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Maximal tubular phosphate reabsorption capacity corrected for changes in glomerular filtration rate (TmP/GFR) was taken as a measure of renal phosphate handling in patients with good and stable functioning kidney allografts. TmP/GFR values were within the normal range in only one-fifth of the patients. Eighty per cent had an abnormally low renal phosphate threshold concentration. Persistent hyperparathyroidism was the causative factor of this diminished tubular reabsorption in less than half of these patients, the majority of them showing an iPTH independent phosphate leak. Although glucocorticoids, azathioprine and tubular damage of the graft in the perioperative phase may contribute to this iPTH independent phosphate wasting, no single causative factor could be identified. Cases with hypophosphataemia should be treated in order to avoid symptoms of phosphate depletion. Active Vitamin D metabolites would be the therapy of choice by suppressing the parathyroid glands ("chemical PTX") and by directly enhancing tubular phosphate reabsorption. In persistent hyperpathyroidism with hypercalcaemia, surgical parathyroidectomy must be considered. Therapy with phosphate salts is only symptomatic and should be used only as an adjunct.

Aluminium kinetics in patients with endstage renal failure and chronic intermittent haemodialysis have been studied. All patients revealed elevated predialytic serum aluminum levels. Because of a significant correlation between daily intake of aluminiumhydroxyd and serum aluminium levels it is concluded that the intestinal aluminium absorption plays an etiological role in the development of hyperaluminaemia. Plasma aluminium levels at the end of a regular dialysis procedure are significant lower compared to predialytic values. Similarly a significant decrease of aluminium concentration was observed in the plasma after passage through the dialyzer. This is due to the fact that the aluminium content of the dialysate used in our unit (0.1-0.3 mumol/l) is lower than the ultrafiltrable fraction of the plasma aluminium measured in vivo. Therefore a negative aluminium-balance during haemodialysis has to be assumed in our patients. Extreme aluminium-accummulation seems to be avoided and we therefore never experienced aluminium intoxication and dialysis dementia in our center. To assess a negative aluminium balance during haemodialysis, because of high protein binding of aluminium, a dialysate with an extreme low aluminium content has to be recommended.

In order to evaluate the potential role of parathyroid hormone on glucose metabolism in patients on chronic hemodialysis hyperglycemic clamp studies were performed in 7 parathyroidectomized and 11 nonparathyroidectomized patients on chronic hemodialysis and in healthy controls. There were no significant differences in the peripheral glucose uptake of the 3 groups. The beta cell response to hyperglycemia during the early phase as well as during the steady state was almost identical in controls and in nonparathyroidectomized uremics, whereas in the parathyroidectomized group a markedly enhanced insulin secretion was found. Calculated tissue sensitivity to insulin therefore was equal in controls and in nonparathyroidectomized uremics, whereas patients after parathyroidectomy had peripheral insulin resistance. Our results demonstrate that patients on chronic hemodialysis apparently have normal peripheral glucose uptake. The subgroup of patients who have undergone parathyroidectomy, however, show an enhanced insulin response to hyperglycemia suggesting peripheral insulin resistance. We conclude that longstanding and severe secondary hyperparathyroidism--the usual cause for parathyroidectomy in these patients--results in irreversible insulin resistance with a compensatory increase of insulin secretion.

The acute renal response to 1,0 g Prednisolon i.v. in kidney transplant recipients and normal controls was investigated. The results indicate an acute suppression of glomerular filtration rate (CIN, CCR) and effective plasma flow (CPAH). The reabsorption of sodium in the proximal tubule was shown to be impaired as a direct effect of the steroid infusion, as well as there was an increase in the filtered fraction of potassium. The creatinine clearance under treatment of high doses of steroids does not reflect the actual changes in glomerular filtration rate

Reduced carbon monoxide diffusing capacity of the lung (DLCO) is reported in patients with impaired renal function. Since DLCO also depends on the pulmonary capillary blood volume the role of renal anaemia was evaluated. Measurements were carried out in 43 azotaemic patients [serum creatinine (SKr) 1.5 to 14.0 mg/100 ml], without evidence of cardiovascular or pulmonary complications of uraemia, of SKr, haemoglobin concentration (Hb) and steady state DLCO. In the case of DLCO values allowance was made for body surface area and thoracic gas volume. The relation was studied of the corrected DLCO to SKr and to Hb. There was a higher statistical correlation between DLCO and Hb than between DLCO and SKr. After additional correction of DLCO for Hb, no correlation to SKr was found. It is concluded that the reduction in DLCO in uraemia is due largely to a low Hb and, hence, to renal anaemia rather than to uraemic damage of interstitial lung tissue.

Thirty four children, aged 2 to 15 years, were treated by haemodialysis between 1967 and 1978. Eleven children suffered from acute renal failure. Twenty three children with end-stage chronic renal disease were treated over periods ranging from 1 week to 19 months. All children were dialysed in a renal unit for adult patients awaiting renal transplantation. Our results refer especially to the technical equipment for paediatric dialysis and to the problems of blood access. The medical problems of chronic uraemia and chronic intermittent haemodialysis in children are discussed. From our experience we conclude that a sufficient degree of rehabilitation can be reached only in a paediatric dialysis unit.

