H.K. Stummvoll

Abnormalities in the Hypothalamic-Pituitary-Adrenocortical Axis in Patients With Chronic Renal Failure

The recently described human corticotropin-releasing factor was administered to eight patients with chronic renal failure in order to assess hypothalamic-pituitary-adrenocortical (HPA) function. Acute administration of corticotropin-releasing factor lead to a diminished increase of the basally elevated levels of ACTH and beta-endorphin immunoreactivity in patients on chronic hemodialysis. Basal plasma cortisol concentration was normal in end-stage renal disease; however, considering the corresponding elevated ACTH concentrations, cortisol levels were inadequately low. Thus, the hypothalamus as well as the adrenal gland seems to contribute to the alterations in HPA function observed in patients with chronic renal failure; involvement of the pituitary gland and effects of metabolic alterations cannot be ruled out.

Glucose Intolerance and Hemoglobin A, in Chronic Renal Insufficiency

Glycosylated hemoglobin A (HbA1), a proposed indicator of the integrated plasma glucose concentration over a long period of time, was investigated in patients with various degrees of renal

Enhanced 6-oxo-PGF1α levels in plasma during hemodialysis

Abstract The activation of platelets due to foreign surface interaction is a well known fact. Earlier, we found an increase of circulating platelet microaggregates (method of Wu and Hoak) during hemodialysis. Since this phenomenon might cause a PGI 2 -release by lung and/or vascular tissue, we studied the plasma 6-oxo-PGF 1α -levels in 6 patients during hemodialysis. We found an initial increase of plasma 6-oxo-PGF 1α . Coincidently, hypoxemia, fall in platelet and lekocyte count and a decrease in platelet count ratio were observed. An effect of heparin was excluded in a control group. The findings support the hypothesis that PGI 2 acts as a defense mechanism against platelet deposition on vascular wall by a temporary increased synthesis which could be monitored by a temporarily enhanced plasma 6-oxo-PGF 1α -level during the initial phase of hemodialysis.

Renal Phosphate Wasting after Successful Kidney Transplantation

1α-hydroxycholecalciferol was tried as a therapy for renal phosphate wasting in kidney allograft recipients with normal parathyroid gland activity. During a 3-week period of treatment we observed a si

Zirkulierende Thrombozytenaggregate während Hämodialyse

SummaryIn eight chronically haemodialysed patients a significant increase of circulating platelet aggregates (method of Wu and Hoak) was observed immediately after starting haemodialysis. The number of aggregates decreased at the end of haemodialysis reaching the starting values after 360 min. The platelet interaction with the dialysis membrane surface might cause this phenomenon. Anticoagulation with heparin alone was insufficient in preventing aggregate formation during haemodialysis.ZusammenfassungBei acht Patienten, die sich im Dauerdialyseprogramm befanden, wurde unmittelbar nach Anschluß an den Hämodialysator eine massive Zunahme von zirkulierenden Thrombozytenaggregaten mit der Methode nach Wu und Hoak gefunden. Die Zahl der Aggregate war noch während der Hämodialyse rückläufig, wobei nach 360 min der Ausgangswert wieder erreicht wurde. Als auslösende Ursache muß die Interaktion der Thrombozyten mit der Membranoberfläche des Dialysators gesehen werden. Antikoagulierung mit Heparin allein ist nicht ausreichend, um eine Mikroaggregatbildung während Hämodialyse zu verhindern.In eight chronically haemodialysed patients a significant increase of circulating platelet aggregates (method of Wu and Hoak) was observed immediately after starting haemodialysis. The number of aggregates decreased at the end of haemodialysis reaching the starting values after 360 min. The platelet interaction with the dialysis membrane surface might cause this phenomenon. Anticoagulation with heparin alone was insufficient in preventing aggregate formation during haemodialysis.

Dialysis and psoriasis.

Excerpt To the editor: Since the amelioration of psoriasis during dialysis was first described (1), a number of reports of positive effects of dialysis on this troublesome and often therapy-resista...

Cimetidine in Secondary Hyperparathyroidism

Excerpt To the editor: After anecdotal reports on a decrease of immunoreactive paraphyroid hormone (PTH) levels due to the administration of cimetidine in primary hyperparathyroidism (1,2), therape...

