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Luan D Truong

Publications and source records attributed to Luan D Truong.

At least 19 recordsLinked to original sources
PubMed2006

Immunoglobulin therapy for plasma cell-rich rejection in the renal allograft.

Plasma cell-rich acute rejection (PCAR) is associated with poor allograft outcome in renal transplantation. Previous studies report a graft half-life of six months after a single PCAR episode. However, the management of this condition is unclear. Intravenous immunoglobulin (IVIG) therapy, by virtue of its immunomodulating properties, and its influence on B-cell maturation into plasma cells, may be a good candidate for reversing this type of rejection. We report four episodes of PCAR in two patients who responded well to IVIG with improvement in renal function.

Adult↗
PubMed2006

Granulomatous pyelitis associated with urinary obstruction: a comprehensive clinicopathologic study.

Urinary obstruction is rarely associated with a distinct granulomatous inflammation, which involves the pyelocalyceal system and closely simulates infectious conditions including tuberculosis. Its clinicopathologic features, however, have not been adequately studied since there are only seven isolated reported cases. In a comprehensive study of 112 kidney specimens with urinary obstruction, we identified five cases of granulomatous pyelitis. The features of these cases were detailed and compared with the previously reported cases. Among the five identified subjects, three patients had history of urolithiasis and two had ureteral stenosis and all had stent placement 7 weeks to 12 years before nephrectomy for relief of the unilateral urinary obstruction. The age distribution was between 38 and 81 years. Two had end-stage renal disease or chronic renal failure. The pyelocaliceal system showed frank hydronephrosis (1 case) or partial dilatation (4 cases) and contained cheesy and gritty material in its lumen. Each case showed severe granulomatous inflammation, which was limited to the pelvic wall and closely associated with calcified debris, necrotic inflammatory cells, and material consistent with Tamm-Horsfall protein. The kidney showed chronic tubulointerstitial nephritis but without granulomas. Cultures of urine, blood, and the renal pelvic content, and special stains of tissue sections did not show fungi or mycobacteria in any case. Many of these features were also observed in previously reported cases. Granulomatous pyelitis is a rare but distinct cliniocopathologic entity characterized by severe noninfectious granulomatous inflammation limited to the renal pelvis, which is uniformely asociated with urinary obstruction and pyelocalyceal dilatation and may develop in response to accumulated calcified material in the renal pelvis. Awareness of this entity and its characteristic clinicopathologic features also helps eliminate an infectious etiology with obvious treatment and prognostic implications.

Adult↗
PubMed2006

Essential role of Smad3 in angiotensin II-induced vascular fibrosis.

Angiotensin II (Ang II) plays a pivotal role in vascular fibrosis, which leads to serious complications in hypertension and diabetes. However, the underlying signaling mechanisms are largely unclear. In hypertensive patients, we found that arteriosclerosis was associated with the activation of Smad2/3. This observation was further investigated in vitro by stimulating mouse primary aorta vascular smooth muscle cells (VSMCs) with Ang II. There were several novel findings. First, Ang II was able to activate an early Smad signaling pathway directly at 15 to 30 minutes. This was extracellular signal-regulated kinase 1/2 (ERK1/2) mitogen-activated protein kinase (MAPK) dependent but transforming growth factor-beta (TGF-beta) independent because Ang II-induced Smad signaling was blocked by addition of ERK1/2 inhibitor and by dominant-negative (DN) ERK1/2 but not by DN-TGF-beta receptor II (TbetaRII) or conditional deletion of TbetaRII. Second, Ang II was also able to activate the late Smad2/3 signaling pathway at 24 hours, which was TGF-beta dependent because it was blocked by the anti-TGF-beta antibody and DN-TbetaRII. Finally, activation of Smad3 but not Smad2 was a key and necessary mechanism of Ang II-induced vascular fibrosis because Ang II induced Smad3/4 promoter activities and collagen matrix expression was abolished in VSMCs null for Smad3 but not Smad2. Thus, we concluded that Ang II induces vascular fibrosis via both TGF-beta-dependent and ERK1/2 MAPK-dependent Smad signaling pathways. Activation of Smad3 but not Smad2 is a key mechanism by which Ang II mediates arteriosclerosis.

