident in patients with more advanced stages of the disease.
The presence of renal failure does not modify the response of the tumor to chemotherapy and is not a mortality prognostic factor. 95% of patients recover kidney function in the four months following the diagnosis and only 1% requires permanent renal replacement therapy. In the initial management of patients should be deemed the use of plasmapheresis and chemotherapy in high doses seeking to avoid irreversible renal failure.
In those patients with controlled disease and without significant comorbidity must be considered, if necessary, renal replacement therapy including the kidney transplant.
Kidney failure is the single factor with most unfavorable prognostic influence. However, the most important prognostic factor is the sensitivity of cloned it mielomatosa to cytostatic treatment. With chemotherapy is reached an objective response in about 50% of patients persisting for 1-2 years, out of which usually occurs a relapse. The response to treatment is less durable. Infection is the most common cause of death.