|Nefrologia 2011;31(2):233-234 | Doi. 10.3265/Nefrologia.pre2010.Nov.10668|
|Multiple myeloma, severe hypercalcaemia, acute renal failure and multiple organ failure due to calcinosis|
|Mieloma múltiple, hipercalcemia severa, insuficiencia renal aguda y fallo multiorgánico por calcinosis|
|Enviado a Revisar: 26 Oct. 2010 | Aceptado el: 16 Nov. 2010 | En Publicación: 22 Mar. 2011|
|J.G. Martínez Mateu, G.P. Losada González, M.A. Munar Vila , M. Uriol Rivera, G. Gómez Marqués, A.C. Tugores|
|Departamento de Nefrología. Hospital Son Dureta. Palma de Mallorca, Islas Baleares (Spain)|
|Correspondencia para J.G. Martínez Mateu, Departamento de Nefrología, Hospital Son Dureta, Palma de Mallorca, Islas Baleares|
To the Editor,
Renal failure in multiple myeloma is frequent; it is found in 20%-40% of cases at diagnosis and is an unfavourable prognostic factor. Myeloma kidney and hypercalcaemia are the most frequent causes. Other contributing factors are dehydration, hyperuricaemia, nephrotoxic drugs and iodine contrasts. Repeated episodes of hypercalcaemia can produce calcium salt deposits in tissues, especially those with an alkaline medium, such as kidneys, lungs or gastric mucosa. We present the case of a 38-year-old man, with multiple myeloma, severe hypercalcaemia, acute renal failure, metastatic calcinosis and multiple organ failure.
The patient had no pathological history, was a smoker of 40 cigarettes/day, and an alcohol consumer. He visited the emergency department with general polymyalgia, nocturia, and oedemas around the ankles for one week. For 48 hours before his visit, he had taken paracetamol every 8 hours.
In the physical examination he had mucocutaneous paleness. Blood pressure: 120/70; temperature: 37.4ºC; auscultation: normal. Abdominal palpation: no findings. Lower limbs had no oedemas.
Laboratory tests showed creatinine: 9.8mg/dl; urea: 198mg/dl; haemoglobin: 9.8g/l; potassium: 4.7mEq/l; sodium: 134mEq/l; haemoglobin: 9.6mg/dl; haematocrit: 27%; leukocytes: 15 900 with 71% neutrophils; platelets: 135 000; creatine phosphokinase (CPK): 4.62IU/l; calcium: 15mg/dl; ionic calcium: 7.71mg/dl. Sediment: proteinuria: 300mg/dl; red blood cells: 5/10/high power field (HPF); leukocytes: 0-5/HPF. The kidney ultrasound showed that the kidneys were of normal size, no hydronephrosis, and increased echogenicity. The chest X-ray was normal. Tests pointed towards acute renal failure with severe hypercalcaemia. Daily haemodialysis was started with low calcium concentrations in the solution and subcutaneous calcitonin. On the third day after admission, the patient developed acute respiratory failure and neurological deterioration. He was therefore transferred to the ICU, with suspected tumoural hypercalcaemia requiring thoracic and cranial CT scans and proteinogram. We observed bilateral alveolar infiltration, right fronto-tempo-parietal subdural haematoma with subfalcine and transtentorial herniation. The haematoma was surgically drained and the patient died 8 hours after the intervention. Monoclonal IgG kappa was detected in the proteinogram. An autopsy was carried out, diagnosing multiple myeloma kappa, affecting the bone marrow; metastatic calcification mainly in the kidneys, stomach, lungs, liver and vessels, and pulmonary haemorrhage with respiratory distress.
Hypercalcaemia is produced in patients with multiple myeloma due to the increased bone resorption caused by osteoclast activation, especially due to the hyperactivity of the RANK/RANK-L receptor. Kidney failure is produced by lesions on the renal tubular epithelium, which alters the ability to concentrate urine and sometimes causes epithelial cell necrosis and obstruction of the tubules. This can then lead to stasis and calcium deposits in the kidney. Treatment should be started quickly, ensuring the patient is hydrated and using anti-myeloma therapy, including steroids. Calcitonin inhibits bone resorption without risk of nephrotoxicity, but its hypocalcaemic effect is modest and transitory. Bisphosphonates, potent osteoclast inhibitors, are very effective for severe hypercalcaemia, but are a risk for kidney toxicity and hypocalcaemia. The most used are pamidronate, and zoledronic acid, but the latter is not recommended when creatinine levels are above 3mg/dl. Some studies recommend using ibandronate for patients with renal failure, as it is less nephrotoxic, and some authors have even used ibandronate for patients with myeloma and renal failure caused by hypercalcaemia or nephrocalcinosis, recovering renal function and calcium levels. Haemodialysis must be started for oliguric renal failure cases. In our case, we started treatment with calcitonin and daily haemodialysis, but the patient’s condition progressed rapidly, with multiple organ failure and respiratory distress due to tumoural calcinosis. In conclusion, we must highlight the need to closely monitor calcium levels in patients with multiple myeloma and start therapeutic measures early. For cases of malignant hypercalcaemia, we recommend bisphosphonates as be the most effective therapy, and for renal failure the least nephrotoxic drugs at an adjusted dosage.
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