Adult↗
PubMed2006

Advanced glycation end products activate a chymase-dependent angiotensin II-generating pathway in diabetic complications.

BACKGROUND: Angiotensin II is a key mediator of diabetes-related vascular disease. It is now recognized that in addition to angiotensin-converting enzyme, chymase is an important alternative angiotensin II-generating enzyme in hypertension and diabetes. However, the mechanism of induction of chymase in diabetes remains unknown. METHODS AND RESULTS: Here, we report that chymase is upregulated in coronary and renal arteries in patients with diabetes by immunohistochemistry. Upregulation of vascular chymase is associated with deposition of advanced glycation end products (AGEs), an increase in expression of the receptor for AGEs (RAGE), and activation of ERK1/2 MAP kinase. In vitro, AGEs can induce chymase expression and chymase-dependent angiotensin II generation in human vascular smooth muscle cells via the RAGE-ERK1/2 MAP kinase-dependent mechanism. This is confirmed by blockade of AGE-induced vascular chymase expression with a neutralizing RAGE antibody and an inhibitor to ERK1/2 and by overexpression of the dominant negative ERK1/2. Compared with angiotensin-converting enzyme, chymase contributes to the majority of angiotensin II production (>70%, P<0.01) in response to AGEs. Furthermore, AGE-induced angiotensin II production is blocked by the anti-RAGE antibody and by inhibition of ERK1/2 MAP kinase activities. CONCLUSIONS: AGEs, a hallmark of diabetes, induce chymase via the RAGE-ERK1/2 MAP kinase pathway. Chymase initiates an important alternative angiotensin II-generating pathway in diabetes and may play a critical role in diabetic vascular disease.

Adult↗
PubMed2006

Prostatic involvement by transitional cell carcinoma in patients with bladder cancer and its prognostic significance.

To study the importance of prostatic involvement by transitional cell carcinoma (TCC) in patients with bladder cancer, we examined the entire prostates by whole-mount sections from 214 radical cystoprostatectomy specimens for detailed patterns of involvement by TCC and correlated the results with lymph node metastasis and patients' survival. Prostatic involvement by TCC was detected in 69 (32%) of 214 cases. Among them, 30 (43%) patients had carcinoma in situ (CIS) and the other 39 (57%) were invasive TCC. Carcinoma in situ occurred in either prostatic urethra (n = 6, 20%) or, more commonly, in prostatic ducts/acini (n = 14, 47%), and in a combination of prostatic urethra and ducts (n = 10, 33%). Ten (26%) of the invasive TCC resulted from direct penetration from the primary tumor in the bladder, and the remaining 29 (72%) cases arose from prostatic urethra/ducts, of which 11, 13, and 5 invaded the lamina propria, prostatic stroma, and periprostatic or seminal vesical tissue, respectively. Both prostatic TCC involvement and nodal metastasis were highly significant prognostic factors for patients' survival and the survival significance of prostatic TCC involvement still existed regardless of lymph node status. Furthermore, the presence of prostatic CIS and degrees of prostatic invasion are associated with nodal metastasis and survival. Patients with prostatic CIS or urethral lamina propria invasion had a similar, but higher incidence of lymph node metastasis and lower long-term and 5-year survival than those patients without prostatic involvement. Similarly, prostatic stromal invasion and periprostatic/seminal vesical invasion had a similar, but much higher nodal metastasis and worse survival than patients with only prostatic CIS or urethral lamina propria invasion. In summary, presence of prostatic TCC involvement and levels of involvement are significant prognostic factors in patients with bladder cancer.

Adult↗
PubMed2006

Renal failure and nephrocalcinosis associated with oral sodium phosphate bowel cleansing: clinical patterns and renal biopsy findings.