Tubulärer Phosphattransport nach erfolgreicher Nierentransplantation

SummaryDisturbances in phosphate homeostasis are almost universally present in patients with chronic renal failure. They consist of phosphate-accumulation, hyperphosphatemia, extraosseous calcifications, hyperparathyroidism and disturbances in Vitamin-D metabolism. After successful transplantation these disturbances are believed to resolve quickly, but sometimes phosphate wasting occurs in the early post-transplant phase. This study was determined to investigate phosphate handling by the transplanted kidney in 42 patients with longterm good and stable transplant function (serum creatinine (Cr) <2,0 mg/100 ml, graft survival >6 months). Calcium (Ca), inorganic phosphorus (P), creatinine was measured in plasma and urine, maximal tubular reabsorption capacity for phosphorus (phosphate threshold, TmP/GFR) was calculated using Walton and Bijvoets [21] nomogram; immunoreactive parathyroid hormone (iPTH) was determined using an antibody against the C-regional part of the PTH-molecule.Only 8 patients (19%) showed normal renal phosphate handling as indicated by normal plasma-phosphate, normal TmP/GFR and normal iPTH. 34 patients (81%) had a decreased TmP/GFR. This phosphate leak was due to persistant hyperparathyroidism in 15 patients, 4 of them showing additionally hypophosphatemia and hypercalcemia. In the remaining 19 patients there was a PTH-independent phosphate leak as indicated by a decreased TmP/GFR despite normal iPTH values. In this group 9 patients had a decompensated phosphate leak leading to hypophosphatemia. The results show a high incidence of abnormalities in renal phosphate handling even after successful kidney transplantation with longterm surviving good and stable functioning allografts. To prevent osteomalacia and other symptomes of the phosphate depletion syndrome, means should be undertaken to increase plasma phosphate levels by lowering PTH-levels in the patients with the PTH-dependent phosphate leak (active Vitamin D analogues, parathyroidectomy) whereas sufficient phosphate suplementation (oral phosphate and/or also active Vitamin D analogues) is necessary in patients with PTH-independent decompensated phosphate leak.ZusammenfassungStörungen der Phosphathomöostase werden nahezu obligat bei Patienten mit chronischer Niereninsuffizienz beobachtet. Sie bestehen in einer Hyperphosphatämie, extraossären Verkalkungen, sekundärem Hyperparathyreoidismus und gestörtem Vitamin D-Metabolismus. Nach erfolgreicher Nierentransplantation soll es zu einer raschen Normalisierung des gestörten Phosphatstoffwechsels kommen. Trotzdem findet sich manchmal ein renaler Phosphatverlust in der frühen postoperativen Phase. Ziel dieser Untersuchung war es, den tubulären Phosphattransport der transplantierten Niere bei 42 Patienten mit guter und stabiler Transplantatfunktion zu untersuchen (Serum-Kreatinin (Cr) <2,0 mg/100 ml, ml, Transplantatüberlebensdauer >6 Monate). Calcium (Ca), anorganischer Phosphor (P) und Kreatinin wurden im Plasma und Harn gemessen, die maximale tubuläre Phosphatrückresorptionsrate (Phosphat-threshold, TmP/GFR) unter Verwendung von Walton und Bijvoets Normogramm [21] errechnet; das immunreaktive Parathormon wurde mittels einem gegen das C-regionale Ende des Parathormonmoleküls reagierenden Antikörper bestimmt.Nur 8 Patienten (19%) zeigten einen normalen renalen Phosphatstoffwechsel, definiert durch normalen Plasma-Phosphorspiegel, normale TmP/GFR und normales iPTH. 34 Patienten (81%) hatten eine erniedrigte TmP/GFR. Dieser renale Phosphatverlust war bei 15 Patienten mit einem persistierenden Hyperparathy-reoidismus vergesellschaftet, wobei bei 4 Patienten zusätzlich eine Hypophosphatämie und Hypercalcämie bestand. Die verbleibenden 19 Patienten wiesen einen von der Epithelkörperchenfunktion unabhängigen renalen Phosphatverlust auf, welcher durch eine verminderte TmP/GFR bei normaler Parathormonkonzentration definiert wurde. In dieser Patientengruppe wiesen 9 Patienten einen zur Hypophosphatämie führenden dekompensierten renalen Phosphatverlust auf.Die Resultate zeigen einen hohen Prozentsatz von Störungen des Phosphatstoffwechsels nach erfolgreicher Nierentransplantation mit guter und stabiler Transplantatfunktion auf. Um der Entstehung einer Osteomalazie und anderen Zeichen des Phosphatdepletionssyndroms vorzubeugen, steht die Erhöhung des Plasma-Phosphats durch Supprimierung der Parathormonsekretion bei der Patientengruppe mit dem parathormonabhängigen renalen Phosphatverlust (aktive Vitamin-D-Metabolite, Parathyreoidektomie) bzw. ausreichende Phosphatsupplementation (Phosphor oral und/oder gleichfalls aktive Vitamin D-Metabolite) bei der anderen Patientengruppe im Mittelpunkt des therapeutischen Interesses.