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Angioplasty was performed in 16 patients with renal artery occlusion. It was successful in each of six acute occlusions, although four patients died later of their underlying disease. Two patients are long-term survivors and have normal or compensated renal function up to three years postoperatively. Vessel reconstruction was successful in eight of ten patients with chronic occlusion. In seven there was definite improvement or normalization of the hypertension, in six renal function returned to normal. Thus the success rate as to organ preservation with improvement in pressure and function was 60%.

In 67 patients thought to have renovascular hypertension, plasma renin activity was measured in both renal veins and peripherally (common femoral v.) before and after administration of 25 mg captopril. Other antihypertensive medication, except diuretics and ACE inhibitors, had been discontinued. The renin ratio, renin secretion indices before and after ACE inhibition, as well as the percentage rise in peripheral plasma renin activity, after captopril were calculated from the measured data. The diagnostic and prognostic value of the various calculation models were compared on the basis of blood pressure changes in 29 patients after intervention (28 operations, one percutaneous transluminal angioplasty). Of the various calculations the renin ratio after ACE stimulation--measuring plasma renin activity separately for each side--was of the greatest value in discriminating for renovascular hypertension (sensitivity 89%, specificity 100%). Comparable results in the discrimination for renovascular hypertension were achieved by determining the rise in peripheral plasma renin activity after captopril. This method is, therefore, a simple, noninvasive test for diagnosing renovascular hypertension with great accuracy even while existing medication is being continued.

Treatment of diabetics with end-stage renal failure is still a hazard. We report on 33 insulin-dependent diabetic patients who were treated with CAPD over a period of up to 70 months. Seven of them have been transplanted. The evaluation of the clinical and biological parameters serum protein, phosphate, calcium, revealed acceptable values. Hemoglobin rose during the treatment period. Hypertension improved and medication was reduced. HbAlc levels were near normal with subcutaneous application of insulin. Peritonitis rate was 1/18 patient-months. Survival rate was comparable with other centers with 83% in the first and 62% in the second year. In 7 patients that have been transplanted no CAPD-related problems arose after transplantation. 6 of them are still doing well; one returned to CAPD because of graft failure. In conclusion, because of good control of hypertension, blood glucose and anemia and the avoidance of fluctuating volumes, we think CAPD to be the best method for diabetics awaiting transplantation and for those that cannot be transplanted.

With a daily maintenance dose of 0.1 mg digitoxin a mean steady state digitoxin serum concentration of 17.0 +/- 3.2 ng/ml was measured in 10 male probands. When 750 mg of quinidine bisulphate were administered at the same time digitoxin concentration increased significantly to 22.4 +/- 4.2 ng/ml (P less than 0.0005). The serum half life of digitoxin during quinidine treatment was significantly increased to 10.8 +/- 2.1 days compared to a control group with 7.6 +/- 1.6 days (P less than 0.0025). Protein binding of digitoxin, renal digitoxin excretion and renal digitoxin clearance were equally uninfluenced by quinidine as were endogenous creatinine clearance and sodium and potassium excretion in urine. In two patient with cardiac insufficiency there was likewise a significant increase in digitoxin serum concentration. For clinical application of combined therapy of quinidine and digitoxin the danger of digitalis intoxication seems to be less in comparison to digoxin as increase of digitoxin concentration in serum is lower than of digoxin.

It has been shown that fatal "poisoning" with the mushroom species Paxillus involutus is caused by antibodies against the fungus in sensitized patients. Because circulating immune complexes play an important role, therapeutic procedures which can eliminate those complexes could stop immune hemolysis. A 37-year-old patient became severely ill after repeated ingestion of sufficiently cooked Paxillus involutus. As a result of hemolysis with reversible shock symptoms, acute renal failure developed. Plasma exchange with 3,000 ml albumin 5% was carried out daily during the first 3 days after admission. Each plasma exchange lowered free hemoglobin and immune complex levels by 60%-75%. Acute renal failure was successfully treated with hemodialysis. Specific IgG-antibodies against membrane particles of Paxillus involutus were detected by hemagglutination tests in the serum of the patient. The sequence of reactions resulting from the testing procedures strongly suggests the formation of immune complexes. These complexes are likely to bind to erythrocytes acting as innocent bystanders. Activation of the complement system finally results in hemolysis and shock. In addition to adequate shock treatment elimination of these immune complexes by plasma separation seems to be the therapy of choice.

Sixty-four percutaneous renal biopsies under ultrasound guidance done in 60 patients with renal impairment are compared with 33 open, operative biopsies. In 62 percutaneous biopsies (96.8%), more than 3 glomeruli could be obtained. Eight biopsies (12.5%) presented with minor complications afterwards. All of them were spontaneously reversible. In the operative biopsy group, there were complications in 6 patients (18.2%). In 2 cases, operative revision was necessary. In conclusion, percutaneous ultrasound guided biopsy in experienced hands offers several advantages in patients with renal impairment. It must be kept in mind that from a minority of patients only an operative biopsy can be taken due to certain risks.

