肾移植术后移植肾功能延迟恢复的处理(附14例报告)

目的探讨肾移植术后移植肾功能延迟恢复（DGF）的原因及处理措施。方法通过对发生DGF的14例患者临床表现、血肌酐、环孢素A（CsA）血浓度、彩色多普勒超声、移植肾细针穿刺吸抽细胞学检查（FNAB）等分析，诊断移植肾静脉栓塞1例，CsA中毒性肾损害2例，急性肾小管坏死（ATN）6例，急性排斥反应（AR）5例。分别予血液透析、手术探查、调整免疫抑制剂种类或剂量等处理。结果1例移植肾静脉栓塞患者行移植肾切除术；13例患者9—27d尿量增多，术后1个月复查肾功能良好。结论DGF原因包括技术性并发症、CsA中毒性肾损害、ATN、排斥反应等，应结合临床表现及辅助检查，早期诊断，及早采取血液透析、手术探查、调整免疫抑制剂种类或剂量等措施，可取得良好效果。     

Histological Features of Acute Tubular Necrosis in Native Kidneys and Long-Term Renal Function

There are few studies on the relationship between the morphology of acute tubular necrosis (ATN) in native kidneys and late functional recovery. Eighteen patients with acute renal failure (ARF) who had undergone renal biopsy were studied. All had the histological diagnosis of ATN and were followed for at least six months. Clinical characteristics of ARF were analyzed, and histological features were semi-quantitatively evaluated (tubular atrophy, interstitial inflammatory infiltrate, interstitial fibrosis, and ATN). According to the maximal GFR achieved during the follow-up, patients were divided into two groups: complete recovery (GFR ≥ 90 mL/min/1.73 m²) and partial recovery (GFR < 90 mL/min/1.73 m²). Only 39% of the patients achieved complete recovery. Patients with partial recovery achieved their maximal GFR (63 ± 9 mL/min/1.73 m²) 37 ± 14 months after ARF, a period of time similar to those patients with complete recovery (i.e., 54 ± 22 months). Patients with partial recovery had more severe ARF: oliguria was more frequent (90 versus 17%, p < 0.01), and they had higher peak creatinine (13.85 ± 1.12 versus 8.95 ± 1.30 mg/dL, p = 0.01), and longer hospitalization (45 ± 7 versus 20 ± 4 days, p = 0.03). No single histological parameter was associated with partial recovery, but the sum of all was when expressed as an injury index [4.00 (2.73–5.45) versus 2.00 (1.25–3.31), p < 0.05]. In conclusion, among patients with atypical ATN course, those with more severe ARF and tubule-interstitial lesions are more prone to partial recovery.     

急性肠系膜上动脉栓塞病程中的甲状腺激素水平

目的：探讨急性肠系膜上动脉栓塞患者血清甲状腺素水平及治疗后的变化规律。方法：选择42例急性肠系膜上动脉栓塞患者,于治疗前和治疗后1、3、7、14、30 d抽取空腹静脉血,利用放射免疫测定方法检测血清FT3、FT4、T3、T4、TSH水平;选择同龄同性别健康查体人员作为对照组。结果：治疗组血清FT3、FT4、T3、T4均明显低于正常对照组,且以肠坏死组最明显（P＜0.05）;治疗后血清甲状腺素降低,30 d后接近正常水平。结论：急性肠系膜上动脉栓塞患者存在低甲状腺素血症,且以肠坏死患者最明显,治疗后随病情逐渐恢复。     

Acute Tubular Necrosis Associated with Non-Hemorrhagic Dengue Fever: A Case Report

Dengue fever (DF) is an arthropod-born viral infection affecting humans. Dengue viruses are transmitted through the bites of the mosquito Aedes aegypti. Acute renal failure (ARF) is reported in patients who are affected mainly with Dengue hemorrhagic fever (DHF), which is a severe presentation of the disease. We report the case of a 24-year-old Omani female with no past history of particular medical problems. She was referred to our hospital for the further management of acute renal failure. She had clinical features of DF without DHF. The kidney biopsy showed features of acute tubular necrosis (ATN). She had a complete recovery after 25 days and required three sessions of hemodialysis. We conclude that DF even without DHF may lead to ATN and ARF. Clinicians should be aware of this etiology. Treatment is supportive and may require dialysis. The prognosis could be favorable.     

