Forty-nine paediatric patients at different stages of chronic renal failure were followed until adult height was attained. Mean age at completion of growth was close to normal. Adult height was evaluated against population-specific standards. It was less than 2 SD under the mean in two of 18 patients on conservative treatment, five of 18 during dialysis and none of 13 after transplantation, but correlation with mode of treatment did not reach significance. These findings contradict previous data stating that most of these children become small adults. Although analysis of the data suggests that many children with renal failure remain below their genetic potential of growth, final stunting appears infrequent.
Out of 58 consecutive cadaveric renal allograft recipients whose initial immunosuppression was cyclosporine (Cys) and prednisolone, 18 were converted to prednisolone and azathioprine. Of these all four patients converted because of rejection lost their grafts. Renal function improved in seven patients converted because of nephrotoxicity and in six out of seven patients converted for miscellaneous reasons. Out of five patients converted electively at three months, one died of infection and three developed acute rejection episodes.
Plasma renin activity (PRA) and aldosterone concentrations were measured simultaneously with urinary excretion of kallikrein and of four prostaglandins (PGE2, PGF2 alpha, 6-keto-PGF1 alpha and TXB2) in 23 patients with pregnancy-induced hypertension (PIH; 17 with permanent PIH (PH) and six with labile PIH (LH), i.e. patients whose hypertension was controlled only by home bed-rest) and in 16 normotensive pregnant women. Plasma renin activity was lower in PH than in controls or in LH. No difference between the three groups was observed for plasma aldosterone and urinary excretion of kallikrein and prostaglandins except that TXB2 was higher in LH than in PH. Thus patients with LH have a different biological profile from that of PH, since they have higher PRA and higher TXB2 excretion, an association that suggests a more pronounced ureteral compression by the gravid uterus in this group. Although no decreased synthesis of vasodilating prostaglandins was found in PH, a dysregulation of the renin-angiotensin-prostacyclin loop is suggested by a negative correlation between PRA and 6-keto-PGF1 alpha. An independent vasopressive substance which would stimulate PGI2 and suppress renin secretion is therefore postulated.
Haemodialysis was performed in non-uraemic dogs with equipment coated with a stable heparin. During a three hour dialysis a constant blood flow of 205 ml/min was easily maintained. There was no increase in whole blood coagulation time and no heparin release from the surface. The platelet count was initially reduced by 15 per cent, but remained constant at this value throughout the dialysis. No increase in FPA concentration was detected. Heparin coating on inherently thrombogenic materials enables haemodialysis in the absence of systemic anticoagulation and without measurable activation of the haemostatic mechanism.
Four patients are described with pneumatosis intestinalis following cadaveric kidney transplantation, all with severe cytomegalovirus (CMV) infection. Two patients had a primary infection and 2 patients had a reactivation of CMV. One patient died because of disseminated CMV infection. Multiple inclusion bodies were found at postmortem examination in lungs and liver, and at the site of the ulcers in the gastrointestinal tract. Two patients had, concomitantly, an active, nonobstructive duodenal ulcer. In a control population of 17 patients who suffered from a duodenal ulcer post-transplant without any evidence of CMV-infection, we could not demonstrate pneumatosis intestinalis. We suggest a possible causal relationship between pneumatosis intestinalis and active CMV infection. The mechanisms that could be responsible for this relationship are discussed.
Sodium acetate (SA) has been implicated in hypotensive episodes of haemodialysis because of its vasodilatory effects. The haemodynamic correlates of the changes in blood pressure, cardiac output (CO) and total peripheral resistance (TPR) are well known but the site of action of SA (i.e. arteriolar, venular or both) is not yet clarified. We thus studied the changes in CO, TPR and mean arterial pressure (MAP) induced by four graded doses of SA (0.034 to 0.300 mEq/kg/min) in seven normal dogs. To evaluate the site of vasodilation we also measured the changes in cardiopulmonary volume (CPV), mean pulmonary artery pressure (MPAP) and mean transit time (MTT). From control to the highest infusion rate, CO increased from 1.63 +/- 0.20 to 3.59 +/- 0.38L/min (p less than 0.001), TPR decreased from 78.2 +/- 11.3 to 36.4 +/- 4.8A.U. (p less than 0.001). MAP rose significantly from 107.2 +/- 4.0 to 116.5 +/- 8.5 mmHg (p less than 0.05) and stroke volume was maintained (17.2 +/- 2.3 to 19.6 +/- 2.1 ml, NS) in spite of the marked tachycardia observed (heart rate from 106.1 +/- 7.6 to 194.8 +/- 9.1bpm, p less than 0.001). This was associated with increases in MPAP (from 13.3 +/- 0.7 to 19.6 +/- 2.1mmHg, p less than 0.01) and CPV (from 195.0 +/- 21.3 to 224.4 +/- 24.3ml, p less than 0.01) and marked decrease in MTT (from 7.74 +/- 0.73 to 3.78 +/- 0.22 sec, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetic donors are still reluctantly accepted as potential organ donors because of supposed poor graft function caused by diabetic lesions. The results of transplantation of six kidneys from three donors with insulin dependent diabetes mellitus are reported. All three donors had a normal creatinine clearance and absence of proteinuria. Renal biopsies were taken. Five grafts are still functioning, six months to two years after transplantation with a mean creatinine clearance of 69ml/min (range 51-95). Three of five biopsies taken six months after transplantation showed marked decrease of the diabetic lesions. On the basis of these findings it seems justified to accept kidneys from diabetic donors for transplantation.
Microcytic, hypochromic anaemia is a feature of aluminium toxicity. To detect the possible influence of aluminium on erythropoiesis in a general haemodialysis population we studied the evolution of red blood cell parameters and aluminium status in 30 patients (27 without aluminium toxicity symptoms). Aluminium status was assessed by serum aluminium measurements before (BAl) and after (PAl) a desferrioxamine infusion. The evolution with time (delta) of PAl and DAl (= PAl - BAl) during the prospective study inversely correlated with delta mean corpuscular volume (2 alpha less than 0.01) and delta mean corpuscular haemoglobin (2 alpha less than 0.001). Patients with DAl greater than 180 micrograms/L had lower mean corpuscular haemoglobin values (p less than 0.05). These findings suggest that aluminium inhibits haemoglobin synthesis even in haemodialysis patients free of aluminium toxicity symptoms.
In order to develop an experimental IgA nephropathy, C3H/HeJ mice, high producers of IgA, were strongly immunised orally by ferritin and compared to C3H/eB mice. After immunisation, serum IgA and IgG titres increased significantly only in C3H/HeJ mice. Specific antiferritin antibody could be detected in the serum. Mesangial IgA deposits were present in most of C3H/HeJ mice after immunisation and were significantly higher than in C3H/eB mice. No ferritin deposits could be detected in the kidney. No clinical manifestation appeared in these animals.