Chronic progressive of relapsing inflammatory polyneuropathy (CRIP) can be treated effectively with immunosuppressive drugs and/or plasma exchange (PE). This report describes a patient who responded dramatically and reproducibly to PE during four successive relapses and remained in remission while on medical immunosuppression with azathioprine and corticosteroids. The clinical course was closely correlated with electrophysiologic parameters such as compound muscle action potential amplitudes and distal latencies. The purified IgG fraction of PE filtrate bound to rat and human sciatic nerve on immunohistochemistry. Furthermore, a similar staining pattern was achieved by purified Fab fragments, which was absent in all control preparations. These findings support the hypothesis that circulating plasma factors may play a role in CRIP and that one of these factors may be an IgG antibody to peripheral nerve components.

Renin activity, angiotensin-II concentration and venous aldosterone concentration were measured in 20 healthy subjects and 18 hypertensives before and after stimulation of the renin-angiotensin-aldosterone system. The test did not distinguish between the two groups: in the individual case there was no relationship between renin-activity, angiotensin-II concentration and aldosterone concentration in peripheral venous blood. Stimulation of the system without sodium balance is not a reliable screening test for hypertension.

Four patients with severe hypnotic intoxication, twice after suicidal intake of barbital, once of barbital, methaqualone and carbromal, and once of carbromal, were treated with six activated charcoal haemoperfusions. Three patients showed rapid improvement in the level of consciousness followed by complete recovery. One female patient died in cerebral coma due to complete acute cerebromalacia following hypoxia. Serious complications due to the haemoperfusion did not occur. Correct use of activated charcoal haemoperfusion enriches the therapeutic spectrum of severe exogenous intoxications.

Combined oral therapy with digoxin (0.375 mg/dl) and disopyramide (300 and 600 mg/dl) in nine subjects did not alter steady-state digoxin serum concentrations just before the daily single digoxin dose. Digoxin and creatinine clearances were not changed. After a bolus IV dose of 0.8 mg digoxin, volume of distribution (from 672 +/- 176 l to 407 +/- 153 l) and elimination t1/2 beta of digoxin were reduced significantly in five subjects after 600 mg oral disopyramide daily (from 40.2 +/- 11.7 hr to 22 +/- 7.3 hr). Total clearance and digoxin distribution t1/2 alpha did not change significantly. The clinical significance of this interaction is not clear.

Since dialysis solutions in CAPD are now nearly aluminum free, the only source for elevated aluminum levels are aluminum-containing phosphate binders. Elimination with CAPD is insufficient to prevent aluminum accumulation. Therefore, we investigated a phosphate binder consisting of calcium alginate, a natural polyuronic acid, containing 100 mg calcium/g substance in 14 patients on CAPD over a period of one year. The patients had previously been treated with aluminum-containing phosphate binders for a period of 24.3 +/- 21.3 months. During a period of 3 weeks before changing to the new phosphate binder the mean (+/- SD) serum phosphorus concentration was 1.8 +/- 0.4 mmol/l, while at the end of one year of treatment with calcium alginate the concentration was 1.6 +/- 0.4 mmol/l. In order to lower serum phosphorus to this level, it was necessary to increase the mean (+/- SD) amount of calcium alginate from 6.9 +/- 1.3 g per day at the beginning of the study to 8.3 +/- 2.1 g per day at the end. The mean (+/- SD) serum calcium concentration did not change throughout the study period. Serum levels of alkaline phosphatase, 1.25 (OH)2 vitamin D3, and intact parathyroid hormone did not change as well. The mean (+/- SD) serum aluminum level declined from 36.0 +/- 20 to 14.0 +/- 11.3 micrograms/l after 6 months (p less than 0.001). In conclusion, calcium alginate is a good alternative to aluminum-containing phosphate binders and to phosphate binders on a calcium base as it does not lead to hypercalcemia. It prevents aluminum intoxication and has no serious side effects.

After full digitalisation, 11 healthy subjects received 0.375 mg digoxin daily as maintenance dose. Under steady-state conditions and determination of serum concentration and renal clearance of digoxin, they were then given 500 or 1000 mg quinidine daily in addition to the digoxin. While serum concentration of digoxin rose significantly from 0.75 +/- 0.2 ng/ml after one week on 500 mg quinidine, and to 1.8 +/- 0.6 ng/ml after 1000 mg of quinidine, renal digoxin clearance fell from 186.2 +/- 67.4 to 125.4 +/- 61.8 ml/min after 500 mg of quinidine. Raising quinidine dosage to 1000 mg daily caused no further digoxin clearance reduction. During the total experimental period endogenous creatinine clearance remained unchanged. The results indicate that the rise in serum digoxin concentration on simultaneous quinidine administration is largely due to reduction in renal digoxin clearance. A clinical observation confirms the considerable practical importance of this interaction.

