Blunted renal dopaminergic system activity in puromycin aminonucleoside-induced nephrotic syndrome.

BACKGROUND: A primary tubular sodium handling abnormality has been implicated in the edema formation of nephrotic syndrome. Dopamine synthesized by renal proximal tubules behaves as an endogenous natriuretic hormone by activating D(1)-like receptors as a paracrine/autocrine substance. METHODS: We examined the time courses of the urinary excretion of sodium, protein and dopamine in puromycin aminonucleoside (PAN)-treated and control rats. The rats were sacrificed during greatest sodium retention (day 7) as well as during negative sodium balance (day 14) for the evaluation of renal aromatic l-amino acid decarboxylase (AADC) activity, the enzyme responsible for the synthesis of renal dopamine. Also, the influence of volume expansion (VE) and the effects of the D(1)-like agonist fenoldopam (10 microg/kg bw/min) on natriuresis and on proximal tubular Na(+),K(+)-ATPase activity were examined on day 7. RESULTS: The daily urinary excretion of dopamine was decreased in PAN-treated rats, from day 5 and beyond. This was accompanied by a marked decrease in the renal AADC activity, on days 7 and 14. During VE, the fenoldopam-induced decrease in proximal tubular Na(+),K(+)-ATPase activity was more pronounced in PAN-treated rats than in controls. However, the urinary sodium excretion during fenoldopam infusion was markedly increased in control rats but was not altered in PAN-treated animals. CONCLUSION: PAN nephrosis is associated with a blunted renal dopaminergic system activity which may contribute to enhance the proximal tubular Na(+),K(+)-ATPase activity. However, the lack of renal dopamine appears not to be related with the overall renal sodium retention in a state of proteinuria.     

肾综合征出血热发病机制研究进展

肾综合征出血热发病机制至今仍未完全阐明,病毒、病毒受体、细胞因子、自由基、特异性CTL反应、HLA差异性均可能与发病有关.此文对近年来的研究进展进行了综述.     

慢性肾衰竭急性加重的临床特征及相关因素分析

目的：探讨慢性肾衰竭（CRF）急性加重因素及其治疗措施对预后的影响。方法：对2001年1月～2005年6月住院治疗的CRF急性加重患者42例，按其加重原因、基础疾病、治疗方式和疗效进行回顾性总结。结果：CRF急性加重因素依次为各种感染（45．2％）、原发病加重（19．0％）、高血压未控制（14．3％）、水电解质紊乱（11．9％）、肾毒性药物（11．9％）、心功能不全（9．5％）、尿路梗阻（4．8％）、血高粘滞状态（2．4%），7例同时存在≥2种上述病因（16．7％）。CRF急性加重原发病以慢性肾小球肾炎（52．4％）和糖尿病肾病（11．9％）为主。积极治疗后肾功能恢复达到或接近原来水平者40例，死亡2例，死亡2例的年龄均在60岁以上。结论：对于CRF肾功能急剧恶化的患者，应积极寻找其加重因素，并采取非透析和透析相结合治疗，改善肾功能，降低病死率，延长患者生命。     

Cardiovascular calcification in end-stage renal disease.

Cardiovascular diseases are common in patients with end-stage renal disease (ESRD) and cardiovascular morbidity and mortality among dialysis patients are substantially higher than in the general population. The reasons for this high incidence are multiple. They include traditional factors such as hypertension, diabetes, dyslipidaemia, sodium overload, and elevated homocysteine levels as well as disturbances of mineral metabolism, specifically abnormalities in phosphorus and calcium homeostasis. This review will describe the specific cardiovascular complications related to calcifications in ESRD, the implications of the abnormalities of mineral metabolism in its pathogenesis and the current imaging techniques available for the detection of cardiovascular calcifications. Excess of calcium load contributes to the development of cardiac calcifications; therefore, alternative strategies to diminish exogenous calcium load should be considered in patients with ESRD.     

