Lactate stress test in the diagnosis of mitochondrial myopathy.

The aim of the study was to determine the sensitivity and specificity of the lactate stress test in the detection of mitochondrial myopathies. Thirty one healthy subjects, 10 patients with non-mitochondrial myopathy and 26 patients with mitochondrial myopathy underwent lactate stress testing at a standardized workload of 30 W during 15 min on a bicycle ergometer. Lactate was determined before the exercise (R1), 5, 10, 15 min after starting the exercise (S5, S10, S15) and 15 min after finishing the exercise (R2). A result was interpreted as pathologic if more than two of the five lactate values were above the corresponding upper reference limits. The upper reference limits for the venous lactate at R1, S5, S10, S15 and R2 were 1.9, 2.0, 2.1, 2.0 and 1.7 mmol/l respectively. The lactate stress test was pathologic in 1/10 of the non-mitochondrial myopathies and in 18/26 of the mitochondrial myopathies. The sensitivity of the lactate stress test was 69%. The specificity of the test was 90%. In conclusion, the lactate stress test proved to be helpful for evaluating the integrity of the oxidative metabolism in the majority of patients with mitochondrial myopathy.

The kidney and primary hypertension: contributions from renal transplantation studies in animals and humans.

CLINICAL STUDIES: In clinical renal transplantation studies, recipients of a renal graft from a donor with a genetic predisposition to hypertension had higher blood pressures and required more antihypertensive treatment than recipients of a renal graft from a normotensive donor. In addition, blood pressure normalization in patients suffering from essential hypertension by bilateral nephrectomy and subsequent transplantation of a kidney from a normotensive donor has been reported. The interpretation of these data may be limited by the large number of different factors that can contribute to post-transplantation hypertension in human renal transplant recipients. EXPERIMENTAL STUDIES: In experimental renal transplantation studies the contribution of individual factors to post-transplantation hypertension can be independently assessed. Besides immunological graft rejection and hypertension-induced damage to the renal graft, a genetic predisposition to hypertension in the kidney donor has been demonstrated to be associated with post-transplantation hypertension in the recipient. Thus, normotensive recipients of a renal graft from a genetically hypertensive donor consistently developed post-transplantation hypertension in four different animal models of genetic hypertension. Furthermore, in genetically hypertensive rats bilateral nephrectomy together with transplantation of a kidney from a normotensive donor has been shown to be associated with a decrease in blood pressure. CONCLUSIONS: Hypertension following renal transplantation may be due to a variety of factors, including immunological graft rejection, hypertension-induced damage to the renal transplant and a genetic predisposition to hypertension of the kidney donor. The finding that blood pressure is transplanted with the renal graft in genetic hypertension suggests a genetically determined alteration to the kidney as a major factor in the aetiology of primary hypertension. The nature of this factor is just beginning to be understood. Renal transplantation studies in rat models of genetic hypertension, combined with the tools of molecular biology, may help to provide further insights into the role of the kidney in primary hypertension.