In this collaborative study 9 cases of intractable ascites in chronic hemodialysis patients are evaluated. Six patients died within 14, two more within 18 months after onset of ascites. Possible causes of the pathogenesis (repeated fluid overload, hydrostatic and oncotic pressure flux forces, alteration of membrane permeability) are discussed. Renal homograft transplantation seems to be the only successful treatment.

The neuropathological features are presented of an autopsy series of 43 renal transplant recipients. Inflammatory CNS lesions were found in 18 cases and were attributable to secondary CNS involvement in bacterial or fungal septicaemia (8 cases) or in localized extraneural infections (5 cases). Mixed bacterial-fungal infection and bacterial-fungal-viral triple infection were seen in one case each. Isolated toxoplasmic granulomas were observed in two cases. No tissue changes typical of CNS viral infections, including cytomegaly, were found except for small glial nodules in the brain stem in 7 cases. Massive intracerebral haemorrhages were seen in 2 cases after haemodialysis; subdural haematoma occurred once. Non-specific changes including brain oedema and diffuse glial poliodystrophy were found in many cases; vascular lesions and purpura occurred only seldom. A meningocerebellar malignant lymphoma, probably of metastatic origin was found in one case. Clinico-pathological correlation was poor in 5 cases; this is considered to be due to immunosuppressive therapy, which may mask either clinical expression of severe CNS lesions or morphological expression of viral encephalitis.

A 47 year-old male presented with increased stool frequency, abdominal discomfort and weight loss. Two sonographers found independently a "mass" in the region of the head of the pancreas. 8 years before the patient had had a Billroth-II-surgery. Laparatomy revealed a chronic periduodenitis as sonographic substratum. Therefore, basing on sporadic reports, an anamnestic finding of a Billroth-II-surgery should be kept in mind in differential diagnosis of a tumor of the head of the pancreas when employing sonography as a diagnostic tool.

An artificial kidney (HFAK 5) was evaluated as an ultrafiltration device and was found to efficiently remove water from fluid-overloaded patients. The fluid removal rate was quantitated on a chronically hemodialyzed patient and an example of clinical application on a patient without renal insufficiency, is reported. It is suggested that ultrafiltration is a helpful method for treating refractory edematous states.

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.

Although numerous in vitro experiments demonstrated a variable degree of urate bound to human serum albumin and other macromolecules of human plasma, only few data are available on in vivo bound urate. Extracorporal clearances of uric acid, urea nitrogen, creatinine and phosphorus were performed at the beginning, the midtime and the end of 10 hours of hemodialysis. A continuous decrease of uric acid clearance was observed in ratio with the capacity of the artificial kidney used. In contrast to uric acid the clearances of urea nitrogen, creatinine and phosphorus remained constant during the time of dialysis. From the fall of uric acid clearance, the authors conclude a partial binding of uric acid in human plasma.

During the past 2 years 7 children received kidneys from cadaveric donors. 2 transplants had to be removed because of irreversible chronic rejection and 1 recipient died on the 4th day after surgery. The remaining 4 recipients are doing well. In the evaluation of the results special emphasis is placed on the normalization of growth and puberty. The difficulties of psychosocial rehabilitation are stressed.

The clinical observation of 6 out of 250 renal transplant patients showed that acute renal rejection may lead to reversible acute tubular necrosis (ATN) necessitating intermittent haemodialysis treatment. Despite missing early response to high-dose (methyl-) prednisolone therapy (during a mean period of 4.7 days) all 6 patients developed spontaneous diuresis 14.5 days on average after onset of rejection while on maintenance immunosuppressive therapy. From the clinical course the conclusion was drawn that in severe cases of renal rejection with arteriographic and histological findings consistent with acute tubular necrosis, prolonged therapy with high doses of (methyl-) prednisolone is not desirable, since after reversal of immunological rejection the onset of spontaneous diuresis will be determined mainly by the duration of the healing and recovery phase of acute tubular necrosis.

26 hypertensive patients groupded according to the severity-index and the WHO-index were treated with pindolol (monotherapy, 15 mg daily). The response of blood pressure depression was statistically significant, although not always sufficient when judged by clinical parameters. Plasma renin activity responded variably to the treatment in different patients and different groups. In 18 patients a statistically significant increase of serum potassium could be observed. No major side effects of therapy were encountered.

Urinary enzymes were studied in 15 patients subjected to kidney transplantation. The investigation was initiated immediately after operation and was continued for a period of between 2 and 8 weeks. There was a significant increase in urinary MDH activity in 94.2% of cases, of LDH activity in 95,65% and of gamma-GT activity in 95,17% of the cases. This detected increase in urinary enzyme activities preceded the clinical diagnosis of rejection by activities preceded the clinical diagnosis of rejection by at least 24 hours. Determination of these enzymes provides a reliable tool for the early detection of rejection crises.

In three patients with advanced renal disease (inulin clearance, 4.6 to 9.1 ml/min) and systemic manifestations of secondary hyperparathyroidism, concentrations of serum calcium and phosphorus were maintained within our normal limits (9 and 3.5 mg/100 ml, respectively) with phosphate-binding antacids and orally given calcium carbonate. The result was progressive disappearance of symptoms related to secondary hyperparathyroidism, healing of osteitis fibrosa, and normalization of serum concentrations of immunoreactive parathyroid hormone.