成人型主动脉弓中断一例

患者男,24岁。体检发现心脏杂音6年,无明显临床症状,有长期高血压病史。入院查体:脉搏120次/分,左上肢、右上肢、左下肢、右下肢的血压分别为147/96 mm Hg、143/89mm Hg、123/74 mm Hg和116/71 mm Hg。发育正常,口唇无紫绀;心尖搏动位置正常,心界大小正常,P2亢进。肝肾功能、     

孤立性右锁骨下动脉1例

病儿男,4岁.发现右上肢体脉搏弱1年.查体:发育可,右上肢血压50/30mm Hg(1 mm Hg=0.133 kPa),左上肢血压95/60 mm Hg,右下肢血压115/75 mm Hg,左下肢血压130/70 mm Hg;心前区未闻及杂音.X线胸片示两侧肺血不对称,右侧偏多,主动脉结不宽,肺动脉段平直,心胸比率0.55.     

孤立性右锁骨下动脉1例

病儿男,4岁.发现右上肢体脉搏弱1年.查体:发育可,右上肢血压50/30mm Hg(1 mm Hg=0.133 kPa),左上肢血压95/60 mm Hg,右下肢血压115/75 mm Hg,左下肢血压130/70 mm Hg;心前区未闻及杂音.X线胸片示两侧肺血不对称,右侧偏多,主动脉结不宽,肺动脉段平直,心胸比率0.55.     

孤立性右锁骨下动脉1例

病儿男,4岁.发现右上肢体脉搏弱1年.查体:发育可,右上肢血压50/30mm Hg(1 mm Hg=0.133 kPa),左上肢血压95/60 mm Hg,右下肢血压115/75 mm Hg,左下肢血压130/70 mm Hg;心前区未闻及杂音.X线胸片示两侧肺血不对称,右侧偏多,主动脉结不宽,肺动脉段平直,心胸比率0.55.     

孤立性右锁骨下动脉1例

病儿男,4岁.发现右上肢体脉搏弱1年.查体:发育可,右上肢血压50/30mm Hg(1 mm Hg=0.133 kPa),左上肢血压95/60 mm Hg,右下肢血压115/75 mm Hg,左下肢血压130/70 mm Hg;心前区未闻及杂音.X线胸片示两侧肺血不对称,右侧偏多,主动脉结不宽,肺动脉段平直,心胸比率0.55.     

孤立性右锁骨下动脉1例

病儿男,4岁.发现右上肢体脉搏弱1年.查体:发育可,右上肢血压50/30mm Hg(1 mm Hg=0.133 kPa),左上肢血压95/60 mm Hg,右下肢血压115/75 mm Hg,左下肢血压130/70 mm Hg;心前区未闻及杂音.X线胸片示两侧肺血不对称,右侧偏多,主动脉结不宽,肺动脉段平直,心胸比率0.55.     

孤立性右锁骨下动脉1例

病儿男,4岁.发现右上肢体脉搏弱1年.查体:发育可,右上肢血压50/30mm Hg(1 mm Hg=0.133 kPa),左上肢血压95/60 mm Hg,右下肢血压115/75 mm Hg,左下肢血压130/70 mm Hg;心前区未闻及杂音.X线胸片示两侧肺血不对称,右侧偏多,主动脉结不宽,肺动脉段平直,心胸比率0.55.     

孤立性右锁骨下动脉1例

病儿男,4岁.发现右上肢体脉搏弱1年.查体:发育可,右上肢血压50/30mm Hg(1 mm Hg=0.133 kPa),左上肢血压95/60 mm Hg,右下肢血压115/75 mm Hg,左下肢血压130/70 mm Hg;心前区未闻及杂音.X线胸片示两侧肺血不对称,右侧偏多,主动脉结不宽,肺动脉段平直,心胸比率0.55.     

孤立性右锁骨下动脉1例

病儿男,4岁.发现右上肢体脉搏弱1年.查体:发育可,右上肢血压50/30mm Hg(1 mm Hg=0.133 kPa),左上肢血压95/60 mm Hg,右下肢血压115/75 mm Hg,左下肢血压130/70 mm Hg;心前区未闻及杂音.X线胸片示两侧肺血不对称,右侧偏多,主动脉结不宽,肺动脉段平直,心胸比率0.55.     

孤立性右锁骨下动脉1例

病儿男,4岁.发现右上肢体脉搏弱1年.查体:发育可,右上肢血压50/30mm Hg(1 mm Hg=0.133 kPa),左上肢血压95/60 mm Hg,右下肢血压115/75 mm Hg,左下肢血压130/70 mm Hg;心前区未闻及杂音.X线胸片示两侧肺血不对称,右侧偏多,主动脉结不宽,肺动脉段平直,心胸比率0.55.     

