[Progress of diagnosis and treatment of hypertensive renal damage by Chinese medicine].

Hypertensive renal damage is based on the extent and duration of hypertension, renal damage caused by varying severity. Hypertensive renal damage due to various causes imbalance of vascular active substances, renal arteriosclerosis, so that the abnormal renal hemodynamic, renal ischemia, low specific gravity of urine, low osmotic pressure and urine. The rapidly increasing incidence of hypertensive renal damage has become one of the most important reasons of end stage renal disease (ESRD). Effective treatment of hypertension is limited by poor compliance and significant adverse reaction of antihypertensive drugs. Therefore, some patients have turned to Chinese medicine (CM), hoping that such treatments might improve the efficiency. The author reviews relevant theory and the latest researches, on the basis of combining diseases and syndrome, discusses state and achievement of hypertensive renal damage with Chinese herbal medicines from fundamental and clinical research and action mechanism from standpoints of Chinese herbal compound and herbal effective chemical composition to take future research for important reference.

[Hereditary hyperferritinemia cataract syndrome]. / Das hereditäre Hyperferritinämie-Katarakt-Syndrom.

HISTORY: A 42-year-old man was found to have a four to six fold increase in the level of plasma ferritin since four years. In the age of 10 he had undergone unilateral resection of a dysplastic kidney associated with systemic hypertension. He had also developed recurrent venous thromboses caused by atresia of the inferior vena cava with azygos continuation, known since 23 years. Iron overload or hemochromatosis had been excluded, but despite numerous investigations the exact cause of the hyperferritinemia had not been elucidated. The patient, his grandfather, his mother and a brother had undergone cataract surgeries in both eyes. He presented at admission with prominent veins over the abdomen a postthrombotic syndrome. INVESTIGATION: Laboratory tests revealed a ferritin level 6 times above the upper limit of normal, but iron, transferrin saturation, and transferrin levels were normal. The patient was on oral anticoagulation (INR 2.2). Molecular genetic tests revealed heterozygous mutation IRE+ 32 G > T. DIAGNOSIS, TREATMENT AND COURSE: The findings indicated a hereditary hyperferritinemia cataract syndrome with an autosomal dominant trait. As functions of other organs are not affected, bilateral cataract surgery is "curative". CONCLUSION: Early and correct diagnosis avoids unnecessary diagnostic and therapeutic interventions, such as extended and repeated laboratory tests, liver biopsies, phlebotomies and chelation therapy.

[Scleroderma renal crisis]. / Crise rénale sclérodermique.

Scleroderma renal crisis (SRC) occurs in patients with systemic sclerosis (SSc) and is defined by otherwise unexplained rapidly progressive renal insufficiency associated with oliguria or rapidly progressive arterial hypertension or both. SRC is a rare and severe complication of SSc, most often encountered during the first 4 years of disease, almost only in patients with diffuse SSc. Factors predicting SRC were identified, including high-dose corticosteroid administration. Use of angiotensin-converting enzyme inhibitors (ACEI) has dramatically impressed the prognosis of SRC, but it mortality rate is still high. Treatment aims at normalizing blood pressure as soon as possible. ACEI should always be used, and additional anti-hypertensive agents, including calcium channel blockers and alpha- and beta-blockers, may be useful. Renal replacement therapy may be needed, but often (for almost half of patients) only temporarily.

Elevated serum activity of N-acetyl-beta-glucosaminidase in essential hypertension: diagnostic value and reversal to normal values after antihypertensive therapy.

Previous studies have shown that urinary N-acetyl-beta-glucosaminidase (NAG) is elevated in patients with hypertension, even without renal disease. To elucidate the value of measuring NAG, both in urine and serum of hypertensive patients, we measured NAG activity in the serum, plasma, and 24-hour urine by the fluorimetric method in 84 patients with uncomplicated essential hypertension before and after 6 months of effective treatment. NAG activities of these hypertensive patients were compared with those of 102 healthy normotensive subjects and 97 patients with various renal diseases and controlled hypertension. Serum NAG activity was clearly greater in patients with essential hypertension (427 +/- 124 U/mL) than in normotensive subjects (380 +/- 109 U/mL) or patients with renal disorders (393 +/- 115 U/mL) (P less than or equal to 0.004). The greater was the diastolic pressure in the hypertensive group, the greater was serum NAG activity (r = +0.30, P = 0.004). Hypertensive patients with high serum NAG activity were further characterized by a more exaggerated increase in systolic pressure (34 +/- 16 v 25 +/- 15 mm Hg, P = 0.051) and total peripheral resistance (19% +/- 18% v 12% +/- 13%, P = 0.042) in response to the cold pressor test and by a greater increase in systolic pressure (56 +/- 15 v 45 +/- 13 mm Hg, P = 0.009) and diastolic pressure (11 +/- 7 v 6 +/- 9, P = 0.043) in response to bicycle exercise testing than the group with low serum NAG activity. In contrast, urinary NAG activity tended to be only slightly higher in patients with essential hypertension than in the normotensive control group (33 +/- 31 v 23 +/- 29 U/mg creatinine [cr], P = 0.062), whereas patients with renal diseases had clearly increased urinary NAG activity (87 +/- 105 U/mg cr) (P less than 0.001). Following effective antihypertensive therapy, serum NAG activity decreased in patients with essential hypertension to values of normotensive control subjects (from 427 +/- 124 U/mL to 386 +/- 106 U/mL, P less than 0.01). A significant decrease in serum NAG activity was observed in patients with both initially high as well as low pretreatment serum NAG activities (P less than 0.001 and P less than 0.02, respectively). Urinary NAG activity overall was unchanged by antihypertensive treatment. We conclude that in patients with mild essential hypertension, serum NAG activity was already elevated (whereas urinary NAG activity was not) and was normalized by effective antihypertensive treatment.(ABSTRACT TRUNCATED AT 400 WORDS)

Diagnosis of angiotensinogenic hypertension: the complementary roles of renal scintigraphy and the saralasin infusion test.

A recently developed 1-day screening procedure for angiotensinogenic ("high-renin") hypertension is based on (A) a fall in blood pressure in response to intravenous infusion of the angiotensin antagonist, saralasin (P-113), and (B) peripheral venous renin assays by radioimmunoassay, in a sodium-depleted state. Out of 700 hypertensive patients screened by these tests, 160 had renal imaging performed with technetium-99m glucoheptonate and iodine-131 Hippuran. The P-113 infusion test proved superior to peripheral venous renin assays for the detection of angiotensinogenic hypertension. Positive infusion tests correlated well with renal vein renin assays. Frequently, however, both these tests were positive with bilateral renal disease and/or malignant hypertension. While renal imaging proved valuable in indicating which patients had a unilateral abnormality, it frequently could not distinguish unilateral renovascular disease from unilateral parenchymal disease unrelated to angiotensinogenic hypertension. Twenty-five patients in this series had arteriographic renal artery stenosis, of whom 3 had false negative P-113 infusion tests, 9 had negative peripheral renin assays, and 3 had no imaging abnormalities. This study indicates that scintigraphy is a useful procedure for the investigation of hypertensive patients when the initial P-113 infusion test is positive, or discordant with other findings. By imaging, angiotensinogenic hypertension due to bilateral renal disease can be distinguished from unilateral renovascular disease, and the site of the ischemic renal tissue can usually be identified.