Seyhun Kürşat

Nocardiosis in renal transplant patients.

Ercan Ok, Nefroloji Bilim Dah, Ege Üniversitesi, Tip Fakültesi, TR-35100 Bornova/İzmir (Turkey) Dear Sir, Nocardiosis is a life-threatening infection in immunosuppressed patients. The prevalence of the disease was reported to be 2.3-5% in renal allograft recipients [1, 2]. It frequently causes cutaneous disseminated form, localized suppurative subcutaneous lesion, pulmonary involvement and metastat-ic cerebral abscess form, the worst of all central nervous system involvement with a mortality ratio exceeding 80% [3]. Mono-poly-clonal antilymphocyte serum therapies, pulse methylprednisolone treatments, CMV disease, posttransplant diabetes mellitus, and splenectomy are well-known predisposing factors to all posttransplant infectious complications [4]. Six (1.7%) nocardia infections were diagnosed between 1.1.1987 and 1.7.1995 Table 1. Presenting symptoms, signs, chest X-ray findings, involved sites, suspected predisposing factors and outcome of the patients with nocardiosis Case Presenting symptoms Chest X-ray findings No. and signs Sites Suspected involved predisposing factors Outcome

The Unmasking of Hyperreninemic Hypovolemia by Captopril Test in a Hypertensive HD Patient Unaccompanied by Autonomic Neuropathy

Accessible online at: www.karger.com/journals/nef Dear Sir, The cause of hypertension in end-stage renal failure is hypervolemia in a vast majority of patients. It is easily controlled by volume reduction [1]. However in a small percentage of patients, hypertension persists despite the achievement of ‘dry weight’. In such cases angiotensin-converting inhibitors (ACEI) are usually effective [2]. Supine hypertension and orthostatic hypotension caused by autonomic neuropathy can coexist in end-stage renal failure patients caused by diabetic nephropathy [3]. Autonomic neuropathy can cause excessive hypotensive response to captopril administration. In this case report we would like to present a hypertensive nondiabetic hemodialysis (HD) patient who responded to captopril administration with symptomatic hypotension and having no signs of autonomic neuropathy suggesting that the cause of hypertension was hypovolemic hyperreninism. A 59-year-old male HD patient presented with headache to our HD department. His blood pressure (BP) was 177/116 mm Hg. He had been on HD for 6 years. His primary disease was hypertensive nephropathy evidenced by renal biopsy. He had been anuric since the first months of HD. EMG detected mild mix neuropathy involving mainly the lower extremities but not autonomic neuropathy evidenced by normal sympathetic dermal responses, besides normal changes in RR intervals determined by EKG in response to hyperventilation and Valsalva maneuver. No renal artery stenosis was detected with Doppler ultrasonography, Increased resistive indices of 0.75 and 0.82 regarding left and right kidney respectively was consistent with small vessel disease due to hypertensive nephropathy. The patient had normal cardiothoracic index (CTI) and echocardiographic parameters (table 1) at the end of a HD session, and though hypertensive, a captopril test (CT) was performed 1 day after HD. CT protocol: BP was measured every 10 min in the sitting position in a quiet environment. After 1 h baseline period, 25 mg captopril dissolved in 10 ml of water was given to the patient and BP measurements were continued for another 90 min. A decrease in systolic and diastolic pressures 110 mm Hg compared to the mean baseline value was considered positive. First CT resulted in a symptomatic BP drop to 60/40 mm Hg. Since hypovolemia was thought to be the causative factor, 1.5 liters of saline was infused. Still hypertensive, the patient did not give a positive response to the second CT which was also performed 1 day after HD. After an ultrafiltration session the patient lost 1 kg of body weight. At that point, 0.5 kg above the origi-

Prevalence of Anti-HCV Positivity in Hemodialysis Patients

Accessible online at: www.karger.com/journals/nef Dear Sir, Hepatitis C viruses (HCV) play important roles in the genesis of both acute and chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma. The most frequent modes of transmission of this virus are via blood and blood products and via body secretions such as semen, saliva, and sweat. For this reason, hemodialysis (HD) patients undergoing repeated venipunctures and frequent blood transfusions constitute one of the most important risk groups [1]. In this study, 85 HD patients were screened for anti-HCV antibody positivity; the factors that were thought to cause this positivity were also investigated. Anti-HCV positivity was detected by using third-generation enzyme-linked immunosorbent assay kits (Sorin Biomedica). The data thus obtained were processed with the aid of the SPSS version 6 package program using chisquare and Student’s t tests where appropriate. Thirty-three out of total 85 HD patients were women, the remaining 52 were men. Their average age was 49 B 14.4 (range 20– 79) years. Thirty-three out of 85 patients were found to be anti-HCV positive (38.8%). HCV RNA could not be detected because of financial problems. While a statistically significant correlation was found between antiHCV positivity and HD duration (p = 0.001), anti-HCV positivity could not be found to be correlated with factors such as age, number of blood transfusions, number of HD sessions per week, and alanine aminotransferase level elevations (p 1 0.05). The prevalence of anti-HCV positivity when compared with the healthy population and blood donors living in the same geographic region is considerably higher. While the prevalence of anti-HCV positivity in the general population of Turkey is below 1%, this figure shows an enormous increase in the different HD populations, ranging from 14.4 to 79.1% [2]. The prevalence of antiHCV positivity in our HD patients is an intermediate one. A number of studies were conducted in order to elucidate the factors responsible for this high anti-HCV prevalence. While some studies underlined the importance of blood transfusions, others insisted that the number of blood transfusions is not important, the duration of dialysis being the vital determinant. In our study, too, an important correlation was observed with regard to the dialysis duration (p = 0.001) but not for the number of blood transfusions. The probable reason for this was thought to be the widespread use of recombinant human erythropoietin and the screening of blood and blood products for HCV. The correlation with the duration of dialysis tempted us to assume that the HD procedure itself could constitute a risk factor for the transmission of HCV. Sampietro et al. [3] insisted on the possibility of a nosocomial transmission as a result of the observation of a relative homogeneity and a rare variance of HCV strains in their HD facility. In concordance with this hypothesis is the fact that the prevalence of anti-HCV positivity is relatively lower in continuous ambulatory peritoneal dialysis and home HD patients. The most probable route of transmission in HD units is said to be the dialysis procedure itself not performed under strict infection control precautions and asepsis, via materials contaminated with infectious blood [4]. In conclusion, HD patients must be screened for hepatitis B surface antigen and anti-HCV positivity periodically and in the case of positivity, if possible, must be dialyzed in different rooms by different personnel. The patients must be kept informed about the modes of transmission and the outcome of these infections.

