PD treatment for severe congestive heart failure.

Our objective was to evaluate if peritoneal dialysis (PD) could improve survival of patients with progressive severe congestive heart failure resistant to drug therapy. The patients were selected by the cardiologist in cooperation with a nephrologist, including patients not responding to conventional medication with an expected fatal outcome within the next months. The study included 16 consecutive patients with a chronic progressive severe refractory heart failure (sHF) of NYHA class III (n = 6) or IV (n = 10) who did not respond to diuretics and angiotension converting enzyme (ACE) inhibitors. They had a mean age of 60 years (+/- 14, range 30-75, median 62 years). Nine of the patients had sHF as the only reason for initiating PD (all NYHA IV), while 7 also needed dialysis due to uremia. Five of 7 had been on hemodialysis but switched to PD due to a progressive congestive sHF. In 2 patients, PD was decided already at start of dialysis therapy due to the severity of their heart failure. The reason for sHF was: valvular dysfunction (n = 5) with defect prosthesis (n = 3); in the course of a myocardial infarction (n = 4); and cardiomyopathy (n = 4). Tenckhoff catheters were inserted under local anesthesia and ultrafiltration was started and maintained until discharge. The survival time and change in heart size by x-ray was used for analyses. All patients improved their stage of congestive heart failure by NYHA classification already during the first month. Six patients died during the follow-up period due to cardiac reasons (sudden death, relapse of sHF) after a mean of 10.7 months (+/- 3.7, range 1-24 months). Ten were alive after a median observation period of 10 months (+/- 12.5, range 1-36 months). Heart size was reduced in 15 of the patients. Three of the patients with sHF but without uremia could stop the PD. The results showed that ultrafiltration by PD was easy to perform despite low initial blood pressure. The sHF was reduced and life span was prolonged with improved quality of life.

Nutritional magnesium supplementation does not change blood pressure nor serum or muscle potassium and magnesium in untreated hypertension. A double-blind crossover study.

The aim of this study was to evaluate if a nutritional dose of magnesium given orally changes the blood pressure in untreated hypertensive patients and if orally-given magnesium had any influence on serum and muscle magnesium and potassium. A randomized, double-blind crossover study design was followed with magnesium 15 mmol/day or placebo treatment for two months. Thirty-nine patients aged 20-59 years, were treated. Samples for magnesium and potassium in blood, muscle and urine were taken at entry time, after two months (crossover time) and after four months (end of study). Systolic and diastolic supine and standing blood pressures were measured at the same times. No significant change in blood pressure, serum or muscle concentrations of electrolytes were observed on magnesium treatment. Urine magnesium rose significantly on magnesium, and it decreased significantly on placebo. Therefore results suggest that 15 mmol magnesium/day, given to untreated mild-to-moderate hypertensives does not alter blood pressure nor the concentrations of magnesium and potassium in serum and muscle, in patients with normal magnesium turnover.

Nutritional dose of magnesium in hypertensive patients on beta blockers lowers systolic blood pressure: a double-blind, cross-over study.

OBJECTIVES: To evaluate if magnesium alters blood pressure in hypertensive patients treated with beta blockers and if such effect can be coupled to a change in potassium and magnesium levels in muscle, serum and urine. DESIGN: A randomized double-blind, cross-over study with magnesium and placebo taken orally, each for 8 weeks. SETTING: Outpatient clinic, University Hospital, Umeå, Sweden. SUBJECTS: Thirty-nine patients aged 26-69 years with moderate essential hypertension, treated before entry and during the study with continuous, unchanged beta blockers completed the study. INTERVENTIONS: Random allocation to receive magnesium aspartate or placebo. Daily magnesium dose was 15 mmol (365 mg) distributed three times a day over 8 weeks. MAIN OUTCOME MEASURES: Blood pressure, serum, urine and muscle magnesium and potassium. Measurements performed at the start, after 8 and 16 weeks. RESULTS: Systolic supine and standing blood pressure significantly decreased when magnesium was supplemented following placebo but not when magnesium was given at start. When magnesium and placebo groups were independently compared there was no significant change in supine and standing systolic and diastolic pressure. Serum and urine magnesium and serum potassium were significantly higher after magnesium treatment, whilst no change was present in urine potassium or in muscle magnesium and potassium. CONCLUSIONS: This study showed that 15 mmol magnesium day-1 given to mild to moderate hypertensive patients treated with beta blockers could be the cause of a significant decrease in supine and standing systolic blood pressure.