Selenium Deficiency and Thyroid Function in Acute Renal Failure

The lethality of acute renal failure exceeds 50% due to multiorgan dysfunction. In such critically ill patients a reduction of thyroid hormone concentrations without clinical symptoms or laboratory evidence of hypothyroidism frequently occurs. Selenium has recently been shown to play a major role in thyroid hormone metabolism. The aim of this study was to investigate the possible influence of selenium on thyroid hormone metabolism in acute renal failure. Changes in thyroid metabolism were related to the severity of multiorgan failure and to the clinical course. Thyroxine (T4), tri-iodothyronine (T3), free-T4, free-T3, thyrotropin (TSH), serum creatinine, and plasma selenium concentrations in 28 patients (mean age 60 ± 13) with acute renal failure and multiple-organ dysfunction syndrome were determined initially, and every 3 days after hospital admission. The plasma selenium concentration was found to be reduced compared to normal controls (32 ± 14 vs. 70–120 μg/L). T4 (56 ± 15 nmol/L, normal range 64–148), T3 (1.31 ± 0.38 nmol/L, normal range 1.42–2.46), free-T3 (3.1 ± 1.0 pmol/L, normal range 4.7–9.0), and free-T4 (10.8 ± 4.0 pmol/L, normal range 10.3–25.8) values were low in 50–70% of the patients at the time of presentation. Plasma TSH concentrations were within the normal range (0.59 ± 0.79 mU/L, normal range 0.25–3.1), and no clinical symptoms of hypothyroidism were observed. T4 concentration was higher in patients who survived acute renal failure compared to nonsurvivors (62 ± 22 vs. 51 ± 16 nmol/L, p < 0.05). Plasma selenium concentration was lower in patients with a severe organ dysfunction syndrome (36 ± 10 vs. 29 ± 19 μg/L) and correlated with the number of organ failures in these patients (r = –0.247, p < 0.05). T4 and free-T4 values paralleled decreasing selenium concentrations (r = 0.35, p < 0.05). Thyroid hormone levels were reduced in patients with acute renal failure without an increase in TSH. An increase in T4 concentrations became apparent during treatment and may be related to a favorable outcome in acute renal failure. Thyroid hormone concentrations paralleled plasma selenium levels, indicating a possible influence of selenium on thyroid function in acute renal failure.     

Relation of Thyroid Disfunction,Thyroid Autoantibodies,and Renal Function

Fifty-eight patients with thyroid dysfunction were included, comparing 27 healthy subjects to evaluate the relationship between thyroid autoimmunity, thyroid functional status, and renal function. Regardless of clinical status, hypothyroidism was defined as T3–T4 < normal limits and TSH>upper limit of normal, and hyperthyroidism was defined as T3–T4>normal limits and TSH < 0.1 mcU/mL. In all participants, serum antithyroperoxidase level, serum antithyroglobulin level, creatinine clearance (CC), and urinary albumin excretion rate (UAER) in 24-h urine collections were measured. Of 85 persons, 41 patients ages 20 to 71 years (median; 44) had hypothyroidism, 17 patients ages 22 to 56 years (median; 32) had hyperthyroidism, and 27 subjects ages 20 to 67 years (median; 50) were normal. Regarding thyroid autoantibody positiveness, the positive group had a higher UAER than the negative group (30.2 mg/day, 20.8 mg/day, respectively; p = 0.05). In hypothyroid patients, UAER was significantly higher than in hyperthyroid patients and control subjects (30.1 mg/day, 11.8 mg/day, 10.5 mg/day, respectively; p < 0.001). In the hypothyroid population, with regard to UAER and CC, we could not find a significant difference between the thyroid autoantibody positive and negative groups. In view of CC, hypothyroid patients had significantly lower CC than the hyperthyroid group (79.0 mL/min, 86.5 mL/min, respectively; p < 0.01). A careful control of the renal function in thyroid diseases should be evaluated. Renal dysfunction seems to be secondary to hypothyroidism rather than thyroid autoimmunity.     

