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Nephrol Dial Transplant (1998) 13: 2703–2714

Nephrology Dialysis Transplantation

Letters Henoch–Scho¨nlein purpura nephritis associated with methicillin-resistant Staphylococcus aureus infection Sir, Environmental agents reported to be associated with the pathogenesis of Henoch–Scho¨nlein purpura nephritis (HSPN ) include viral antigens, bacterial antigens, drugs. A high incidence of upper respiratory tract infections preceding HSPN was also reported [1,2]. On the other hand, patients with HSPN did not have an increased frequency of positive cultures for haemolytic streptococci in a carefully controlled study [3]. HSPN associated with other bacterial antigen has been reported, however, we have been unable to find a report of HSPN after staphylococcal infection. The present paper describes a case of HSPN, with rapidly progressive glomerulonephritis, associated with methicillin-resistant Staphylococcus aureus (MRSA) infection. A 60-year-old Japanese man, who had a subphrenic abscess after an operation for acute appendicitis, developed proteinuria and haematuria. He also complained of arthralgia, and areas of purpura were seen over his extremities. Urinary protein excretion was 5–7 g/day, occult blood in urine was

detected, and creatinine clearance was about 50 ml/min. The levels of serum CRP, IgA and immune complexes were highly elevated. Bacteriological analysis showed coagulase type II MRSA producing staphylococcal enterotoxin A and C. Analysis of peripheral lymphocyte subsets using 3-colour flow cytometry showed increased the ratios of some variable parts of b-chain ( Vb) of T cell receptor ( TCR) positive T-cells (Figure 1). Histopathological findings demonstrated focal mesangial and endocapillary proliferative glomerulonephritis with crescent formation and tubulointerstitial nephritis. On immunofluorescence examination, IgA, IgG and C 3 were intensely positive in both the mesangium and peripheral capillary wall. Leukocytoclastic vasculitis was also observed on skin biopsy. We promptly administered antibiotic therapy consisting of vancomycin. However, the patient had persistent complaints of purpura and arthralgia, levels of CRP was not normalized, MRSA remained detectable, proteinuria did not decrease, and kidney function rapidly worsened. After 4 weeks, the serum creatinine level was 7.1 mg/dl, and the patient needed dialysis therapy. About 4 weeks after the initiation of haemodialysis, purpura and arthralgia disappeared, the CRP level normalized, MRSA was no longer

Fig. 1. PBMC were isolated from the patient’s peripheral blood by density centrifugation at the on-set of HSPN. PBMC were stained with phycoerythrin, biotin or FITC-labelled monoclonal antibodies and stained cells were analyzed by three-colour staining with a fluorescenceactivated cell sorter. FITC-conjugated anti-T cell receptor Vb antibodies (x-axis) and phycoerythrin-conjugated anti-CD3 antibody (y-axis) fluorescence profiles plotted on a logarithmic scale. This analysis shows increased the ratios of Vb 5.2+5.3-, Vb8 family-, and Vb12.1-positive cells. © 1998 European Renal Association–European Dialysis and Transplant Association

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detectable, and the ratios of enhanced TCR Vb-positive cells were decreased. However, the patient could not discontinue haemodialysis therapy. Staphylococcal enterotoxins have been called ‘superantigens’ because of their efficient activation of T lymphocytes and because of the stimularity of the mechanism of T-cell stimulation to antigen recognition [4]. The interaction sites on the major histocompatibility complex molecule and on the TCR Vb. Staphylococcal enterotoxins have been reported to play a role in the pathogenesis of numerous human diseases, including toxic shock syndrome [5], with an increase in specific TCR Vb+T cells. On the other hand, it recently has been reported that clonal expansion of T cells occurs in peripheral blood mononuclear cells (PBMC ) and in local lesions of rheumatoid arthritis [6,7], Sjo¨gren’s syndrome [8] and Kawasaki disease [9] as a result of variable-diversityjoining gene combinations or complementarity-determining region 3 according to TCR analysis. In the present case, HSPN developed after the MRSA infection and an increase in specific TCR Vb+cells was elevated after the onset of HSPN and reduced during vancomycin treatment. This suggested that superantigens and/or conventional antigens might be involved in the pathogenesis of HSPN. Acknowledgements. Supported in part (to Dr A. Koyama) by Grantsin-aids for Scientific Research from the Ministry of Education, Science and Culture, Japan and by Progressive Renal Disease from the Specially Selected Disease Project of the Ministry of Health and Welfare, Japan. Department of Internal Medicine Institute of Clinical Medicine University of Tsukuba Ibaraki Japan

Kouichi Hirayama Masaki Kobayashi Makoto Kondoh Kaori Muro Satoshi Iwabuchi Keigyo Yoh Takashi Ishizu Shuichi Kikuchi Naoto Yamaguchi Sohji Nagase Akio Koyama