The Simultaneous Appearance of Alport Syndrome in a Renal Transplant Donor and the Recipient as Primary Disease Recurrence

This article is also accessible online at: http://BioMedNet.com/karger Dear Sir, Alport syndrome is a hereditary nephropathy characterized by sensorineural hearing deficit, typical ocular abnormalities, microscopic hematuria and proteinuria that may be followed by renal insufficiency [1]. In X-linked Alport syndrome, male patients almost always exhibit hematuria and proteinuria and develop renal insufficiency [2]. Boys who are free of hematuria during the first 10 years of life are unlikely to be affected [2]. Females who are heterozygous for X-linked Alport syndrome are affected to a lesser degree, having only intermittent microscopic hematuria in 90% of cases or no hematuria at all [3]. Both males and females with autosomal recessive Alport syndrome appear to progress to end-stage renal disease during the 2nd and 3rd decades of life, with persistent hematuria [1]. Autosomal recessive Alport syndrome should be suspected when an individual exhibits the typical clinical and pathologic features of the disease but lacks a positive family history, especially when a young female has findings indicative of severe disease such as deafness, renal insufficiency or nephrotic syndrome [1]. The diagnosis of Alport syndrome was made in a female patient with end-stage renal disease who was born in 1971, because of microscopic hematuria, sensorineural hearing deficit, anterior lenticonus, posterior polymorphous corneal dystrophia and perimacular stippling. The patient received an allograft from her mother in 1990 and was treated with triple immunosuppression. Pretransplant evaluation of the donor did not show any sign of hereditary nephropathy such as hypertension, urinary sediment abnormalities, renal failure (creatinine clearance 128 ml/min), hearing deficit (tested audiometrically) and ocular abnormalities. Microscopic hematuria appeared in the recipient in the 4th posttransplant year. There was no hypertension, renal insufficieny or proteinuria. The donor developed persistent microscopic hematuria at the same time but also had proteinuria (1 g/day). In the 5th year after transplant, while having a serum creatinine level of 1.7 mg/dl (150 Ìmol/l), an ACE inhibitor and hydrochlorothiazide combination was begun because of hypertension. Though normotension was achieved, the serum creatinine level increased further to 2 mg/dl (177 Ìmol/l) in the 6th year and is 2.3 mg/dl (203 Ìmol/l) at the 7th posttransplant year. Urinary protein excretion is 2 g/day. Regarding Alport syndrome, the recipient still has microscopic hematuria as the sole abnormality. Pedigree analysis showed that the 17year-old sister of the recipient also had microscopic hematuria, proteinuria, sensorineural hearing deficit, and perimacular stippling but no renal failure. No sign of hereditary nephropathy was observed in her 50year-old father, 15-year-old brother and 30year-old elder sister. The fact that neither father nor mother had any relative with signs of the hereditary nephritis suggests that the hereditary form of Alport syndrome in this family was of recessive pattern. The probability of the X-linked recessive form is extremely weak in the face of the lack of any finding indicating hereditary nephritis in the 15-year-old boy, who certainly would have microscopic hematuria in the second decade of his life. The only remaining possibility is the autosomal recessive form. The most interesting feature in this family is the late appearance of hypertension, microscopic hematuria, nephrotic-range proteinuria and renal insufficiency in the 5th decade in the donor, although the syndrome was fully developed in the recipient in the second decade. The features of the donor and the recipient at the time of transplantation were consistent with the autosomal recessive form [1]. Hyperfiltration was thought to be the responsible factor in both the primary disease recurrence in the recipient and the so-called late-onset Alport syndrome in the donor. Though hypertension, proteinuria and renal insufficiency in a donor candidate are absolute contraindications for kidney transplantation, at present some transplant centers approve microscopic-hematuric persons for organ donation. It is obvious that such persons develop renal failure with a greater probability than others who do not have microscopic hematuria [1]. As in the family described here, donors who have not even microscopic hematuria before transplantation, may exhibit the features of Alport syndrome at some time after transplantation. This report suggests that our policy regarding kidney transplantation in Alport syndrome families must be reviewed.