Acute renal failure (ARF) is rarely reported after bowel preparation with sodium phosphate. We report a patient with mild Crohn disease (in remission), without history of renal disease, and with normal baseline renal function, who developed ARF 14 days after bowel preparation for colonoscopy with oral sodium phosphate. A renal biopsy showed multifocal calcium phosphate deposition in the renal tubules against a background of diffuse chronic tubulointerstitial injury. Review of the literature suggested 2 distinct patterns of ARF in the context of sodium phosphate bowel cleansing. One pattern is characterized by ARF, which develops a few hours or days after sodium phosphate administration, as a component of a systemic syndrome associated with severe hyperphosphatemia and hypocalcemia. Correction of these electrolyte abnormalities was frequently associated with rapid recovery of renal function. The cause of ARF in this context was not clear because the favorable outcome negated the need for renal biopsy. In the second pattern, exemplified by the current patient, ARF was identified incidentally. These patients did not have any features of an acute syndrome immediately after sodium phosphate administration and presented much later (usually weeks) with mild, nonspecific symptoms. At the time of presentation, the serum calcium and phosphate levels were normal. The renal biopsies in each of these patients showed nephrocalcinosis as the possible cause of ARF. The renal failure improved at least partially in most of these patients, but persisted in rare cases.

Administration, Oral↗
PubMed2006

Are gadolinium-based contrast media nephrotoxic? A renal biopsy study.

Gadolinium-based contrast media were originally introduced as alternatives to iodinated media for magnetic resonance imaging. Although originally thought to be nonnephrotoxic, gadolinium-based contrast media have recently been reported to be associated with acute renal failure; the mechanism and the underlying renal injury are not completely understood. We report what is, to our knowledge, the first renal biopsy in this context. A 56-year-old patient underwent 2 consecutive vascular imaging procedures in conjunction with gadolinium-based contrast medium administration. A few days later, the patient developed acute renal failure. A renal biopsy showed acute tubular cell injury including patchy tubular cell necrosis, tubular cell degeneration, and marked proliferation of tubular cells, together with mild interstitial edema and interstitial inflammation, but without significant glomerular or vascular changes. During supportive therapy, renal function was partially regained. This case emphasizes the potential nephrotoxicity of gadolinium-based contrast media and suggests that the nephrotoxicity is related to potentially reversible acute tubular cell injury.

Biopsy↗
PubMed2005

The utility of B72.3, carcinoembryonic antigen, and Leu M-1 in cell blocks: an adjunct to fine-needle aspiration diagnosis of bronchioloalveolar carcinoma of the lung.

BACKGROUND: The distinction of bronchioloalveolar carcinoma (BAC) from atypical adenomatous hyperplasia (AAH) or reactive alveolar cell hyperplasia (RAH) can be difficult on aspiration cytology, even when cell block preparations are available. The authors evaluated the usefulness of B72.3, carcinoembryonic antigen (CEA), and Leu M-1 immunostains in differentiating BAC, AAH, and RAH. METHODS: Immunostains for B72.3, CEA, and Leu M-1 were performed on cell block sections from 11 lung lesions that were diagnosed cytologically as BAC (6 lesions) and "atypical cells, cannot exclude BAC" (5 lesions). Ten histologic sections of AAH and 8 histologic sections of RAH also were stained. RESULTS: Among the six lesions that had an unequivocal cytologic diagnosis of BAC, all sections were positive for two of three immunostains. Tissue follow-up confirmed BAC in all six lesions. Among the five lesions that were diagnosed as "atypical cells, cannot exclude BAC," four lesions were positive for two of three immunostains, and one lesion was negative for all three immunostains. Subsequent tissue follow-up confirmed BAC in four of these lesions. Follow-up histology of the wedge resection on the lesion in the atypical category that was negative for B72.3, CEA, and Leu M-1 showed only AAH. All 10 lesions that had a histologic diagnosis of AAH and 8 lesions that had a histologic diagnosis RAH were negative for B72.3, CEA, and Leu M-1. CONCLUSIONS: Positive staining for at least 2 immunostains among B72.3, CEA, and Leu M-1 provided strong supportive evidence for the diagnosis of BAC, and a negative result for all 3 immunostains was helpful in excluding BAC and in differentiating BAC from AAH and RAH.

Adenocarcinoma, Bronchiolo-Alveolar↗
PubMed2005

Signaling mechanism of TGF-beta1 in prevention of renal inflammation: role of Smad7.

