Mucormycosis-induced hypercalcemia: a case report.

Hypercalcemia is a vital laboratory marker because it can show underlying severe diseases like cancer and infections. Of all the causes of hypercalcemia, primary hyperparathyroidism, and malignancies are the most common, but granulomatous diseases, such as certain fungal infections, can also be the cause. Here we describe the case of a 29-year-old woman, an insulin-dependent diabetic, found unconscious and tachypneic at home. In the emergency room, the medical team diagnosed diabetic ketoacidosis (DKA) and acute kidney injury (AKI). During hospitalization, despite resolving acidemia, persistent hypercalcemia attracted attention. Laboratory tests showed decreased parathyroid hormone (PTH) levels, confirming non-PTH-dependent hypercalcemia. Computed tomography (CT) of the chest and abdomen demonstrated no alterations, but an upper digestive endoscopy revealed an ulcerated and infiltrative lesion in the stomach. A biopsy showed a granulomatous infiltrate due to mucormycosis infection. The patient received liposomal amphotericin B for 30 days and isavuconazonium for two months. Serum calcium levels improved during treatment. Inquiry of the etiology of hypercalcemia should begin with the PTH assay; high levels are consistent with hyperparathyroidism; low levels, with calcium or vitamin D intoxication, malignancies, prolonged immobilization, and granulomatous diseases. In the latter cases, the overproduction of 1-alpha-hydroxylase by the granulomatous tissue increases the conversion of 25(OH)vitamin D into 1-25(OH)vitamin D, which causes the intestinal absorption of calcium. We have described the first hypercalcemia related to mucormycosis infection in a young diabetic patient, although case presentations associate other fungal infections with elevated serum calcium.

Pharmacotherapy of chronic kidney disease and mineral bone disorder.

INTRODUCTION: Disturbances of the bone and mineral metabolism are a common complication of chronic kidney disease (CKD); these disturbances are known as CKD-mineral bone disorder (CKD-MBD). A better understanding of the pathophysiological mechanisms of CKD-MBD, along with its negative impact on other organs and systems, as well as on survival, has led to a shift in the treatment paradigm of this disorder. The use of phosphate binders changed dramatically over the last decade when noncalcium-containing phosphate binders, such as sevelamer and lanthanum carbonate, became possible alternative treatments to avoid calcium overload. Vitamin D receptor activators, such as paricalcitol and doxercalciferol, with fewer calcemic and phosphatemic effects, have also been introduced to control parathormone production and the interest in native vitamin D supplementation has grown. Furthermore, a new drug class, the calcimimetics, has recently been introduced into the therapeutic arsenal for treating secondary hyperparathyroidism. AREAS COVERED: This review discusses the advantages and disadvantages of the above pharmacological options to treat CKD-MBD. EXPERT OPINION: The individual-based use of phosphate binders, vitamin D and calcimimetics, separately or in combination, constitute a reasonable approach to treat CKD-MBD. These treatments aim to achieve a rigorous control of phosphorus and parathormone levels, while avoiding calcium overload.

Over 500 pancreas transplants by a single team in São Paulo, Brazil.

Pancreas transplantation (PT) remains a developing practice in Latin America. From 1996 to 2009, 506 PTs were performed by our team in the following categories: simultaneous pancreas-kidney (SPK), simultaneous deceased donor pancreas and living-donor kidney (SPLK), pancreas after kidney (PAK), and pancreas transplant alone (PTA). Enteric drainage was preferred for SPK and bladder drainage for solitary PT or SPLK. Immunosuppression was with tacrolimus, mycophenolate mofetil, and steroids, and anti-lymphocytic drugs were used to induce solitary PT and SPLK. The series includes 254 SPK, 60 SPLK, 94 PAK, and 98 PTA. The one-yr patient survivals were 82% for SPK, 90% for SPLK, 95% for PTA, and 93% for PAK. The one-yr pancreas graft survivals were 70% for SPK, 86% for SPLK, 86% for PAK, and 77% for PTA. The one-yr kidney graft survivals were 77.5% for SPK and 89% for SPLK. This represents the largest reported PT series in Latin America. Results comparable to those of developed countries were achieved, with the exception of the SPK category. This has led our program to prioritize solitary PT and SPLK.

Urothelial carcinoma transmission via kidney transplantation.

Transmission of urothelial carcinoma via solid organ transplant has never been reported in the literature to our knowledge. We report a case of transmission of this tumour to a kidney recipient. The donor was a 37-year-old woman, victim of a subarachnoid haemorrhage. The recipient was a 21-year-old girl, with a history of chronic kidney disease secondary to neurogenic bladder. This fatality has been rarely described in literature, but never with this histological type of cancer. Nowadays, with the expanded criteria for donation, older people are accepted as donor because of the shortage of organs. However, this may increase the likelihood of the number of cancer transmission.

Electrolyte disturbances and acute kidney injury induced by imatinib therapy.

Imatinib mesylate is an anticancer agent that selectively inhibits protein kinases involved in the pathophysiology of cancer. It is now the first-line therapy for patients with chronic myeloid leukaemia (CML) and is generally well tolerated. Here, we describe a case of a patient receiving imatinib for CML. The patient developed renal failure accompanied by severe hypophosphataemia, hypokalaemia and hypomagnesaemia. We discuss the pathophysiological characteristics of imatinib-induced renal injury, and we demonstrate that these electrolyte disturbances were caused by increased urinary excretion of phosphate and potassium. Early diagnosis and correction of imatinib-induced renal injury and electrolyte disorders can improve clinical outcomes.