Ileal Tuberculosis Causing Hypercalcemia and Renal Failure.

Hypercalcemia rarely causes acute pancreatitis due to secretory block in the pancreas and damage by accumulated proteases. Hypercalcemia, though described in granulomatous disorders, is uncommon in tuberculosis. Acute kidney injury is known to occur with acute pancreatitis, secondary to sepsis and septic shock; however, acute pancreatitis resulting in acute cortical necrosis is very rare. We report a 22-year-old woman, who presented with pain abdomen and vomiting. She was found to have features of acute pancreatitis, both biochemically and radiologically. She had hypercalcemia on presentation and this was attributed to be the cause for pancreatitis as other causes were ruled out. 1, 25-dihydroxyvitamin D level was high with normal parathyroid hormone level. Whole-body positron emission tomography-computed tomography showed increased fluorodeoxyglucose uptake in the terminal ileum and histology from that area showed noncaseating granuloma with acid-fast bacilli in the tissue. She was treated with antituberculosis therapy; hypercalcemia improved over a period of time and pancreatitis resolved. She developed anuric renal failure, and kidney biopsy showed patchy acute cortical necrosis. She is dialysis dependent at the end of 6 months. To the best of our knowledge, this is the first case report of a patient with ileal tuberculosis presenting with hypercalcemia and acute pancreatitis. This case is reported due to the rarity of extrapulmonary tuberculosis presenting with symptomatic hypercalcemia, acute pancreatitis, and acute renal cortical necrosis.

Lactate levels and risk of lactic acidosis with metformin in diabetic kidney disease patients.

Metformin as an oral antidiabetic drug (OAD) is not recommended in renal failure due to the presumed risk of lactic acidosis though it has advantages in cardiovascular protection with a low risk of hypoglycemia. Few studies have measured lactic acid blood levels in patients with diabetic kidney disease on metformin and demonstrated lactic acidosis. The aim of our study is to see if patients with diabetic kidney disease are at risk of elevated lactate blood levels and lactic acidosis. Lactate levels and blood pH were estimated in patients with type 2 diabetes mellitus receiving metformin in different stages of chronic kidney disease (CKD) and were compared with a similar group not receiving metformin. Patients with diabetic kidney disease, with estimated glomerular filtration rate <60 mL/min who were previously receiving metformin started in centers elsewhere and referred here were studied and compared with a similar group taking other OADs or insulin. Independent sample t-test or ANOVA were used to compare quantitative variables between groups. Pearson correlation was used to analyze association between quantitative variables and linear regression analysis and was employed to note the relationship between quantitative variables. Of 57 patients who received a mean dose of 1.134 grams of metformin, 33 (55.9%) were in stage 3, 16 (28.1%) in stage 4, and 8 (14%) in stage 5 CKD. Mean serum pH (P = 0.572), bicarbonate (P = 0.978), and plasma lactate (P = 0.449) levels in those taking and not taking metformin were comparable. There was no difference in the plasma lactate levels in different stages of CKD in the metformin group (P = 0.498) although there was significant correlation with metformin dose (P <0.05). Blood lactate levels were not elevated in patients with diabetic kidney disease at a daily dose of metformin <1 g.

Combined surgical and immunosupressive therapy for encapsulating peritoneal sclerosis.

Encapsulating peritoneal sclerosis (EPS) is an infrequent but serious complication of long-term peritoneal dialysis with 50% mortality and lack consensus on treatment. The pathogenesis of EPS is ill understood, and diagnosis lacks specificity and relies on clinical, radiographic and microscopic evaluation. Since there is no general agreement on managing EPS, we report a case treated successfully with surgery followed by immunosuppressive therapy with tamoxifen and steroids. He later successfully underwent deceased donor renal transplantation.