急性髂股静脉血栓形成血清甲状腺激素测定的临床意义

作者对３２例髂股静脉血栓形成病人及３０例同龄健康人进行血清Ｔ３、Ｔ４、ｒＴ３和ＴＳＨ测定，结果表明，所有病人均存在低Ｔ３、低Ｔ４高ｒＴ３血症，同时表明血清甲状腺激素同病情轻重、病人预后及转归密切相关，血清Ｔ３低于０．５ｎｍｏｌ／Ｌ者病情危重，血清Ｔ４低于５０ｎｍｏｌ／Ｌ者预后不良。本研究表明，血清甲状腺激素测定可作为急性髂股静脉血栓形成、病情轻重和预后判断的实验室指标。     

Carboxypeptidase Z (CPZ) Links Thyroid Hormone and Wnt Signaling Pathways in Growth Plate Chondrocytes

Carboxypeptidase Z (CPZ) removes carboxyl‐terminal basic amino acid residues, particularly arginine residues, from proteins. CPZ contains a cysteine‐rich domain (CRD) similar to the CRD found in the frizzled family of Wnt receptors. We have previously shown that thyroid hormone regulates terminal differentiation of growth plate chondrocytes through activation of Wnt‐4 expression and Wnt/β‐catenin signaling. The Wnt‐4 protein contains a C‐terminal arginine residue and binds to CPZ through the CRD. The objective of this study was to determine whether CPZ modulates Wnt/β‐catenin signaling and terminal differentiation of growth plate chondrocytes. Our results show that CPZ and Wnt‐4 mRNA are co‐expressed throughout growth plate cartilage. In primary pellet cultures of rat growth plate chondrocytes, thyroid hormone increases both Wnt‐4 and CPZ expression, as well as CPZ enzymatic activity. Knockdown of either Wnt‐4 or CPZ mRNA levels using an RNA interference technique or blocking CPZ enzymatic activity with the carboxypeptidase inhibitor GEMSA reduces the thyroid hormone effect on both alkaline phosphatase activity and Col10a1 mRNA expression. Adenoviral overexpression of CPZ activates Wnt/β‐catenin signaling and promotes the terminal differentiation of growth plate cells. Overexpression of CPZ in growth plate chondrocytes also removes the C‐terminal arginine residue from a synthetic peptide consisting of the carboxyl‐terminal 16 amino acids of the Wnt‐4 protein. Removal of the C‐terminal arginine residue of Wnt‐4 by site‐directed mutagenesis enhances the positive effect of Wnt‐4 on terminal differentiation. These data indicate that thyroid hormone may regulate terminal differentiation of growth plate chondrocytes in part by modulating Wnt signaling pathways through the induction of CPZ and subsequent CPZ‐enhanced activation of Wnt‐4.     

Biopsy Proven Acute Tubular Necrosis Associated with Vancomycin in a Child: Case Report and Literature Review

Vancomycin-related nephrotoxicity typically manifests as acute tubulointerstitial nephritis. The drug does appear, however, to increase the nephrotoxicity of concurrently administered aminoglycosides. The extent of direct tubular toxicity attributable to vancomycin, especially in the absence of aminoglycoside treatment, does not appear to have been previously described. We report a case of biopsy-proven acute tubular necrosis secondary to vancomycin toxicity in a 13-year-old boy where there was no likely alternate explanation for toxic or ischemic injury. No hemodialysis was required, and the patient made a full recovery with subsequently regained renal function.     