1. Meadow SR, Glasgow EF, White RHR et al. Scho¨nlein–Henoch nephritis. Quart J Med 1972; 41: 241–258 2. Allen DM, Diamond LK, Howell DA. Anaphylactoid purpura in children (Scho¨nlein–Henoch syndrome). Am J Dis Child 1960; 99: 833–854 3. Ayoub EM, Hoyer J. Anaphylactoid purpura: streptococcal antibody titers and b 1c-globulin levels. J Pediatr 1969; 75: 193–201 4. White J, Herman A, Pullen AM et al. The Vb-specific superantigen staphylococcal enterotoxin B: stimulation of mature T cells and clonal deletion in neonatal mice. Cell 1989; 56: 27–35 5. Choi Y, Lafferty JA, Clements JR et al. Selective expansion of T cells expressing Vb2 in toxic shock syndrome. J Exp Med 1990; 172: 981–984 6. Goronzy JJ, Bartz-Bazzanella P, Hu W, Jendro MC, WalserKuntz DR. Dominant clonotypes in the repertoire of peripheral CD4+ T cells in rheumatoid arthritis. J Clin Invest 1994; 94: 2068–2076 7. Ikeda Y, Masuko K, Nakai Y et al. High frequencies of identical T cell clonotypes in synovial tissues of rheumatoid arthritis patients suggest the occurrence of common antigen-driven immune responses. Arthritis Rheum 1996; 39: 446–453 8. Matsumoto I, Tsubota K, Satake Y et al. Common T cell receptor clonotype in lacrimal glands and labial salivary glands from patients with Sjo¨gren’s syndrome. J Clin Invest 1996; 97: 1969–1977 9. Choi IH, Chwae YJ, Shim WS et al. Clonal expansion of CD8+ T cells in Kawasaki disease. J Immunol 1997; 159: 481–486

Treatment of progressive renal failure in idiopathic membranous nephropathy with azathioprine and prednisolone Sir, We agree with the conclusion of Brown et al. [1] that azathioprine and prednisolone treatment is of benefit in patients with idiopathic membranous nephropathy and significant renal impairment. We write to draw attention to our own findings [2] in, admittedly, a smaller number of patients with this condition, in whom serum creatinine concentration had risen by 90 mmol/l or more to reach a concentration of 300 mmol/l or more over a 12-month period of observation and in whom proteinuria of nephrotic proportions was present. Treatment with azathioprine and prednisolone was associated with a significant reduction in serum creatinine concentration at 1 year with a decline in proteinuria. A small number of patients fulfilling the above criteria who were not so treated suffered progressive deterioration in renal function. We agree with Brown et al. that such improvement is not normally to be expected in this situation and is likely to have been a consequence of treatment, although formal proof of benefit must await data from a prospective controlled trial. We agree that side-effects with prednisolone and azathioprine may well be less severe than with regimens employing cyclophosphamide or chlorambucil and, as they and we point out, prednisolone and azathioprine treatment has the additional advantage of being familiar to nephrologists. St Bartholomew’s Hospital L. R. I. Baker West Smithfield B. Tucker London EC1A 7BE I. C. Macdougall UK R. Oommen 1. Brown JH, Douglas AF, Murphy BG et al. Treatment of renal failure in idiopathic membranous nephropathy with azathioprine and prednisolone. Nephrol Dial Transplant 1998; 13: 443–448 2. Baker LRI, Tucker B, Macdougall IC, Oommen R. Treatment of progressive renal failure and nephrotic syndrome with azathioprine and prednisolone. Postgrad Med J 1997; 73 (864): 647–648

Mesangial hyperplasia in a patient with renovascular hypertension and proteinuria Sir, We have read with interest the report of Bhowmik et al. [1] describing renal-artery stenosis and focal segmental glomerulosclerosis in the contralateral kidney. In recent years similar cases have been reported [2–5]. Recently a 17-yearold female patient with hypertension 170/120 mmHg (while under antihypertensive treatment) and 2.5 g/24 h proteinuria was admitted to our Nephrology Clinic. The patient’s history was unremarkable. She seemed to have been well until 2 weeks prior to admission, when she suddenly complained of headaches, dizziness, and palpitations. Her physician detected hypertension (240/130 mmHg) and subnephrotic proteinuria. Administration of methyldopa, propranolol, and diuretics did not provide significant improvement. On admission we confirmed hypertension with hypertensive retinopathy, hypertensive concentric LVH, impaired LV diastolic performance as evidenced by ECG and ultrasound, and 1.8 g/24 h proteinuria. Treatment with clonidine, propranolol, nifedipine, and diuretics did not result in normalization of the blood pressure.