TGF-beta has been shown to play a critical role in anti-inflammation; however, the signaling mechanisms of TGF-beta in anti-inflammatory response remains largely unclear. This study reported that mice that overexpress latent TGF-beta1 on skin are protected against renal inflammation in a model of obstructive kidney disease and investigated the signaling mechanism of TGF-beta1 in inhibition of renal inflammation in vivo and in vitro. Seven days after urinary obstruction, wild-type mice developed severe renal inflammation, including massive T cell and macrophage infiltration and marked upregulation of IL-1beta, TNF-alpha, and intercellular adhesion molecule-1 (all P < 0.001). Surprising, renal inflammation was prevented in transgenic mice. This was associated with an increase in latent TGF-beta1 in circulation (a 10-fold increase) and renal tissues (a 2.5-fold increase). Further studies showed that inhibition of renal inflammation in TGF-beta1 transgenic mice was also associated with a marked upregulation of renal Smad7 and IkappaBalpha and a suppression of NF-kappaB activation in the diseased kidney (all P < 0.01). These in vivo findings suggested the importance of TGF-beta-NF-kappaB cross-talk signaling pathway in regulating renal inflammation. This was tested in vitro in a doxycycline-regulated Smad7-expressing renal tubular cell line. Overexpression of Smad7 was able to upregulate IkappaBalpha directly in a time- and dose-dependent manner, thereby inhibiting NF-kappaB activation and NF-kappaB-driven inflammatory response. In conclusion, latent TGF-beta may have protective roles in renal inflammation. Smad7-mediated inhibition of NF-kappaB activation via the induction of IkBalpha may be the central mechanism by which latent TGF-beta prevents renal inflammation.

Animals↗
PubMed2005

Kidney-specific cadherin, a specific marker for the distal portion of the nephron and related renal neoplasms.

Renal cell neoplasms are presumably derived from different cell types of the nephron. Clear cell and papillary renal cell carcinoma (RCC) are thought to be of proximal tubular origin, whereas oncocytoma and chromophobe RCC are derived from intercalated cells of distal nephron. A few molecules, such as RCC marker and CD10, have been shown to be markers for clear cell RCC and papillary RCC. Such markers are not yet available for renal tumors presumably of the distal nephron. The expression of kidney-specific (Ksp) cadherin, a recently cloned gene thought to be transcribed exclusively in the kidney, was studied in normal human kidney, as well as in 105 primary renal neoplasms, including 42 clear cell RCC, 30 papillary RCC, 13 chromophobe RCC, and 20 oncocytomas. The expression patterns were compared with those of RCC marker. The Ksp-cadherin expression was noted preferentially in distal convoluted tubules with a basolateral membrane stain in normal kidney. All 13 chromophobe RCC and 19 of 20 oncocytomas showed diffuse and strong immunoreactivity for Ksp-cadherin, while only 14% clear cell RCC and 13% papillary RCC showed focal positivity. The RCC marker expression was detected in 85%, 98%, 15% and 0% of clear cell RCC, papillary RCC, chromophobe RCC, and oncocytoma, respectively. A few clear cell RCC and papillary RCC showed dual expression of both RCC marker and Ksp-cadherin, which appear to have distinct histologic features. These results demonstrated high sensitivity and specificity of Ksp-cadherin for distal convoluted tubules, which can be used as adjunct for diagnosis of chromophobe RCC.

Adenocarcinoma, Clear Cell↗
PubMed2005

Calcium oxalate deposition in renal cell carcinoma associated with acquired cystic kidney disease: a comprehensive study.