动员自体骨髓干细胞对大鼠急性肾小管坏死的治疗

目的：观察粒细胞集落刺激因子联合干细胞因子动员骨髓干细胞的作用、骨髓干细胞是否具有向损伤肾组织归巢的能力及其在肾脏组织中的分布,初步探讨粒细胞集落刺激因子联合干细胞因子是否具有促进急性肾小管坏死修复的作用。方法：160只8～10周龄雄性SD大鼠随机分为4组：对照组,模型组、G-CSF＋SCF治疗组、G-CSF＋SCF对照组,检测：（1）外周血白细胞总数及单个核细胞中CD34＋细胞百分比的变化;（2）尿NAG酶检测;（3）肾脏组织病理学改变;（4）肾组织CD34＋细胞表达变化。结果：（1）G-CSF＋SCF治疗组和G-CSF＋SCF对照组外周血中白细胞数、CD34＋细胞百分比于第5天达高峰,与对照组、模型组相比,差异有统计学意义（P〈0.05）,以后逐渐下降;相应地,G-CSF＋SCF治疗组肾组织内CD34＋细胞较对照组、模型组也明显增多（P〈0.05）。（2）手术后第5、10、17天,G-CSF＋SCF治疗组尿NAG酶、肾脏病理学改变均明显好于模型组（P〈0.05）。第24天G-CSF＋SCF治疗组尿NAG酶、肾脏病理学改变基本恢复正常,而模型组仍异常。第31天各组间尿NAG酶、肾脏病理学改变其差异无统计学意义。结论：（1）粒细胞集落刺激因子和干细胞因子联合应用对缺血再灌注损伤诱发急性肾小管坏死大鼠的骨髓干细胞有显著的动员作用。（2）骨髓干细胞能在损伤的肾小管归巢和定居,并可能参与损伤肾组织的修复。（3）粒细胞集落刺激因子和干细胞因子联合应用能在一定程度上加速急性肾小管坏死后肾功能的修复。     

Acute Renal Failure as a Complication of Acute Pancreatitis

To assess the prevalence of acute renal failure (ARF) inpatients with acute pancreatitis, as well as the factors predictive of a lethal outcome, we retrospectively studied the data of all patients admitted to our hospital over a 5-year period. Between 1989 and 1993, 554 patients presented with acute pancreatitis, of which 24 (4.4%) subsequently developed ARF. Death occurred in 14/24 (58%) of patients with ARF, and was associated with an increased incidence of multiorgan failure. There was no statistically significant difference in the age, admission blood pressure, or admission pulse rate of the patients who survived and those who died. In contrast, death was associated with a higher Ranson score, and the increased prevalence of multiorgan failure. The length of hospitalization of the nonsurviving group was significantly shorter. Acute renal failure is not a common finding in patients with acute pancreatitis. However, when it occurs, it is associated with a poor prognosis, and is predicted by a higher Ranson score and the presence of multiorgan failure.     

Plasmapheresis in Treatment of Acute Oligoanuria in Crescentic Glomerulonephritis

Plasmapheresis therapy can provide an approach in the treatment of crescentic glomerulonephritis by mechanically removing nephritogenic factors from the circulation, both antiglomerular basement membrane antibodies and circulating immune complexes as well as antineutrophil cytoplasmic antibodies (ANCAs). We present our experience with plasmapheresis treatment in patients with acute oligoanuria caused by crescentic glomerulonephritis. We used membrane plasmapheresis to treat 11 patients with crescentic glomerulonephritis with more than 80% crescent formation on biopsy and with acute onset of the disease and acute oligoanuria. The immune complex form of the disease was documented in 7, the anti-glomerular basement membrane antibodies mediated (anti-GBM) form in 2, the ANCA-associated form in 1 case, and the recurrent anti-GBM form in 1 patient. Plasmapheresis was performed 2–3 times weekly using Bellco BL 500 and Gambro 2000 PF plasma filters. The total number of plasma exchanges (2,000–2,200 ml each) for each patient was 5–9. The treatment was associated with steroids and cyclophosphamide. The improvement of renal function with the start of diuresis and significant decrease of creatinine from the range of 786–1,301 μ M at the start of the treatment was noted in 5 of the 11 patients. The duration of remission without hemodialysis was 6–12 months. Treatment with plasmapheresis in cases with recurrent anuria was without benefit. We can conclude that plasmapheresis can delay end-stage renal failure in cases with acute onset of crescentic glomerulonephritis.     

Recombinant Tissue‐Type Plasminogen Activator in the Treatment of Acute Renal Artery Thrombosis After Kidney Transplantation

Acute arterial thrombosis is an uncommon but potentially devastating consequence of kidney transplantation. Early recognition followed by thrombectomy may salvage the graft. We present a case of acute renal artery thrombosis after a living‐related kidney transplant with successful treatment with operative thrombectomy and intraarterial infusion of recombinant tissue‐type plasminogen activator.     

