代谢评估在泌尿系结石诊治中的应用

泌尿系结石为泌尿外科的常见病之一,其5年复发率高达50%。系统性地治疗泌尿系结石,除了通过药物或手术治疗清除结石,全面地评估患者有无代谢异常也是必不可少的。结石患者的代谢评估主要包括结石成分分析,血生化检查以及24h尿液成分分析。本文拟结合最新的泌尿系结石诊治指南,分析代谢评估在泌尿系结石诊治中的作用及其进展。     

尿流改道术后并发泌尿系结石的研究进展

泌尿系结石是根治性膀胱切除尿流改道术后常见的远期并发症之一,严重影响着患者的健康及生活质量,此类结石与常规泌尿系结石的病因及治疗有很大不同,已引起临床工作者的关注。根治性膀胱切除并行尿流改道后发生泌尿系结石主要因素包括代谢因素、感染因素以及术后的解剖因素,尿流改道后泌尿系结石的治疗方式主要有体外冲击波碎石术、经皮肾镜取石术、顺行或逆行输尿管镜碎石取石术及开放手术。本文对其发病因素及其治疗方法作一综述,以探讨尿流改道术后并发泌尿系结石的原因及治疗。     

甲状旁腺增生致反复泌尿系结石1例报告并文献复习

目的：总结甲状旁腺增生导致的反复泌尿系结石的诊断和治疗经验，提高泌尿外科医师对此病的认识、分析和治疗水平。方法：回顾性分析1例由甲状旁腺增生导致的反复泌尿系结石患者的临床资料：因反复泌尿系结石伴双上肢骨痛十余年，反复行体外冲击波碎石、输尿管镜碎石及相关骨科治疗，症状控制不理想。本次就诊时在详细追问病史下经科室会诊考虑为甲状旁腺机能亢进导致的泌尿系结石，遂经实验室检查证实。联合甲状腺乳腺外科进行手术。结果：术后患者症状明显缓解，病理检查结果为甲状旁腺增生。泌尿外科遂为患者清除输尿管结石。术后随访2年，未再发结石和骨痛。结论：泌尿外科医师在接诊反复结石患者时应考虑有甲状旁腺机能亢进的可能性；甲状旁腺激素检查有助于临床诊断；多学科团队模式可提高该类患者的诊疗效果。     

B超定位体外冲击波碎石术治疗泌尿系结石1000例分析

目的:探讨B超定位体外冲击波碎石(ESWL)治疗泌尿系结石的技术特点治疗效果及适应症.方法:对ESWL治疗的泌尿系结石结石1000例患者的临床资料进行分析和总结.结果:碎石治疗3个月排净结石956例,占95.6％;部分排除的41例,占4.1％;完全无变化的3例,占0.3％.结论:ESWL治疗泌尿系结石,疗效好,副作用小,并发症少,对大多数的泌尿系泌尿系结石疗效满意,但对输尿管结石合并重度肾积水或者肾萎缩的疗效较差,因此对那些结石过大,结石滞留输尿管时间过长致患侧肾脏受损严重的,不宜勉强行ESWL治疗.     

尿流改道后输尿管结石的处理（附8例报告）

目的：评价尿流改道后输尿管结石的治疗方案。方法：回顾性分析8例尿流改道后输尿管结石的处理方法,术前泌尿系腹部平片、泌尿系彩超、肾输尿管膀胱CT平扫明确为输尿管结石,所有患者对症治疗,随访观察1周,患者如结石未自行排出,行体外冲击波碎石术（ESWL）或逆行输尿管镜钬激光碎石。结果：2例患者输尿管结石自行排出;3例患者行ESWL,1例碎石后结石成功排出;5例行逆行输尿管软镜碎石成功。8例患者结石治疗后均未出现并发症。结论：尿流改道后输尿管结石的处理包括短期随访观察、ESWL及逆行输尿管软镜碎石治疗。逆行输尿管软镜碎石是安全有效的,可作为尿流改道患者输尿管结石的理想治疗方法之一。     

ESWL治疗输尿管结石失败原因分析

目的：分析32例输尿管结石ESWL治疗失败的原因。方法：应用Dorniercompact DeltaⅡ型体外冲击波碎石机对416例输尿管结石患者行ESWL治疗,其中32例经2～3次碎石后,结石未排出而改用输尿管镜或腹腔镜手术治疗。结果：32例失败患者中,22例结石全部粉碎或部分粉碎,因输尿管病变未排除;10例未击碎。结论：ESWL治疗输尿管结石必须严格选择病例,聚焦定位必须准确;结石长期固定输尿管同一位置致中重度肾积水患者,若首次治疗无结石排除,应及时改变治疗方法,避免过度治疗。     

