Renal water handling in rats with decompensated liver cirrhosis.

The present study was performed to investigate the renal handling of water in rats with decompensated liver cirrhosis. Liver cirrhosis was induced by intraperitoneal administration of carbon tetrachloride twice weekly for 16 wk. Control rats were treated with vehicle. The cirrhotic rats developed severe disturbances in water homeostasis: urine production was decreased and hyperosmotic, the rats had significantly decreased plasma sodium concentration and ascites, and the ability to excrete an intravenous water load was significantly impaired. Plasma concentrations of vasopressin and aldosterone were increased. Mean arterial pressure, glomerular filtration rate (GFR), and fractional lithium excretion were decreased. Acute vasopressin type 2-receptor blockade with the selective nonpeptide antagonist OPC-31260 (800 microg. kg(-1). h(-1)) was performed during conditions whereby volume depletion was prevented by computer-driven, servo-controlled intravenous volume replacement with 150 mM glucose. The aquaretic response to OPC-31260 was similar in cirrhotic and control rats. However, the OPC 31260-induced rises in fractional water excretion (delta V/GFR; +24%) and fractional distal water excretion (delta V/C(Li); +46%) were significantly increased in the cirrhotic rats, where V is flow rate and delta is change. This suggests that vasopressin-mediated renal water reabsorption capacity was increased in the cirrhotic rats. Semiquantitative immunoblotting revealed that the expression of the vasopressin-regulated water channel aquaporin-2 was unchanged in membrane fractions of both whole kidney and inner medulla from cirrhotic rats. Together, these results suggest a relative escape from vasopressin on collecting duct water reabsorption in rats with decompensated liver cirrhosis.

The natural history of insulin-dependent diabetes in Denmark: 2. Long-term survival--who and why.

Forty per cent of all Danish insulin-dependent diabetic (IDDM) patients survive for at least 40 years after diagnosis. In an attempt to identify factors influencing the probability of surviving for 40 years or more, we followed all IDDM patients diagnosed before 1943 and admitted to the Steno Memorial Hospital. Patients surviving greater than or equal to 40 years were compared with patients dying within 35 years of diabetes diagnosis. Patients dying within 35 years were characterized by male preponderance (p less than 0.01), poor metabolic control (p less than 0.05), and by less frequent attendance at a specialized care unit (p less than 0.0001). Death due to uraemia/diabetic nephropathy was also characterized by male preponderance, poor metabolic control, and few contacts with a specialized care unit but in patients dying from cardiovascular disease (CVD), no effect of sex was found, indicating that the protection from CVD found in the female non-diabetic population is absent in IDDM patients. We conclude that long-term survival with IDDM may be determined by factors susceptible to intervention such as metabolic regulation and patient attitude to their disease.

The natural history of insulin-dependent diabetes mellitus in Denmark: 1. Long-term survival with and without late diabetic complications.

All 906 patients with insulin-dependent diabetes mellitus (IDDM) diagnosed before the age of 31 years, prior to 1943, and admitted to the Steno Memorial Hospital were followed until death or until 1 January 1984. In an attempt to identify factors of prognostic importance, we compared patients dying within 35 years of the onset of diabetes with patients surviving for 40 years or more. Three hundred and seventy-seven patients survived for 40 years or more; of these 224 were still alive and invited to a re-examination, in which 184 participated. After 40 years of diabetes, the most frequent complications were impaired vision (due to diabetic retinopathy) and persistent proteinuria. However, 53% had no major complications despite 40 years with IDDM. The 184 re-examined patients (median age 60 years, median diabetes duration 47 years) were all genuine IDDM patients, as defined by stimulated C-peptide levels. Proliferative retinopathy or visual impairment was found in 56% of the 184 patients, abnormal ECG or amputations in 26%, and elevated urinary albumin excretion rate (AER) greater than or equal to 30 mg/24 h) in 45%. Twenty-five per cent had none of these complications. Proliferative retinopathy was associated with elevated AER and raised systolic blood pressure, macroangiopathy with the use of antihypertensive drugs, and proteinuria with low age at diagnosis, large increase in systolic blood pressure, smoking, and insulin-binding antibodies. Sex, age and diabetes duration were not associated with any of these three late diabetic complications.

Serum amylase during recovery from diabetic ketoacidosis.

To elucidate the mechanism of the hyperamylasaemia which is often found in diabetic ketoacidosis, 9 patients who were admitted in this disease state were studied. Blood samples were taken every 4 hours for the first 24 hours and thereafter daily for 7 days. Serum amylase concentration increased gradually in all patients, from 256 (65-1155) U/1 at the initial sampling to a maximum of 1160 (210-2670) U/1 20-24 hours later (p. greater than 0.01), median values with 95% confidence limits. Simultaneously, plasma inorganic phosphate concentrations decreased from a median value of 1.35 mmol/l to 0.45 mmol/l (p less than 0.01), and a significant negative correlation was found between the changes in these parameters in 5 patients. Isoenzyme analysis in 8 of the patients showed that hyperamylasaemia was of the "salivary type" in two and of the "pancreatic type" in two. None of the patients had clinical signs of pancreatitis. It is concluded that in diabetic ketoacidosis, the increase in serum amylase concentration observed in all patients is closely related to the action of insulin in the majority of these, and some possible mechanisms are discussed.

Non-traumatic perforation of gastric ulcer in a hiatal hernia to the pericardium.

A patient with ulcer in a hiatal hernia with perforation to the pericardial sac is reported. The symptoms and signs of non-traumatic perforation from esophagus or stomach to the pericardium or heart are described on the basis of a brief review of the literature. A prominent feature of our patient was long-standing pain in the left shoulder. We suggest that this symptom may be a warning of threatening pericardial perforation.