Parathyroid Hormone as a Marker for the Differential Diagnosis of Acute and Chronic Renal Failure

It is often difficult to distinguish acute renal failure clinically from chronic renal failure, especially in patients who do not have records of their medical history. We investigated the magnitude of iPTH increase in ARF and the potential role of iPTH as a marker for differential diagnosis of ARF and CRF in new patients referred to our renal unit. We prospectively analyzed 122 (ARF n?=?64, CRF n?=?58) patients referred to our renal unit with serum creatinine higher than 2 mg/dL. ROC curve analysis was performed to investigate role of iPTH for differentiating ARF from CRF. The sensitivity, specificity, and positive predictive value of iPTH in discrimination of ARF and CRF were calculated. There was no statistically significant difference regarding the means of age, sex distribution, and serum chemistry between patients with ARF or CRF. But serum iPTH (p < 0.0001) levels were lower in patients with ARF than in those with CRF. A cutoff, set at 170pg/mL for iPTH to discriminate patients with CRF, yielded a sensitivity of 88% and a specificity of 89%. This study confirms that the iPTH measurement is of clinical value in differentiating acute from chronic renal failure.     

Impact of Early or Delayed Cyclosporine on Delayed Graft Function in Renal Transplant Recipients: A Randomized, Multicenter Study

The benefit of delayed cyclosporine in reducing risk of delayed graft function (DGF) is not clearly established. This study compared early vs. delayed cyclosporine microemulsion (CsA-ME) in de novo renal transplant patients. Patients were randomized to early (day 0, n = 97) or delayed (day 6, n = 100) CsA-ME at an initial dose of 8 mg/kg/day with dose adjusted according to C₂ level. All patients received enteric-coated mycophenolate sodium (EC-MPS), steroids and an anti-interleukin-2 receptor antibody. In both groups, 33% of patients were at high risk of DGF; 26 patients (26.8%) in the early CsA-ME group and 23 patients (23.0%) in the delayed CsA-ME group experienced DGF (n.s.). Renal function at 3 months was comparable (creatinine clearance 51.1mL/min with early CsA-ME and 53.8 mL/min with delayed CsA-ME), and remained similar to 12 months. Treatment failure, defined as biopsy-proven acute rejection, graft loss or death, did not differ significantly at 12 months (23.7% with early CsA-ME vs. 29.0% with delayed CsA-ME). Biopsy-proven acute rejection occurred in 15.5% of early CsA-ME and 26.5% of delayed CsA-ME patients (n.s.). Both regimens were well tolerated. These data suggest that early or delayed introduction of CsA-ME results in similar renal function in renal transplant patients regardless of DGF risk level.     

Mortality in Elderly Patients with Acute Renal Failure

In a retrospective study, we identified 55 elderly patients with acute renal failure (ARF) admitted to our hospital during an 8-year period from 1985 to 1993. Information about the etiology, complications, laboratory data, and treatment course were obtained from the clinical history. Of the 200 patients with ARF admitted to the hospital during this period, 28% were patients more than 60 years old (41 male and 14 female) with an average age of 68.5 ± 7 years. The main causes of ARF were sepsis, volume depletion, low cardiac output, arterial hypotension, nephrotoxicity by antibiotics, and obstructive uropathy. The global mortality of elderly patients with ARF was 53%. The mortality rate of the different types of the ARF were: prerenal 35%, intrinsic 64% (oliguric 76%, nonoliguric 50%), and postrenal 40%. Mortality as a result of sepsis occurred in 18 patients (62%), by cardiovascular disease in 4 patients (13%), by acute respiratory failure in 2 patients (7%), and by other causes in 5 patients (18%). In the cases of sepsis, Pseudomonas was detected in 7 cases (39%), Escherichia coli in 2 cases (11%), Gram-negative nonspecific in 3 cases (17%), Klebsiella in 1 case (5%), and in 5 cases (16%), the hemoculture was negative. The patient survival rate was 47% (26 of 55 patients). Of these patients, 19 recovered their normal renal function (73%), but 7 patients remained with renal failure (27%). In conclusion, the global mortality in the elderly patients without considering the types of ARF was 53%. The oliguric form had the highest mortality rate with 76%. The main causes for mortality were sepsis with 62%, cardiovascular disease with 13%, and other causes 18%.     

