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.
Dialysis between two flowing, miscible fluids without an intervening membrane enhances both the transport rate and biocompatibility. Unfortunately, it also presents serious challenges, including the loss of pressure as a driving force for volume transport, the need for sterile dialysate in greater quantity than in conventional dialysis, the possibility of unacceptable protein loss, and even the possibility of blood cell loss. This paper quantifies these advantages and disadvantages, and evaluate the means by which the latter might be surmounted. Preliminary data are provided to show that stable flows of one fluid sheathing another, miscible fluid are achievable and that molecular exchange between the fluids is orderly and in qualitative agreement with the theory. Extension of the concept to other blood purification tasks, especially in the treatment of liver failure and various macromolecular separations, is also discussed. In conclusion, membraneless separations will require a secondary process and a recycle stream. Under these conditions, its advantages can be preserved and its disadvantages controlled.
The first study compared two groups on dialysis: 25 patients with diabetes mellitus and 25 matched non-diabetic patients, in relation to the presence of signs of hyperparathyroidism, to assess the reported low incidence of hyperparathyroidism in these patients. The diabetic group showed significantly lower values of PTH, Alk phosphatase, percentage of patients requiring vitamin D treatment, and less evidence of hyperparathyroidism on X-ray and in bone histomorphometry. In the second study 16 patients with chronic renal failure due to diabetic nephropathy were compared to 27 patients with the same degree of renal failure of other origin, the diabetic nephropathy group showed no increase in PTH, with falling creatinine clearance. Despite this low PTH, the phosphaturia was higher in the diabetic nephropathy group (Tm PO4/C Cr: 1.94 +/- 0.43 vs 2.5 +/- 0.68). In conclusion, patients with diabetes mellitus are less prone to develop hyperparathyroidism in progressive renal failure. This could be due to a relative increase in phosphaturia during declining function.
Six HBsAg negative patients with cirrhosis of the liver (CL) presented with recurrent bouts of palpable purpura in the legs due to small vessel leucocytoclastic vasculitis. In addition, all patients had renal failure, proteinuria and microhaematuria. Renal biopsy disclosed either diffuse proliferative (3 cases) or focal necrotising glomerulonephritis with crescents (2 cases). One patient had IgM-IgG mixed cryoglobulinaemia (type II). Four patients died of complications of their CL. Hepatocellular carcinoma was found in 1 case. In the patient without renal biopsy renal function improved following steroids and cyclophosphamide. The pathogenesis of this syndrome of cutaneous vasculitis with severe glomerular involvement in CL is unknown but could be immune-complex mediated.
We have evaluated the Hickman catheter and Hemasite access port as means to re-establish vascular access in patients lacking veins for conventional arteriovenous fistulae. The Hemasite is more convenient, but is also costlier, requires more surgical skill to implant, and is more frequently associated with major infections. One-half of the Hemasites have failed because of infection. As a result, the long-term survival rate is lower for Hemasite graft, although the differences noted have not yet reached statistical levels of significance.
The bone scans of 32 patients on regular dialysis who received desferrioxamine therapy for fracturing osteomalacia secondary to aluminium intoxication are reviewed. All scans show the same pattern, with lack of tracer deposition in bone and deposition in soft tissues. Therapy with desferrioxamine controlled the aluminium intoxication in all cases, and in 21 patients the bone scan reverted to normal or showed a pattern typical of hyperparathyroidism.
To evaluate the normal haemodynamic and respiratory responses to blood-membrane contact sham-dialysis, i.e. with blood flowing through a dialyser but without dialysate and ultrafiltration, was performed on healthy young men during 150 minutes. Heart rate, cardiac output, arterial blood pressure and pulmonary arterial blood pressure (continuously recorded during the initial 30 minutes) did not change significantly. The white blood cell count fell markedly to a minimum after 20 minutes of blood-membrane contact, then returning to above the baseline values, but PaO2 did not change significantly.
The low molecular weight heparin CY 222 (CHOAY) has been compared to unfractioned heparin (UFH) in patients on chronic haemodialysis and haemofiltration at various doses as regards it biological activity (measured by Activated Partial Thromboplastin Time and by anti-Xa activity) and its clinical effect on clot formation in the blood lines and bleeding at the puncture sites or recent wounds. Compared to UFH, CY 222 has a greater anti-Xa activity for a shorter APTT. This biological difference is of clinical advantage since clotting in lines is comparable or less than with UFH whereas compression time at puncture sites is shorter and recently bleeding wounds in 28 patients did not bleed again. The long half life of CY 222 allows its use as a single priming dose of 300 anti-Xa U/kg in haemodialysis and 450 anti-Xa U/kg in haemofiltration.
In an attempt to define the cellular basis of the uraemic insulin resistance we studied insulin action in adipocytes from eight patients with undialysed chronic uraemia and from eight matched healthy controls. (125I)-insulin binding to fat cells from uraemic patients was normal. In contrast (14C)-D-glucose transport exhibited decreased sensitivity to insulin. The concentrations of insulin that elicited a half-maximal response were 422 +/- 95 pmol/L in uraemic patients and 179 +/- 38 pmol/L in normals (p less than 0.01). The non-insulin and the maximally insulin stimulated glucose transport of adipocytes from uraemic patients was normal. The lipogenesis of fat cells from uraemic patients had depressed sensitivity to insulin (half-maximal stimulation at 38 +/- 8 pmol/L in uraemic patients and at 11 +/- 3 pmol/L in normals, p less than 0.01) with unchanged non-insulin and maximally insulin stimulated lipogenesis. Taken together these results suggest that the insulin resistance of adipocytes from patients with chronic uraemia may be primarily accounted for by post-binding defects localised to glucose transport and metabolism.