The dose-dependent reduction in blood pressure through administration of magnesium. A double blind placebo controlled cross-over study.

Seventeen patients with a diastolic blood pressure over 90 mm Hg were recruited from a running health screening program to participate in a double blind cross-over study of magnesium supplementation (15 mmol Mg2+/day (Emgesan, Kabi Pharmacia) for 3 weeks, followed by 30 mmol Mg2+/day for another 3 weeks, finishing with 40 mmol Mg2+/day for a final 3 weeks). A significant decrease in the mean systolic blood pressure was recorded from 154.0 +/- 10.7 mm Hg to 146.1 +/- 16.9 mm Hg (P = .031) while the mean diastolic blood pressure decreased from 100.2 +/- 4.2 mm Hg to 92.0 +/- 6.6 mm Hg (P = .0001).

Nephrotoxicity of contrast media in patients with diabetes mellitus. A comparative urographic and angiographic study with iohexol and metrizoate.

A double-blind urographic and angiographic study was done with the ionic contrast medium meglumine metrizoate and the non-ionic iohexol in 90 patients with diabetes mellitus. Twenty patients were insulin dependent, and 70 non-insulin dependent diabetics. Diabetic patients with decreased as well as normal renal function prior to the examination sustained a reversible and small increase in the plasma creatinine level postexamination. The small increase caused by meglumine metrizoate was significantly higher than the increase caused by iohexol. There was also a significantly higher increase in plasma creatinine among the patients with diabetic nephropathy compared with those without nephropathy.

Cadmium concentration in human kidney biopsies.

This study reports the cadmium concentration and histopathology of kidney tissue from 29 patients with clinical findings that motivated a diagnostic percutaneous kidney biopsy and/or a history of possible exposure to cadmium. Cadmium was found in all specimens examined including those from controls. In the patients, the mean cadmium concentration was 12.9 (0.6-45.0) micrograms cadmium per g wet kidney tissue. The highest concentrations (30-45 micrograms/g) were found in three patients with morphological and clinical findings of tubulo-interstitial damage. Patients with signs of tubulo-interstitial disease had higher mean cadmium concentrations than those with glomerular changes, and patients with normal blood pressure had higher concentrations than those with diastolic hypertension. In a control group of 22 autopsies, the mean cadmium concentration was 8.7 (2.9-22.4) micrograms/g. The mean difference between the right and the left kidney was 2.3 (0.9-9.6) micrograms/g. Laboratory findings in patients with cadmium nephropathy were nonspecific. Thus, in patients with interstitial nephritis and cadmium exposure, a biopsy for the analysis of kidney cadmium concentration may be motivated. The combination of morphological and clinical findings of interstitial nephritis and a high concentration of cadmium in biopsied kidney tissue indicates cadmium nephropathy.

Arteriographic evaluation of postsurgical stomach.

Visceral arteriography was performed in 35 adult patients who had undergone various types of gastric surgery. Nineteen of these patients had presented with gastrointestinal hemorrhage at different postoperative intervals (4 days-23 years). Arteriography showed the bleeding site in 14 (74%) and permitted its nonoperative control in 8 cases. Diffuse hemorrhage from the gastric pouch as well as localized bleeding from suture line, marginal or stress ulcers, and other sources were recognized. Arteriography was also crucial in the diagnosis of iatrogenic arteriovenous fistulas, telangiectasia in the anastomotic regions, inadvertently ligated arteries, and postoperative changes in the vascular architecture. Value and limitations of arteriography of the postsurgical stomach are presented together with a review of the pertinent literature.

Fatal reaction following renal angiography and biopsy in diabetic patients with Azotemia.

Severe reactions to contrast media in two diabetic patients with azotemia are described. Both patients also showed signs of immunopathy. The reaction was fatal in one of them. Little is known about contrast media reactions and their natural history. Patients with diabetes mellitus and impaired renal function should be studied with caution and with careful consideration of the indication for the procedure. If an examination with contrast media is considered unavoidable, all diabetic patients with renal failure should be supervised closely to detect the development of acute renal failure. Dehydration should be avoided. Careful monitoring of blood glucose, serum electrolytes, serum creatinine and blood pressure will aid in the early detection of the adverse reaction.