糖化血红蛋白及糖化血清蛋白与糖尿病肾功能衰竭患者的血糖监测

糖化血红蛋白(Hb)A1c是血糖监测的苇要指标,反映检测前2～3个月的平均血糖水平.慢性肾功能衰竭(CRF)患者存在贫血、酸中毒、氧化应激、胰岛素抵抗、血液透析及促红细胞生成素(EPO)的应用等因素,对HbA1c的测定会造成影响.糖化血清蛋白(GSP)反映检测前2～3周的平均血糖水平,仅受血浆蛋白的影响,几乎不受血红蛋白和EPO治疗等以上因素的影响,且对短时间内的血糖变化更为敏感.将GSP作为糖尿病肾功能衰竭患者血糖监测指标可能比HbA1c更理想.     

肾综合征出血热患者T细胞亚群数量与白细胞介素2,4水平变化的关系

采用ABC免疫组化染色法及单克隆抗体夹心法ELISA，同步检测了34例肾综合征出血热（HFRS）患者外周血T细胞亚群数量和血清白细胞介素2和4（IL－2、IL－4）水平。发现HFRS病程中各T细胞亚群数量均有不同程度的升高，其中CDS阳性T细胞在各病期均有升高。IL－4水平升高仅见于发热期．而IL－2的升高主要在低血压期和少尿期。病程中有CD4／CD8比值的下降甚至倒置。这种比值的变化与IL－2和IL－4的动态变化有一定的相关性。结果揭示，在HFRS发病机理中存在Thl型和Th2型免疫反应等多种免疫病理机制。     

Neonatal renal failure due to obstructive candidal bezoars

Acute renal failure (ARF) developed in a 7-week-old infant due to bilateral candidal bezoars (fungal balls) causing obstruction at the pelviureteric junction. The baby was born at term with an appropriate birthweight, and had been treated with broad-spectrum antibiotics for respiratory distress and septicemia during the 1st week of life. Recovery from ARF followed renal decompression with bilateral nephrostomy tube placement and parenteral administration of amphotericin B and 5-flucytosine. Received August 21, 1996; received in revised form and accepted January 3, 1997     

Distal Penile Gangrene in a Patient with Chronic Renal Failure

To date, only 10 cases of distal penile gangrene in patients with chronic renal failure have been reported. This rare condition is believed to result from progressive vascular calcification due to secondary hyperparathyroidism in patients with chronic renal failure. We report an additional case of distal penile gangrene in a 41-year-old man who presented with chronic renal disease and pulmonary tuberculosis. Since some authors have emphasized that aggressive surgical treatment in such cases has a significant mortality rate, we took a more conservative approach to treatment.     

Cibenzoline-induced respiratory muscular paralysis in a hemodialysis patient

A 69-year-old man was admitted to our kidney center with endstage renal failure. We started intermittent peritoneal dialysis immediately because of severe azotemia, hyperkalemia, and metabolic acidosis. Two weeks after admission, he developed uremic pericarditis with frequent ventricular premature contractions and supraventricular premature contractions. The intermittent peritoneal dialysis was then replaced by intensive hemodialysis, and oral administration of 300 mg/d of cibenzoline was started. Four days later, he developed thirst, weakness, and dyspnea due to respiratory muscular paralysis. We initiated respiratory support with a respirator because analysis of his blood gases revealed marked hypercapnia and hypoxia. He also developed hypoglycemia and prolonged PQ and QRS intervals on the electrocardiogram, which we believed were due to cibenzoline intoxication; we discontinued the cibenzoline immediately. All symptoms improved, and he was extubated 5 days later. After 2 months, his pericardial effusion disappeared. He now continues maintenance hemodialysis as an outpatient. We suspect that the cibenzoline induced the respiratory muscular paralysis for 2 reasons: 1) the patient experienced the respiratory muscular paralysis, at the same time he also experienced thirst, weakness, hypoglycemia, and prolonged PQ and QRS intervals on electrocardiogram, and all of these symptoms improved after the discontinuation of cibenzoline, and 2) his plasma concentration of cibenzoline became remarkably elevated, to 20 times above the standard therapeutic level. This patient's clinical course indicates that hemodialysis might be superior to intermittent peritoneal dialysis for treatment of cibenzoline intoxication.