The main complication of acquired cystic kidney disease (ACKD) is frequent development of renal tumors, including renal cell carcinoma (RCC). Intratumoral deposition of calcium oxalate (CaOx) is a distinct feature of ACKD-associated RCCs, but several features of this type of RCC are not known. Features of the 30 end-stage renal disease (ESRD)-associated RCCs identified within a 13-year period, including eight with CaOx deposition, were analyzed. Pathologic and clinical features of CaOx positive (+) and negative (-) RCCs were evaluated and compared. The CaOx+ RCCs showed higher tendency for bilaterality and multifocality. Seven tumors displayed distinctive morphologic features characterized by tumor cells with ill-defined cell membrane, abundant granular eosinophilic cytoplasm, large nuclei, and prominent nucleoli. One tumor was of clear cell type. Regardless of histologic type, all tumors displayed a proximal tubular differentiation. No significant difference was noted for tumors' stage, proliferation, and apoptosis rate between the CaOx+ and CaOx- RCCs. CaOx+ RCCs account for a significant portion of all ESRD-associated RCCs. The majority of these RCCs display a distinctive morphologic profile. Proximal tubular cell differentiation in conjunction with ESRD-mediated high serum level may be pathogenetically important for intratumoral CaOx deposition. These RCCs seems to have a relatively good prognosis.

Adult↗
PubMed2005

Chronic allograft nephropathy and nephrotic range proteinuria.

While the association between post-transplant nephrotic range proteinuria (PTx-NP) and chronic allograft nephropathy (CAN) has been described, the factors that determine graft survival in such patients are unclear. We retrospectively identified 30 patients with biopsy-proven CAN who presented with PTX-NP between 1988 and 2002. Patients were stratified into two groups according to PTX-NP onset: <1 yr vs. >1 yr post-transplantation. Both groups were comparable with respect to the degree of renal dysfunction (serum creatinine 4.3 +/- 2.5 mg/dL vs. 3.4 +/- 1.5 mg/dL) and proteinuria (4.7 +/- 1.6 gm/d vs. 5.8 +/- 3 gm/d). After a mean follow-up of 14 months post-biopsy, 87% of patients had lost their grafts in both groups (89% vs. 83%, p = NS). Overall, patients with serum creatinine 2 mg/dL (75% vs. 4%, Fisher Exact Probability p = 0.0038). Using Kaplan-Meier estimate, the 5-yr graft survival rate was 100% for patients with serum creatinine 2 mg/dL (p = 0.06). The magnitude of proteinuria beyond 3 gm/d did not influence graft survival. One-half of the patients (n = 15) received therapy with angiotensin converting enzyme inhibitors (ACEI). Graft survival, however, was not different between the patients who received ACEI compared with the patients who did not receive ACEI (13% vs. 13%). PTx-NP related to CAN was associated with poor allograft survival, irrespective of the time of onset of presentation, especially when renal function was reduced at the time of biopsy.

Adult↗
PubMed2005

Loss of nitric oxide and endothelial-derived hyperpolarizing factor-mediated responses in aging.

BACKGROUND: Aging has considerable structural and functional effects on the vascular system of the kidney. One such effect is an alteration in vascular tone which potentially will initiate renal damage. Vascular tone is determined by the balance between vasoconstrictors and vasodilators. Therefore, we hypothesized that aging attenuates vasodilatory responses in the kidney. These changes may be mediated by a loss of nitric oxide and endothelial-derived hyperpolarizing factor (EDHF). METHODS: The systemic and renal responses of nitric oxide and EDHF were investigated in aging (18 months old) and young (3 months old) Sprague-Dawley rats. RESULTS: We demonstrated a general loss of vasodilatory responses in the aging kidney. In addition, nitric oxide levels were reduced in the serum and kidney cortex of aging versus young animals, although this was not accompanied with a loss of endothelial nitric oxide synthase (eNOS) protein in the kidney cortex. Aging animals also exhibited a loss in EDHF-mediated vasodilation following stimulation with either acetylcholine or bradykinin in the isolated perfused kidney. CONCLUSION: These findings indicate that not only a defect in the nitric oxide pathway, but also a loss of EDHF-mediated responses may be responsible for impaired vasodilation in the aging kidney. This may result in enhanced vasoconstrictive responses in aging which potentially will cause renal damage and ultimately a loss in glomerular filtration rate (GFR).

Acetylcholine↗
PubMed2005

Intraoperative pathology consultation for kidney and urinary bladder specimens.