80例三聚氰胺致婴幼儿泌尿系结石治疗的临床分析

目的回顾性分析80例三聚氰胺致婴幼儿泌尿系结石患儿的临床资料,提高对婴幼儿泌尿系结石的治疗水平。方珐纳入2008年9月-2008年11月在兰州大学第二医院诊治的80例三聚氰胺致婴幼儿泌尿系结石患儿,采用内科保守治疗或外科干预（输尿管镜下碎石及输尿管支架管置人术、微创经皮肾镜碎石术MPcNL）。培杲37例患儿采用内科保守治疗两周后30例结石完全排除,7例结石减小;43例采用外科干预,术后24h内患儿均出现多尿,尿量约为800-2500mL。复查B超,41例结石完全排出,2例结石减小。结论内科保守治疗和外科干预治疗对三聚氰胺致婴幼儿泌尿系结石患儿具有明显疗效,其中微创外科治疗可作为三聚氰胺致婴幼儿泌尿系结石梗阻患儿的首选方法。     

在刚果金的中国人多发泌尿系结石的原因及治疗预防措施

目的:探讨在刚果金的中国人多发泌尿系结石的原因及治疗预防措施.方法:分析在2010年6月～2010年9月21例患泌尿系结石的患者,进行诊断治疗的临床资料.结果:治疗主要是以非手术疗法,对症治疗为主.使用药物进行排石及溶石治疗.结论:在刚果金的中国人多发泌尿系结石的原因有多种,结石可以治愈,以预防为主.     

川西地区500例泌尿系结石成分构成及相关因素分析

目的：探讨川西地区泌尿系结石的成分构成及其相关因素。方法：前瞻性收集2011年11月～2013年11月经确诊为泌尿系结石的患者500例,采用红外光自动分析仪（LIIR一20型）分析结石成分构成。用SPSS13．0软件描述性分析相关研究指标。结果：泌尿系结石患者的性别比（男：女）为1．86：1,且以中青年（29～48岁）居多（46．8％）。少年患者以肾结石为主（55％）,青年、中年和老年患者以输尿管结石为主（分别占69．9％、65．2％和53．6％）。泌尿系结石成分主要为纯一水草酸钙（28．4％）,但青年患者以混合结石（一水草酸钙／二水草酸钙和碳酸）居多（38．2％）。汉族患者结石成分主要为纯一水草酸钙（29．8％、）;藏族多为混合结石（38．0％）。结论：川西地区泌尿系结石成分主要为草酸钙,且具有民族和地区差异,建议针对结石成分的特点采取相应的预防和治疗措施。     

内镜、腹腔镜联合治疗胆囊结石合并胆总管结石(附51例报告)

目的探讨十二指肠镜、腹腔镜联合治疗胆囊结石合并胆总管结石的治疗效果。方法采用十二指肠镜取出胆总管结石后，再用腹腔镜切除胆囊治疗胆囊结石合并胆总管结石病例的方法。结果51例患者的治疗均获得成功。结论胆囊结石合并胆总管结石的病例，通过十二指肠镜取出胆总管结石后，再行腹腔镜胆囊切除术，可避免开腹或腹腔镜胆总管探查等操作较复杂、创伤较大的手术方式。     

A case of incomplete distal renal tubular acidosis undergoing repeated treatment by extracorporeal shock-wave lithotripay and transureteral lithotripsy for recurrent urolithiasis

A 65-year-old woman was referred to our hospital for further examination of recurrent urinary stone formation. She had undergone 49 sessions of extracorporeal shock-wave lithotripay (ESWL) and 3 sessions of transureteral lithotripsy (TUL) under the diagnosis of idiopathic recurrent urolithiasis at another hospital. An excretory urography showed bilateral hydronephrosis and a retrograde urography revealed bilateral lower ureteral stricture. Ammonium chloride loading test demonstrated incomplete distal renal tubular acidosis. Potassium citrate therapy had begun and bilateral nephrostomies were required in order to prevent recurrent urinary tract infection and new stone formation. Literature was reviewed and discussion was made on the ureteral stricture after ESWL and TUL, and on incomplete distal renal tubular acidosis.     