After six years of home haemodialysis and two years of continuous ambulatory peritoneal dialysis a 59-year-old woman developed an aluminium-induced osteopathy, myopathy and normochromic anaemia. She was at first treated with intravenous, then peritoneal, deferoxamine, 1 g every other day. Before treatment, 15.8 micrograms aluminium (Al) had been eliminated daily, with a peritoneal clearance of 0.3 ml/min; after intravenous deferoxamine a mean of 774.3 +/- 102.3 micrograms Al was eliminated per day, after peritoneal deferoxamine 646.7 +/- 89.6 micrograms of Al per day, with a peritoneal clearance of 2.2 +/- 0.9 (intravenous) and 1.9 +/- 0.7 ml/min (intraperitoneal). After four months of deferoxamine administration, mostly intraperitoneally as an out-patient, the osteomalacia clearly improved, as did the myopathy and anaemia.

Aluminum concentrations in the dialysate and serum of 14 patients on CAPD were measured every six months. Additionally, in ten of the patients Al elimination was measured after a bolus ingestion of 1800 mg aluminium-chloride-hydroxide-complex. There was no significant difference between serum Al concentrations initially (47.3 +/- 8.2 micrograms/l), at six months (55.4 +/- 9.5 micrograms/l), and after 12 months (44.3 +/- 10.1 micrograms/l) although the Al concentration in the dialysate had been decreased from 16.6 +/- 2.3 micrograms/l to 1.5 +/- 0.2 in the last six months. The Al concentrations in the effluent dialysate were 14.5 +/- 1.3 micrograms/l initially, 15.6 +/- 1.2 micrograms/l after six months and 11.9 +/- 2.6 micrograms/l after 12 months. During kinetic studies a constant rise of serum Al concentration was found until the fifth hour, from 29.9 +/- 2.5 to 42.5 +/- 4.0, and a decline after 24 hours to 32.4 +/- 3.0 micrograms/l. The quantity of Al eliminated was 41.1 +/- 8.7 micrograms/24 h, equivalent to 1.2% of the ingested dose. In patients with residual renal function, renal Al clearance was almost double the peritoneal one. These results indicate that Al elimination by CAPD is not efficient and ingestion of Al-containing phosphate binders can result in Al accumulation.

The physiological role of inactive renin, especially the question of whether and how a conversion to active renin takes place in vivo, remains controversial. In order to show the dynamic alterations from inactive to active renin following acute ACE-inhibition, both forms of renin were investigated in both renal veins and the peripheral circulation of 20 patients with essential hypertension and 20 patients with renovascular hypertension before and 1 h after 25 mg of captopril. Active and inactive renin were determined indirectly as plasma renin activity (PRA, unit: ng/ml x h). In vitro activation of inactive renin was achieved with trypsin (1 mg/ml plasma), followed by a further determination of PRA (= total renin). Subtraction of the active renin from the total renin yields the amount of inactive renin. In patients with essential hypertension, the mean values of active renin increase equally in both renal veins (1.4 and 1.3 before, 1.9 and 1.8 after captopril) and the peripheral circulation (0.9 and 1.3) (p less than 0.002), whereas the inactive renin decreases correspondingly. Renal veins: 7.6 and 8.2 before, 7.2 and 7.6 after captopril; peripheral circulation: 7.7 before and 7.0 after captopril (p less than 0.05). In all patients with renovascular hypertension, there is basally a marked lateralization of active renin (6.4 vs 3.5; p less than 0.01) and inactive renin (20.5 and 18.9, p less than 0.03) towards the side of the ischemic kidney. After captopril, the values for total renin and active renin increase (p less than 0.001), and the side difference for active renin becomes still more pronounced (33.0 vs 14.2; p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

To check the reliability of the captopril test and of quantitative radioisotope techniques for the primary diagnosis of renovascular hypertension the data from 41 patients suspected of this disease were retrospectively analysed. In all cases plasma renin activity (PRA) was assayed in peripheral blood and in renal vein blood before and after 25 mg captopril. Double tracer studies with 131I-hippuran and 99mTc-DTPA were also performed, as was renal arteriography. The postoperative blood pressure plots of 23 patients with unilateral renal artery stenosis (who had subsequently been operated upon) were included in the evaluation. Renovascular hypertension was diagnosed in 21 patients and essential hypertension in 20. Twelve of the 20 patients with essential hypertension had renal artery stenosis, but this had not produced renovascular hypertension. The diagnostic significance of the tests as markers of renovascular hypertension was as follows: captopril test P less than 0.001, glomerular filtration fraction P less than 0.02, hippuran clearance P less than 0.001. The captopril test and the quantitative radioisotope techniques were in agreement in identifying patients with renal artery stenosis and renovascular hypertension. False-positive results due to methodological shortcomings can be avoided by applying both methods in succession.