CONTEXT: Intraoperative pathology consultation for kidney and urinary bladder specimens is relatively infrequent. Scant literature is devoted to this topic. OBJECTIVE: The clinical indications and diagnostic usefulness and pitfalls of intraoperative pathology consultation of kidney and urinary bladder specimens will be reviewed, based on literature and personally encountered cases. DATA SOURCES: The indications for intraoperative pathology consultation for renal lesions included (1) surgical margins in partial nephrectomy specimens, (2) solid renal mass in unusual clinical or radiologic settings, (3) synchronous renal and extrarenal masses, (4) cystic renal lesions, (5) ureteral surgical margin for transitional cell carcinoma, (6) multiple renal masses, (7) solid mass in a diffusely cystic kidney, and (8) evaluation of renal injury. The indications for urinary bladder included (1) status of the surgical margins, (2) diagnosis of bladder tumor biopsy, (3) diagnosis of extravesical tumors with vesical extension, (4) diagnosis of extravesical mass, including pelvic lymph nodes encountered during cystectomy, and (5) status of bladder neck margin during radical prostatectomy for cancer. The frequent problematic areas for the kidney included misdiagnosis or incorrect classification of cystic tumors or spindle cell tumors, and confusion of clear cell renal cell carcinoma with inflammatory lesions. The problematic areas for urinary bladder included the differential diagnoses of high-grade dysplasia/carcinoma in situ with reactive changes at the ureteral or urethral surgical margins. CONCLUSIONS: Distinctive indications and diagnostic pitfalls are recognized for intraoperative consultation of renal or urinary bladder lesions. Awareness of the pertinent problems should improve diagnostic accuracy and facilitate the proper management of these lesions.

Frozen Sections↗
PubMed2004

A truncated-dose regimen of daclizumab for prevention of acute rejection in kidney transplant recipients: a single-center experience.

Daclizumab can decrease the incidence of acute rejection (AR) in renal transplant (RTx) recipients. In this prospective study, 52 RTx patients were divided into two groups according to the dose of daclizumab: 1 mg/kg on day 0 and every 14 days for five doses (group 1, n = 30) or a truncated regimen of 2 mg/kg on day 0 and on the day of discharge (group 2, n = 22). The following variables were recorded: demographics; delayed graft function; AR at 3, 6, and 12 months; time to AR; chronic allograft nephropathy (CAN); and serum creatinine. The overall incidences of AR were 23% and 27% (P = 0.76) in groups 1 and 2, respectively, whereas at 6 months they were 21% and 18% (P = 1.0). Median time to AR was 10 days in group 1 and 94 days in group 2 (P = 0.09). The incidence of CAN was 6.6% in group 1 and 13% in group 2 (P = 0.63). These data suggest that the truncated dose of daclizumab is as effective as the standard regimen for AR prophylaxis.

Antibodies, Monoclonal↗
PubMed2004

AT1A-mediated activation of kidney JNK1 and SMAD2 in obstructive uropathy: preservation of kidney tissue mass using candesartan.

Literature suggests the involvement of the renin-angiotensin system and transforming growth factor (TGF)-beta in the renal injury that follows chronic ureteric obstruction. SMAD proteins and the JNK1 cascade are essential components of TGF-beta signaling machinery, and recent data suggest cooperative interaction between JNK1 and SMAD proteins in TGF-beta-mediated gene expression. We used a rat model of chronic unilateral ureteric obstruction to study the effects of candesartan, an AT(1A)-receptor blocker, on tissue morphology and the activities of JNK1 and SMAD2 protein in the kidney. Ureteric obstruction for 28 days leads to interstitial fibrosis, tubule atrophy, and marked activation of SMAD2 and JNK1, without significant change in p38 kinase or ERK. Candesartan treatment, however, attenuated the chronic tubulointerstitial injury in obstructed kidneys and was associated with significant preservation of kidney tissue mass. Furthermore, treatment with candesartan diminished JNK1 activity and downregulated SMAD2 protein and activity in obstructed kidneys. In conclusion, obstructed kidneys showed chronic tubulointerstitial injury, which was associated with JNK1 and SMAD2 activation. The renoprotective effects afforded by AT(1A)-receptor blockade in obstructive uropathy are consistent with attenuation of JNK1- and SMAD2-mediated renal injury.

Animals↗