Jj Weening

THE EFFECT OF PHLEBOTOMY ON RENAL-FUNCTION AND PROTEINURIA IN A PATIENT WITH CONGENITAL CYANOTIC HEART-DISEASE

The Effect of Phlebotomy on Renal Function and Proteinuria in a Patient with Congenital Cyanotic Heart Disease P.E. de Jong J.J. Weening A.J.M. Donker G.K. van der Hem P. E. de Jong, Department of Medicine, Division of Nephrology, Department of Pathology, State University Hospital, Groningen (The Netherlands), Nephron 1983;33:225-226 Sir, With interest we read the paper of Wilcox et al. [1] on renal function in patients with cor pulmonale and secondary polycythaemia. Effective renal plasma flow (ERPF) was found to be reduced and filtration fraction (FF) to be increased. A few days after haematocrit (Hct) reduction, FF fell in 5 out of 7 patients. Parallel with the decrease in FF, a fall in body weight was seen. The authors suggest that, at least temporarily, the increased postglomerular capillary resistance – which is present in these patients [2] -can be corrected by Hct reduction. We now show another effect of phlebotomy in a patient with congenital cyanotic heart disease. It is known that glomerular lesions can occur in these patients [3, 4]. Spear and Vitsky [3, 4] described glomerular enlargement, congestion and capillary dilatation. There was mesangial hyper-cellularity and focal glomerular sclerosis on light microscopy. On electron microscopy, diffuse thickening of the glomerular basement membrane was found [5]. Besides the abovementioned renal functional abnormalities also proteinuria is a common finding in these patients [4,5], probably as a consequence of the glomerular functional and morphological abnormalities. We recently observed a 36-year-old man, known with tetralogy of Fallot, who underwent a Blalock operation at the age of 6. He was admitted to our hospital because of nephrotic syndrome and hypertension. Hct was 67%. Phlebotomy was carried out and he was instituted on digoxin. Body weight decreased and oedema disappeared but proteinuria persisted. From this period no accurate renal function studies are available. The patient was transmitted to the department of nephrology. At this moment no clinical signs of fluid overload were present and blood pressure was 140/95 mm Hg. Further investigations did not reveal any other abnormality known to cause nephrotic syndrome. Hct was 55%, proteinuria amounted to 4–5 g/ Table I. The effects of phlebotomy in our patient During After 8 weeks observation phlebotomy3, after discharge Body weight, kg 56.7 55.3 59 Haematocrit, % 55 44 59 Serum creatinine, μmol/l 86 77 91 Serum urea, mmol/l 7.7 5.0 5.3 GFR, ml/min 73 101 78 ERPF‚ml/min 132 223 155

Sodium Depletion Enhances the Antiproteinuric Effect of ACE Inhibition in Established Experimental Nephrosis

R.T. Gansevoort, Department of Nephrology, State University Hospital Groningen, The Netherlands Dear Sir, The beneficial effect of angiotensin-I-converting-enzyme inhibition (ACEi) to prevent both a rise in proteinuria as well as progression of renal function loss has been documented in different models of experimental nephrosis [1]. Extrapolation to the human situation however seems rather hazardous, since the majority of these animal studies started ACEi before or immediately after disease induction, whereas treatment in patients is only started at the time that renal disease is fully established. This difference in disease state when starting ACEi may have consequences for the interpretation of data; the level of proteinuria in the animal studies may be an indication of the amount of structural damage to glomeruli, whereas the antiproteinuric effect of ACEi in the human situation, according for instance to its reversibility, is probably due to a functional alteration. Only a few animal studies have, in analogy to the human situation, investigated the effect of ACEi in an established disease state. Some investigators found no effect of ACEi on proteinuria [2-4], while others found a significant decrease [5-7]. In man sodium depletion is necessary to obtain an optimal antiproteinuric effect of ACEi [8]. We hypothesized that differences in sodium intake and volume status between the above-mentioned animal studies could account for the conflicting results. We therefore studied the effect of differences in sodium intake on proteinuria and on the antiproteinuric effect of ACEi in an experimental model of established adriamy-cin nephrosis. Ten male Wistar rats, age 12 weeks, weighing 270 ± 12 g, were injected with adriamycin in a dose of 3 mg/kg i. v. to induce nephrosis. The study consisted of four periods during which 24hour protein was measured twice weekly and blood pressure once weekly. Every period lasted until a stabilization of proteinuria and blood pressure was achieved. Statistical analysis was performed by non-parametric analysis of variance (Kruskall-Wallis) using the last, stable, values of each period. Significance was assumed at p < 0.05. During the first period all rats were fed a low-salt diet, containing 0.05% NaCl. Six weeks were allowed for proteinuria to develop and stabilize. In period 2, lasting 4 weeks, rats were matched for blood pressure and proteinuria and divided into two groups in order to study the effect of different sodium intake on these parameters. One group (n = 5) continued the low-salt diet, while the other group (n = 5) received