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Laboratory investigations did not reveal significant changes: no serum Ig or C3 changes, proteinaemia 7 g/dl with hypoalbuminaemia (44%), normal SLO antibody levels, absence of LE cells, serum urea 20 mg/dl, serum creatinine 0.8 mg/dl, slightly reduced creatinine clearance (69 ml/min). Abdominal ultrasound showed reduced right kidney 85/38 mm and increased left kidney 125/65 mm, with no evidence of occlusive features. Intravenous urography and isotopic nephrogram revealed a largely non-functional left kidney. The aortography showed the left renal artery to have normal origin and size (Figure 1), while the right artery exhibited uniform narrowing with a 2.7-mm lumen in the central portion and a 10-mm-long uniform narrowing (85%)

in the distal portion. PTA was then performed, with a satisfactory outcome, i.e. only 26% residual stenosis. Blood pressure normalized within 36 h without any medication and 72 h after PTA proteinuria was reduced to 0.56 g/24 h. It was still in this range 4 months after PTA. An echo-guided kidney biopsy was performed on the contralateral kidney. The kidney biopsy revealed mesangial hyperplasia, no interstitial infiltrate, and no significant interstitial fibrosis (Figure 2). Renal vascular hypertension associated with moderate to severe proteinuria and FSGS in the contralateral kidney has been reported both in children [6 ] and in people older than 60 [3,4,7]. The authors claimed that these lesions and the proteinuria are the consequences of the glomerular hyperfiltration induced by the angiotensin II. We propose that this mechanism was responsible for our patient’s pathological findings, too. In contrast to the observation of Bhowmik et al. [1] and to [4,8] our patient presented mesangial hyperplasia. In our opinion this raises the question of whether more advanced mesangial lesions are the result of angiotensin-induced hyperfiltration. The lesion seen in our patient may be a precursor to full-blown FSGS, but we acknowledge the possibility that lowering of blood pressure in our patient may have caused reversal of pre-existent lesions. Although the hypertension was chronic and the stenosis of the renal artery was severe, our patient underwent PTA. After angioplasty, the blood pressure normalized, no antihypertensive drugs were administered, and proteinuria declined significantly. Both our case and the others mentioned indicate the need to establish whether there exists a stenosis of the renal artery in patients with severe hypertension and proteinuria. PTA seems to be an appropriate treatment in young patients with severe RVHT and proteinuria.

Fig. 1. Aortography showing normal origin and size of the left renal artery and narrowing of the right renal artery.

1University of Medicine and Pharmacy 2Cardiology Centre Timisoara Romania

Fig. 2. Renal biopsy showing mesangial hyperplasia.

Ad. Schiller1 Gh. Gluhovschi1 D. Gavrilescu2 G. Deutsch1

1. Bhowmik D, Dash SC, Jain D, Agarwal SK, Tiwari SC, Dinda AK. Renal artery stenosis and focal segmental glomerulosclerosis in the contralateral kidney. Nephrol Dial Transplant 1998; 13: 1562–1564 2. Chen R, Novick AC, Pohl M. Reversible renin mediated massive proteinuria successfully treated by nephrectomy. J Urol 1995; 153(1): 133–134 3. Docci D, Moscatelli G, Capponcini C, Baldrati L, Felleti C. Nephrotic range proteinuria in a patient with high renin hypertension: effect of treatment with ACE-inhibitor. Am J Nephrol 1992; 12(5): 387–389 4. Fujii S, Kasahara H, Oguchi H. A case of renovascular hypertension with nephrotic syndrome, accompanied by focal segmental glomerulosclerosis-like lesions in contralateral kidney, Nippon Jinzo Gakkai Shi 1991; 33(10): 1017–1027 5. Ogata H, Ishiyama N, Hamabe K et al. Renovascular hypertension with massive proteinuria, Intern Med (Jpn) 1996; 35(7): 569–573 6. Kaneko K, Shimazaki S, Ino T et al. Severe hyponatremia in a patient with renovascular hypertension: case report, Nephron 1994; 68(2): 252–255 7. Fukushima T, Saiki T, Satoh T, Nomura S, Hirano H, Osawa G. A case of renovascular hypertension with nephrotic syndrome. Nippon Jinzo Gakkai Shi 1995; 37(10): 595–599 8. Thandhani R, Pascual M, Nickeleit V, Tolkoff-Rubin N, Colvin R. Preliminary description of focal segmental glomerulosclerosis in patients with renovascular disease, Lancet 1996; 347(8996): 231–233

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Hydroxyethylstarch-associated transient acute renal failure after epidural anaesthesia for labour analgesia and Caesarean section Sir, The potential effects of hydroxyethylstarch (HES ) on renal function are controversial. Although HES appears to be protective against ischaemic damage in kidney transplants when added to kidney transplant perfusion solutions, rarely it appears to cause acute renal failure [1,2]. We report on two healthy, full-term primigravidae with uneventful pregnancies whose medical histories were unremarkable for renal disease. They developed acute transient non-oliguric renal failure after Caesarean section under epidural anaesthesia. Caesarean section was performed because of failure to progress in association with signs of fetal distress and suspected chorioamnionitis. Blood loss during the Caesarean section was moderate (