Extreme hyperglycemia with ketoacidosis and hyperkalemia in a patient on chronic hemodialysis.

A patient on hemodialysis for end-stage renal disease secondary to diabetic nephropathy was admitted in a coma with Kussmaul breathing and hypertension (232/124 mmHg). She had extreme hyperglycemia (1884 mg/dL), acidosis (total CO(2) 4 mmol/L), hyperkalemia (7.2 mmol/L) with electrocardiographic abnormalities, and hypertonicity (330.7 mOsm/kg). Initial treatment with insulin drip resulted in a decrease in serum potassium to 5.3 mmol/L, but no significant change in mental status or other laboratory parameters. Hemodialysis of 1.75 hours resulted in rapid decline in serum glucose and tonicity and rapid improvement of the acidosis, but no change in mental status, which began to improve slowly after the hemodialysis was stopped, but with ongoing treatment with continuous insulin infusion. The rate of decline in tonicity during hemodialysis (14.5 mOsm/kg/h) was high, raising concerns about neurological complications. In this case, extreme hyperglycemia with ketoacidosis, hyperkalemia, and coma developing in a hemodialysis patient responded to insulin infusion. Monitoring of the clinical status and the pertinent laboratory values is required to assess the need for other therapeutic measures including volume and potassium replacement and emergency dialysis. The indications for and risks of emergency dialysis in this setting are not clearly defined.

Tumoral calcinosis without hyperparathyroidism in a patient on continuous ambulatory peritoneal dialysis.

Reports of tumoral calcinosis (TC) in peritoneal dialysis (PD) patients are rare. Reported PD patients with TC also had hyperparathyroidism. A 67-year-old man on continuous ambulatory PD for almost 3 years developed TC of the right wrist and knee and both shoulders and feet. In the 2 years preceding the diagnosis of TC, this patient's serum parathyroid hormone levels were consistently low (17 +/- 12 pg/ mL). Hypercalcemia had been found in 32% of the serum samples, hyperphosphatemia in 91%, and elevated Ca x P product in 78% of the samples. At presentation with TC, serum C-reactive protein was elevated, and serum levels of vitamin D compounds were below normal. Four months after the diagnosis of TC, the patient died with a combination of gastrointestinal and retroperitoneal bleeding episodes and septic events. Tumoral calcinosis may develop in PD patients without hyperparathyroidism. Sustained hyperphosphatemia and high Ca x P product are important in the pathogenesis of uremic TC. Elevated indices of inflammation may accompany TC. Studies are needed to identify other important factors in the pathogenesis of TC in PD patients and to evaluate treatment methods.