Safety of ultrasound-guided percutaneous renal biopsy-retrospective analysis of 1090 consecutive cases.

BACKGROUND: Ultrasound-guided renal biopsy with an automated spring-loaded biopsy device has become the standard method for kidney biopsy. Information on the success rate and safety of the routine use of this procedure from large series is not available. Such information is of interest for cost benefit considerations and for medicolegal purposes. We performed an audit of this procedure. SUBJECTS AND METHODS: From January 1993 to June 1997, 1090 percutaneous renal biopsies were performed in the renal units of Heidelberg (n = 557) and Karlsruhe (n = 533) using a spring-loaded biopsy device (Biopty; Radiplast AB, Uppsala, Sweden). After intensive local disinfection, biopsies were performed under local anaesthesia and direct visualization by ultrasound (Sonolayer SSH-140 A, Toshiba Inc., Japan). A puncturing adaptor was used (model UAGV 009 A, Toshiba, Japan). Of the 1090 biopsies 114 (10.4%) were performed on renal allografts and 976 (89.6%) on orthotopic kidneys. Biopsies were performed only if patients were strictly normotensive (<140/90 mmHg) and had normal coagulation parameters (PT, PTT, factor VIII, thrombocyte count, and bleeding time). All patients had been advised not to take aspirin or non-steroidal antiinflammatory agents for at least 5 days prior biopsy. We analysed (1) yield of diagnostically useful material, and (2) frequency of postbiopsy complications (e.g. macrohaematuria, haematoma, infections, and AV fistula). RESULTS: Except for one case requiring interventional radiology because of persisting blood loss and three cases requiring blood transfusions, no serious complications were seen in the 1090 consecutive renal biopsies, e.g. death, loss of kidney, life-threatening haemorrhage, or persisting haemodynamically relevant AV fistulae. The frequency of minor haematoma with an extension >2 x 2 cm, but no significant decrease of haemoglobin, was 2.2% (25/1090). Self-limited mild macrohaematuria occurred in 0.8% (9/1090). The incidence of small, haemodynamically irrelevant AV fistulae detected by Doppler ultrasound was 9% (48/533). Sufficient tissue for reliable histopathological diagnosis was obtained in almost all cases (1077/1090 = 98.8%). The median number of glomeruli per biopsy sample was 9 (range 1-37). CONCLUSION: If contraindications, especially high blood pressure and abnormal haemostasis, are respected, ultrasound-guided percutaneous renal biopsy with an automated biopsy device is safe. Skilled operators obtain satisfactory amounts of kidney tissue in almost all cases.

Treatment of severe nephrotic syndrome.

Treatment modalities in severe nephrotic syndrome have to consider (a) the underlying glomerular diseases as well as (b) the extrarenal complications. Occasionally acute renal failure develops on the basis of an unknown nephrotic syndrome; if a primary glomerular disease is diagnosed by biopsy, immunosuppressive therapy is optional. In type I and type II diabetes development of a severe nephrotic syndrome is usually not reversible. To avoid the rapid decline of renal function a consequent antihypertensive therapy is the treatment of choice in this stage of the disease. Treatment of primary glomerular diseases with severe (NS) includes frequently relapsing minimal change nephropathy (MCN) that can be treated with prednisolone 1 mg/kg/day until remission occurs. For prolongation of the remission cyclophosphamide 2 mg/kg/day for eight weeks, or alternatively cyclosporine A 3 to 5 mg/kg/day for six months, can be given. In steroid-resistant focal segmental glomerulosclerosis (FSGS) eight weeks of treatment with cyclophosphamide 2.5 mg/kg/day or six months treatment with cyclosporine A 3 to 5 mg/kg/day can induce a partial or complete remission in up to 20% of the patients. In membranous glomerulopathy with severe NS, one month of therapy with prednisolone followed by chlorambucil for one month (all together 6 months) improves the renal outcome of the patients compared to controls. Alternatively, cyclophosphamide 2 mg/kg/day plus 30 mg prednisolone/day can be given for a couple of months. Extrarenal complications of a severe NS are: (a) edema; (b) thromboembolism; and (c) lipid abnormalities. If nephrotic patients are resistant to orally administered loop diuretics, they should be treated in addition intravenously with hydrochlorothiazide p.o. Nephrotic patients with a serum albumin level < 20 g/liter should be routinely anticoagulated. Extensive hyperlipidemia in severe NS can be treated with HMG-CoA reductase inhibitors.

Immunosuppressive therapy and hepatitis C virus infection: the clinical course of liver disease.

In a retrospective long-term follow-up study the clinical course of liver disease was examined in renal allograft recipients with hepatitis C virus (HCV) infection and negative hepatitis B surface antigen under immunosuppressive therapy. We compared 42 anti-HCV antibody (anti-HCV) positive patients (study group) to 213 anti-HCV negative patients (control group). All patients received immunosuppressive therapy. Measurements were made of the following: aminotransferases, bilirubin, albumin, gammaglobulins, ascites, spleen diameter, HCV RNA, and anti-HCV antibody. We found all but four anti-HCV positive patients to be HCV RNA positive prior to transplantation. There were no differences in overall mortality or mortality secondary to liver disease or sepsis. Normal liver enzymes were found in 13 (31%) anti-HCV positive and in 137 (64%) anti-HCV negative patients during the whole mean observation period of 65 months (range 10-215). Aminotransferase activity decreased in anti-HCV positive and negative patients during the observation period. Liver function with regard to synthesis and excretion was normal in anti-HCV negative and anti-HCV positive patients. No signs of portal hypertension were observed in the anti-HCV positive group. Neither the different immunosuppressive regimens nor the antirejection therapy led to differences between anti-HCV positive and negative groups with respect to liver function and did not alter the clinical course. We conclude that HCV infection in patients under immunosuppressive therapy causes only a mild liver disease, as determined by clinicochemical and clinical parameters, and that mortality rate is not increased.