Case of hypoparathyroidism, deafness and renal dysplasia (HDR) syndrome associated with nephrocalcinosis and distal renal tubular acidosis

Hypoparathyroidism, deafness and renal dysplasia (HDR) syndrome is an autosomal dominant disorder characterized by hypoparathyroidism, sensorineural deafness and renal dysplasia. Herein, we report a case of HDR syndrome associated with nephrocalcinosis and distal renal tubular acidosis. A 34-year-old woman was admitted to investigate recurrent stone formation and bilateral nephrocalcinosis. As a 3-year-old child, she had been diagnosed with HDR syndrome without chromosome evaluation. She had spontaneous stone passages on several occasions. On laboratory examination, serum calcium and intact parathyroid hormone at lower levels. Urinary citrate excretion was extremely low at 51.6 mg/day. On an ammonium chloride loading test, complete distal renal tubular acidosis was proved. To prevent the nephrocalcinosis from deteriorating, she was given potassium-sodium citrate. Since administration, she has not experienced spontaneous stone passage or renal colic. Nephrocalcinosis and recurrent urolithiasis will strongly affect renal prognosis in this case and we consider that citrate medication is an effective therapy in avoiding progress of her nephrocalcinosis.     

Management of urolithiasis with chronic renal failure

PURPOSE OF REVIEW: Epidemiological trends of urolithiasis and the prevalence of renal failure in patients with stones have changed. This is the era of minimally invasive therapy for stone disease. We review the impact of minimally invasive therapy on the management of urolithiasis in patients with renal failure and its outcome. RECENT FINDINGS: The prevalence of urolithiasis has reached its peak and plateaued in Europe and North America while it is still rising in the underdeveloped countries. The prevalence of renal failure in patients with chronic renal failure has reduced by half over the last decade. Minimally invasive therapy like percutaneous nephrolithotripsy has fared better than open stone surgery in all respects. Patients with kidney stones do not have normal renal function. Recently, cystine stones, and stones in patients with renal tubular acidosis and bowel disease were shown to affect renal function significantly. SUMMARY: Management of stones in chronic renal failure is challenging. Efforts should be made to minimize renal injury. Once a 'stone-free' kidney is achieved, steps should be taken to conserve renal function and address the issue of recurrence.     

Screening renal stone formers for distal renal tubular acidosis

A group of 110 consecutive renal stone formers were screened for distal renal tubular acidosis (RTA) using morning fasting urinary pH (mfUpH) levels followed by a short ammonium chloride loading test in patients with levels above 6.0. In 14 patients (12.7%) a renal acidification defect was noted; 13 had incomplete and 1 had complete distal RTA. Distal RTA was found particularly in recurrent stone formers (17%), and especially in those with bilateral stone disease, where a distal renal tubular acidification defect was found in 50%. We have been unable to differentiate primary from secondary RTA in renal stone formers. Regardless of whether the acidification defect is primary or secondary to stone formation, however, all renal stone formers with distal RTA can expect to benefit from prophylactic alkaline therapy and it is recommended that the screening procedure, which is easy to use in daily clinical practice, is applied to all stone formers and not restricted to patients with recurrent stone disease.     

Relationship between metabolic acidosis and calcium phosphate urinary stone formation in women

The relationship between the degree of metabolic acidosis and calcium phosphate stone formation was studied. Furthermore, the reasons why renal tubular acidosis (RTA) and primary hyperparathyroidism (PHPT) dominantly occur in women, and female stone formers more often produce calcium phosphate stone are discussed. Blood was slightly more acidotic in women than in men in both the urolithiasis and the control groups. Likewise, blood was significantly more acidotic and urinary pH significantly higher in patients with PHPT. Patients with RTA had severe metabolic acidosis, and urinary pH was highest among all groups. Calcium phosphate concentration was significantly higher in women than in men, and was also higher in patients with PHPT than in those with urolithiasis. All patients with RTA had pure calcium phosphate stones. The reasons why females are more acidotic and have more calcium phosphate in stones are suspected to be related to progesterone and urinary tract infection.     

Recurrent nephrolithiasis in renal tubular acidosis. Metabolic profiles,therapy and course

13 patients with recurrent urolithiasis and distal renal tubular acidosis (RTA I) were investigated for lithogenic metabolic disorders. Treatment was given and the patients observed for periods of up to 10 years.     