Effects of Thyroid Function on the Course of Experimental Chronic Renal Failure in Rats

Thyroid hormone has been reported to affect renal function. To investigate the effects of thyroid hormone on the progression of renal deterioration, thyroid hormone (dried thyroid) and an antithyroid drug (thiamazole) were administered to adriamycin (ADR)-induced renal failure rats. The rats were divided into four groups, including 1) ADR-DT, given dried thyroid and thiamazole; 2) ADR-T, given thiamazole; 3) ADR; and 4) control. The survival rate at the end of the study (22 weeks) was 62.5% in ADR-DT group and 100% in ADR-T, ADR, and control groups, respectively. There was a significant difference in the body weight and pulse rate between ADR-DT and ADR-T or ADR groups, except for the pulse rate at week 6 (P < 0.05). The creatinine clearance was greater in the ADR-T group than in the ADR or ADR-DT groups at week 22, and was significantly different between the ADR-T and the ADR-DT groups (P < 0.05). The fractional kidney weight and tubular changes were significantly greater in the ADR-DT group than in the ADR-T or ADR groups (P < 0.05). The interstitial volume was significantly greater in the ADR-DT group than in the ADR-T group (P < 0.05). We therefore conclude that a dried thyroid has an aggravative effect in the tubular changes and relative interstitial volume induced by ADR.     

Low free thyroxine concentrations and deficient nocturnal surge of thyroid-stimulating hormone in haemodialysed patients compared with undialysed patients.

BACKGROUND: There is little information on the differences in pituitary-thyroid function between undialysed and haemodialysed patients. METHODS: Serum concentrations of free thyroxine (T(4)) and free triiodothyronine (T(3)), measured by enhanced chemiluminescence immunoassay, and thyroid-stimulating hormone (TSH) were compared in undialysed (n=22) and haemodialysed patients (n=85). The response of the serum TSH concentration to exogenously administered thyrotropin-releasing hormone (TRH) and circadian variation in serum TSH were also studied in the two groups. RESULTS: Serum free T(4) concentration was significantly lower in haemodialysed than in undialysed patients (1.02+/-0.02 vs 1.33+/-0.06 ng/dl, P<0.0001). Serum concentrations of free T(3) and TSH were essentially the same for the two groups. The response of serum TSH concentration to TRH was basically the same. Serum TSH concentration in undialysed patients during the night and in the morning were 142.4+/-15.4% and 121.7+/-4.1% of that during the day, the differences being significantly different. A nocturnal surge of TSH was not observed in haemodialysed patients. CONCLUSIONS: Low serum free T(4) concentration and a deficient nocturnal surge of TSH were found in haemodialysed patients compared with undialysed patients. The deficient nocturnal surge of TSH may contribute to the lower serum free T(4) concentration in haemodialysed patients.     

Acute Ureteral Obstruction and Glomerulotubular Function in Rats

Urinary tract obstruction is a common cause of acute renal failure (ARF). During unilateral ureteral obstruction (UUO) arteriolar vasoconstriction, increase in tubular pressure, and ultrafiltrate retrodiffusion occur. We studied renal function of rats with surgical UUO for 24 hr. After this period of UUO, the contralateral kidney was removed and the right ureter was deobstructed. The control uninephrectomized group consisted of normal rats submitted to left uninephrectomy (UNx). Functional studies were performed 12 and 24 hr, and 7 days after deobstruction and UNx. We measured creatinine clearance, and fractional excretion of sodium and lithium. Using conventional formulas we calculated fractional proximal and distal sodium reabsorption. Initially we observed a reduction in glomerular filtration rate (GFR) after deobstruction (12 and 24 hr). However, after 7 days, the GFR was significantly higher in deobstructed rats than in controls (340.3 ± 18.3 vs. 286.4 ± 9.3 μL/min/100 g, p < 0.01). The dry kidney weight was also increased in these rats. The fractional sodium excretion was increased in deobstructed rats, mainly in early studies (12 and 24 hr). Whereas fractional proximal reabsorption was reduced in both groups, the fractional distal reabsorption was significantly decreased in the deobstructed group compared to UNX controls (93.9 ± 0.9 vs. 98.9 ± 0.1% after 24 hr, p < 0.01). Our data showed that UUO influenced both glomerular and tubular functions. A salient finding was the overcorrection of GFR 7 days after deobstruction. The renal release of hormones and growth factors could mediate these alterations in renal function through their vascular, tubular, and proliferative actions.