[Determination of renal function in clinical routine: which is the best method?]. / Bestimmung der Nierenfunktion im klinischen Alltag--welche Methode ist die beste?

BACKGROUND AND OBJECTIVE: Accurate quantification of renal function is important for diagnosing and monitoring progression of renal diseases and for calculating adequate doses of drugs that are excreted by the kidneys. Gold-standard procedures are too complex for routine clinical use. At the moment there are several formulae to choose from, all said to estimate renal function precisely enough for clinical purposes. It was the aim of this study to compare the accuracy of several of these in clinical routine. PATIENTS AND METHODS: The results of inulin clearance were compared with those calculated by the Cockcroft-Gault formula (CGF), abbreviated diet modification of renal disease (MDRD) formula, the Mayo formula and the cystatin C-based formula as proposed by Larsson et al. Included were 189 in-patients (aged 20-87, 40% of them women, range of inulin clearance 8-244 ml/min/1,73m). In addition, inulin clearance was compared with creatinine clearance in 142 patients (aged 20-87 years, 42% women. Inulin clearance 13-244 ml/min/1,73m). Bland-Altman diagrams were drawn and mean bias and standard deviation of the formulae were compared with inulin clearance, as were sensitivity and specifity for diagnosing reduced renal function. RESULTS: All formulae underestimated glomerular filtration rate (GFR), with CGF and MDRD formulas giving the best results. These formulae had a mean bias of -16.2 (SD 24.8) and -18.2 (SD 25.6) ml/min/1,73m (2) , respectively. All creatinine-based formulae showed a high sensitivity and specifity for diagnosing a GFR below 60 ml/min/1,73m (2). CONCLUSION: None of the estimating formulae can replace inulin clearance with adequate accuracy. In our patients the cystatin C formula of Larsson et al showed no advantage. But the MDRD formula, which can be calculated without knowing body weight, is as accurate and precise as CGF.

Ten years of laparoscopic living donor nephrectomy: retrospect and prospect from the nephrologist's point of view.

The laparoscopic living kidney donor nephrectomy introduced in 1995 has become an accepted method of kidney harvest for transplantation. The method has proven its usefulness as well as its superiority compared to open donor nephrectomy. Based on the results of a decade, an overview from a nephrologist's point of view is presented here in; a view that is known to be quite different from (and sometimes contrary to) the surgeon's approach. While urologists and surgeons focus more on the technique and complication rates, the nephrologist tends to estimate the new procedure with regard to his dialysis patients' outcomes (ie, whether it will result in an increased number of kidney transplantations in the long term). The latter aspect has to be the benchmark in the estimation of the effects of this procedure; it is the ultimate goal of every surgery in kidney transplantation. The 10-year results are more than encouraging, but nevertheless it will take at least one more decade for a valid evaluation.

[Abscettic pneumonia in a renal transplantation female patient]. / Abszedierende Pneumonie bei einer nierentransplantierten Patientin.

A 39-year old female patient who was kidney transplanted three years ago was admitted to hospital with fever of unknown origin for several days. Blood samples revealed decreased renal function and increased inflammation parameters. Chest X-ray and CT scan showed multiple cavernous structures, some with liquid. Staphylococcus aureus was detected in blood culture samples. With the aid of these results Staphylococcus pneumonia with multiple abscesses was diagnosed. The treatment consisted of removal of the infectious focus and a systemic antibiotic therapy corresponding to the microbiologic results. We describe a case of Staphylococcus pneumonia caused by a infected vascular prosthesis under consideration of immunosuppression in a renal transplanted patient.

Cardiac beta-adrenoceptors in chronic uremia: studies in humans and rats.

OBJECTIVES: The purpose of this study was to elucidate whether cardiac beta-adrenergic effects may be blunted in patients on maintenance hemodialysis (HD) and may help to explain autonomic dysfunction. BACKGROUND: Patients on HD often suffer from autonomic dysfunction. METHODS: We investigated the cardiovascular response of five HD patients (age: 46.1+/-7.9 years) and six healthy volunteers (age: 48.2+/-7.5 years) to isoprenaline, pirenzepine and phenylephrine. For analysis of underlying mechanisms of beta-adrenoceptor hyporesponsiveness, six-week-old male Wistar rats were rendered uremic by 5/6-nephrectomy (n = 9; SNX) and were killed for removal of the heart after six to seven weeks. Sham-operated rats (n = 15) served as controls. RESULTS: In the patient study, isoprenaline (3.5, 7, 17, 35 ng/kg/min, i.v.) led to an increase in heart rate, and shortening of the heart rate corrected duration of the electromechanical systole (QS2c), both of which were significantly reduced in HD patients. Baroreflex sensitivity was significantly reduced in HD patients. The response to low parasympathomimetic doses of pirenzepine was unchanged. In the rat study, left ventricular strips were placed in an organ bath, electrically driven and exposed to isoprenaline (10(-11) to 10(-6) mol/liter). While pD2 values were unchanged, maximum effect at the highest concentration was significantly reduced in SNX rats. The response to carbachol was not altered, nor was the M2-cholinoceptor density. There was no difference in beta-adrenoceptor density, or in immunodetectable amount of Gs and Gi protein. Activation of adenylyl cyclase evoked by isoprenaline was significantly reduced in left ventricular membranes of SNX rats, whereas effects of 10 micromol/liter GTP, 10 mmol/liter NaF, 10 micromol/liter forskolin and 10 mmol/liter Mn2+ were not altered. CONCLUSIONS: Cardiac beta-adrenergic responses are blunted in chronic uremia due to reduced isoprenaline-dependent activation of adenylyl cyclase. This might be caused by an "uncoupling" of the receptor or by an inhibition of the receptor by uremic toxins.