Prevention of recurrent calcium stone formation with potassium citrate therapy in patients with distal renal tubular acidosis

Distal renal tubular acidosis is a common cause of intractable calcium nephrolithiasis. We examined the effect of oral potassium citrate therapy in 9 patients with incomplete distal renal tubular acidosis diagnosed on the basis of an abnormal response to an oral ammonium chloride load. Patients were studied during a control phase and after 3 months of potassium citrate treatment (60 to 80 mEq. daily). Potassium citrate caused a significant increase in urinary pH and urinary citrate, and a decrease in urinary calcium. The urinary relative saturation ratio of calcium oxalate significantly decreased during treatment, while that of brushite did not change. Potassium citrate also was shown to inhibit new stone formation. During a mean treatment period of 34 months none of the 9 patients had new stones, although 39.3 plus or minus 79.7 (standard deviation) stones per patient formed during the 3 years preceding treatment. The results support the potential clinical advantage of potassium citrate therapy in patients with distal renal tubular acidosis and recurrent calcium nephrolithiasis.     

Effect of oxalate on the growth of renal tubular epithelial cells

PURPOSE: Until recently, oxalate was considered merely as a major component of calcium oxalate stones, forming crystals in the lumen of the renal tubules. However, new evidence suggests that oxalate is not only a major constituent of calcium oxalate stones but also has effect on renal tubular epithelial cells, affecting the pathogenesis of nephrolithiasis. We tried to elucidate the effect of oxalate on the growth of renal tubular epithelial cells of different species and locations and also to interpret the possible role of the oxalate in the pathogenesis of urolithiasis. MATERIALS AND METHODS: Porcine proximal renal tubular epithelial cells (LLC-PK1) and canine distal renal tubular epithelial cells (MDCK) were incubated with different concentrations of oxalate, and the effect of oxalate on the growth of the cells was assessed by methylthiazoletetrazolium assay. RESULTS: Growth of the renal tubular epithelial cells was inhibited with increasing concentrations of oxalate in both proximal and distal lines. CONCLUSION: Oxalate may cause stone formation by affecting the growth of renal tubular epithelial cells as well as by providing a constituent of calcium oxalate stones.     

Alkali action on the urinary crystallization of calcium salts: contrasting responses to sodium citrate and potassium citrate

Alkali therapy is used commonly to prevent recurrent stone formation in patients with distal renal tubular acidosis. We compared the effects of potassium citrate to those of sodium citrate in 6 well defined cases of incomplete distal renal tubular acidosis. The patients were studied during a control phase, during potassium citrate treatment (80 mEq. per day) and during sodium citrate treatment (80 mEq. per day) chosen in random order. Potassium citrate caused a decrease in urinary calcium and a significant increase in urinary citrate that resulted in a significant decrease in the urinary saturation of calcium oxalate. It did not alter the saturation of brushite and sodium urate. However, while sodium citrate also was able to increase the urinary citrate level, there was no decrease in the urinary calcium (owing to the increased sodium load). Thus, the urinary saturation of calcium oxalate did not decrease as much as with potassium citrate and the saturation of brushite increased significantly. Moreover, the urinary saturation of sodium urate increased significantly owing to the enhanced sodium excretion. The results suggest that potassium citrate therapy may retard the crystallization of calcium oxalate and may not cause calcium phosphate crystallization. In contrast, sodium citrate may have no effect or it sometimes may accentuate the crystallization of calcium salts. Thus, our study supports the potential clinical advantage of potassium citrate therapy over sodium alkali treatment in patients with incomplete distal renal tubular acidosis and recurrent calcium nephrolithiasis.     

Microlith Formation In Vitro by Madin Darby Canine Kidney (MDCK) Cells

Background : The mechanism of renal stone genesis as well as the location of stone crystal formation in the kidney remains unclear. Possible sites of stone generation are either in the tubular lumen or tubular cell. Methods : We cultured Madin Darby canine kidney (MDCK), LLC-PK1 and Magen Krebs Niigata-28 (MKN-28) cells in DMEM + 10% FBS medium in a well without passage for 30 days. Results : MDCK cells produced microliths at the basolateral side but not on the lumen side of these cells. The other two cell lines did not form microliths. Conclusion : Our data show that microlith formation is a characteristic of MDCK cells and that biological mineralization of MDCK cells may serve as a human urolithiasis model in vitro. The findings support a significant role of the renal distal convoluted tubule and collecting ducts in the in vitro generation of urinary stones.