Influences of renal stone surgeries on renal function--evaluation of renal function with 99mTc-DMSA renal scintigraphy]

From 1984 to 1990, 99mTc-DMSA renal scintigraphy was performed before and after nephrolithotomy (15 cases), pyelolithotomy (15 cases), percutaneous nephrolithotripsy (PNL: 15 cases) and extracorporeal shock wave lithotripsy (ESWL: 16 cases, 17 kidneys) in order to evaluate of influences of renal stone surgeries on split renal function. DMSA renal uptake change ratio of treated kidneys of nephrolithotomy (-24.94 +/- 5.60%) was significantly lower than that of PNL (-0.06 +/- 3.92%), pyelolithotomy (-4.08 +/- 4.79%) (p less than 0.01) and ESWL (-7.72 +/- 3.87%) (p less than 0.05). The average change ratios of contralateral kidneys were as follows: PNL 4.80 +/- 4.21% nephrolithotomy 4.67 +/- 4.73%, pyelolithotomy -1.46 +/- 5.39% and ESWL -2.02 +/- 4.44%. One to 3 weeks after PNL, the cold area on the renal image was found in 10 (66.7%) of 15 cases. In cases of ESWL, DMSA renal uptake decreased even 4-10 weeks (mean 7 weeks) after treatment. In conclusion, possivility of deterioration of renal function after ESWL was suggested.     

Transplantation of renal primordia: renal organogenesis

Dialysis and allotransplantation of human kidneys represent effective therapies to replace kidney function, but the former replaces only a small component of renal function, and the latter is limited by lack of organ availability. Xenotransplantation of whole kidneys from nonprimate donors is complicated by humoral and severe cellular rejection. The use of individual cells or groups of cells to repair damaged tissue (cellular therapies) offers an alternative for renal tissue replacement. However, recapitulation of complex functions such glomerular filtration and reabsorption and secretion of solutes that are dependent on a three-dimensionally integrated kidney structure are beyond the scope of most cellular replacement therapies. The use of nonvascularized embryonic renal primordia for transplantation circumvents humoral rejection of xenogeneic tissue and ameliorates cellular rejection. Renal primordia are preprogrammed to attract a vasculature and differentiate into a kidney and in this manner undergo organogenesis after transplantation into the mesentery of hosts. Here we review a decade’s progress in renal organogenesis.     

AusDiab renal study: indicators of renal disease

SUMMARY: The Australian Diabetes, Obesity and Lifestyle Study (AusDiab) was designed to determine the prevalence of diabetes and abnormal glucose metabolism, lifestyle and health behaviours and early indicators of renal disease in Australian adults. the study screened 11247 adults aged ≥ 25 years residing in randomly selected districts in all States and Territories of Australia between April 1999 and December 2000. Diabetes and hypertension were detected in 7.5% and 28.8%, respectively. Proteinuria was detected in 2.5% of subjects tested and serum creatinine was elevated in 1.06%. Dipstick screening followed by analysis of a mid-stream urine sample revealed haematuria in 6.8% of subjects tested. Body mass index scores indicated that 48.2% of all men screened were overweight, and a further 19.1% were obese. of the women, 30.2% were overweight and 21.8% obese. the results of the AusDiab study suggests one-third of the Australian adult population have at least one indicator of renal disease.     

Preservation of renal reserve in chronic renal disease

Protein-induced increases in glomerular filtration rate (GFR), termed renal reserve, is said to be abrogated with the onset of renal disease. However, this notion is inconsistent with the results from animal studies which suggest that alterations in protein intake modulate the glomerular hemodynamics in experimental renal disease. Accordingly, 12 normal subjects and 15 patients with renal disease received a protein meal providing 1 g/kg body weight protein. The subjects were pretreated with either placebo or an angiotensin I converting enzyme inhibitor, enalapril. A significant (P less than 0.05) increase in inulin and para-aminohippurate (PAH) clearance was noted in normal subjects as well as in patients with renal disease. The increase in GFR over basal values in normal subjects (28 +/- 9%), patients with moderate renal failure (20 +/- 13%), and advanced renal failure (21 +/- 14%) was not different. Plasma renin activity was unchanged following protein meal in the placebo studies although it increased following enalapril administration. Enalapril pretreatment did not alter the glomerular vasodilation and hyperfiltration following protein meal. We conclude that protein meal induces glomerular hyperfiltration in renal disease and that this protein-induced hyperfiltration is not mediated by angiotensin II. Because glomerular hyperfiltration is implicated in the progression of renal disease, these data suggest that even in patients who have advanced renal failure, high-protein diets may exert a detrimental effect on the kidney.